israel journal of psychiatry and related sciences

israel journal of

psychiatry

In schizophrenia, how do you get from here

Vol. 48 - Number 4 2011

ISSN: 0333-7308

227

Editorial: Commentary on Israel’s Psychiatric Rehabilitation Law Robert E. Drake et al.

Volume 48, Number 4, 2011 Israel Journal of Psychiatry and Related Sciences

230

to here?

Xeplion®, a new once-monthly injectable schizophrenia therapy,1 significantly reduces relapse.2 With early onset of efficacy3,4 and good tolerability,1–6 Xeplion can help your patients shape a future in a way that they wish.

The Mortality Risk Among Persons with Psychiatric Hospitalizations Ziona Haklai et al.

240

Schizophrenia: It’s Broken and It Can’t Be Fixed. A Conceptual Analysis at the Centenary of Bleuler’s Dementia praecox oder Gruppe der Schizophrenien

Jan Dirk Blom and Herman M. van Praag

252

Religion and Psychological wellbeing and distress in israeli Jews: Findings from the Gallup World Poll Jeff Levin

262

Post-discharge Contact with Mental Health Clinics and Psychiatric Readmission: A 6-month Follow-up Study Alexander Grinshpoon et al.

268

“Transferred to Another Institution”: Clinical Histories of Psychiatric Patients Murdered in the Nazi “Euthanasia” Killing Program Florian Steger et al.

275

Anti-ribosomal P antibody in schizophrenia Yaron Gilat et al.

Preventing relapse, enabling futures

For comprehensive information please refer to full Prescribing information as approved by the Israeli Health Authority.

References: 1. Xeplion prescribing information. 2. Hough D et al. Schiz Res 2010; 116: 107-117.

3. Pandina GJ et al. J Clin Psychopharmacol 2010; 30: 235-244. 4. Kramer M et al. Int J Neuropsychopharmacol 2010; 13: 635-647. 5. Gopal S et al. J Psychopharmacol Online First, published on July 8, 2010 as doi:10.1177/0269881110372817. 6. Hoy SM et al. CNS Drug Rev 2010; 24(3): 227-244.

280

Evidence-Based Treatment for Pediatric ObsessiveCompulsive Disorder Lindsay Brauer, et al.

)GAD( ‫וחרדה‬

‫לטיפול בדכאון‬ 1 ‫עוצמה כפולה כבר מההתחלה‬

‫מהיר יותר‬ ‫ מצב רוח וכאב‬,‫הקלה בתסמיני חרדה‬ 2 ‫מהשבוע הראשון‬ 7 ‫שיפור במדדי התפקוד‬

‫בטוח יותר‬ ‫בקשישים ובחולים עם גורמי סיכון‬ 5,6 ‫קרדיווסקולרים‬

‫פשוט ונוח יותר‬ ‫ מג' ליום מהיום הראשון‬60 ‫מינון קבוע של‬

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‫מוכח יותר‬ ‫בהקלה על התסמינים הנפשיים והתסמינים‬ 3 ‫הכואבים הנלווים לדכאון‬

‫ אלי לילי ישראל‬:‫ יבואן‬,‫ ספרד‬,‫ לילי בע"מ‬:‫; יצרן‬Duloxetine as hydrochloride '‫ מג‬60 -‫ מג' ו‬30 ‫ כמוסות של‬:‫ מינונים‬,Duloxetine as HCL :‫ חומר פעיל‬,Cymbalta :‫שם התכשיר‬ ‫ למידע מלא נא עיין בעלון מידע לרופא כפי שאושר ע"י משרד הבריאות‬,‫בע"מ‬ :‫התוויות מאושרות‬

 Cymbalta is indicated for the treatment of major depressive episodes.  Cymbalta is indicated for the management of neuropathic pain associated with diabetic peripheral neuropathy.  Cymbalta is indicated for the treatment of generalized anxiety disorder (GAD)  Cymbalta is indicated for the management of fibromyalgia (FM) .

References: 1. Bymaster et al, Current Pharmaceutical Design, 2005. 11:1475-1493; 2. Brannan et al. J Psych Res 2005; 39: 161-172; 3. Brecht S, et al. J Clin Psychiatry. 68:1707- 1716. 2007; 4. Cymbalta PI; 5. Raskin J et al, Am J Psychiatry 2007; 164:900–909; 6. Wernicke J, et al. Drug Safety 2007;30 (5):437-455; 7. Wohlreich MM, et al. J Clin Psychopharmacol 2005; 25: 552-560 CY081030

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‫נוחות ויעילות על קצה הלשון‬

‫משפר את ההיענות לטיפול‬

1. San L. et al, CNS Neuroscience and Therapeutic 14 (2008) 203-214*Zyprexa® is indicated for the acute and maintenance treatment of Schizophrenia.*Zyprexa® is indicated for the management of the manifestations of psychotic disorders.*Zyprexa® is indicated for the treatment of acute mixed or manic episodes associated with Bipolar Disorder.*Zyprexa® is indicated for the prevention of recurrence in Bipolar Disorder.*Zyprexa® IM is indicated for the treatment of agitation associated with Schizophrenia and Bipolar Mania.*Zyprexa®: 5mg, 7.5mg, 10mg*Zyprexa® VeloTab™: 5mg, 10mg*Zyprexa® IM: 10mg Manufacture: Eli Lilly and Company | License holder: Eli Lilly Israel Ltd. P.O. Box 2160 Herzliya Pituach 46120

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NEW TREATMENT FOR Schizophrenia and Bipolar I Disorder 1 Proven Efficacy in all Symptom Clusters 2,3,4,5

ABI-08-10

References: 1. Aripiprazole (AbilifyÂŽ) Physician Prescribing Information Leaflet approved by Israeli Ministry of Health. 2. Kane JM et al. Efficacy and Safety of Aripiprazole and haloperidol vs placebo in patients with schizophrenia and schizoaffective disorder. J Clin Psychiatry ,2002; 63(9):763-771. 3. Kasper S et al. Efficacy and safety of aripiprazole vs haloperidol for long-term maintenance treatment following acute relapse of schizophrenia. Int. J Neuropsychopharmacol ,2003; 6 (4):325-337. 4. Volavka J et al; Efficacy of aripiprazole against hostility in schizophrenia and schizoaffective disorder: data from 5 double blind studies. J Clin Psychiatry ,2005; 66(11):1362-1366. 5.

Lieberman JA. Dopamine partial agonist: A new class of antipsychotic. CNS Drugs ,2004; 18(4):251-267.

Biotis is an exclusive representative of selected brands of BMS Biotis Ltd. 22 Hamelacha St. P.O.Box 11372 Rosh Ha’Ayin, 48091 Israel. Tel: +972-3-9002005. Fax: +972-3-9002029 www.biotis.co.il Please refer to Abilify approved Physician Prescribing Information

israel journal of

psychiatry and related sciences EDitor

David Greenberg DEPUTY EDITORS

David Roe Rael Strous Gil Zalsman

Book reviews editor

Yoram Barak PAst Editor

Eli L. Edelstein Founding Editor

Heinz Z. Winnik Editorial Board

Alean Al-Krenawi Alan Apter Elliot Gershon Talma Hendler Ehud Klein Ilana Kremer ltzhak Levav Yuval Melamed Shlomo Mendlovic Ronnen Segman Eliezer Witztum Zvi Zemishlany International Advisory Board

Yoram Bilu Aaron Bodenheimer Carl Eisdorfer Julian Leff Margarete Mitscherlich-Nielsen Peter Neubauer Phyllis Palgi Leo Rangell Melvin Sabshin Robert Wallerstein Myrna Weissman

227 > Editorial: Commentary on Israel’s Psychiatric Rehabilitation Law

Robert E. Drake, Michael F. Hogan, Mike Slade and Graham Thornicroft

230 > The Mortality Risk Among Persons with Psychiatric Hospitalizations Ziona Haklai, Nehama Goldberger, Nechama Stein, Inna Pugachova and Itzhak Levav

The Official Publication of the Israel Psychiatric Association Vol. 48 - Number 4 2011

268 > “Transferred to Another Institution”: Clinical Histories of Psychiatric Patients Murdered in the Nazi “Euthanasia” Killing Program

Florian Steger, Andreas Görgl, Wolfgang Strube, Hans-J. Winckelmann and Thomas Becker

275 > Anti-ribosomal P antibody in schizophrenia

Yaron Gilat, Yehuda Shoenfeld, Moshe Kotler and Iulian Iancu

240 > Schizophrenia: It’s Broken and It Can’t Be Fixed. A Conceptual Analysis at the Centenary of Bleuler’s Dementia praecox oder Gruppe der Schizophrenien

280 > Evidence-Based Treatment for Pediatric Obsessive-Compulsive Disorder

248 > Commentary

288 > Book reviews

Jan Dirk Blom and Herman M. van Praag

Lindsay Brauer, Adam B. Lewin and Eric A. Storch

Assen Jablensky

Assaf Shelef, David Greenberg, Leah Rossman

250 > Authors’ response

291 > Correspondence

Jan Dirk Blom and Herman M. van Praag

252 > Religion and Psychological well-being and distress in israeli Jews: Findings from the Gallup World Poll Jeff Levin

262 > Post-discharge Contact with Mental Health Clinics and Psychiatric Readmission: A 6-month Follow-up Study Alexander Grinshpoon, Yaacov Lerner, Tzipi Hornik-Lurie, Nelly Zilber and Alexander M. Ponizovsky

Primary Delusional Parasitosis Treated Effectively with Paliperidone Yakup Albayrak, Okan Ekinci and Sena Yenel Özbay

293 > Obituaries 294 > List of reviewers for Israel Journal of Psychiatry, 2011 Hebrew Section

295 > News and Notes 298 > Abstracts

Assistant Editor

Joan Hooper

Marketing: MediaFarm Group

+972-77-3219970 23 Zamenhoff st.

Tel-Aviv 64373, Israel

amir@mediafarm.co.il www.mediafarm.co.il

The photos were taken by participants in a photography master class run by Alex Levak, winner of the Israel Prize for photography in 2005, together with the staff photo therapist, Essie Haus, and with the support of the Association of Friends of Lev Hasharon Mental Health Center headed

by Orly Dankner.

The patients photographed their world both at the hospital and at home on leave. The photos open windows to their inner worlds and provide a voice to their authentic selves and use photographs as a means of transference of their unique experiences. The participants in the class developed a close and unique bond.

Isr J Psychiatry Relat Sci - Vol. 48 - No 4 (2011)

Editorial: Commentary on Israel’s Psychiatric Rehabilitation Law Robert E. Drake, Michael F. Hogan, Mike Slade and Graham Thornicroft

The first 10 years of Israel’s Psychiatric Rehabilitation Law represent the successful first stage in system change – an array of community rehabilitation services has been created. Although it has increased client-centeredness, moved some rehabilitation services into the community, and increased social inclusion, a number of next steps might be considered.

In October of 2010 the Israeli national health/mental health leadership met in a special workshop sponsored by the Israel National Institute for Health Policy Research to review the 2000 Psychiatric Rehabilitation Law. Four international consultants who participated in the workshop offered the following suggestions for potential next steps in Israel.

Individual Recovery Goals

The concepts of client-centeredness and recovery have evolved over several decades with increasing focus on helping people to define and develop a life they consider meaningful, elucidating the process of and techniques for honoring and supporting their individualized journeys, and challenging traditional mental health attitudes and procedures (1). People with lived experience have emphasized the centrality of hope, identity, meaning, and personal responsibility (2-5). In Israel the involvement of service users has given voice to many individuals, but the next stage may require developing egalitarian partnerships that go beyond traditional clinical relationships (6). True partnerships require sharing power in all aspects of defining goals and making decisions.

Israel’s Psychiatric Rehabilitation Law enshrines the treatment and support rights of individuals. The next policy evolution may make more explicit that these services and supports should be offered in the service of the individual’s life goals, rather than being given in their best interests – a subtle distinction with profound implications (7).

These ideas will affect the process and content of mental health care also. The danger here is viewing services as an end in themselves, so that “compliance” and “adherence” are seen as desirable. A pro-recovery 226 227

approach to clinical care, by contrast, emphasizes coherence, values, alliance, choice and empowerment (8).

Community Integration and Discrimination

People need to be in the community to pursue their journeys, to reach their functional goals, to be included in society, and to live independently. Rehabilitation services must therefore be delivered in the community (9).

True community integration and social inclusion depend upon having opportunities available in the mainstream society outside of the mental health system.

Overcoming discrimination is therefore as important as providing clinical services (10). The most powerful antidote for discrimination is close social contact – people drop their false prejudices when they know or work with someone who has a mental illness (11).

Recent research demonstrates that anti-discrimination programs can be effective, through the direct involvement of consumers as teachers interacting with the public (12). Thus Israel might consider adding an antidiscrimination campaign to enhance its efforts to move rehabilitation services into the community.

Evidence-based Interventions

Interventions that are demonstrably effective are termed evidence-based practices. By definition, they are clearly defined (in a manual, book, video and other guidelines), replicable (usually based on training and a fidelity measure), and supported by rigorous research (typically more than one randomized controlled trial) (13).

Evidence-based psychiatric rehabilitation interventions help people with mental illnesses to achieve functional goals that they define as personally meaningful, such as independent living, competitive employment, mainstream education, friendships outside of the mental health system, and managing their own illnesses (14).

Dependence on the mental health system is of course not anyone’s rehabilitation goal.

Several evidence-based rehabilitation practices promote recovery goals. Supported housing and assertive community treatment help people to avoid hospitalizations and homelessness and to succeed in independent

Robert E. Drake et al.

community living settings (15, 16). Supported employment and education help them to attain mainstream jobs and educational experiences in the community (17). Illness management interventions help them to manage their illnesses in the community using natural supports (18). Family interventions help them to improve relationships with their families (19).

Evidence-based psychiatric rehabilitation interventions embody several common features. Multidisciplinary teams deliver the interventions, always focusing on the client’s goals, using a process of shared decision-making, aiming at inclusion in the mainstream community, embracing natural supports, and helping people to acquire the skills they need to succeed in environments of their choice.

Measurement

Using evidence-based practices requires a complementary insistence on measurement and outcomes research.

Rehabilitation addresses functional outcomes that are observable and measurable. Documenting the proportion of people who are living independently, attending school, working in competitive jobs, avoiding social isolation, and managing their own symptoms is relatively straightforward. Standardized measures exist for each of these areas (20), and the field is rapidly developing benchmarks (21). Without outcome measurement and benchmarks, program leaders do not know whether clients are recovering, and providers naturally drift toward offering traditional services within clinics – not optimal for pursuing recovery. Outcomes show clearly whether or not clients are meeting their goals.

Measuring process, usually in the form of fidelity to evidence-based practices, is as important as measuring outcomes (22). Outcomes are often skewed by selection bias because programs tend to provide services for clients who are easier to treat and more likely to achieve good outcomes, thereby neglecting the most needy clients (23). Process measures ensure that high-quality services are in place.

Community-based research also enhances quality.

Evidence-based practices must be tested and adapted to local cultural and economic contexts, and Israel would be well served by expanding its current research on community-based care and outcomes (e.g., 24).

System Change

Implementing evidence-based practices on a large scale and ensuring sustainability require widespread dissemi-

nation, training, adoption, monitoring and feedback (25, 26). Research on implementation, despite a paucity of controlled trials, clearly establishes that training alone is insufficient to put in place and sustain an evidence-based practice. Instead, an effective approach should involve stakeholders at many different levels: e.g., regional mental health authorities attending to financial incentives and accountability, technical assistance centers providing training and fidelity assessments, clinic directors overseeing workforce requirements and medical records, team leaders using field-based supervision and data to reinforce clinicians, and clinicians learning new skills and helping each other. Strong leaders prioritize the new practice, actively overcome whatever barriers are encountered, redesign the flow of work to support the new practice, and reinforce change through measurement and feedback.

Currently the most widely used mechanism for implementation of evidence-based practices is the regional technical assistance center (27). In this strategy experts provide consultation to administrators, training and longitudinal supervision to clinicians, and monitoring and feedback to programs via fidelity visits. A more recent approach, the learning collaborative model (28), involves multidisciplinary teams from several practice sites meeting with researchers to discuss their processes of care and desired improvements. After agreeing on goals and strategies for change, they help each other and monitor key outcomes. In the future, implementation is likely to rely more on information technology (29).

Several approaches are developing and being tested rapidly: distance learning, telemedicine, mobile technology, self-treatment programs and electronic decision support systems (30). Each shows great promise thus far.

Conclusions

Israel’s Psychiatric Rehabilitation Law has inspired hope by establishing a right to rehabilitation services and a record of early implementation success. Suggested next steps include fully incorporating recovery values, emphasizing community integration and social inclusion, adopting evidence-based practices, measuring process and outcomes, and planning widespread dissemination and implementation.

References 1. Slade M. Personal recovery and mental illness. A guide for mental health professionals. Cambridge: Cambridge University, 2009.

2. Deegan P. Recovery: The lived experience of rehabilitation. Psychosoc

228 227

Editorial: Commentary on Israel’s Psychiatric Rehabilitation Law

Rehabil J 1988; 11:11-19.

3. Fisher DV. Health care reform based on an empowerment model of recovery by people with psychiatric disabilities. Hosp Community Psych 1994; 45:913-915.

4. Mead S, Copeland ME. What recovery means to us: Consumers perspectives. Community Ment Hlt J 2000; 36:315-328.

5. Ralph RO. Recovery. Psychiatr Rehabil Skills 2000; 4:480-517.

6. Slade M. 100 ways to support recovery. London: Rethink, 2009.

7. Perkins R, Repper J. Social inclusion and recovery. London: Baillière Tindall, 2003.

8. Slade M. The contribution of mental health services to recovery. J Ment Health 2009; 18:367-371.

9. Corrigan PW, Mueser KT, Bond GR, Drake RE, Solomon P. The principles and practice of psychiatric rehabilitation. New York: Guilford, 2008.

10. Thornicroft G, Brohan E, Rose D, Sartorius N, Leese M. Global pattern of experienced and anticipated discrimination against people with schizophrenia: A cross-sectional survey. Lancet 2009; 373:408-415.

11. Henderson C, Thornicroft G. Stigma and discrimination in mental illness: Time to change. Lancet 2009; 373:1928-1930.

12. Pinfold V, Thornicroft G, Huxley P, Farmer p. Active ingredients in anti-stigma programmes in mental health. Int Rev Psychiatry 2005; 17:123-131.

13. Drake RE. Principles of evidence-based mental health. In: Drake RE, Merrens M, Lynde D, editors. Evidence-based mental health: A textbook. New York: John Wiley, 2005: pp. 45-65.

14. New Freedom Commission on Mental Health. Achieving the promise: Transforming mental health care in America. Final Report. Rockville, Md.: US Department of Health and Human Services. Publication SMA03-3832, 2003.

15. Phillips SD, Burns BJ, Edgar ER, Mueser KT, Linkins KW, Rosenheck RA, et al. Assertive community treatment: Moving an evidence-based intervention into standard practice. Psychiatr Serv 2001; 52: 771-779.

16. Tsemberis S, Gulcur L, Nakae M. Housing first, consumer choice, and harm reduction for homeless individuals with a dual diagnosis. Am J Public Health 2004; 94:651-656.

17. Bond GR, Becker DR, Drake RE, Rapp CA, Meisler N, Lehman AF, et al. Implementing supported employment as an evidence-based practice.

Psychiatr Serv 2001; 52:313-322.

18. Mueser KT, Corrigan PW, Hilton DW, Tanzman B, Schaub A, Gingerich S, et al. Illness management and recovery: A review of the research.

Psychiatr Serv 2002; 53:1272-1284.

19. Dixon L, McFarlane WR, Lefley H, Lucksted A, Cohen M, Falloon I, et al. Evidence-based practices for services to families of people with psychiatric disabilities. Psychiatr Serv 2001; 52:903-910.

228 229

20. Tansella M, Thornicroft G, editors. Mental health outcome measures, 3rd ed. Edited by M. London: Gaskell, Royal College of Psychiatrists, 2009.

21. Becker DR, Drake RE, Bond GR. Benchmark outcomes in supported employment. Am J Psychiatr Rehabil. In press for 2011.

22. Bond GR, Evans L, Salyers MP, Williams J, Kim H. Measurement of fidelity in psychiatric rehabilitation. Ment Hlt Serv Res 2000; 2:75-87.

23. Shen Y. Selection incentives in a performance-based contracting system.

Health Serv Res 2003; 38:535-552.

24. Hasson-Ohayon I, Roe D, Kravetz S. A randomized controlled trial of the effectiveness of the illness management and recovery program.

Psychiatr Serv 2007; 58:1461-1466.

25. Drake RE, Bond GR. Implementing integrated mental health and substance abuse services. J Dual Diagnosis 2010; 6:251-262.

26. Torrey WC, Bond GR, McHugo GJ, Swain K. Evidence-based practice implementation in community mental health settings: The relative importance of key domains of implementation activity. Administration and Policy in Mental Health. DOI 10.1007/s10488-011-0357-9.

27. Rapp CA, Goscha RJ, Carlson LS. Evidence-based practice implementation in Kansas. Community Ment Hlt J 2010; 46:461-465.

28. Becker DR, Drake RE, Bond GR, Haslett W, Nawaz S, Martinez RA. A mental health learning collaborative on supported employment.

Psychiatr Serv 2011; 62:704-706.

29. Institute of Medicine Committee on Quality of Health in America: Improving the quality of health care for mental and substance use conditions. Washington, DC: National Academies Press, 2006.

30. Cartreine JA, Ahern DK, Locke SE. A roadmap to computer-based psychotherapy in the United States. Harvard Rev Psychiat 2010; 18:80-90.

Contact information for Authors:

Robert E. Drake Dartmouth Psychiatric Research Center, Lebanon, NH, USA

Robert.E.Drake@Dartmouth.edu

Michael F. Hogan Office of Mental Health, Albany, NY, USA

Mike Slade Health Service and Population Research Department, Institute of Psychiatry, King’s College London, London, UK

Graham Thornicroft Health Service and Population Research Department, Institute of Psychiatry, King’s College London, London, UK

‫דיכאון ביפולרי ‪ -‬עזור למטופל שלך להתקדם אל עתיד בהיר יותר‬ ‫‪The one and only‬‬ ‫התרופה היחידה שנבדקה ואושרה לטיפול בהתקפי דכאון‬ ‫בהפרעה ביפולרית (כמונותרפיה ובשילוב עם מייצב)*‬

‫ה‪ NEJM -‬המליץ על ‪ Seroquel‬כקו ראשון‬ ‫‪1‬‬ ‫לטיפול בדכאון ביפולרי‬

‫(מבין‪ :‬מייצבי מצב רוח‪ ,‬נוגדי דכאון ותרופות אטיפיות)‬

‫‪...‬זה הזמן לשקול מחדש את הטיפול‪...‬‬

‫‪08-12-SER-11-IL-021‬‬

‫לפני מתן מרשם יש לעיין בעלון לרופא כפי שאושר ע"י משרד הבריאות‬

‫‪Reference: 1. Frye MA (2011) NEJM; 364:51-9. 2. Seroquel XR MoH approved Prescribing Information.‬‬ ‫‪SeroquelXR® is a redistered trademark of AstraZeneca group of companies. The AstraZeneca logo is a redistered trademark of AstraZeneca group of companies.‬‬

‫* על פי סקירת עלונים לרופא המאושרים בישראל ובארה"ב‬ ‫אסטרהזניקה (ישראל) בע"מ‪ ,‬ת‪.‬ד‪ 4070 .‬א‪.‬ת‪ .‬רעננה ‪ ,43656‬טלפון‪ ,09-7406528 :‬פקס‪ ,09-7406527 :‬דוא"ל‪israel.infoisrael@astrazeneca.com :‬‬

‫חדש‬ ‫מאושרת בישראל‬ ‫כטיפול ‪add-on‬‬ ‫לחולי ‪MDD‬‬ ‫עם תגובה‬

‫‪sub-optimal‬‬

‫לטיפול נוגד דכאון‬

‫‪2‬‬

Isr J Psychiatry Relat Sci - Vol. 48 - No 4 (2011)

The Mortality Risk Among Persons with Psychiatric Hospitalizations Ziona Haklai, MA,1 Nehama Goldberger, MSc,1 Nechama Stein, MA,1 Inna Pugachova, MPH,2 and Itzhak Levav, MD3 1

Department of Health Information, Ministry of Health, Jerusalem, Israel Department of Information and Evaluation, Mental Health Services, Ministry of Health, Jerusalem, Israel 3 Mental Health Services, Ministry of Health, Jerusalem, Israel 2

ABSTRACT Background: Persons affected by severe mental disorders have a higher mortality risk than the general population.

Objectives: To investigate the overall mortality and selected natural and external causes of death by age, gender and mental health-related variables among persons who were ever admitted to psychiatric inpatient services.

Methods: This cohort study compared the mortality risk among Israeli Jews aged 18 and over who were ever hospitalized in psychiatric facilities until 2006, as recorded in the Psychiatric Case Register (PCR), with never- hospitalized subjects. The national database on causes of death was linked to the PCR. Analysis: Mortality rates were computed by age, gender and psychiatric diagnosis, while proportions of deaths were computed by time from discharge. Rates were also analyzed by time-periods of date of death to check for possible association with mental health policy decisions. Age-adjusted and age-specific mortality rates and rate ratios (RR) were computed for persons in the PCR compared with those never hospitalized.

Results: The age-adjusted mortality rate of hospitalized psychiatric persons was double that of the nonhospitalized, RR = 1.98 (95% CI 1.96-2.00). The rate was higher in both genders and for persons of all age groups, particularly for the young. The highest RRs were found for external causes of death, in particular suicide (RR = 16.34, 95% CI 15.49-17.24). Natural causes also showed higher risk, except for malignancies (RR = 1.13, 95% CI 1.10-

Address for Correspondence:

230

1.16). The risk for death was highest for persons admitted for substance abuse, while it was almost equal for those diagnosed with either schizophrenic or affective disorders. The rate ratios were not observed to change as a result of policy decisions, e.g., dehospitalization and the introduction of the atypical antipsychotics. A third of all deaths and 62% of suicides occurred before discharge or within a year from discharge.

Conclusions: This study highlights the importance for advancing programs of both preventative and curative medical care among persons who had psychiatric inpatient care.

Persons with psychiatric disorders have an enhanced risk for comorbid physical diseases (1-3). Yet, for a number of reasons (4), medical care for persons with severe psychiatric disorders is often found to be substandard (5). As a result, their mortality risk, particularly for severe mental disorders, is higher than that of the general population (cf. 6-11). Studies ascertaining this risk were conducted in a number of countries, among them, the U.S. (6), Canada (7), Scandinavia (8-10), the U.K. (11), and in Israel over two decades ago (12).

Despite those uniform findings some questions may be raised: First, are persons hospitalized in Israeli psychiatric institutions in recent years partially or fully free from the same mortality risk? Although research has noted that the Israeli health system has deficiencies (13), the country has a highly developed and nationally-insured medical care system implemented in 1995, as well as free

I. Levav, MD, 29 Rivka Street, Jerusalem, Israel

  Itzhak.Levav@moh.health.gov.il

Ziona Haklai et al.

inpatient and community-based (for curative and rehabilitation care) psychiatric facilities (14). Conceivably, these factors could lead to timely access to medical care, and, as a result, to the possible reduction of the untreated incidence and prevalence of comorbid physical disorders and subsequent mortality.

Admittedly, years ago Israel was not found at a comparative advantage with regard to the control of natural causes of death (12), but since the first study was conducted positive changes have taken place in the health system that could have reduced the risk. Is this indeed the current case in Israel when in countries with well developed health services, e.g., Scandinavia (8-10), the mortality risk for persons hospitalized for psychiatric disorders was found higher than among suitable comparison groups?

Second, is the risk for suicide different from the countries cited above since its overall rate is lower in Israel (15)?

Past studies have shown that increased overall mortality risks are present for all psychiatric disorders, although not equally. For example, Hiroeh et al. (16, 17) showed an enhanced risk of dying by homicide in men with a diagnosis of schizophrenia and in individuals with affective psychosis. The authors also found that the highest risk of death by homicide and accidents was among persons abusing substances, while the highest risk to die by suicide was among persons using drugs. Hoyer et al. (8) found in a study restricted to persons hospitalized for affective disorders that the risk of mortality was increased overall, but in a slightly different proportion among the affective subgroups. Honkonen et al. (9) found that the highest risk for death from external causes was in persons admitted with mood disorders, while for natural causes the risk was higher in persons diagnosed with schizophrenia spectrum disorders. However, they also concluded that “alcohol consumption plays a major role in causing excess deaths that could be potentially avoided.”

Zilber et al. reported that in Israel the highest risk was for hospitalized persons diagnosed with ICD-9 drug addiction and, in descending order, alcoholism, organic disorders, personality disorders, neuroses, schizophrenia and affective disorders (12).

Importantly for our study, Israel offers several methodological advantages for an unbiased exploration of the mortality risk and relevant associations among persons affected with severe mental disorders, since their hospitalizations are registered by law in a nationwide database.

This almost eliminates the possibility of missing subjects who are admitted. Also, among Israel-born Jews (18) a study showed that most or all of the affected persons with

schizophrenia are hospitalized in psychiatric facilities, thus reducing or eliminating selectivity factors. In addition, Israel possesses both an updated register of mortality and yearly estimates of the general population.

Objective This cohort study explored the death risk among JewishIsraelis who were ever hospitalized in psychiatric facilities for different disorders by age, gender and psychiatric diagnoses for overall mortality and by selected causes of death. In addition, it explored the time of death (before or after discharge), and number and length of their hospitalizations. It also examined differences in risk over the years, to assess whether it was modulated following service-related policy decisions: 1) By the National Insurance Law, which entered into effect in 1995 assuring universal access to medical care; 2) By the generalized administration of the second generation of antipsychotics since 2000, given their possible adverse health side-effects, such as diabetes (19); 3) By the coming into effect of the rehabilitation law implemented since 2000, that facilitates the ongoing process of dehospitalization through the provision of a “basket” of services to the persons discharged from inpatient psychiatric facilities (20); and 4) By the possible impact of the publication of Zilber et al.’s study in 1989 (12) on policy decisions seeking to reduce the identified mortality risk.

Methods We utilized the national psychiatric case register (PCR) to identify all Jewish-Israelis over the age of 18 who were ever admitted to psychiatric in-patient facilities (including some day-hospital units) from the beginning of the PCR (in the early 1950s) and every year henceforth until the end of 2006.

The PCR cumulatively enters all admissions and discharges to all psychiatric inpatient facilities using a unique identification number. As noted above, the reporting is mandated by law (21). It is a reasonable assumption that all Jewish-Israelis with a severe psychiatric disorder were hospitalized, particularly in the early years of the study when the supply of beds was relatively high (22). In contrast, the Arab-Israeli minorities, particularly women, use the psychiatric inpatient services considerably less (22). To avoid a biased sample, the latter group was not included in this study.

231

The Mortality Risk Among Persons with Psychiatric Hospitalizations

The PCR includes the respective dates and diagnosis made by a clinical psychiatrist upon admission and discharge, and socio-demographic information. Diagnoses are recorded according to ICD-10; those made prior to the last WHO classification have been updated. We grouped the cases by the psychiatric diagnosis at discharge (whether the person was alive or deceased) during the last admission (given the higher diagnostic reliability the longer the period of observation) as follows: drug and alcohol addiction (F10-F19); all non-affective psychotic disorders (including schizophrenia) (F20-F29); affective disorders (F30-F39); organic brain disorders (F00 – F09, G40); and others (F40-F99, Z03, Z032, Z04, Z046).

The nationwide database of causes of death is under the responsibility of the Central Bureau of Statistics (CBS). During the years 1981-1997, the causes of death were coded according to the 9th edition of the International Classification of Diseases and according to the 10th edition since 1998. The mortality records with causes of death for the years of our study, 19812006, were linked with the PCR. The causes of death were grouped as follows (with ICD-10 codes, equivalent ICD-9 codes were used before 1998): 1) Natural causes: infectious diseases (A00-B99); cancer (C00-C97); diabetes (E10-E14); heart diseases (I00I09, I11, I13, I20-I51); cerebrovascular diseases (I60-I69); respiratory diseases (J10-J18, J40-J47); and other, 2) external causes: accidents (V01-X59, Y85-Y86), suicide (X60X84, Y870); homicide (X85-Y09, Y871); and other. Total deaths comprise natural, external and missing causes.

For all those on the mortality file found in the PCR, the respective dates of admission and discharge for first and last hospitalization were added to the file. Time to death was calculated as the difference between the dates of death and of the last discharge. If the death was recorded as having taken place on discharge date, the death could have occurred following the release procedures, or during the hospital stay, or while the person was on leave or with the status of runaway, or in the general hospital where the person may have been transferred for specialized medical or surgical care. This risk-period of death was grouped as follows: on the day of discharge; less than three months; three months–one year; and over a year.

In this study we followed up all subjects who ever had a psychiatric hospitalization since the beginning of 1981 until the end of 2006 to check for their mortality. To be included in the follow up, persons hospitalized before 1981 had to be alive at the beginning of that year. The denominator, based on the total Jewish population for each year by 232

age and gender, was extracted from data provided by the Central Bureau of Statistics (CBS), while the total number of persons ever hospitalized for each year by gender, age and psychiatric diagnosis was extracted from the PCR. For comparison of deaths during different years, the following periods were used: 1981-1985; 19861990; 1991-1995; 1996-2000; and 2001-2006. Age was grouped into ages 18-44, 45-64 and 65 and over.

Confidentiality was strictly assured since the authors who analyzed the data had no access to the identity of the persons linked by both databases.

Analysis Gender and age-specific and age-standardized mortality rates were calculated using the direct method based on the 1996 total Jewish population as standard, for persons ever hospitalized in psychiatric facilities (hospitalized) and for those never hospitalized (non-hospitalized).

Rate ratios (RR) and their respective 95% confidence intervals (CI) were calculated as well.

Results The number of persons aged 18 and over who were ever hospitalized in psychiatric facilities from the 1950s until the end of 2006, and who were alive at the beginning of 1981 (for those hospitalized before that year) was 136,687 (men, 52.4%; women, 47.6%). The accumulated number of deaths for the hospitalized persons during the years 19812006 was 42,836. The total number of deaths of the JewishIsraeli population during those 25 years was 752,600.

The age distribution and psychiatric diagnoses of the total population of the ever hospitalized, alive each year between 1981-2006, by gender and age, are shown in Table 1. Diagnoses of organic and affective disorders were more prevalent at age 65 and over (13.6% and 34.6%, respectively), while the diagnosis of non-affective psychotic disorders was more prevalent at younger ages. The percent of women diagnosed with drug and alcohol addiction (1.1%) was lower than of men (5.3%), but higher for affective disorders (women, 23.4%; men, 12.0%). The average age of women was higher than for men (37.9% of them were aged 18-44 compared to 50.9% for men.)

Mortality risk by cause and psychiatric diagnosis

Table 2 shows the age-adjusted mortality rates by causes of death for all hospitalized and non-hospitalized subjects. The total age-adjusted mortality rate per 100,000

Ziona Haklai et al.

Table 1. Psychiatric diagnoses by average age and gender of Jewish Israelis aged 18 and over who ever had a psychiatric hospitalization, 1981-2006* (%) Age/Psychiatric diagnosis at discharge

Organic disorders

Drug and alcohol addiction

Non-affective psychotic disorders

Affective disorders

Other disorders

Men

All diagnoses

Â

Unknown

Total

18-44

50.9

45-64

35.3

2.8

5.1

52.4

6.8

31.4

1.5

100.0

4.6

6.0

46.6

13.3

26.0

3.5

100.0

65+ Total

13.8

14.3

4.7

32.4

28.0

17.0

3.6

100.0

100.0

5.0

5.3

47.6

12.0

27.5

2.5

100.0

18-44

37.9

2.4

1.6

52.6

13.0

28.7

1.8

100.0

45-64

37.2

3.9

1.0

49.5

23.9

18.3

3.5

100.0

65+

24.9

13.2

0.6

33.6

38.5

11.0

3.1

100.0

Total

100.0

5.6

1.1

46.7

23.4

20.4

2.7

100.0

18-44

44.7

2.6

3.6

52.4

9.3

30.3

1.6

100.0

45-64

36.2

4.2

3.5

48.0

18.5

22.2

3.5

100.0

65+

19.1

13.6

2.1

33.2

34.6

13.3

3.3

100.0

Total

100.0

5.3

3.3

47.2

17.5

24.1

2.6

100.0

WomenÂ

Total

*Computed from total yearly population of those who ever had a psychiatric hospitalization and were alive for each year.

persons aged 18 and over during the follow-up years (1981-2006) for the ever-hospitalized group was twice as high as that of the never-hospitalized persons in psychiatric facilities, RR = 1.98 (95% CI 1.96-2.00).

Higher rate ratios were found for various specific natural causes among the ever-hospitalized group, except for cancer. The highest rate ratios were found for infectious, RR = 2.38 (95% CI 2.24-2.52), and respiratory diseases, RR = 2.40 (95% CI 2.31-2.50).

The rate ratios for external causes of death were markedly higher than for natural causes among the ever-hospitalized group, for suicide, RR= 16.34 (95% CI 15.4917.24); homicide, RR = 3.60 (95% CI 2.92-4.42); accidents, RR = 2.63 (95% CI 2.50-2.77); and other external causes, RR = 4.58 (95% CI 4.17-5.03). We also calculated rate ratios for both genders and found them to be similar, except for suicide, where the RR was particularly high for women, RR = 28.07 (95% CI 25.43-30.99) compared to men, RR = 12.32 (95% CI 11.55-13.14).

Table 2 also shows the age-adjusted rates by causes of death and different psychiatric disorders. The ageadjusted mortality rates were highest for persons diagnosed with organic disorders (4138, 95% CI 4026-4250), followed by those with drug and alcohol addiction (3474, 95% CI 3313-3635). Age-adjusted rates for those with drug and alcohol addiction were about twice as

high as those for persons diagnosed with non-affective psychotic (1695, 95% CI 1666-1724) or affective disorders (1583, 95% CI 1545-1621). Mortality rates for the latter two diagnoses were similar. All rates were calculated by 100,000 persons.

Among natural causes of death, rates were higher for those with organic disorders followed by those with drug and alcohol addiction except for diabetes, where the rate for persons with drug and alcohol addiction (75, 95% CI 53-102) was close to those diagnosed with non-affective psychotic (77, 95% CI 71-83) and affective disorders (66,95% CI 59-72). Among the total external causes of death, those with organic disorders (250,95% CI 209-291) had rates close to those with non-affective psychotic (232, 95% CI 221-244) and affective disorders (249, 95% CI 226-271), while persons with drug and alcohol addiction had rates about twice as high (520, 95% CI 450-590) as those in the other diagnostic groups. All rates were calculated per 100,000 persons.

Suicide rates were highest among persons with affective disorders (161,95% CI 142-181), followed by those with drug and alcohol addiction (156,95% CI 116-204), and about a quarter higher than those with non-affective psychotic disorders (129,95% CI 120-138). The mortality rate from accidents was much higher among those with drug and alcohol addiction disorders (186, 233

The Mortality Risk Among Persons with Psychiatric Hospitalizations

Table 2. Age-adjusted rates for Jewish-Israelis aged 18 and over who ever had a psychiatric hospitalization by psychiatric diagnosis and cause of death and RRs compared with non-hospitalized subjects, 1981- 2006. Rates per 100,000 persons Psychiatric diagnosis at discharge Causes of death/ psychiatric diagnosis

Organic disorders

Drug or alcohol addictions

Non-affective psychotic disorders

Affective disorders

Other disorders

All psychiatric diagnoses**

Nonhospitalized

Rate ratio#

Infectious diseases

148.8

80.3

41.6

36.7

39.5

52.3

22.0

2.4

Cancer

399.2

443.1

224.1

240.3

231.6

261.6

232.1

1.1

Diabetes

173.2

74.5

76.7

65.5

71.8

84.9

40.6

2.1

Heart diseases

932.6

524.4

368.3

373.2

323.6

451.9

283.5

1.6

Cerebrovascular diseases

380.1

172.8

104.3

117.8

95.2

143.8

88.3

1.6

Respiratory diseases

271.5

206.8

106.3

72.7

83.4

116.7

48.6

2.4

Other natural causes

1574.4

1433.9

530.8

419.1

409.3

622.1

229.9

2.7

Total natural causes

3879.9

2935.7

1452.2

1325.3

1254.5

1733.4

945.0

1.8

Accidents

133.2

185.6

77.4

66.9

58.1

82.7

31.4

2.6

Suicide

81.4

155.9

128.9

161.4

86.6

121.5

7.4

16.3

Homicide

..

43.0

3.5

..

8.9

6.5

1.8

3.6

Other external causes

33.1

135.3

22.6

20.0

21.7

27.6

6.0

4.6

Total external causes

249.8

519.8

232.4

248.6

175.3

238.4

46.7

5.1

Total*

4138.1

3474.0

1695.0

1583.2

1440.9

1983.0

1002.5

2.0

Rate ratio: all hospitalized/non-hospitalized. .. Rates based on less than 5 cases. #

* Total rates include missing death causes. ** Rates for all diagnoses include missing recorded diagnoses

95% CI 145-226) than for all other diagnoses. All rates were calculated per 100,000 persons.

Table 3 shows mortality rates by age group and causes of death for all hospitalized and the never-hospitalized subjects, and for different psychiatric disorders. Age-specific RRs for all causes were higher in the younger groups. The RRs for total mortality ranged from 1.55 (95% CI 1.531.57) for persons aged 65 and above, to 7.07 (95% CI 6.86-

7.30) for persons aged 18-44. RRs were higher for external than for natural causes of death in all age groups. The rate ratios for both genders were found to be similar, except for external causes of death at younger ages, 18-44, where the RRs for women, 15.13 (95% CI 13.77-16.61) were considerably higher than for men, 6.54 (95% CI 6.19-6.92).

Rates for total natural causes of death for persons diagnosed with organic disorders were over twice as high as

Table 3. Death rates for Jewish-Israelis aged 18 and over who ever had a psychiatric hospitalization by psychiatric diagnoses, age groups and causes of death, and for non-hospitalized, 1981-2006. Rates per 100,000 persons Psychiatric diagnosis at discharge Causes of death

Age group

Organic disorders

Drug or alcohol addictions

Non-affective psychotic disorders

Affective disorders

Other disorders

All psychiatric diagnoses**

Nonhospitalized

Rate ratio#

Total natural causes

18-44

917.0

1170.6

251.2

167.0

229.2

290.6

45.1

6.4

45-64

3330.5

3442.2

1331.0

1108.9

1020.3

1426.6

490.4

2.9

65+

15039.6

8546.0

5762.8

5603.5

5114.6

7153.1

4667.0

1.5

Total external causes

18-44

202.3

593.5

250.7

224.3

157.8

202.3

26.7

8.7

45-64

211.0

463.9

182.5

240.6

157.9

211.0

31.0

6.5

65+

472.9

342.9

241.4

374.7

264.1

472.9

138.1

2.4

Total*

18-44

1119.3

1783.8

507.1

396.4

392.1

526.9

74.5

7.1

45-64

3548.3

3926.8

1522.6

1358.2

1195.5

1639.7

531.5

3.1

65+

15551.4

8915.3

6035.3

6006.4

5401.8

7515.7

4844.0

1.6

Rate ratio: all hospitalized/non-hospitalized. * Total rates include missing death causes. ** Rates for all diagnoses include missing recorded diagnoses. #

234

Ziona Haklai et al.

among those with non-affecTable 4. Rate ratios of age-adjusted death rates for Jewish-Israelis aged 18 and over who tive psychotic and affective ever had a psychiatric hospitalization compared with non-hospitalized subjects by causes of disorders at all ages. For total death, selected psychiatric diagnoses and period of death, 1981–2006 external causes of death, the Years of deaths age group 18 - 44 had lower

1981-1985 1986-1990 1991-1995 1996-2000 2001-2006 1981-2006 rates, while for those aged 45 Causes of death Rate ratios all hospitalized/non-hospitalized - 64 the rates were similar to Infectious diseases 3.66 2.76 2.10 2.39 1.95 2.38 those with non-affective psyCancer 0.99 1.11 1.11 1.18 1.15 1.13 chotic and affective disorders.

Diabetes 2.36 2.25 2.04 1.97 2.07 2.09 The mortality rate among Heart diseases 1.70 1.57 1.60 1.56 1.60 1.59 persons with drug and alcohol Cerebrovascular diseases 1.86 1.86 1.56 1.46 1.52 1.63 abuse was higher than other Respiratory diseases 3.01 2.40 2.14 2.26 2.32 2.40 diagnostic categories for all Other natural causes 3.15 2.99 2.84 2.54 2.43 2.71 causes. This was found in parTotal natural causes 2.00 1.89 1.78 1.79 1.79 1.83 ticular for all natural causes of death in the 18-44 age group, Accidents 2.97 2.24 2.42 2.67 2.96 2.63 where the rate was 1171 (95% Suicide 21.48 18.05 13.05 15.26 16.24 16.34 CI 1053-1298), almost five Other external causes 5.14 4.98 3.34 5.16 3.75 4.35 times higher than among those Total external causes 5.51 4.73 4.58 5.35 5.37 5.10 with non-affective psychotic Total* 2.16 2.05 1.91 1.93 1.93 1.98 disorders (251,95% CI 230Rate ratios for persons with non-affective psychotic disorders/non-hospitalized

266); seven times higher than Diabetes 2.24 2.03 1.90 1.77 1.78 1.89 for those with affective disorTotal natural causes 1.41 1.55 1.55 1.54 1.60 1.54 ders (167,95% CI 40-198); and Total external causes 5.30 4.68 4.15 5.28 5.42 4.97 26 times higher than for nonTotal 1.65 1.78 1.71 1.68 1.74 1.71 hospitalized persons. All rates

Rate ratios for persons with affective disorders/non-hospitalized were calculated per 100,000 Diabetes 0.96 1.50 1.60 1.79 1.65 1.61 persons.

The mortality rate for perTotal natural causes 1.22 1.37 1.33 1.49 1.49 1.40 sons with affective disorders Total external causes 5.56 4.49 5.44 5.47 5.61 5.32 was similar or lower than for Total 1.47 1.60 1.56 1.63 1.64 1.60 those with non-affective psy- * Total rates include missing death causes chotic disorders. The excepreduction in RR during the period 1981 - 2006 occurred tion was for all external causes of death at older ages, in for infectious diseases, where the RR in 2000 - 2006 was particular for persons aged 65 and over, where the rate was almost half that in 1981-1985. The RR for respiratory dis375 (95% CI 341-409) for those with affective disorders eases also was reduced by about a quarter during the same compared to 241 (95% CI 214-271) for those with nonyears. We further investigated the source of this decrease affective psychotic disorders. All rates were calculated per by checking individual infectious disease groups, and 100,000 persons. found this decrease reflected in septicaemia (which conOverall and specific mortality risks by time period stitutes about 70% of infectious disease mortality in recent The RRs of mortality among the ever-hospitalized years) where the RR fell from 3.84 (95% CI 3.25-4.54) in persons compared to the never hospitalized have been 1981-1985, to 1.97 (95% CI 1.72-2.25) in 2000-2006. Most stable since the beginning of the 90s, RR = 1.91 (95% CI of the decrease occurred until 1995. Similarly, we checked 1.87-1.95) in 1991-1995, compared with slightly higher subgroups of respiratory diseases, and found that the rate ratios for earlier years, RR = 2.05 (95% CI 2.00mortality rates from influenza and pneumonia among the 2.10) in 1986-1990, and RR = 2.16 (95% CI 2.11-2.21) hospitalized have also decreased greatly over the period in 1981-1985 (Table 4). investigated, the RR fell from 4.19 (95% CI 3.74-4.70) Among specific natural causes of death, the greatest in 1981-1985, to 2.27 (95% CI 1.98-2.59) in 2000-2006.

235

The Mortality Risk Among Persons with Psychiatric Hospitalizations

In contrast, rates for chronic lower respiratory diseases remained stable, with the RR increasing slightly.

The RR for diabetes has remained stable after a small initial reduction from the period of 1980-1985. As for suicide, the RR in 1991-2000 decreased by about a third compared to the years 1981-1985 (Table 4).

The RRs for diabetes has declined steadily for persons diagnosed with non-affective psychotic disorders, while for those diagnosed with affective disorders it has generally increased. Analogously for the total natural causes of death, the RR has been relatively stable for those with non-affective psychotic disorders but increased somewhat for those with affective disorders.

In-hospital death and time from hospital discharge until death

Overall, a larger proportion of deaths occur before or, particularly, soon after discharge among younger patients than among older ones. One fifth (20%) of deaths for persons aged 18-44 took place before discharge from the psychiatric facilities compared to 17%, among those aged 45-64, and 12%, among those aged 65 and over. For those aged 18-44, 54% of deaths occurred before discharge from hospital or during the first year thereafter, compared to 37%, for those aged 45-64 and 29%, for those aged 65 and over (Figure 1). Proportions for men and women were found to be similar.

As for different causes of death, more suicides occur in hospital or on the day of recorded discharge than for deaths due to natural causes or other external causes. Two thirds, 62%, of suicides occurred before discharge from hospital or during the first year thereafter, compared to 42%, from other external causes and 32%, from natural causes of death (Figure 2). This was found, in particular, in hospitalized persons aged 18-44, where 25% of suicides occurred before or on the recorded day of discharge, and 70% before discharge or within the first year.

A larger proportion of deaths occur in hospital or on the recorded day of discharge for persons with the diagnosis of non-affective psychosis, 25%, than for those with affective disorders, 7%, or with other diagnoses, 11% (Figure 3).

Discussion Our findings clearly replicated those reported by the literature. Those findings were made in studies conducted in different countries, including Israel over two decades ago, using different methods and procedures, 236

Figures 1-3. Proportion of deaths by time elapsed since discharge for Jewish-Israelis aged 18 and over who were ever hospitalized in psychiatric facilities, 1981 â&#x20AC;&#x201C; 2006 (% of total deaths) (N=42,836) Before/on day of discharge < 3 month

3 month-1 year Over 1 year

Figure 1. By age groups 100% 90% 80% 70%

46.0% 63.2% 71.2%

60% 50% 40% 30%

16.7% 9.0%

17.6%

10% 0%

7.4%

10.5%

20% 19.7%

17.3%

18-44

45-64

8.8% 12.6%

65+

Figure 2. By age death 100% 90% 80%

37.8%

70% 60%

58.1% 68.3% 18.5%

50% 40% 30%

8.1%

20%

9.4%

10% 0%

66.7%

suicide

8.7%

15.9%

10.1%

11.1%

14.5%

other exernal

total

21.5%

14.2%

natural

14.9%

22.2%

Figure 3. By psychiatric diagnoses 100% 90% 80% 70%

56.3%

60%

77.9%

50% 40%

8.4%

30%

10.7%

20% 10% 0%

69.0%

9.5%

24.7%

7.6% 8.0%

non affective psychotic disorders

affective disorders

6.5%

10.7% 10.9%

other

Ziona Haklai et al.

e.g., hospital- and community-based individuals, and measures to ascertain risk (6-12). We, as others, found a higher risk for overall mortality and for specific causes of death, except for cancer, among the psychiatrically hospitalized population. Suicide rates, too, were much higher in the hospitalized group. Relatively high RRs of all external causes of death were found among both men and, particularly, among women. This gender difference could be partially attributed to their lower risk among women than men in the general population.

The mortality risk was higher among the younger groups, 18-44, suggesting that psychiatric hospitalizations serve as a risk indicator (23) among individuals who have yet to reach the age where death is more frequent. Importantly, the external causes of death, such as accidents, homicide and suicide have higher RRs than those linked to natural causes, as shown by Hiroeh et al.

(16) in a study based on the Danish Psychiatric Register.

The case of homicide in our study, although based on a relatively small number of events, is of interest, since the notion of dangerousness is often ascribed to people with severe mental disorders but hardly raised with regard to their own victimization.

Like Hiroeh et al. in Denmark (17) and Zilber et al. in Israel (12), but in contrast with Kisely et al. in Canada (7), we found that the mortality risk for cancer did not differ from the general population. This negative finding is consistent with results obtained in a large Israeli study in which the cancer risk among persons hospitalized for schizophrenia (24) and in their parents (25) was found lower than in the general population.

Another negative finding was observed, and this is the reduction of mortality due to infectious and some respiratory diseases (pneumonia and influenza) over the study period, which perhaps reflects increased hygiene and better and timely prevention and treatment of infections.

The risk of mortality in our study was present among hospitalized persons diagnosed with all disorders, and, as noted earlier in Finland, among both persons with short- (9) and long-stays in hospital (26). Importantly, for the younger adults (18-44), the risk period of death by suicide in particular was at the time the person was registered as still being in hospital (this includes those who left the premises on account of authorized or non-authorized leave of absence, or discharges against medical advice) or within the year following discharge.

Several “negative” findings in our study are of marked interest:

1. The process of deinstitutionalization that accompanies the decade-old law on the “Rehabilitation of Persons with Psychiatric Disabilities in the Community” (20) does not seem to have raised the overall mortality risk.

Note that the reduction in beds in psychiatric institutions was 10.7%, in the years 1986-1990; 4.7%, in the years 1991-1995; and 17.8%, in the years 1996-2000. In the years 2001-2006, when the law entered into effect, the reduction escalated to 40.5%. Assuming that the reduction in beds over time determined that persons with more severe disorders were admitted, the “negative” finding is of even greater interest.

2. For suicide, the findings prompt cautious surveillance of the risk, in view of a relatively recent study conducted in Denmark which showed an increased risk for suicide coinciding with a 50% reduction in the number of in-patient beds (8). In Israel, the RRs for suicide in the years 2001-2006 were lower than in the years 1981-1990, but slightly higher than in the intermediate years, 1991-2000.

3. The introduction of atypical antipsychotics in the treatment of persons with non-affective psychosis has not increased the risk for deaths caused by diabetes and other natural causes of death. This negative finding requires surveillance as well, to check for deaths among persons who had received those antipsychotics for a longer period of time than we observed. The need for surveillance is further highlighted by the fact that the RR for diabetes among those hospitalized with non-affective psychotic diagnosis for the years 2001-2006 is slightly higher, 1.78, than for the total natural causes, 1.60. The respective RRs for the same period for those diagnosed with affective disorders were 1.65 and 1.49.

4. As noted above, in our study the mortality risk for cancer was not different than for the general population.

5. The previous Israeli report on mortality among hospitalized persons was published in 1989 (12). The study used the same database we did and included all people who had a recorded hospitalization in 1978 (N= 16,147). Their deaths were followed up until 1983 (N = 2427). It is clear from our results that any decline in the risk for death started before publication of those results, and did not become accelerated following it (Table 4).

Our findings pose a considerable challenge for medical and psychiatric services, in terms of their interpretation and required actions. Several putative factors have 237

The Mortality Risk Among Persons with Psychiatric Hospitalizations

been raised to account for the elevated mortality risk that, acting singly or in combination, affect all four groupings of psychiatric disorders we investigated, such as inactive lifestyle, risk-taking, smoking, diet, medication, neurohumoral mechanisms and inadequate self- and medical services care (3). The relative weight of each factor towards explaining the findings has not been determined. Clearly, however, active programs are undoubtedly required, as proposed by all researchers who have investigated this subject, as follows: First, advocacy targeting the health system is required.

We know by now that persons with schizophrenia carry an unhealthy life style (27), yet programs of health promotion (3), particularly tailored for these persons, are rare or totally absent in the health and mental health systems in Israel.

Second, self- and service-based stigmatic attitudes and behaviors constitute barriers to the adequate care of persons with mental disorders in the general health services (3-5). programs to address both types of stigma-related problems are wanting. Admittedly, stigma is not the sole barrier to adequate care, since persons with severe and persistent mental disorders may neglect medical treatment once a problem had been identified and treatment begun. Therefore, both service and patient-related factors need to be addressed by well-formulated health education programs, including the active involvement of the primary health care practitioners and the organizations of service users and their families.

Third, preventive and curative-oriented programs aimed at the natural causes of mortality should preferably be started while the affected persons are in hospital, and, subsequently, be continued in the psychiatric and substance abuse clinics and, as noted above, involve the service users and their families.

Fourth, the heightened risk for deaths from external causes calls for assertive programs of intervention that may reduce such a risk. Obviously, a fully rational formulation of such a program requires comprehensive research, including the reconstruction of the way the service operates, and the individual-, family- and community-related events that may have triggered the decision to commit suicide or lead to self-endangering behavior.

Our epidemiological study has merely indicated the existence of the heightened risk of potentially preventable factors. The national program of suicide prevention (28) is a timely development, inasmuch as it attempts to provide interventions to individuals at increased risk, such as those who were the subject of this study.

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There are some limitations to our inquiry: 1) For diagnoses of both the mental disorders and causes of death we relied on two databases that collect clinical and not research diagnoses; 2) to explore the possible effect of the new generation of antipsychotics we had to rely on a proxy, the year of their introduction into the services, since we lacked direct access to the patientsâ&#x20AC;&#x2122; prescriptions; and 3) we did not include minority groups of the general population. However, with regard to the latter limitation, we have no grounds to assume that the results may not apply to those groups as well.

Yet, we believe that the limitations are balanced out by several strengths: 1) Most likely, we had a complete enumeration of persons diagnosed with schizophrenia (18); and 2) in contrast to the previous local study (12), we had a considerably longer period of observation, and a much larger number of followed-up persons. These enabled us to conduct a more adequate examination of the effect of different variables, such as age, gender and causes of death and time-periods of risk.

Conclusion This study has again raised a case for action that requires the assertive involvement of the health services (general and psychiatric) as well as family and service user organizations to modify the current situation. Conceivably, the announced transfer of the responsibility for ambulatory care to the four national health providers may facilitate the medical care that this population requires. But short of targeted action, such as health education for service users and families, and programs for the reduction of stigma among health agents, we may find that a mere organizational procedure may fail to change the serious risk that we, and many others before us, have shown. As a model of care for people with mental disorders (e.g., depression) in the primary health setting, we refer the reader to a recently published study showing how treatment of patients with poorly controlled diabetes, coronary heart disease or both, were successfully assisted by a specially designed nurse-based program (29).

References 1. Jeste DV, Gladsjo JA, Lindamer IA, et al. Medical comorbidity in schizophrenia. Schizophr Bull 1966; 22: 423-430.

2. Phelan M, Stradins L, Morrison S. Physical health of people with severe mental illness. BMJ 2001; 322: 443-444.

3. Raphael B, Schmolke M, Wooding, S. Links between mental and physical health and illness. In Herrman H, Saxena S, Moodie R, editors.

Promoting mental health. Concepts. Emerging evidence. Practice.

World Health Organization: Geneva, 2005.

Ziona Haklai et al.

4. Osborn DPJ. The poor physical health of people with mental illness.

West J Med 2001; 175: 329-332.

5. Cradock-Oâ&#x20AC;&#x2122;Leary J., Young AS, Yano EM, et al. Use of general medical services by VA patients with psychiatric disorders. Psychiatr Serv 2002; 53, 874-878.

6. Piatt EE, Munetz MR, Ritter Ch. An examination of premature mortality among decedents with serious mental illness and those in the general population. Psychiatr Serv 2010; 61: 663-668.

7. Kisely S, Sadek S, MacKenzie A, et al. Excess cancer mortality in psychiatric patients. Can J Psychiatry 2008; 53: 753-761.

8. Hoyer EH, Mortensen PB, Olesen AV. Mortality and causes of death in a total national sample of patients with affective disorders admitted for the first time between 1973 and 1993. Br J Psychiatry 2000; 176: 76-82.

9. Honkonen H, Mattila AK, Lehtinen K, et al. Mortality of Finish acute psychiatric hospital patients. Soc Psychiatry Psychiatr Epidemiol 2008; 43: 660-666.

10. Tidemalm D, Waern M, Stefansson C-G, et al. Excess mortality in persons with severe mental disorder in Sweden: A cohort study of 12,103 individuals with and without contact with psychiatric services.

Clin Pract Epidemiol Ment Health 2008;4:23.

11. Harris EC, Barraclough B. Excess mortality of mental disorders. Br J Psychiatry 1998; 173: 11-53.

12. Zilber N, Schufman N, Lerner Y. Mortality among psychiatric patients The groups at risk. Acta Psychiatr Scand 1989; 79: 248-256.

13. Epstein L, Horev T. Inequalities in health and in the health system.

Presentation of the problem and guidelines for policy correction.

Jerusalem: Merkaz Taub, 2007 (Hebrew).

14. Levav I, Grinshpoon A. Mental health services in Israel. Int Psychiatry 2004; 4: 10-14.

15. www.health.gov.il/suicides. Accessed on July 13, 2010.

16. Hiroeh U, Appleby L, Mortensen PB, et al. Death by homicide, suicide and other unnatural causes in people with mental illness: A population-

based study. Lancet 2001; 358: 2110-2112.

17. Hiroeh U, Kapur N, Webb R, et al. Deaths from natural causes in people with mental illness: A cohort study. J Psychosom Res 2008; 64: 275-283.

18. Levav I, Kohn R, Dohrenwend BP, et al. An epidemiological study of mental disorder in a 10-year cohort of young adults in Israel. Psychol Med 1993; 23:3, 691-708.

19. Whyte S, Penny C, Phelan M, et al. Quality of diabetes care in patients with schizophrenia and bipolar disorder: Cross sectional study. Diabet Med 2007; 24: 1442-1448.

20. Lachman M, Hadass-Lidor N. Rehabilitation of persons with psychiatric disabilities in the community: From de-hospitalization to recovery and inclusion. Hadea Harevaja ICSW 2003;35:14-17 (Hebrew).

21. Lichtenberg, P, Kaplan Z, Grinshpoon A, et al. The goals and limitations of Israelâ&#x20AC;&#x2122;s psychiatric case register. Psychiatr Serv 1999; 50, 1043-1048.

22. Ministry of Israel, Mental Health in Israel. Statistical Annual 2003.

Mental Health Services, Department of Information and Evaluation, Jerusalem, 2003.

23. Burt BA. Definitions of risk. J Dental Educ 2001; 65: 1007-1008.

24. Grinshpoon A, Bar-Hana M, Levav I, et al. Cancer in schizophrenia: Is the risk higher or lower? Schizophr Res 2005; 73:2-3; 333-341.

25. Levav I, Lipshitz I, Nobikov I, et al. Cancer risk among parents and siblings of patients with schizophrenia. Br J Psychiatry 2007; 190: 156-161.

26. Rasanen S, Hakko H, Villo K, et al. Excess mortality among long-stay psychiatric patients in Northern Finland. Soc Psychiatry Psychiatr Epidemiol 2003; 38: 297-304.

27. Brown S, Birtwistle J, Roe L, et al. The unhealthy lifestyle of people with schizophrenia. Psychol Med 1999; 29, 697-701.

28. Goldberg Y. The National Program of Suicide Prevention. Personal communication, 2010.

29. Katon WJ, Lin EHB, Michael Von Korff M, et al. Collaborative care for patients with depression and chronic illnesses. N Engl J Med 2010; 363:2611-2620.

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Isr J Psychiatry Relat Sci - Vol. 48 - No 4 (2011)

Schizophrenia: It’s Broken and It Can’t Be Fixed. A Conceptual Analysis at the Centenary of Bleuler’s Dementia praecox oder Gruppe der Schizophrenien Jan Dirk Blom, MD, PhD, 1,2 and Herman M. van Praag, MD, PhD3 1

Parnassia Bavo Group, The Hague, The Netherlands Department of Psychiatry, University of Groningen, Groningen, The Netherlands 3 Department of Psychiatry and Neuropsychology, Maastricht University, Maastricht, The Netherlands 2

ABSTRACT Background: In 1911 Bleuler’s Dementia praecox oder Gruppe der Schizophrenien served to launch schizophrenia as a group of nosological entities characterized by a “splitting of the psychic functions.”

Today, at the centenary of this opus magnum, we find that the term is still in force but not the concept originally envisaged by Bleuler.

Method: For the sake of this conceptual analysis a literature search was carried out in PubMed, Embase, and the historical literature.

Results: The current schizophrenia concept, as operationalized in the DSM and other psychiatric classifications, is primarily indebted to Kraepelin and his degenerationist take on psychopathology. That approach is now obsolete, but the product still prevents us from moving beyond the notion of schizophrenia as a single-disease concept with multiple etiologies, multiple clinical expressions, and an unfavorable outcome.

Conclusions: If we aim to investigate the biological underpinnings of psychotic symptoms, first a deconstruction of the schizophrenia concept will need to take place. In this paper we highlight a method - called functionalization - which allows for such a deconstruction.

Limitations: Functionalization will probably require a new scientific language, which will be largely discontinuous with our current nosological and diagnostic systems.

Background In 2011 it was 100 years ago that the Swiss psychiatrist Eugen Bleuler (1857-1939) published his famous book Dementia praecox oder Gruppe der Schizophrenien (1). The term schizophrenia had been introduced by him three years prior, in a rather inconspicuous paper entitled Die Prognose der Dementia praecox (Schizophreniegruppe) (2), but it was his impressive 420page monograph with its myriad clinical descriptions that would propagate the name and promote its acceptance throughout the world. As indicated by the APA’s status reports on the development of the new Diagnostic and Statistical Manual of Mental Disorders (DSM-5), to be published in 2013, the name will be here to stay for the foreseeable future (3). But the concomitant concept of a “split” or “fragmented” personality, as originally envisaged by Bleuler, was discarded a long time ago.

Paradoxically, our present schizophrenia concept bears the name coined by Bleuler, although it is based on the body of thought of Emil Kraepelin (1856-1926). That body of thought derived to a significant extent from the 19th-century degeneration theory, a poorly discussed doctrine which no longer serves as a source of inspiration for psychiatry’s scientific discourse, but that exerts its influence upon our thinking about psychotic disorders up until the present day (4-6).

Aims In this paper we offer a concise reconstruction of the early developmental history of the schizophrenia concept.

Our primary aim is to demonstrate that the 19th-century

Address for Correspondence: Jan Dirk Blom, MD, PhD, Assistant Professor of Psychiatry, Director of the Residency Training Program, Parnassia Bavo Group, Paradijsappelstraat 2, 2552 HX The Hague, The Netherlands jd.blom@parnassiagroep.nl

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Jan Dirk Blom and Herman M. van Praag

degeneration theory should be granted a more significant role in its shaping than has hitherto been customary, and that this indebtedness constitutes the major reason why psychiatry does not succeed in moving beyond the paradoxical notion of a single-disease concept with multiple etiologies, multiple clinical expressions, and an unfavorable outcome. Our secondary aim is to explore possible directions for the concept’s future development.

Method For the sake of this conceptual analysis, a literature search was carried out in the English, German, French, and Dutch historical literature, PubMed, and Embase (up to October, 2010), using the search terms “schizophrenia,” “dementia praecox,” “Bleuler,” and “Kraepelin.”

Results The genesis of Bleuler’s schizophrenia concept

In 1908 Bleuler introduced the term schizophrenia because he was dissatisfied with the nomenclature used by Kraepelin. As he argued, dementia praecox - as Kraepelin called it - was neither characterized by an unavoidable dementia, nor by an unavoidable praecocitas. “For this reason,” Bleuler wrote, “and because of the fact that one cannot derive adjective and substantive noun modifiers from the expression dementia praecox, I take the liberty of using the word schizophrenia to designate the Kraepelinian notion” (2). Three years later he added, “I call dementia praecox ‘schizophrenia’ because (as I hope to demonstrate) the ‘splitting’ of the different psychic functions is one of its most important characteristics. For the sake of convenience, I use the word in the singular although it is apparent that the group includes several diseases” (1). Thus he suggested that the two terms were interchangeable, and that they referred to a single nosological category or group of disorders.

The term schizophrenia (from the Greek words σχιζειν and φρην) was carefully chosen. It sought to reflect the patient’s peculiar loss of unity of the self, or “splitting of the psychic functions,” as Bleuler called it, and the ensuing emergence of isolated complexes which take turns controlling the personality. In Bleuler’s view, without a proper integration into the rest of the personality, these complexes are bound to result in a fragmentation of the patient’s personality. As he asserts, “Thus the patient appears to be split into as many different persons or personalities as they have complexes” (1). According to Bleuler, this “split-

ting of the psychic functions” may result in an interruption of the normal process of association: “Thus the process of association often works with mere fragments of ideas and concepts. This results in associations which normal individuals will regard as incorrect, bizarre, and utterly unpredictable. Often thinking stops in the middle of a thought; or in the attempt to pass to another idea, it may suddenly cease altogether, at least as far as it is a conscious process (blocking). Instead of continuing the thought, new ideas crop up which neither the patient nor the observer can bring into any connection with the previous stream of thought” (1). To Bleuler these two basic mechanisms constituted the heart of that which he called schizophrenia. He gave the ensuing symptoms, including hallucinations and delusions, the status of “secondary” or - from a slightly different vantage point – “accessory” symptoms.

As regards the etiology of schizophrenia, Bleuler took a well-considered position in which both organic and psychological factors were taken into account (7). As to its prognosis and outcome, he showed himself somewhat more optimistic than Kraepelin. Whereas Kraepelin reported an inevitable decline in 87 per cent of individuals with dementia praecox, Bleuler spoke of periods of remission and exacerbation (1, 8). Nonetheless, Bleuler was convinced that the underlying “schizophrenic process” had a strong tendency to persist, even when superficially the patient might appear to be “sane.”

The notion of an alleged correspondence between Bleuler’s schizophrenia concept and Kraepelin’s dementia praecox concept has proved to be quite resistant (9).

Apart from Bleuler, who characterized his work on schizophrenia as “nothing less than the application of Freud’s ideas to dementia praecox,” Kraepelin added to the myth of compatibility through numerous references to “schizophrenia” and “schizophrenic symptoms” in his later work (1, 8). On closer inspection, though, Bleuler’s concept differed more from Kraepelin’s than the two men would openly admit. Thus Bleuler rejected the very foundation of Kraepelin’s dementia praecox concept, i.e., the notion of an inevitable deterioration towards dementia. However, the greatest source of tension between the two concepts would seem to lie in their level of operationalization. Kraepelin conceptualized dementia praecox as a syndrome-course unit, defining it in terms of overt clinical features developing in a certain direction over time, whereas Bleuler considered it basically as a weakness of association, i.e., a disturbance of mental functioning which might or might not become manifest in overt clinical features. To him 241

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overt psychotic symptoms, so important to Kraepelin’s concept, were merely of secondary importance.

Schizophrenia in the DSMs

The initial reception of Bleuler’s schizophrenia concept was one of indifference (10). It took six years before it elicited any significant response from beyond the circle of Bleuler’s personal collaborators. But during the 1920s, the usage of the term schizophrenia gradually surpassed that of “dementia praecox,” and finally came to replace it.

In 1952, when the first DSM appeared, Bleuler’s concept had been fully incorporated into American psychiatry (11). Apart from a reference to Menninger’s concept of reaction types, derived from the latter’s work with soldiers in World War II, the name “schizophrenic reactions” featuring in the first DSM was a tribute to Bleuler’s idiom (12). Nevertheless, the disorder’s operational definition was chiefly a kraepelinian affair. As the authors of the first DSM stated unambiguously, “This term [i.e., schizophrenic reactions] is synonymous with the formerly used term dementia praecox” (12). The operational definition of schizophrenia in the DSM-IV-TR may be considered a direct descendent of the 1952 version, in which the bleulerian themes “weakness of association” and “splitting of the psychic functions” are again nowhere to be found (4, 13).

In conformity with Kraepelin’s approach, schizophrenia is rather defined in the current DSM as a heterogeneous cluster of overt psychopathological symptoms (A criterion), with a sublimated version of the “inevitable decline” notion in the form of the requirement that the symptoms be present for at least six months (B criterion) (14).

The origins of Kraepelin’s dementia praecox concept

If we wish to become acquainted with the ideas that infused our current schizophrenia concept, it is Kraepelin to whom we must turn. Historical accounts tend to emphasize three major influences upon his work on dementia praecox. The first of these is the syndrome-course unit, as exemplified by Kahlbaum’s catatonia concept, which Kraepelin incorporated in the fourth edition of his textbook as a conceptual mould for dementia praecox (15-17).

Secondly, it has been argued that the concept of General Paralysis of the Insane (GPI) served a similar purpose (18). The third influence was Kraepelin’s own catamnestic study, which he devised to provide empirical confirmation for the theoretical notion of the syndrome-course unit.

This study involved the use of Zählkarten (i.e., “counting vouchers”), with which Kraepelin kept track of his clinical patients, and sorted out those with a favorable prognosis 242

(subsequently diagnosed with manic-depressive illness) and those with an unfavorable one (referred to as the dementia praecox group) (19).

Kraepelin’s ideas on degeneration

A fourth, and poorly discussed influence upon Kraepelin’s conceptualization of dementia praecox was the 19th-century degeneration theory, a pseudo-scientific doctrine which represented the opposite of evolutionary progress, and which dominated scientific thinking at the time (4-6). This idea of a regression towards earlier developmental stages was quite a common notion at the time, one which both troubled and delighted 19thcentury Western society. It was troubling because of its association with impending doom, based on the notion that Man, occupying the top rung of the recently discovered evolutionary ladder, could also take a tumble. On the other hand, the idea was welcomed, because it provided “normal” citizens with an explanatory model for the occurrence of all kinds of misfortune and wickedness in society. In the classic reading of Morel, degeneration involved a transgenerational process of physical, mental, and moral decline, bound to end in extinction of the family line within four generations (20, 21). In the words of Alexander and Selesnick, “One generation might be simply nervous, for example; the next generation would be more nervous; the third might be entirely psychotic; the fourth generation would exhibit a full-blown degenerate state; and any future generations would be so demented that the family would become extinct” (22). Kraepelin was fascinated from an early age onwards with evolutionary theory, and later in life he wrote extensively on the merits of the degenerationist approach (23-26). He shared with Morel the lamarckian notion that physical and mental disorders, but also addiction and immoral behavior, might affect Man’s hereditary material, and that this dystrophic material might subsequently be passed on to its offspring. As he wrote, “Even worse than the immediate effects of alcohol and syphilis is the germ damage [German: Keimschädigung] they bring about, which may cause the degeneration of entire generations… At any rate, the number of mental defectives, epileptics, psychopaths, of criminals, prostitutes, and tramps, who descend from alcoholic and syphilitic parents, and pass on their inferiority to their offspring, is interminable” (23). He considered degeneration such a hazard to society, that he urged the German government to promote scientific research “to throw light on the degeneration issue, to chart the nature and magnitude of this threat, and to

Jan Dirk Blom and Herman M. van Praag

establish which measures can be taken to avert it.” As he continued, “The signs are certainly ominous enough; it is up to us to alert the people and the government, and to show them the way that should be taken to restore the health of our race” (23).

With this recommendation, Kraepelin did not skate on thin ice. Over the years he had become an expert on degeneration, ending up with a somewhat subtler version of the doctrine than Morel, in the sense that he envisaged a certain protective influence from Nature itself against this invisible but devastating process, speculating that the dystrophic material running in families might become “diluted” by admixture with “healthy blood,” and arguing that “the damage will be partially compensated for by [the degenerate’s] reduced life expectancy” (25). And yet his fear of degeneration seemed to be even more acute than Morel’s. In addition to its direct threat through the propagation of acquired pathogenic characteristics, he discerned an indirect threat posed by “domestication” (23,25,26,27).

As he wrote, “A second major type of cultural damaging can be summarized under the common name of domestication, a breaking away from the natural conditions of life” (25). As Kraepelin explained, Man’s increasing dependency upon community life turned him into a dependent and helpless creature, unaccustomed to physical strain and to the hardships encountered in a natural environment (25, 26). In his opinion, this entailed a state of Verweichlichung, i.e., a general weakening of the body, of which the weakening of the brain was only a single aspect. This would in turn lead to a further susceptibility to degeneration through reduced fertility and life expectancy, reduced resistance against disease, increase of sexual aberrations, and increase of suicidal ideations (27).

From 1899 onwards, Kraepelin arranged the nosological categories in his psychiatric classification in accordance with their supposed indebtedness to degeneration, arguing that all mental disorders are caused by it to a greater or lesser extent (27). In an effort to neutralize this virtually omnipresent threat, he called for immediate action from the government, the scientific community, and society at large, advocating large-scale epidemiological surveys and all kinds of preventive measures, ranging from the abstinence of alcohol to positive eugenic measures (24, 25, 27).

Kraepelin’s ideas on eugenics

These eugenic measures involved a program of racial selection, aimed at the sustenance and promotion of the talents of the German race (26). As Kraepelin wrote in his

posthumously published ego document, Persönliches, “All measures which have as their goal an improvement of our race, must… be directed at future rather than present generations, and seek to prevent the accumulation of an unfavorable hereditary constitution, germ damage, and developmental disorders… From all these considerations followed the exceptional meaning I had to attribute to determined racial selection. Apart from many other unfavorable influences, of which I here only mention the undermining of natural selection through economic measures, and the burdening of competent individuals with the responsibility for the incompetent ones, it seemed precarious to me for the future of our people that our own nature was threatened ever more by Jewry. It was the often discernable inclination of the Semitic race to strive forwards not for the sake of intrinsic gratification, but for the sake of external advantages; their deftness, toughness, industriousness, self-abnegation, the indissoluble solidarity; on the other hand, also the ruthlessness in the pursuit of goals and the choice of resources, which made it understandable that they gained victories at the cost of their more indolent, peculiar, dreamy, indecisive, and agreeable compatriots.

Anxiously I saw how in science, too, the influence of the Jews far surpassed their share in the population, and how disastrous this was in so far as here also the pursuit of success and recognition came to the fore rather than the pursuit of truth and knowledge. That is why, although I had personal contacts with many Jews, and had a high regard for many of them, I could only look upon them as the salt of the earth which may well have been necessary for the development of our own powers. A preponderant influence of the Jewish spirit upon German science, which unfortunately became ever more appreciable, appeared to me an exceptionally grave hazard, which should especially be countered through the systematic sustenance of the undeniable talents of the German race” (27, translation: JDB).

These words, written down around 1924, indicate the extent to which Kraepelin had committed himself to degenerationism. With hindsight now, it may be hard to look past the ideas that helped the U.S. government around 1900, as well as the Nazis during World War II, to justify the negative eugenic measures they undertook against population groups designated by them as “degenerative” (28). But this is not the issue that should concern us here, nor are we to judge the way Kraepelin’s ideas may or may not have been misused by others. Instead, we should keep firmly in mind that 243

Schizophrenia: It’s Broken and It Can’t Be Fixed

his version of the theory had its roots in contemporary evolutionary thought, that his ideas on degeneration and racial selection were not as extreme as those of many of his contemporaries, and that, in his writings at least, he never advocated any negative eugenic measures against any population groups. And yet we cannot avoid the question whether these private reflections indicate that he had given in to the belief that certain groups of people can be intrinsically inferior to others, in a moral as well as a psychophysical sense, and that individuals within these groups may well be beyond help, simply because of their membership of the groups in question.

Which, if true, would be a far cry from the basic principles of natural science defended by him so vehemently throughout the rest of his work.

Degeneration and dementia praecox

Kraepelin’s thinking was steeped in degenerationism, like that of so many of his contemporaries. But how exactly did that affect his conceptualization of dementia praecox?

Kraepelin claimed that the disorder’s chief characteristic was its unfavorable outcome, and that he had established that fact by empirical means, with the aid of his Zählkarten.

During the 1970s the International Follow-up Study of Schizophrenia (29) famously challenged the notion that deterioration was characteristic of schizophrenia, but it was also contested by Kraepelin’s contemporaries. As stated by men such as Meschede, Mendel, Siemerling, Jolly, and Grashey, his approach entailed a circular argument in which clinical diagnosis served as a prognostic tool, and prognosis as a diagnostic tool (4, 19). This methodological fallacy was discussed at length by Boyle, who explained that Kraepelin did not follow the correspondence rules for inferring hypothetical constructs, and that his concept was therefore invalid (30). Boyle also observed that each edition of his textbook allowed for more and more symptoms associated with the disorder, thus steadily enlarging the group of matching cases without making the case for the concept itself any stronger. Table 1 reflects the accompanying increase in the number of diagnoses of dementia praecox among inpatients at Kraepelin’s clinic (31).

Table 1. The prevalence of dementia praecox among inpatients at Kraepelin’s clinic between 1892 and 1900 (adapted from Kuilman 1971) 1892

5%

1895

25%

1900

50%

244

It has been argued that these figures may well reflect a genuine increase in the prevalence of the disorder, but they would seem to follow naturally from the increasing looseness of Kraepelin’s diagnostic criteria. In any case, within 20 years what started out as an intriguing but rarely diagnosed disorder had grown into the most common diagnostic category in clinical psychiatry. Meanwhile, as Boyle noted, it was as if everyone, including Kraepelin himself, had lost sight of the concept’s shaky foundations (30). A man as brilliant as Kraepelin must have known that his critics were right. In the light of the above reflections there is good reason to believe, then, that the dementia praecox concept was designed as a prime example of degeneration. As Kraepelin wrote to Wundt as early as 1881, he was from the outset determined “to operationalize the notion of degeneration in psychophysical terms” (32). Accordingly, he introduced dementia praecox in the fourth edition of his textbook under the heading of the psychische Entartungsprocesse (i.e., “mental degenerative processes”) (17). Although it would take another 15 years before Bleuler would pitch the term schizophrenia, it was there and then, in 1893, that the schizophrenia concept commenced its long and prosperous life (27).

The quest for a lathomenology

The 19th-century degeneration theory has long ceased to be a source of inspiration for psychiatry’s scientific discourse. However, if it is true that this pseudo-scientific doctrine helped to shape the dementia praecox concept, which in turn served as a conceptual mould for the first DSM’s “schizophrenic reactions,” the diagnostic features of our current schizophrenia concept are still largely clustered together in a degenerationist fashion. Owing to the APA’s measure to allow no changes in the operational definitions of the DSM’s diagnostic categories without any substantial support from empirical research findings, Kraepelin’s degenerationist outlook is exerting its influence up until the present day. This is why, on the eve of the DSM-5 era, psychiatry finds itself holding a rich legacy of empirical data in the one hand, and a neodegenerationist concept in the other, asking itself how to relate the two. Which is an impossible task, as numerous authors have pointed out (4, 5, 30, 33-40).

Andreasen aptly portrays schizophrenia research as a quest for the disorder’s lathomenology (41). That is to say, as the search for a neurobiological “lath” or narrow bottleneck that connects the established etiologies and risk factors for the development of psychosis with the signs and symptoms observed at the phenomenologi-

Jan Dirk Blom and Herman M. van Praag

cal level. So far, this search for a final common pathway has proved to be rich yet unsatisfactory. One reason for this may be the lack of specificity of the empirical “facts” assembled over the past century (33, 42-45). One of the painful conclusions from a meta-analysis of the results of 20 years of empirical research into the neurobiological and neuropsychological correlates of schizophrenia is that the effect size of these findings is very small, and that findings presented as “typical” for schizophrenia can also be found in individuals with entirely different disorders, or with no psychiatric disorder at all (42). For this reason, current empirical research tends to focus more and more on subtypes and (endo-)phenotypes of schizophrenia, as well as on individual signs and symptoms (46-48).

However, the more important reason why psychiatry is waiting in vain for a proper lathomenology would seem to be that the constellation of signs and symptoms as produced by Kraepelin’s degenerationist approach cannot be reproduced via alternative approaches such as the dopamine hypothesis or, for that matter, any other nondegenerationist approach (4, 49).

Directions for future development

At this stage it would seem paramount that the scientific community formulate a blueprint for programs that encourage further progress in schizophrenia research (33).

To dispose of the concept altogether, or to exchange it for a purely dimensional approach, would not seem to be an appropriate solution. After all, an important virtue of the DSM and related psychiatric classifications is that they provide psychiatry with a common language and uniform diagnostic criteria, which are both prerequisites for any coordinated international research program. Therefore, rather than getting rid of the notion schizophrenia, it would seem advisable to work towards an awakening to the concept’s legitimate status, namely, that it is nothing more and nothing less than a working hypothesis.

In this context we may remind ourselves that Bleuler himself was not too confident about the epistemic value of his schizophrenia concept. As he wrote in 1911, he had proposed the name for lack of a better one, meanwhile realizing that it might well have bearing on a group of disorders rather than on a single disease. The history of psychiatry has proved Bleuler right, in the sense that empirical findings and conceptual considerations have yielded a gradual fragmentation of the original concept into smaller, separate concepts. Some classical examples of such “splinter” concepts are dementia paralytica, dissociative identity disorder, autism, and alcohol-induced

psychotic disorder. More recent attempts to nibble away parts of the territory traditionally attributed to schizophrenia include a proposal to grant catatonia an independent nosological status (50), and the introduction of the notion non-affective acute remittent psychosis (NARP) for a prognostically favorable subgroup of psychotic disorders (51). In addition, schizophrenia’s conceptual boundaries have been called in dispute because of its overlap with other psychiatric disorders and with experiences of individuals without any psychiatric diagnosis (52-54). In the light of today’s technological advances there is good reason to expect an acceleration of schizophrenia’s conceptual deconstruction in the near future (55, 56). Neuroimaging techniques, as well as localizing techniques such as electro-encephalography (EEG) and magneto-encephalography (MEG), have brought back a lively interest in classical syndromes such as Capgras’ syndrome and other misidentification syndromes (57), autoscopy and out-of-body experiences (58), hallucinations (59), and metamorphopsias (60), which would all seem to have neurobiological correlates that defy the boundaries of diagnostic categories as defined in the DSM and related classifications. Along with the promises of molecular biology, genetics, epidemiology, psychopharmacology, and neuropsychiatry, these techniques hold the promise of generating a wealth of fresh data in the near future that may serve as the raw material for a new understanding of the biological underpinnings of mental pathology.

Practically, there are a number of conceivable ways to deconstruct “schizophrenia” and arrive at empirically validated disease entities, syndromes or psychopathological dimensions. They all involve the letting go of psychiatric nosological categories as they are currently defined, and a shift of our scientific focus towards underlying levels of conceptualization such as clinical symptomatology, neuropsychology, neurophysiology, psychopharmacology, and molecular biology. Starting from those levels, there are basically two different approaches, which we call the bottom-up and top-down research paradigms. The bottom-up research paradigm is exemplified by genomics, with its search for locations in the genome that are associated with diseases. By taking patterns in the genome as its point of departure, this procedure is capable of detecting abnormalities which may subsequently turn out to have consequences at the level of clinical psychopathology. It is unlikely that such abnormalities will ever be linked one-on-one to any psychiatric disorder as we know them today, but they 245

Schizophrenia: It’s Broken and It Can’t Be Fixed

are nevertheless highly informative. The clinical presentation of the 22q11 deletion syndrome, for example, is far from identical with that of schizophrenia or autism.

And yet this genetic disorder is associated with an elevated risk for both psychotic and autistic symptoms, and may thus yield novel insights into their mediation (61).

Likewise, the study of 5-hydroxytryptamine metabolism has yielded important novel insights into mood, aggression, and anxiety regulation, with all due consequences for our understanding of disorders as diverse as schizophrenia, depression, anxiety disorders, and alcoholism, without pretending to throw light on each and every aspect of them (62).

Functionalization

The top-down research paradigm involves a dissection of diagnostic categories into their constituent parts, and a subsequent search for relationships between psychological and biological dysfunctions. We wish to illustrate this paradigm by highlighting a method called functionalization, introduced in 1965 by Van Praag and Leijnse (63). Functionalization, or functional psychopathology, involves a stepwise diagnostic procedure which allows for a gradual transition from clinically relevant to scientifically relevant foci. It comprises (i) clinical diagnosis, (ii) syndrome diagnosis, (iii) functionalization of the diagnosis, and (iv) linkage to biological determinants. The first step, clinical diagnosis, is the one used by psychiatrists in their day-to-day practice. It involves the assignment of given mental states to preconceived diagnostic categories such as schizophrenia, depression or ADHD, i.e., what doctors call “diagnosis,” and biologists “identification.” The second step, syndrome diagnosis, represents a departure from the traditional quest for an underlying substrate of nosological entities such as these. Rather than aiming at unraveling the biological underpinnings of whole “disease packages,” it involves the assessment of the symptoms or syndromes involved.

Examples of these are highly specific ones such as verbal auditory hallucinations, misidentification and mania, but also rather unspecific ones such as anxiety, fatigue, apathy and insomnia. The third step, functionalization of the diagnosis, is the cardinal one. It involves the listing of the psychopathological symptoms constituting the syndrome, and the examination, and – if possible – quantification of the psychic dysfunctions involved in their mediation (33, 64). After all, psychopathological symptoms – so important to kraepelinian nosology – are considered expressions of their underlying psy246

chic dysfunctions. This is what Bleuler meant when he designated hallucinations and delusions as symptoms “secondary” to thought disorders. But the method of functionalization goes one step further, in the sense that in the final assessment, it seeks to link psychic dysfunctions to their biological determinants, which, after all, are more likely to correspond with disturbances in psychological regulatory systems than with largely mandesigned categorical entities (34).

Because this method cuts across existing nosological categories such as schizophrenia, depression, bipolar disorder, autism, and so on, it has been proven to be much more fruitful than the search for biological determinants of psychiatry’s nosological categories (65). Ultimately, it might well allow us to attain a psychiatric physiology, i.e., a detailed chart of brain dysfunction underlying abnormally functioning psychological regulatory systems (33).

Thus it holds the promise of rooting psychiatric diagnosis much more firmly in its scientific discourse, and doing much more justice to the individual patient with his or her unique psychopathology. The same holds true for treatment, which might benefit from this approach by the possibility to offer tailor-made drug treatment, psychotherapy, and physical treatment, aimed at specific symptoms and psychic dysfunctions rather than at “disease packages.” An obvious drawback is that this method will force clinicians and researchers to learn a new scientific language which will be largely discontinuous with our current nosological and diagnostic systems. Nosological categories such as “schizophrenia” and “depressive disorder” will need to be replaced by categories such as “hallucinatory syndrome with excess dopaminergic activity,” “hallucinatory syndrome with sensory deprivation and deafferentiation,” “mood disorder with serotonergic dysregulation,” and “mood and anxiety disorder with excess dopaminergic activity,” to name a few hypothetical examples. Combined functional-biological categories such as these will not feature in the upcoming DSM-5. But if we succeed in identifying them, DSM-6 might well come to represent a first step towards a truly biologically based psychiatry. In that case, health insurance companies and governments will be forced to develop new ways to decide which treatments will be refunded for which indications, and which ones will not. In short, life will become more complex for professionals and health insurers alike. But the individual patient will no longer need to hear about a so-called disease with multiple etiologies, multiple clinical expressions, and an unfavourable outcome – which certainly strikes us as a goal worth pursuing.

Jan Dirk Blom and Herman M. van Praag

Conclusion As Bleuler spoke wisely, “Errors are the greatest obstacle to the progress of science; it is of greater practical value to correct them than to achieve new knowledge” (66). One hundred years after the publication of Dementia praecox oder Gruppe der Schizophrenien, psychiatry should face the fact that its schizophrenia concept is heavily indebted to the 19th-century degeneration theory, and that empirical research into the nature and biological underpinnings of psychosis is irreconcilable with its ongoing use. Bleuler’s initial intention was to grant the term schizophrenia nothing but the status of a working title. There should be no reason for us to do otherwise, meanwhile allowing the concept’s gradual deconstruction to take place while novel empirical and conceptual insights become available. The method we advocate to speed up the process of deconstruction is functional psychopathology or functionalization. Meanwhile, there would seem to be little harm in maintaining the term schizophrenia for clinical purposes as long as we bear in mind its preliminary status.

References 1. Bleuler E. Dementia praecox oder Gruppe der Schizophrenien. Leipzig: Franz Deuticke, 1911.

2. Bleuler E. Die Prognose der Dementia praecox (Schizophreniegruppe).

Allgemeine Zeitschrift für Psychiatrie und psychischgerichtliche Medizin 1908;65:436-464.

3. www.dsm5.org/ProposedRevisions/Pages/SchizophreniaandOther PsychoticDisorders.aspx 4. Blom JD. Deconstructing schizophrenia. An analysis of the epistemic and nonepistemic values that govern the biomedical schizophrenia concept. Amsterdam: Boom, 2003.

5. Blom JD. Honderd jaar schizofrenie. Van Bleuler naar de DSM-V. Tijdschr Psychiatr 2007;12:887-895.

6. Pick D. Faces of degeneration. A European disorder, c. 1848-c. 1918.

Cambridge: Cambridge University Press, 1989.

7. Bleuler E. Lehrbuch der Psychiatrie. Sechste Auflage. Berlin: Julius Springer, 1937.

8. Kraepelin E. Psychiatrie. Ein Lehrbuch für Studirende und Ärzte.

I. Band: Allgemeine Psychiatrie. Sechste, vollständig umgearbeitete Auflage. Leipzig: Johann Ambrosius Barth, 1899.

9. Adityanyee [no initials], Aderibigbe YA, Theodoridis D, Vieweg WVR. Dementia praecox to schizophrenia: The first 100 years. Psychiatry Clin Neurosci 1999;53:437-448.

10. Müller C. Rezeption der Bleuler’schen Schizophrenielehre in der zeitgenössischen Fachliteratur. In Hell D, Scharfetter C, Möller A, eds.

Eugen Bleuler. Leben und Werk. Bern: Hans Huber, 2001.

11. Kline NS. Synopsis of Eugen Bleuler’s Dementia praecox or the group of schizophrenias. New York, N.Y.: International Universities Press, 1952.

12. American Psychiatric Association. Diagnostic and statistical manual: Mental disorders, Washington, DC: American Psychiatric Association, 1952.

13. Tandon R, Nasrallah HA, Keshavan MS. Schizophrenia, “just the facts” 4. Clinical features and conceptualization. Schizophr Res 2009;110:1-23.

14. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. Fourth edition, text revision. Washington, DC: American Psychiatric Association, 2000.

15. Kraepelin E. Psychiatrie. Ein Lehrbuch für Studirende und Ärzte. III. Band. Klinische Psychiatrie. II. Teil. Achte, vollständig umgearbeitete Auflage. Leipzig: Johann Ambrosius Barth, 1913.

16. Kahlbaum KL. Die Katatonie oder das Spannungsirresein. Berlin: Verlag von August Hirschwald, 1874.

17. Kraepelin E. Psychiatrie. Ein kurzes Lehrbuch für Studirende und Ärzte. Vierte, vollständig umgearbeitete Auflage. Leipzig: Verlag von Ambrosius Abel, 1893.

18. Peters UH. The German classical concept of schizophrenia. In Howells JG, editor. The concept of schizophrenia: Historical perspectives.

Washington, DC: American Psychiatric Press, 1991.

19. Berrios GE, Hauser R. The early development of Kraepelin’s ideas on classification: A conceptual history. Psychol Med 1988;18:813-821.

20. Morel B-A. Traité des dégénérescences physiques, intellectuelles et morales de l’espèce humaine. Paris: Baillière, 1857.

21. Hermle L. Die Degenerationslehre in der Psychiatrie. Fortschr Neurol Psychiatr 1986;54:69-79.

22. Alexander FG, Selesnick ST. The history of psychiatry. An evaluation of psychiatric thought and practice from prehistoric times to the present.

Northvale, N.J.: Jason Aronson, 1966.

23. Kraepelin E. Zur Entartungsfrage. Centralblatt für Nervenheilkunde und Psychiatrie 1908;19:745-751.

24. Kraepelin E. Die Erscheinungsformen des Irreseins. Zeitschrift für die gesamte Neurologie und Psychiatrie 1920;62:1-29.

25. Kraepelin E. Hundert Jahre Psychiatrie. Ein Beitrag zur Geschichte menschlicher Gesittung. Berlin: Verlag von Julius Springer, 1918.

26. Kraepelin E. Persönliches. Selbstzeugnisse. Burgmair W, Engstrom EJ, Weber MM, editors. Munich: belleville Verlag, 2000.

27. Van Bakel AHAC. Kraepelin over zichzelf. Een becommentarieerde uitgave van "Persönliches." Amsterdam: Uitgeverij Candide/Wrede Veldt, 2001.

28. Meyer J-E. The fate of the mentally ill in Germany during the Third Reich. Psychol Med 1988;18:575-581.

29. World Health Organization. Schizophrenia. An international follow-up study. New York, N.Y.: John Wiley & Sons, 1979.

30. Boyle M. Schizophrenia. A scientific delusion? Second edition. London: Routledge, 2002.

31. Kuilman M. Klinische en psychopathologische beschouwingen over de endogenie. Een literatuurstudie met betrekking tot de endogene psychosen. Lochem: De Tijdstroom, 1971.

32. Kraepelin E. Letter to Wundt, 1881. Universitätsarchiv Leipzig, WundtNachlaß, letter 299. Quoted in Van Bakel AHAC. Een psychologie van de endogenie. Over de theoretische pijlers van de Kraepeliniaanse nosologie. Tijdschr Psychiatr 1998;40:752-764.

33. Van Praag HM. “Make believes” in psychiatry or the perils of progress.

Clinical & experimental psychiatry monograph no. 7. New York, N.Y.: Brunner/Mazel, 1993.

34. Shorter E, Van Praag HM. Disease versus dimension in diagnosis. Can J Psychiatry 2010;55:59-64.

35. Fischer AA. About concept formation in relation to treatment in schizophrenia. Some considerations from the viewpoint of the theory of science. In Lader MH, editor. Studies of schizophrenia. Ashford: Headley Brothers, 1975.

36. Bentall RP, editor. Reconstructing schizophrenia. London: Routledge, 1992.

37. Escher ADMAC. Making sense of psychotic experiences. Maastricht: University of Maastricht, 2005.

38. Romme MAJ. Een kritische beschouwing over de keuze van de diagnose schizofrenie als uitgangspunt van richtlijnen voor de behandeling.

247

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Tijdschr Psychiatr 2005;47:837-845.

39. Van Os J, Tamminga C. Deconstructing psychosis. Schizophr Bull 2007;33:861-862.

40. Van Praag HM. About the impossible concept of schizophrenia. Compr Psychiatry 1976;17:481-497.

41. Andreasen NC. Understanding schizophrenia: A silent spring? Am J Psychiatry 1988;155:1657-1659.

42. Heinrichs RW. In search of madness. Schizophrenia and neuroscience.

Oxford: Oxford University Press, 2001.

43. Wyatt RJ, Alexander RC, Egan MF, Kirch DG. Schizophrenia, just the facts. What do we know, how well do we know it? Schizophr Res 1988;1:3-18.

44. Tandon R, Keshavan MS, Nasrallah HA. Schizophrenia, “Just the facts”: What we know in 2008. Part 1: Overview. Schizophr Res 2008;100:4-19.

45. Tandon R, Keshavan MS, Nasrallah HA. Schizophrenia, “Just the facts”: What we know in 2008. 2. Epidemiology and etiology. Schizophr Res 2008;102:1-18.

46. Braff DL, Freedman R, Schork NJ, Gottesman II. Deconstructing schizophrenia: An overview of the use of endophenotypes in order to understand a complex disorder. Schizophr Bull 2007;33:21-32.

47. Lenzenweger MF. Schizophrenia: Refining the phenotype, resolving endophenotypes. Behav Res Ther 1999;37:281-295.

48. Cloninger CR. A new conceptual paradigm from genetics and psychobiology for the science of mental health. Aust N Z J Psychiatry 1999;33:174-186.

49. Zubin J, Oppenheimer G, Neugebauer R. Degeneration theory and the stigma of schizophrenia. Biol Psychiatry 1985;20:1145-1148.

50. Fink M, Taylor MA. The catatonia syndrome: Forgotten but not gone.

Arch Gen Psychiatry 2009;66:1173-1177.

51. Susser E, Finnerty MT, Sohler N. Acute psychoses: A proposal for ICD11 and DSM-V: The acute psychoses. Psychiatr Q 1996;67:165-176.

52. Tien AY. Distributions of hallucinations in the population. Soc Psychiatry Psychiatr Epidemiol 1991;26:287-292.

53. Van Os J, Hanssen M, Bijl RV, Vollebergh W. Prevalence of psychotic disorder and community level of psychotic symptoms: An urban-rural

Schizophrenia: Cracked but on the Way to Repair Assen Jablensky, MD, Perth, Australia assen@cyllene.uwa.edu.au

The provocative title and “deconstructivist” discourse on schizophrenia in the article by Blom and van Praag invites a commentary. Basically, the authors’ conceptual analysis is focused on: (i) a juxtaposition of Kraepelin’s original ideas about the nature of dementia praecox and Bleuler’s reformulation of the latter under the name schizophrenia; (ii) a critique of the DSM-IV definition and diagnostic criteria of schizophrenia (it remains unclear why the authors make no reference to ICD-10); and (iii) a proposal of “deconstructing” schizophrenia by means of a “functionalization” of the diagnostic approach.

While agreeing with the general tenor of the article, and 248

comparison. Arch Gen Psychiatry 2001;58:663-668.

54. Van Os J, Kapur S. Schizophrenia. Lancet 2009;374:635-645.

55. Heckers SH. Making progress in schizophrenia research. Schizophr Bull 2008;34:591-594.

56. Kapur S, Mizrahi R, Li M. From dopamine to salience to psychosis linking biology, pharmacology and phenomenology of psychosis.

Schizophr Res 2005;79:59-68.

57. Hudson AJ, Grace GM. Misidentification syndromes related to face specific area in the fusiform gyrus. J Neurol Neurosurg Psychiatry 2000;69:645-648.

58. Blanke O, Mohr C. Out-of-body experience, heautoscopy, and autoscopic hallucination of neurological origin. Implications for neurocognitive mechanisms of corporeal awareness and self-consciousness. Brain Res Rev 2005;50:184-199.

59. Blom JD. A dictionary of hallucinations. New York, N.Y.: Springer, 2010.

60. ffytche DH, Blom JD, Catani M. Disorders of visual perception. J Neurol Neurosurg Psychiatry 2010;81:1280-1287.

61. Vorstman JA, Morcus ME, Duijff SN, Klaassen PW, Heinemande Boer JA, Beemer FA, Swaab H, Kahn RS, Van Engeland H. The 22q11.2 deletion in children: High rate of autistic disorders and early onset of psychotic symptoms. J Am Acad Child Adolesc Psychiatry 2006;45:1104-1113.

62. Van Praag HM, Kahn RS, Asnis GM, Wetzler S, Brown SL, Bleich A, Korn ML. Denosologization of biological psychiatry or the specificity of 5-HT disturbances in psychiatric disorders. J Affect Dis 1987;13:1-8.

63. Van Praag HM, Leijnse B. Neubewertung des Syndroms. Skizze einer funktionellen Pathologie. Psychiatr Neurol Neurochir 1965;68:50-66.

64. Van Praag HM, De Kloet R, Van Os J. Stress, the brain and depression.

Cambridge: Cambridge University Press, 2004.

65. Van Praag HM. Anxiety/aggression-driven depression. A paradigm of functionalization and verticalization of psychiatric diagnoses. Prog Neuropsychopharmacol Biol Psychiatry 2001;12:28-39.

66. Bleuler E. Das autistisch-undisziplinierte Denken in der Medizin und seine Überwindung. Vierte Auflage. Berlin: Julius Springer, 1927.

with many of the authors’ specific points, I find some of their statements concerning Kraepelin’s work to be tenuous or wanting in factual accuracy. They seem to overplay the influence of the mid-19th century theory of degeneration on Kraepelin’s outlook. Indeed, like many of his contemporaries, Kraepelin used arguments broadly derived from degeneration theory but he remained ambivalent towards its highly speculative character (1). The authors’ claim that the placement of dementia praecox under the heading of mental degeneration (psychische Entartungsprocesse) in the 4th edition of Kraepelin’s textbook was definitive needs to be corrected. In fact, dementia praecox was removed from “degeneration” and placed under “metabolic diseases” in the 5th edition of 1896 (2). Far from being an inveterate “degenerationist,” Kraepelin was much more “Darwinian” in his theoretical allegiance and can be regarded, with some justification, as the progenitor of evolutionary psychiatry.

In one of his late articles – Patterns of Mental Disorders (Die Erscheinungsformen des Irreseins) (3), he referred to

Jan Dirk Blom Assen andJablensky Herman M. van Praag

phylogenetically ancient, preformed brain mechanisms of reaction that could be released by pathological processes and find expression in three hierarchically ordered classes, or “registers” of symptoms and syndromes, including affective, schizophrenic and encephalopathic forms. This construct bears close resemblance to Hughlings Jackson’s theory of dissolution of higher nervous function (4) with which Kraepelin undoubtedly was familiar. But, while heeding to such meta-theories, Kraepelin essentially remained an empirical scientist in his attempts at “bringing order to the confusing diversity of mental disorders” and “understanding their essential structure” (3). Thus, he adopted Kahlbaum’s proposal for a syndrome-course entity as the basic unit of a ‘natural’ classification of mental disorders but elaborated it further by blending into it the role of pathoplastic factors including, above all, personality traits, age and cognition.

Kraepelin’s concept of dementia praecox was conceived, in its early versions, as an amalgamation of Kahlbaum’s catatonia, Hecker’s hebephrenia, and Morel’s dementia paranoides – all three developing in the course of time an irreversible pattern of cognitive deficit and personality deterioration. The criterion of outcome, defined in terms of “curability” and “incurability” was the cornerstone of his nosological system and was largely a matter of convenience – he realized that knowledge of aetiology and brain pathology at the time could offer little guidance, while outcome was a variable accessible to the clinician and could be described with considerable refinement. Later on, Kraepelin acknowledged the diversity of the clinical pictures subsumed under dementia praecox and articulated nine different “clinical forms,” ranging from dementia praecox simplex to circular, agitated and periodic forms, thus anticipating what today is labelled as schizoaffective disorder. This certainly widened the scope of the original concept, and Kraepelin was faced with the boundary issue between dementia praecox and manic-depressive insanity. In his 1920 article (3), he acknowledged that “it is becoming increasingly clear that we cannot distinguish satisfactorily between these two illnesses and this brings home the suspicion that our formulation of the problem may be incorrect.” The solution of the problem was in recognizing that “the affective and schizophrenic forms of mental disorder do not represent the expression of particular pathological processes, but rather indicate the areas of our personality in which these processes unfold…it is conceivable that these two illnesses may…at times spread beyond the framework of their usual syndromes.” This was the first acknowledgement of the existence of a continuum of psychoses, con-

sistent with his hypothesis about hierarchically structured “registers” of syndromes that might recombine in their clinical presentation in a “lawful” manner, determined by the hypothetical extent of “destruction of nerve tissue” – the “encephalopathic” forms could easily incorporate features of the schizophrenic and affective “registers,” but the reverse was not true – i.e., a primary affective disorder could only occasionally attract symptoms belonging to the underlying “schizophrenic” register and never symptoms from the “encephalopathic” register. This was retained as the Schichtenregel (the strata rule - that has been completely lost in the DSM “atheoretical approach” to psychopathology). Thus, Kraepelin’s long journey from the initial formulation of dementia praecox to the later and wider view of the complexity of the manifestations of the “forms” of mental illness remain pertinent for the research agenda today, along with Bleuler’s reformulation of the concept to include non-psychotic (latent) forms and the important distinction between fundamental and accessory symptoms.

Regarding the statement of Blom and van Praag that Kraepelin’s “degenerationist” approach to the classification of psychoses cannot be reproduced via alternative approaches, I should mention that back in 1987, I was granted access to the Kraepelin archive at the Munich Department of Psychiatry. With my collaborators (5) we selected one volume of Kraepelin’s counting cards (Zählkarten) filled in for all 721 admissions to the department during the year 1908, the time when his nosological system was already mature. Notably, only 53 (7.4%) of the patients were diagnosed as dementia praecox, as compared to 134 (18.6%) cases of manic-depressive insanity. The majority (66.3%) of these cases were first admissions, and with the exception of 13 forensic patients, were voluntary admissions. It is important to note that Table 1 in the Blom and van Praag article, which shows increasing proportions of inpatients being diagnosed as dementia praecox from 1892 to 1900 and is claimed to reflect “the increasing looseness of Kraepelin’s diagnostic criteria,” is based on data from the Heidelberg clinic where all admissions were involuntary (Kraepelin left Heidelberg for Munich in 1903). We analyzed the content of the 187 cards for the two disorders by coding the symptoms and any other recorded clinical features using the syndrome checklist and glossary definitions of the Present State Examination (PSE) and processed the data with the CATEGO computer classification algorithm which assigned ICD-9 diagnoses to the cases (6). We found an overall concordance of 80.2% between Kraepelin’s original diagnoses and the computer-assigned ICD-9 diagnoses.

Furthermore, stepwise discriminant analysis revealed that 249

Schizophrenia: Schizophrenia: authors' Cracked It’s Broken response butand on the It Can’t Way to Be Repair Fixed

flat affect, fantastic delusions and catatonic signs had the highest discrimination weights in the separation of dementia praecox from manic-depressive insanity (5). At a next step, we applied grade of membership analysis (a form of latent class analysis which generates “pure types”) to obtain a purely statistical grouping of the patients based on their symptom profiles and ignoring the original diagnoses (7).

This independent taxonomic analysis produced three “pure types,” clearly corresponding to bipolar disorder, recurrent unipolar depression, and dementia praecox, suggesting a consistent “goodness of fit” between Kraepelin’s typology and the actual clinical material on which it was based.

Finally, is the diagnostic concept of schizophrenia really “broken” beyond repair? Despite the ever-increasing volume of research data, the search for causes of schizophrenia remains inconclusive and this raises doubts about the validity of the diagnostic concept as presently defined.

Such doubts are not without reason. However, simply dismantling the concept is unlikely to result in an alternative model that could account for the host of clinical phenomena and research data consistent with a working hypothesis of schizophrenia as a broad syndrome comprising aetiologically different subtypes, as anticipated by Bleuler. The dissection of the syndrome with the aid of intermediate phenotypes is beginning to be perceived as a viable strategy, and a recent proposal (8) to link genomics and neural circuit functioning as “hubs” for a range of

phenotypes cutting across the conventional classificatory categories may be a signpost for future developments. As suggested by Blom and van Praag, the mapping of clinical phenomenology on specific brain dysfunction is becoming feasible and the resulting functional psychopathology may in the future help recast the present nosology (9).

Functionalization Revisited.

A Reply to Jablensky’s “Schizophrenia: Cracked but on the Way to Repair”

criteria. Unfortunately, however, such a clinical and statistical “goodness of fit” does not suffice to remedy the lack of validity of the schizophrenia concept. On the basis of Jablensky’s work we are convinced that, in clinical practice, Kraepelin applied his own typology of psychotic disorders with unwavering rigor, and that he indeed lent the highest discrimination weights to flat affect, fantastic delusions, and catatonic signs in his attempts to distinguish between dementia praecox and manic-depressive insanity. And yet we wonder whether Kraepelin himself was aware of the extent to which he relied on this diagnostic algorithm. If so, he might well have designated the symptoms at hand as “first rank symptoms” in the vein of Kurt Schneider, or he might at least have mentioned them as symptoms of particular diagnostic value – which he never did.

But let us assume, for argument’s sake, that the triad of flat affect, fantastic delusions, and catatonic signs might indeed help us to devise a nosology of psychotic disorders similar to Kraepelin’s, and that we would

Jan Dirk Blom and Herman M. van Praag

We are grateful to Professor Jablensky for bringing to our attention his own reanalysis of the data derived from Kraepelin’s Zählkarten, the outcome of which beautifully demonstrates the remarkable concordance between the diagnoses established by Kraepelin in 1908 and the way they can be established on the basis of ICD-9 criteria (1). We consider that concordance as further proof of the extent to which our current schizophrenia concept is indebted to Kraepelin’s nosological work, not only when it is operationalized in terms of DSM criteria but also when this is done in terms of ICD 250

References 1. Hoff P. Kraepelin and degeneration theory. Eur Arch Psychiatry Clin Neurosci 2008; 258 (Suppl 2): 12-17.

2. Kraepelin E. Psychiatrie. Ein Lehrbuch für Studirende und Aerzte.

Fünfte, vollständig umgearbeiterte Auflage. Leipzig: Barth, 1896.

3. Kraepelin E. Die Erscheinungsformen des Irreseins. Zeitschrift für die gesammte Neurologie und Psychiatrie 1920; 62:1-29. English translation

by Marshall H. patterns of mental disorder. In Hirsch SR, Shepherd M, editors. Themes and Variations in European Psychiatry. Bristol: John Wright & Sons, 1974: pp. 7-30.

4. Jackson J Hughlings. Remarks on evolution and dissolution of the nervous system. J Ment Sci 1887; 33:25-48.

5. Jablensky A, Hugler H, von Cranach M, Kalinov K. Kraepelin revisited: A reassessment and statistical analysis of dementia praecox and manicdepressive insanity in 1908. Psychol Med 1993; 23:843-858.

6. Wing JK, Cooper JE, Sartorius N. Measurement and Classification of Psychiatric Symptoms. An Instruction Manual for the PSE and Catego Program. London: Cambridge University Press, 1974.

7. Jablensky A, Woodbury MA. Dementia praecox and manic-depressive insanity in 1908: A Grade of Membership analysis of the Kraepelinian dichotomy. Eur Arch Psychiatry Clin Neurosci 1995; 245:202-209.

8. Cuthbert BN, Insel TR. Toward new approaches to psychotic disorders: The NIMH Research Domain Criteria project. Schizophr Bull 2010; 36:1061-1062.

9. Jablensky A. The diagnostic concept of schizophrenia: Its history, evolution, and future prospects. Dialogues Clin Neurosci 2010; 12:271-287.

Jan Dirk Blom and Herman M. van Praag

thus be able to “reproduce” the operational criteria of dementia praecox (or “schizophrenia”) without taking recourse to any speculations about an unavoidable unfavorable outcome, whether inspired by degenerationism or not. Would that help us to increase the validity of the dementia praecox concept? Or of our current schizophrenia concept? And even more importantly, perhaps, would it alter the historical facts about the concept’s indebtedness to Kraepelin’s degenerationist outlook?

Jablensky expresses his concern that we may well have overplayed the influence of the 19th-century degeneration theory on Kraepelin’s work. We will leave it up to the reader to decide whether that is what we did. We agree with Jablensky that Kraepelin was thoroughly darwinian in his theoretical allegiance. He was introduced to evolutionary thought by his brother Karl while he was still in elementary school, only a few years after the first German translation of the Origin of Species had been published.

That introduction, along with the enthusiasm for evolutionary thought expressed by his later teacher Wilhelm Wundt, sparked a life-long fascination with the subject (2). But at the time evolutionary thought was tightly interwoven with the degeneration theory, and Kraepelin freely mixed up elements from both discourses in his theoretical work. This is especially clear in his later writings, such as his 1920 article Die Erscheinungsformen des Irreseins (“The manifestations of madness”), in which he unfolds his ideas on human evolution and on the role of remnants from earlier developmental stages in the mediation of psychopathological symptoms (3). An overview of his ideas on the nature and causes of degeneration is to be found in his 1908 essay Zur Entartungsfrage (“On the question of degeneration”) (4), as well as in his ego document, Persönliches (5), written only a few years before his death. It is unfortunate that van Bakel’s richly annotated translation of that ego document (2) was only published in Dutch, because in that edition we find an extensive treatment of Kraepelin’s reflections on the causes and nature of degeneration, as well as on the threats it allegedly posed to public health. It may be true that Kraepelin remained ambivalent about the doctrine’s speculative character, and that empirical science is the field with which he deserves to be associated foremost in our collective memory. After all, he was an exceptionally gifted and versatile man: a clinician, empirical scientist, taxonomist, progenitor of evolutionary psychiatry, transcultural psychiatrist, philosopher, poet, musician, husband, father, and networker avant la lettre (6). But however ambivalent he may have been about the degeneration theory, it did not keep him

from writing extensively on the subject, and from publicly warning the German government that something should be done about it to avert its disastrous effects.

All in all we are grateful to Jablensky for his thoughtful commentary on our conceptual analysis of the biomedical schizophrenia concept. Elsewhere, the concept was designated by him as “an overinclusive diagnostic category for which no specific biological substrate is identifiable, probably because of admixture between different underlying disease subtypes” (7). That characterization pretty much sums up our own position on the subject, although we would like to add that at present even the existence of “underlying disease subtypes” must be considered uncertain. Maybe, and hopefully, such subtypes will be identified in the near future. But for as long as the concept has been around, clinicians and researchers have been forced to do their jobs without having them at their disposal. For that reason, the method of functionalization that we advocate seeks to link psychic dysfunctions rather than “disease subtypes” to their biological determinants. This method, described in some detail in our paper (8), does not involve a quest for a novel nosological concept but rather a sophistication of our current diagnostic approach. In the everyday practice of cardiologists a diagnosis of myocardial infarction serves as a starting point for a detailed analysis of its biological determinants. Functionalization seeks to allow for similar analyses in the area of psychiatric symptoms, thus paving the way for tailor-made treatments for individual patients, aimed at alleviating their specific symptoms and psychic dysfunctions rather than broad “disease packages” such as “schizophrenia” or any of its alleged “endophenotypes.”

References 1. Jablensky A, Hugler H, von Cranach M, Kalinov K. Kraepelin revisited: A reassessment and statistical analysis of dementia praecox and manicdepressive insanity in 1908. Psychol Med 1993;23:843-858.

2. van Bakel AHAC. Kraepelin over zichzelf. Een becommentarieerde uitgave van "Persönliches." Amsterdam: Uitgeverij Candide/Wrede Veldt, 2001.

3. Kraepelin E. Die Erscheinungsformen des Irreseins. Zeitschrift für die gesamte Neurologie und Psychiatrie 1920;62:1-29.

4. Kraepelin E. Zur Entartungsfrage. Centralblatt für Nervenheilkunde und Psychiatrie 1908;19:745-751.

5. Kraepelin E. Persönliches. Selbstzeugnisse. Burgmair W, Engstrom EJ, Weber MM, eds. Munich: belleville Verlag, 2000.

6. Blom JD. Deconstructing schizophrenia. An analysis of the epistemic and nonepistemic values that govern the biomedical schizophrenia concept. Amsterdam: Boom, 2003.

7. Jablensky A. Resolving schizophrenia’s CATCH 22. Nat Genet 2004;36: 674-675.

8. Blom JD, Van Praag HM. Schizophrenia: It’s broken and it can’t be fixed.

A conceptual analysis at the centenary of Bleuler’s Dementia praecox oder Gruppe der Schizophrenien. Isr J Psychiatry Relat Sci 2011;48:229-247.

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Isr J Psychiatry Relat Sci - Vol. 48 - No 4 (2011)

Religion and Psychological well-being and distress in israeli Jews: Findings from the Gallup World Poll Jeff Levin, PhD, MPH Professor of Epidemiology and Population Health and Director of the Program on Religion and Population Health, Institute for Studies of Religion, Baylor University, Waco, Texas, U.S.A

ABSTRACT Background: This study investigates religious predictors of psychological well-being and psychological distress in a five-year national probability sample of Israeli Jews (N = 4,073). Data were taken from the 2006-2010 annual surveys of Israel as a part of the multinational Gallup World Poll.

Methods: Analyses identified religious predictors of five-item scales of well-being and distress, adjusting for effects of several covariates, including health satisfaction.

Additional analyses examined differences in religion, well-being and distress, and their interrelationships by categories of Jewish religious identity and observance (hiloni, masorti, dati, and haredi).

Results: Levels of religiousness and of well-being increase as one moves “rightward” across Jewish observance. Selfratings of importance of religion and religious attendance are significantly associated with well-being, overall, and a religious harmony scale is associated with both wellbeing (positively) and distress (inversely), and with these measures’ respective items, overall and across Jewish observance.

Conclusions: Religious indicators are significant predictors of both psychological well-being and psychological distress in Israeli Jews, regardless of Jewish religious observance.

INTRODUCTION Over two decades of research has identified religious correlates or determinants of mental health and psycho-

logical well-being (1). This association works two ways: greater religiousness, variously assessed, as protective against psychological distress and psychiatric diagnoses (e.g., mood disorders such as depressive symptoms and anxiety) and promotive of psychological well-being (e.g., happiness, life satisfaction, positive affect). As in all epidemiologic studies, these findings are expressed on average and at the population level; there are, of course, exceptions to these trends. This literature also includes findings from clinical and community studies, social and behavioral research by gerontologists, and other population-based research by psychiatric and psychosocial investigators.

Despite the volume of work that has accumulated, the research literature is homogeneous in an important way.

Published results overwhelmingly draw on samples of Christians, of one denomination or another, from North America. There are fewer international studies and very few studies of Jews, from Israel or the diaspora. This is ironic, as important early research on religion and mental health derived from samples with substantial Jewish respondents, such as the Midtown Manhattan Study of the 1950s (2).

Research on religious factors in Jewish mental health conducted since then comprises population-based studies of diagnosed psychiatric disorders and self-reports of dimensions of psychological well-being and distress.

U.S. studies are few and mostly compare prevalence rates between Jews and non-Jews (3); similarly, Israeli studies tend to compare population subgroups, such as immigrant and native-born Jews (4, 5). This work is instructive, as mental health is a significant predictor of health-related quality of life among adult Israeli Jews (6). Yet while Jewish self-identification is a variable in these studies, for the sake of comparisons, Jewish religious beliefs or practices are not a focus of analysis.

Address for Correspondence: Dr. Jeff Levin, Institute for Studies of Religion, Baylor University, One Bear Place #97236, Waco, TX 76798, U.S.A. jeff_levin@baylor.edu.

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A few Israeli studies have explored the impact of religiousness, broadly defined, on indicators of mental health or well-being. A longitudinal study of retirees found a self-rating of religiosity, defined as observance of religious rituals, to be mildly protective against psychological distress (7). This result was complicated by the observation that religiosity itself increased in response to declines in well-being. A national probability survey of adult Israeli immigrants found that religiosity, defined as observance of religious traditions, was strongly associated with a measure of life satisfaction among immigrants both from the West and from the former Soviet Union (8).

Stratification of respondents by categories of Jewish identity and observance familiar in Israel but not in the diaspora (e.g., secular, traditional, religious, Orthodox) yields additional information, but inconsistent results.

A study of elderly Israelis found greater life satisfaction and health among “religiously observant” rather than “traditionally observant” respondents (9). By contrast, in a nationally representative sample of middle-aged urban Israeli Jews, “observant” (i.e., traditional) Jews reported lower scores than “secular” Jews on the SF-36 mental health scale (10). In a sample of Jewish Israeli college students, scores on a Jewish religious beliefs index were associated with greater well-being and less distress, but only among “secular” and “religious” Jews, not among an intermediate category of “traditional” Jews (11).

Studies among the most Orthodox and ultra-Orthodox categories of Israeli Jews suggest some level of protection, epidemiologically, for mental health and well-being. In a study of matched “secular” and “religious” kibbutzim, religious kibbutz members reported a greater “sense of coherence” and less hostility, leading the authors to conclude that “Jewish religious observance may enhance the formation of certain protective personality characteristics” (12, p. 185). Likewise, in a sample of West Bank and former Gaza settlers, the higher the religiosity the less the demoralization, according to the PERI-D Scale (13). Respondents who self-identified as “national-religious” or “national-ultrareligious” had significantly less psychological distress than either “traditional” or “secular” Jews. In another kibbutz study, belonging to a “religious” rather than “secular” community served to mitigate psychological distress and promote better health (14). The authors concluded that “the regulative and integrative function of belonging to a religious community” (p. 119) contributed most to its salutary impact.

Studies of diaspora Jews mostly validate the relative protection afforded Orthodox and ultra-Orthodox Jews for various mental health outcomes. Most notable is a recent series of psychological studies conducted

by Rosmarin and colleagues in the U.S. This work has established that higher levels of trust in God (15), beliefs affirming God’s benevolence (16), general religiousness and religious practices (17), and gratitude (18) are significantly protective against anxiety and depression among Orthodox Jews. Moreover, high levels of spiritual struggles are associated with poorer physical and mental health among Jews, in general, but with better physical and mental health among the Orthodox (19). An earlier series of British studies of anxiety (20), stress (21), and depression (22) among “strictly orthodox” and “traditionally orthodox” Anglo-Jews explored significant themes related to sociocultural context, but did not identify consistent epidemiologic differences between these groups.

Whether these findings translate to Israel, or to elsewhere in the diaspora, is an open question for several reasons. First, the possibility of “a strong taboo surrounding mental illness” among the ultra-Orthodox (23, p. 1516) may complicate interpretation of results due to underreporting of symptoms. To be fair, if true, this may affect some types of studies and not others, depending upon the mode of assessment; moreover, it is unclear that this would be more or less salient an issue in Israel. Second, the possibility of gender differences in mental health or in putative effects of religion for mental health among the haredim has been only minimally explored (24). Third, there is the confusing matter of how U.S. and diaspora categories of religious identity, observance, and affiliation do and do not correspond to Israeli categories (25).

Finally, there is evidence that more religiousness, regardless of affiliation or level of observance, is salutary for Jewish mental health. A small study of Jewish adults from Washington, DC, found that religious indicators (interest in broad Jewish topics, commitment to religious traditions, holiday celebration, Jewish organizational activism, and personal belief in God) were associated with higher scores on one or more well-beings scales (26).

Each group of studies tells us something important, but cannot tell us other things. Some make simple comparisons between Jews and non-Jews, others look at intra-Jewish differences, according to various taxonomies. A few examine effects of religiousness among Jews, but most do not. Where they do, religious assessment is minimal. Not all focus on Israeli Jews. Not all are based on large national probability samples. Studies typically 253

RELIGION & WELL-BEING IN ISRAELI JEWS

do not assess both positive and negative polarities of well-being. In sum, we must piece together evidence from various sources, each contributing something but none providing a full picture.

The present study makes use of an underutilized data resource in order to extend this prior work.

Serendipitously, this source, the Israel sample of the Gallup World Poll (GWP), contains four religious measures and respective indices of psychological well-being and distress, thus enabling a closer look at this subject with populationwide data. While these measures assess neither the fullness of religious experience, Jewish or otherwise, nor the many dimensions and domains of mental health, they provide an opportunity to examine their interrelationship among Israelis and Jews in a way heretofore impossible. Inclusion of a categorical measure of Jewish religious identity and observance (with distinct self-reported categories of hiloni, masorti, dati, and haredi; for an explanation, see Measures) also permits a stratified look at this issue and enables validation of recent studies.

Based on prior results, modest as they are, and on the extensive literature on religion and mental health, a few findings are expected. First, greater religiousness is expected to be promotive of well-being and protective against distress. There is mixed evidence from prior studies as to whether certain religious measures exhibit contemporaneous or longitudinal effects on specific types of psychological outcomes in particular populations (27).

In light of prior research, a salutary effect is anticipated.

However, the Israeli experience differs in norms of Jewish religious expression from the diaspora, including the U.S. Socioeconomic and cultural correlates of religiousness, even how religiousness is defined, differ substantively and incorporate social and political realities and tensions that may deleteriously impact on well-being. In other words, the construction of Jewish identity in Israel differs from the denominational typology found in the diaspora. The categories used in the GWP do not map easily onto respective Jewish movements in, for example, the U.S. Religious involvement thus may not be as uniformly salutary exposure for well-being, epidemiologically, as it appears to be in some U.S. studies. Religion may be more or less salient a correlate of well-being or distress depending upon the extent of one’s involvement in Judaism.

Second, less research has been conducted on the mental health impact of religious beliefs, attitudes, or practices relative to studies of overall self-reports of practicing or observing Judaism. So for the religious items included in the GWP battery (see Measures), the 254

present study is somewhat exploratory. Nonetheless, affirmation of greater religiousness, however defined — valuation of religion, attendance at worship service, belief in God — is expected to be salutary, whether through association with well-being or through protecting against distress.

Third, it is also anticipated that the salience of these effects — that is, their magnitude and statistical significance — will be more pronounced as one moves “rightward” across categories of Jewish religious identity and observance (i.e., from secular to Orthodox). Based on prior findings, including the studies of Rosmarin and colleagues, there is reason to expect something of a “dose-response” gradient for well-being and distress as well as for the impact of religiousness on these outcomes. Recent U.S. findings confirm such a gradient for self-assessments of physical health, such that salutary religious effects were observed primarily among Orthodox and Conservative Jews and less so or not at all among Reconstructionist, Reform, or secular Jews (28).

In the present study, this would imply greater well-being and less distress moving from hiloni to haredi Jews, and stronger associations of religion with well-being and distress moving in the same direction.

METHODS The Gallup World Poll (GWP)

These data come from the Israeli sample of the Gallup World Poll (GWP), a continual cross-sectional survey of the adult population of over 150 countries using randomly selected, nationally representative samples (29). Most GWP samples comprise 1,000 people per country per round and use a standard set of core questions, supplemented by additional country-specific or region-specific items. These surveys have been conducted annually, with plans for quarterly surveys in many countries. Data are generally collected via face-to-face interviews, although in some countries telephone interviews are used.

Data were collected in Israel in July, 2006 (N = 1,002); August, 2007 (N = 1,001); September-October, 2008 (N = 1,001); October-November, 2009 (N = 1,000); and October-November, 2010 (N = 1,000). All interviews were conducted in person in Hebrew (or in Arabic or Russian, if needed). The present study uses a combined five-year sample (N = 5,004) and limits analyses to the survey’s Jewish respondents (N = 4,073), constituting 81% of the Israeli sample aged 15 and over. For selected analyses, the available sample size is smaller, due to three

Jeff Levin

study variables being available only in certain rounds of data collection (explained in Data Analysis). To be clear, each year’s GWP is a separate cross-sectional survey; this is not a single multi-wave panel and thus all respondents in the combined sample are unique.

Typical of large-scale social surveys, the GWP contains hundreds of items and scales assessing domains of social, political, and economic life. The GWP is best known for its many indices used in aggregate (countrylevel) analyses, such as national rankings of personal economy, corruption, violence, food and shelter, law and order, optimism, and other constructs (30), as well as in studies of global health and its determinants (31).

The GWP also contains item sets assessing psychological well-being and distress, personal health, and religiosity—thus enabling its use here.

The GWP is a promising but largely untapped resource for systematic empirical research, both multinationally and within respective countries, such as Israel. There is also, incidentally, a distinct “Palestinian Territories” sample, enabling future comparative research. The GWP data are not publically available, but accessible to a select group of consulting research scholars, including the present author, who has a research interest in the health of Jews. The GWP’s Israeli sample has, to now, been mostly unutilized. The present paper, it is expected, will be the first of a series of analyses using these data.

Measures

The GWP Israeli sample contains a few binary religious items. These include importance of religion (“Is religion an important part of your daily life?”; recoded as: 0 = no, 1 = yes), religious attendance (“Have you attended a place of worship or religious service within the last seven days?”; recoded as: 0 = no, 1 = yes), and God directly involved (“Do you believe God is directly involved in things that happen in the world, or not?”; recoded as: 0 = no, 1 = yes).

Five additional Likert items (coded from 1 = strongly disagree to 5= strongly agree) were combined into a religious harmony scale (α = .69): “I always treat people of other religious faiths with respect,” “Most religious faiths make a positive contribution to society,” “I would not object to a person of a different religious faith moving next door,” “People of other religious faiths always treat me with respect,” and, “In the past year, I have learned something from someone of another religious faith.”

There is also a measure of Jewish religious identity and observance (“What specific Jewish denomination are you?”), recoded as: 1 = hiloni (secular; 48.6% of the sam-

ple), 2 = masorti (traditional; 33.2%), 3 = dati (religious; 14.1%), 4 = haredi (Orthodox; 4.1%). These categories, as noted, are not the same as the Jewish movements or “denominations” found in the U.S. and throughout the diaspora. Haredi means more or less what it does elsewhere: religious Jews subscribing to ultra-Orthodox life styles. Dati would be closer to the more strictly Torahobservant side of the diaspora’s Modern Orthodox, but is culturally, socioeconomically, and politically distinct from haredi. Israelis who self-identify as masorti are traditionally religious Jews of non-Ashkenazi origin; there is also a small Masorti (Conservative) movement in Israel, but that means something quite different. Finally, hiloni Jews, while institutionally unaffiliated or non-religious, nonetheless may be considerably more observant in some ways than liberal affiliated Jews in the diaspora. If this taxonomy is confusing to non-Israelis, it just underscores that these categories are not equivalent to the familiar Jewish denominations found in the West. Based on other estimates (32), the proportional breakdown in this sample is representative of the overall population, although underrepresentation of haredim remains a persistent issue in mental health studies.

Outcome measures include two five-item indices constructed for the present study. A psychological well-being scale (α = .52) was constructed from five items developed by the GWP to assess “positive experience,” or “respondents’ experienced wellbeing on the day before the survey.”

As utilized in the present study, this measure comprises a summary of scores on these items (“Did you feel wellrested yesterday?,” “Were you treated with respect all day yesterday?,” “Did you smile or laugh a lot yesterday?,” “Did you learn or do something interesting yesterday?,” and, “Did you experience the following feelings during a lot of the day yesterday? How about enjoyment?”; each recoded as: 0 = no, 1 = yes). Likewise, a psychological distress scale (α = .56) was constructed from five items developed by the GWP to assess the opposite polarity of well-being, termed “negative experience.” These items (“Did you experience the following feelings during a lot of the day yesterday?

How about physical pain?,” “How about worry?,” “How about sadness?,” “How about depression?,” and, “How about anger?”) were recoded and summarized in the same fashion as in the well-being scale. These indices and their respective questions have been used in research on global prosperity and economic development (33).

Covariates include a single-item self-assessment of health satisfaction (“Are you satisfied or dissatisfied with your personal health?”; recoded as: 0 = dissatisfied, 1 = sat255

RELIGION & WELL-BEING IN ISRAELI JEWS

subsamples (34). To facilitate comparison of regression effects across Jewish categories, regression models were also run for the overall sample including a multiplicative interaction term for the Jewish religious identity and observance variable and the respective religious indicator. This provides a de facto test of subgroup differences, indicated by a statistically significant interaction.

A confusing feature of the GWP Israeli data is that not all measures are available at every round of data collection. In the present study, this comes into play as follows. For all analyses reporting findings from the overall sample, in Tables 1 through 3, the full five-year combined sample of Israeli Jews is used (N= 4,073). For all analyses stratifying by Jewish religious identity and observance in these tables, four years of combined data are used, from 2007-2010 (N = 3,247); this variable was not present in the 2006 survey. Two additional sample limitations: the God directly involved variable was only present in the 2009 sample (N = 836) and the religious harmony scale items were only available in the combined 2008-2009 sample (N = 1,596), the latter affecting Table 4 and applicable rows in the other tables.

isfied) and four sociodemographic variables: age (in years), gender (recoded as: 0 = male, 1 = female), marital status (recoded as: 0 = not married and living together, 1 = married and living together; collapsed from 6 categories), and education (recoded as: 1 = elementary: through 8 years, 2 = secondary/tertiary: 9-15 years, 3 = college degree).

Data Analysis

All analyses were conducted using SAS version 9.2.

Descriptive statistics and ANOVA results for differences in study variables by categories of Jewish religious identity and observance were obtained using the UNIVARIATE and GLM procedures, respectively. Psychometric validation of the several scales was conducted using the CORR procedure.

A strategy of two-step OLS regression was used to model effects of the four religious measures separately on each of the two outcome variables, using the REG procedure. In Model I, gross (unadjusted) or bivariate associations were examined. In Model II, each respective analysis was rerun, adding in measures of the covariates (health satisfaction, age, gender, marital status, education), producing net (adjusted) or multivariable associations. Analyses were conducted separately for the wellbeing and distress scales in relation to each religious variable. Results are presented both overall and separately for each category of Jewish religious identity and observance.

Both unstandardized (b) and standardized (β) regression coefficients are reported, enabling comparisons both across different models in different subsamples and for respective religious indicators and within respective

RESULTS For nine of eleven study variables, statistically significant differences are observed across the four categories of Jewish religious identity and observance (see Table 1).

For three of the religious variables (importance of religion, religious attendance, and God directly involved), there is a significant gradient such that scores steadily

Table 1. Descriptive Statistics of Study Variables, Overall and by Categories of Jewish Religious Identity and Observance* Overall Study Variables

Mean

Haredi (sd)

Mean

Dati (sd)

Mean

Masorti (sd)

Mean

Hiloni (sd)

Mean

(sd)

F

p

Importance of Religion

.41

(.49)

.98

(.12)

.92

(.27)

.60

(.49)

.11

(.31)

826.6

<.0001

Religious Attendance

.33

(.47)

.89

(.31)

.80

(.40)

.42

(.49)

.10

(.30)

500.1

<.0001

God Directly Involved

.75

(.43)

1.00

(.00)

.99

(.10)

.92

(.28)

.56

(.50)

62.46

<.0001

Religious Harmony Scale

16.20

(4.17)

13.61

(4.86)

14.81

(4.69)

16.59

(3.88)

16.63

(3.91)

20.64

<.0001

Psychological Well-Being Scale

3.34

(1.34)

3.63

(1.33)

3.41

(1.39)

3.32

(1.32)

3.27

(1.31)

3.32

.019

Psychological Distress Scale

1.46

(1.34)

1.25

(1.44)

1.56

(1.36)

1.52

(1.36)

1.52

(1.30)

1.74

.157

Health Satisfaction

.80

(.40)

.79

(.41)

.81

(.39)

.83

(.37)

.78

(.41)

3.25

.021

Age

40.14

(16.3)

34.20

(12.1)

39.15

(16.0)

39.63

(16.1)

41.79

(16.5)

12.06

<.0001

Female

.54

(.50)

.52

(.50)

.49

(.50)

.54

(.50)

.55

(.50)

1.75

.154

Married

.58

(.49)

.78

(.42)

.65

(.48)

.57

(.50)

.56

(.50)

11.17

<.0001

Education

2.25

(.49)

2.26

(.46)

2.18

(.46)

2.17

(.46)

2.32

(.50)

24.56

<.0001

*ANOVA results for differences by Jewish religious affiliation in each study variable.

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Jeff Levin

Table 2. Regressions# of Psychological Well-Being Scale on Religious Indicators, Overall and by Categories of Jewish Religious Identity and Observance Overall Religious Indicators$

Haredi

Dati

Masorti

Hiloni

β (b)

se

β (b)

se

β (b)

se

β (b)

se

β (b)

se

Model I: Gross resultsd

.04 (.10)*

.05

.01 (.13)

.96

.11 (.54)*

.25

.02 (.05)

.09

-.03 (-.11)

.12

Model II: Net resultsd

.04 (.11)*

.05

.02 (.18)

.93

.10 (.53)*

.26

.02 (.07)

.09

-.01 (-.05)

.12

Model I: Gross results&

.05 (.14)**

.05

-.05 (-.23)

.41

.08 (.27)

.17

.03 (.07)

.09

-.00 (-.01)

.12

Model II: Net results

.05 (.14)**

.05

-.03 (-.11)

.41

.09 (.32)

.18

.04 (.11)

.09

.00 (.02)

.12

Importance of Religion

Religious Attendance &

God Directly Involved Model I: Gross results

.01 (.02)

.11

---

---

-.06 (-.74)

1.3

.02 (.08)

.34

-.02 (-.05)

.13

Model II: Net results

.02 (.07)

.11

---

---

-.04 (-.49)

1.4

.03 (.17)

.33

-.02 (-.05)

.14

Model I: Gross results&

.11 (.04)***

.01

.31 (.08)*

.04

.13 (.04)*

.02

.08 (.03)

.02

.14 (.05)***

.01

Model II: Net results

.12 (.04)***

.01

.39 (.10)*

.04

.14 (.04)*

.02

.08 (.03)

.02

.16 (.05)***

.01

Religious Harmony Scale &

Separate analyses for each of the four religious measures.

Model I = gross (unadjusted) results; Model II = net (adjusted) results, controlling for effects of health satisfaction, age, gender, marital status, and education.

# $

decline as one moves “leftward” in terms of religious observance, from haredi (Orthodox) to dati (religious) to masorti (traditional) to hiloni (secular) Jews. The big drop off is mostly between the Orthodox and religious Jews and the other two categories. For the religious harmony scale, the gradient goes in the opposite direction: hilonim and masortim are most likely to affirm religious tolerance and respect, and datim and haredim less so.

The two outcome measures show mixed evidence of religious differences. For psychological well-being, as hypothesized, there is a modest but distinct and statistically significant gradient from the most to the least religious. Scores decline from haredim (Mean = 3.63) to datim (Mean = 3.41) to masortim (Mean = 3.32) to hilonim (Mean = 3.27); these are not large differences, but are statistically significant (F = 3.32, p = .019). For psychological distress, a data trend is visible such that there appears to be less distress as one moves “rightward” from secular to Orthodox Jews, but this does not attain statistical significance.

Results of regressions of both scales onto the religious measures indicate statistically significant associations between religion and well-being or distress, plus distinctive differences in the salience of religiousness depending upon the category of Jewish religious identity and observance. Three of the four religious indicators (importance of religion, religious attendance, and the religious harmony scale) are significant predictors

*p < .05; **p < .01; ***p < .001.

Statistically significant differences in regression coefficients across Jewish categories.

&

of well-being, overall, even after adjusting for covariate effects (see Table 2). The other religious indicator (God directly involved) is not significantly associated, nor are there subgroup differences. For importance of religion, the greatest net effect is among datim (β = .10, p < .05).

For the religious harmony scale, at the net level, stronger affirmation of this construct is associated with greater well-being among haredim (β = .39, p < .05), datim (β = .14, p < .05), and hilonim (β = .16, p < .001).

Overall, religiousness exhibits a protective effect on distress only through the religious harmony scale (see Table 3). Stronger affirmation of this construct, at the net level, is associated with less distress overall (β = -.16, p < .001) and among datim (β = -.19, p < .01), masortim (β = -.15, p < .001), and hilonim (β = -.17, p < .001); for haredi Jews, the association is not statistically significant.

For religious attendance, despite no overall association with distress, interesting subgroup differences emerged.

Among datim, at the net level, recent attendance at shul is protective against distress (β = -.13, p < .001). (For the haredim, the standardized and unstandardized regression coefficients are even larger, but due to a higher standard error and a smaller available sample size they are not statistically significant.) Among the hilonim, by contrast, at the net level, greater religious attendance was associated with more distress (β = .06, p < .05).

Note that regression estimates for God directly involved among haredim are omitted from both Tables 2 257

RELIGION & WELL-BEING IN ISRAELI JEWS

Table 3. Regressions# of Psychological Distress Scale on Religious Indicators, Overall and by Categories of Jewish Religious Identity and Observance Overall Religious Indicators$

Haredi

Dati

Masorti

Hiloni

β (b)

se

β (b)

se

β (b)

se

β (b)

se

β (b)

se

Model I: Gross results

-.01 (-.04)

.04

-.07 (-.75)

1.0

-.06 (-.31)

.25

-.03 (-.07)

.09

.04 (15)

.11

Model II: Net results

-.01 (-.02)

.04

-.09 (-.98)

.96

-.08 (-.42)

.25

-.03 (-.10)

.08

.04 (.15)

.11

Model I: Gross results&

-.02 (-.07)

.05

-.15 (-.67)

.41

-.13 (-.46)**

.17

-.03 (-.09)

.09

.05 (.23)*

.11

Model II: Net results&

-.01 (-.03)

.04

-.16 (-.69)

.40

-.13 (-.47)**

.16

-.04 (-.11)

.08

.06 (.25)*

.11

Model I: Gross results

-.01 (-.04)

.10

---

---

.03 (.39)

1.3

.03 (.16)

.30

.00 (.00)

.13

Model II: Net results

-.01 (-.02)

.10

---

---

.02 (.29)

1.3

.03 (.12)

.28

.01 (.03)

.13

Model I: Gross results&

-.14 (-.05)***

.01

-.25 (-.08)

.04

-.21 (-.06)**

.02

-.12 (-.04)**

.02

-.15 (-.05)***

.01

Model II: Net results&

-.16 (-.05)***

.01

-.24 (-.07)

.04

-.19 (-.05)**

.02

-.15 (-.05)***

.01

-.17 (-.06)***

.01

Importance of Religion

Religious Attendance

God Directly Involved

Religious Harmony Scale

Separate analyses for each of the four religious measures.

Model I = gross (unadjusted) results; Model II = net (adjusted) results, controlling for effects of health satisfaction, age, gender, marital status, and education.

# $

and 3. They were unevaluable due to an absence of variation in this variable in this subgroup (see Table 1). That is, every single haredi member of the sample affirmed God’s direct involvement in human affairs; not a single respondent answered otherwise. Therefore, the variable is not actually a variable in this group, and structural model estimates are thus not possible. In statistical terms, the model is not full rank and OLS solutions for the parameters are not unique. This is an unusual occurrence and an interesting finding in its own right, underscoring the substantial differences in religious beliefs and practices among these four groups.

DISCUSSION As anticipated, religious indicators are significantly associated with measures of psychological well-being and distress. Also as expected, a gradient is observed in religiousness and in well-being, such that higher levels of well-being are reported as one moves “rightward” from secular to Orthodox, except for the religious harmony scale where the gradient goes in the opposite direction. For the relationship between religious indicators and both outcomes, there is no evidence of a gradient; three of the four religious indicators are each significantly associated with one or both measures overall or in one or more subcategories of Jewish religious 258

*p < .05; **p < .01; ***p < .001.

Statistically significant differences in regression coefficients across Jewish categories.

&

identity and observance. The most substantial and interesting findings involve the religious harmony scale, an index assessing experience with religious tolerance and respect. Overall and within each of the Jewish religious subgroups, the scale is associated with more well-being or less distress or both. These results, along with those of other studies across the religious spectrum (1), challenge longstanding stereotypes of religious participation as uniformly harmful to well-being or necessarily reflective of psychopathology (35).

One limitation of this study is the prevalence-study or cross-sectional design of the GWP. However, this design feature is offset by the advantages of a national probability sample, a large sample size, and the presence of annual samples that soon will enable application of sophisticated methodologies such as time-series analyses. Moreover, this limitation is also negated by the wording of the outcome measures: both the well-being and distress scales inquire about statuses that occurred “yesterday”; the usual uncertainty in temporal order that limits interpretation of results from prevalence studies is thus not as impactful here.

Another limitation is the low internal-consistency reliability estimates of the well-being and distress scales. In the overall GWP sample of 679,145 respondents from 155 countries, these α values are .64 and .68 respectively, considerably higher than among the

Jeff Levin

Jewish respondents in the Israeli sample (reported in Measures). While statistically significant associations were nonetheless observed with the religious variables (shown in Tables 2 and 3), the marginal reliability of these scales may have inhibited other associations and serve to restrict interpretation of these results.

To circumvent this problem and supplement the present analyses, separate sets of regressions were run for each of the ten items constituting the two scales (analyses not reported in the tables). Statistically significant associations were found for importance of religion with the smile or laugh a lot and experience feelings of enjoyment items of the well-being scale; for religious attendance with the same variables plus the learn or do something interesting item; and for God directly involved on the smile or laugh a lot item. For the religious harmony scale, by contrast, statistically significant associations emerged for eight of the ten total scale items, all but the well-rested and learn or do something interesting items. The notable finding here is the near ubiquity of affirmation of the value of religious tolerance and respect as both a correlate of well-being and an ostensibly protective factor against distress. This inspired a more detailed look.

In Table 4, results are presented for gross and net regressions of each of the ten psychological well-being scale and psychological distress scale items on the religious harmony scale, overall and separately by categories of Jewish religious identity and observance. As just noted,

in the overall sample high scores on the religious harmony scale are significantly associated with eight of the ten scale items. Stratifying by Jewish religious identity and observance reveals that these findings are due to strong and consistent effects mostly among hilonim (significant net associations with eight of ten items) and, to a lesser extent, among masortim (significant net associations with three items) and datim (significant net associations with four items). Among the haredim, by contrast, higher scores on the religious harmony scale are of minimal net relevance to particular items, except for a significant association with a single item, smile or laugh a lot. Perhaps this is due to the much smaller subsample size and relatively larger standard errors, as the overall score on this scale is a very strong and significant gross and net correlate of well-being among the haredim (see Table 2).

In sum, results appear consistent and straightforward: affirmation of giving and receiving religious tolerance and respect among Jewish Israelis is positively associated with mental health, regardless of one’s category of religious identity and observance. These results also hold for two of the other three religious variables — importance of religion and religious attendance — although the religious harmony scale exhibits the most across-the-board impact, across outcomes and across categories of Jewish identity and observance.

These results raise important questions that cannot be answered using the present data. For example, what is it about Jewish religious practice that is or should be

Table 4. Regressions# of Psychological Well-Being Scale and Psychological Distress Scale Items on Religious Harmony Scale, Overall and by Categories of Jewish Religious Identity and Observance Overall Scale Items

I

II

Haredi I

II

Dati I

Masorti

II

I

II

Hiloni I

II

Well-Rested

.03

.03

.11

.12

.08

.08

.04

.03

-.01

-.01

Treated with Respect&

.15***

.16***

.05

.13

.22***

.21***

.09*

.10*

.17***

.18***

Smile or Laugh a Lot&

.07**

.08**

.33*

.42**

.14*

.16*

.02

.02

.07

.08*

Learn or Do Something Interesting&

-.00

.01

.11

.16

-.07

-.08

-.02

-.01

.08*

.08*

Experience Feelings of Enjoyment

.05*

.07*

.16

.14

.01

.02

.05

.06

.09*

.12**

Experience Feelings of Pain

-.08**

-.08**

-.16

-.22

-.05

-.05

-.06

-.08

-.08*

-.08*

&

Experience Feelings of Worry

-.05

-.05*

-.17

-.08

-.04

-.03

-.06

-.07

-.06

-.07

Experience Feelings of Sadness

-.11***

-.11***

-.29*

-.26

-.12

-.12

-.08

-.10*

-.12**

-.13***

Experience Feelings of Depression&

-.09***

-.10***

-.04

-.04

-.16*

-.15*

-.11*

-.12**

-.07

-.09*

Experience Feelings of Anger&

-.12***

-.12***

-.14

-.17

-.23***

-.23***

-.09*

-.09

-.11**

-.12**

# Separate analyses for each item of the psychological well-being and psychological distress scales. Reported values are standardized (β) regression coefficients. $ Model I = gross (unadjusted) results; Model II = net (adjusted) results, controlling for effects of health satisfaction, age, gender, marital status, and education.

*p < .05; **p < .01; ***p < .001.

Statistically significant differences in regression coefficients across Jewish categories.

&

259

RELIGION & WELL-BEING IN ISRAELI JEWS

associated with well-being and distress? This is an issue of “mechanisms,” to use the language of sociomedical researchers—or those mediators or moderating variables that account for putative effects of exposure variables (in this instance religiousness) on a given outcome.

In other words, what is it about the observance of one’s religion that ideally would engender a salutary impact on mental health? What are the characteristics, functions, expressions, or manifestations of religion that are or should be promotive of well-being or preventive of distress? In the literature on religion and mental health, these are thought to include reinforcement of norms of healthy behavior, provision of supportive interpersonal and communal relationships, opportunity for prayer and worship experiences that provide channels for cathartic emotional expression, affirmation of systems of belief and worldview that create a sense of meaning and context for the vicissitudes of life, and engendering of hope and optimism and other positive expectations that frame one’s daily experiences (1, 36). Each of these functions of religion is manifestly mental-health impacting, in principle, mostly related to an influence on self-control or self-regulation (37), and each can be recognized in Jewish religious contexts. Certain types of intense religious experience also may be associated with altered states of consciousness which exhibit psychophysiological correlates (38), a subject worth exploring further among Jewish mystics, perhaps.

Such questions are fascinating, but quite beyond the capability of being addressed in existing population surveys. In the GWP, for instance, requisite constructs were not assessed and the prevalence-study design may not be ideal for issues that may require other modes of assessment. Regardless, with the present results in hand, the next step should be to explain, not just to describe.

This mirrors an issue at the forefront of the study of religion and mental health for at least 20 years: researchers have dealt extensively with the “what” question, so to speak, but less so with “how” or “why.” For the present subject, this would require a data source with requisite instruments that: (a) assess dimensions and domains of mental and physical health in a more sophisticated and clinically validated way than through brief collections of well-being/distress items, (b) measure features of Jewish religious observance and Jewish life in general through validated scales and indices used by psychologists and sociologists of religion or by development of new instruments, and (c) address the myriad possible mediating factors or correlates of mental health or 260

Jewish experience that might account for their apparent interconnection.

This is a tall order. Some existing data sources contain one or perhaps two of these features, but too few Jewish respondents or subjects to enable meaningful analyses. A global or diaspora Jewish health survey would be ideal, but would require considerable coordination, perhaps in partnership with a global survey firm and a consortium of Jewish agencies and academics in Israel, the U.S., and throughout the world. In the meantime, existing data sources can continue to be mined for nuggets of information that can help to paint an epidemiologic portrait of the mental health of Jews, including, where possible, identification of correlates and predictors related to Jewish life, as in the present paper. This is not just an academic exercise: religion is an important, and some might say complicating, issue for caregiving with religious Jewish patients (39) and is a factor in the attitudes and behavior of healthcare practitioners, as well (40, 41). Religion has other diverse implications related to mental health: for psychiatric referral patterns (42), for the work of rabbis and pastoral care professionals (43), and for psychiatric-epidemiologic research on patterns and determinants of psychopathology and psychotherapy utilization among Jews (44).

Acknowledgement The author would like to thank Jim Clifton, Chairman and CEO; Dr. Gale Muller, Vice Chairman of Worldwide R&D; and Dr. Jon Clifton, Deputy Director of the Gallup World Poll, all from the Gallup Organization, for providing access to the Gallup World Poll data through the mechanism of a Research Scholar Consulting Agreement. He would also like to thank the two reviewers for their very helpful comments.

References 1. Levin J. Religion and mental health: Theory and research. Int J Appl Psychoanal Studies 2010; 7:102–115.

2. Srole L, Langner T. Religious origin. In: Srole L, Langner TS, Michael ST, Opler MK, Rennie TAC, editors. Mental health in the metropolis: The Midtown Manhattan Study. New York: McGraw-Hill, 1962: pp.

300-324.

3. Yeung PP, Greenwald S. Jewish Americans and mental health: Results of the NIMH Epidemiologic Catchment Area Study. Soc Psychiatry Psychiatr Epidemiol 1992; 27:292-297.

4. Mirsky J, Kohn R, Levav I, Grinshpoon A, Ponizovsky AM. Psychological distress and common mental disorders among immigrants: Results from the Israeli-based component of the World Mental Health Survey. J Clin Psychiatry 2008; 69:1715-1720.

5. Levav I, Kohn R, Dohrenwend BP, Shrout PE, Skodol AE, Schwartz S, Link BG, Naveh G. An epidemiological study of mental disorders in a 10-year cohort of young adults in Israel. Psychol Med 1993; 23:691-707.

6. Shmueli A. Subjective health status and health values in the general population. Med Decis Making 1999; 19:122-127.

7. Anson O, Antonovsky A, Sagy S. Religiosity and well-being among retirees: A question of causality. Behav Health Aging 1990; 1:85-97.

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8. Amit K. Determinants of life satisfaction among immigrants from Western countries and from the FSU in Israel. Soc Indic Res 2010; 96:515-534.

9. Shkolnik T, Weiner C, Malik L, Festinger Y. The effect of Jewish religiosity of elderly Israelis on their life satisfaction, health, function and activity. J Cross Cult Gerontol 2001; 16:201-219.

10. Shmueli A. Health and religiosity among Israeli Jews. Eur J Public Health 2006; 17:104-111.

11. Vilchinsky N, Kravetz S. How are religious belief and behavior good for you?: An investigation of mediators relating religion to mental health in a sample of Israeli Jewish students. J Sci Stud Relig 2005; 44:459-471.

12. Kark JD, Carmel S, Sinnreich R, Goldberger N Friedlander Y. Psychosocial factors among members of religious and secular kibbutzim.

Isr J Med Sci 1996; 32:185-194.

13. Levav I, Kohn R, Billig M. The protective effect of religiosity under terrorism. Psychiatry 2008; 71:46-58.

14. Anson O, Levenson A, Maoz B, Bonneh DY. Religious community, individual religiosity, and health: A tale of two kibbutzim. Sociology 1991; 25:119-132.

15. Rosmarin D H, Pargament KI, Mahoney A. The role of religiousness in anxiety, depression and happiness in a Jewish community sample: A preliminary investigation. Ment Health Relig Cult 2009; 12:97–113.

16. Rosmarin DH, Pirutinsky S, Pargament KI, Krumrei EJ. Are religious beliefs relevant to mental health among Jews? Psychology of Religion and Spirituality 2009; 1:180–190.

17. Rosmarin DH, Krumrei EJ, Andersson G. Religion as a predictor of psychological distress in two religious communities. Cogn Behav Ther 2009; 38:54–64.

18. Rosmarin DH, Krumrei EJ, Pargament KI. Do gratitude and spirituality predict psychological distress? Int J Existential Psychology Psychother 2010; 3:1–5.

19. Rosmarin DH, Pargament KI, Flannelly KJ. Do spiritual struggles predict poorer physical/mental health among Jews? Int J Psychol Relig 2009; 19:244–258.

20. Loewenthal KM, Goldblatt V, Gorton T, Lubitsch G, Bicknell H, Fellowes D, Sowden A. The social circumstances of anxiety and its symptoms among Anglo-Jews. J Affect Dis1997; 46:87-94.

21. Loewenthal KM, Goldblatt V, Lubitsch G, Gorton T, Bicknell H, Fellowes D, Sowden A. The costs and benefits of boundary maintenance: Stress, religion and culture among Jews in Britain. Soc Psychiatry Psychiatr Epidemiol 1997; 32:200-207.

22. Loewenthal K, Goldblatt V, Gorton T, Lubitsch G, Bicknell H, Fellowes D, Sowden A. Gender and depression in Anglo-Jewry. Psychol Med 1995; 25:1051-1063.

23. Devi S. Mental health and religion in Israel’s ultra-Orthodox Jews.

Lancet 2005; 366:1516-1517.

24. Loewenthal KM, Goldblatt V, Lubtish G. Haredi women, haredi men, stress and distress. Isr J Psychiatry Relat Sci 1998; 35:217-224.

25. Don-Yehiya E. Orthodox Jewry in Israel and North American [sic].

Israel Stud 2005; 10:157-187.

26. Ressler WH. Jewishness and well-being: Specific identification and general psychological adjustment. Psychol Rep 1997; 81:515-518.

27. Levin JS, Taylor RJ. Panel analyses of religious involvement and wellbeing in African Americans: Contemporaneous vs. longitudinal effects.

J Sci Stud Relig 1998; 37:695-709.

28. Levin J. Health impact of Jewish religious observance in the USA: Findings from the 2000–01 National Jewish Population Survey. J Relig Health 2011; online prepublication.

29. Gallup. Worldwide Research Methodology and Codebook. [New York]: Gallup, Inc., 2011.

30. Gallup. State of the World: 2008 Annual Report. New York: Gallup Press, 2008.

31. Clifton J, Gingrich N. Are citizens of the world satisfied with their health? Health Affair 2007; 26:545-551.

32. Friedman TL. The Israeli Jews: 4 distinct camps. New York Times, June 29, 1987:A12.

33. Diener E, Ng W, Harter J, Arora R. Wealth and happiness across the world: Material prosperity predicts life evaluation, whereas psychosocial prosperity predicts positive feeling. J Pers Soc Psychol 2010: 99:52-61.

34. Kim J-O, Ferree GD Jr. Standardization in causal analysis. Sociol Method Res 1981; 10:187-210.

35. Ellis A. Is religiosity pathological? Free Inq 1988; 8(2):27-32.

36. Levin JS, Chatters LM. Research on religion and mental health: An overview of empirical findings and theoretical issues. In: Koenig HG, editor. Handbook of religion and mental health. San Diego: Academic Press, 1998: pp. 33-50.

37. McCullough ME, Willoughby BLB. Religion, self-regulation, and selfcontrol: Associations, explanations, and implications. Psych Bull 2009; 135:69-93.

38. Levin JS, Wickramasekera IE, Hirshberg C. Is religiousness a correlate of absorption?: Implications for psychophysiology, coping, and morbidity.

Altern Ther Health M 1998; 4(6):72-76.

39. Bilu Y, Witztum E. Working with Jewish ultra-orthodox patients: Guidelines for a culturally sensitive therapy. Cult Med Psychiatry 1993; 17:197-233.

40. Musgrave CF, McFarlane EA. Israeli oncology nurses’ religiosity, spiritual well-being, and attitudes toward spiritual care: A path analysis.

Oncol Nurs Forum 2004; 31:321-327.

41. Musgrave CF, McFarlane EA. Intrinsic and extrinsic religiosity, spiritual well-being, and attitudes toward spiritual care: A comparison of Israeli Jewish oncology nurses’ scores. Oncol Nurs Forum 2004; 31:11791183.

42. Witztum E, Greenberg D, Dasberg H. Mental illness and religious change. Br J Med Psychol 1990; 63:33-41.

43. Cohen J. Judaism and mental illness. Australian Journal of Pastoral Care and Health 2008; 2(2):1-5.

44. Sanua VD. Studies in mental illness and other psychiatric deviances among contemporary Jewry: A review of the literature. Isr J Psychiatry Relat Sci 1989; 26:187-211.

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Isr J Psychiatry Relat Sci - Vol. 48 - No 4 (2011)

Post-discharge Contact with Mental Health Clinics and Psychiatric Readmission: A 6-month Follow-up Study Alexander Grinshpoon, MD, MHA, PhD,1 Yaacov Lerner, MD,2 Tzipi Hornik-Lurie, MA,2 Nelly Zilber, Dès Sc,2 and Alexander M. Ponizovsky, MD, PhD3 1

Tirat Carmel Mental Health Center and Bruce Rappaport Medical Faculty, Technion, Haifa, Israel Falk Institute for Mental Health Studies, Jerusalem, Israel 3 Department of Mental Health Services, Ministry of Health, Jerusalem, Israel 2

ABSTRACT Background: Continuity of mental health care is a major topic in the post deinstitutionalization era, especially concerning its possible importance as a contributing factor in preventing rehospitalization.

Objectives: To examine a) the association between continuing care and time to rehospitalization; and b) the predictors of time to first outpatient contact after discharge from psychiatric hospital.

Methods: Hospitalization records of all patients discharged from the Tirat Carmel psychiatric hospital in Israel, between January 1, 2006, and December 31, 2006, the National Register of Psychiatric Hospitalizations database and administrative databases of all psychiatric outpatient clinics in this catchment area were used to monitor continuing care and rehospitalization within 180 days from discharge. Predictors of time to rehospitalization and outpatient visits were examined using a Cox proportional hazards regression model.

Results: Out of the 908 discharged inpatients, 29% were rehospitalized and 59% visited an outpatient clinic during the study period. Of those who visited a clinic, 22% were rehospitalized compared with 40% of those who did not visit. Not making aftercare contact with a mental health clinic during the study period and/ or having a history of more than four hospitalizations were significant predictors of earlier psychiatric readmission. Males and patients diagnosed with

schizophrenia or affective disorders made contact with outpatient clinics significantly earlier. Patients who were discharged from the hospital after a daycare period contacted outpatient clinics significantly later than those who were not in daycare.

Conclusions: The findings suggest that psychiatric rehospitalization is associated with discontinuity of contact with psychiatric services but not with diagnosis. Patients with schizophrenia or affective disorders were found to adhere to a greater degree to clinical aftercare, which may explain why they are not rehospitalized earlier than less severe patients.

Introduction Continuity of mental health care is a major topic in the post deinstitutionalization era (1), especially concerning its possible importance as a contributing factor in preventing rehospitalization. Reducing rates of psychiatric rehospitalization has become a focus for policymakers as a way to improve quality of care and reduce costs.

Risk factors for psychiatric rehospitalization can be divided into patient-related and service-related variables. Patient-related risk factors include sociodemographic characteristics, such as male gender (2), older age (3), single or divorced marital status (4), being unemployed (5), and clinical characteristics, such as diagnosis of schizophrenia, schizoaffective disorder

Address for Correspondence: Dr. A.M. Ponizovsky, Mental Health Services, Ministry of Health, 2 Ben Tabai St., Jerusalem 93591, Israel alexander.ponizovsky@moh.health.gov.il

262

Alexander Grinshpoon et al.

(6, 7) or major depression (8, 9), noncompliance with antipsychotic treatment (10), duration of hospital stay (11), and number of previous admissions (12-14).

Service-related risk factors associated with rehospitalization include inadequate hospital-based discharge planning (15-17), referral to aftercare (7, 18), poor adherence to treatment after discharge (19, 20), and unmet needs of inpatients (21, 22).

Thompson et al. (7) explored the relationships between referral to aftercare, duration of hospital stay, and rehospitalization within six months of discharge in a sample of 1,481 psychiatric inpatients, mostly with diagnoses of schizophrenia and schizoaffective disorders. They found that the longer duration of hospital stay and diagnosis of schizophrenia predicted referral to aftercare, but that the referral itself did not mediate the relationship between duration of stay and rehospitalization. Diagnosis of schizoaffective disorder, a high number of previous admissions and referral to aftercare altogether significantly increased the risk of rehospitalization.

In the U.S.A., Prince (23) examined the predictors of inpatient readmission within three months of psychiatric hospital discharge of patients with a diagnosis of schizophrenia. He found that interventions addressing service continuity, symptom education and daily structure of activities were effective in preventing rehospitalization only among individuals with four or more prior hospitalizations. However, as a recent review of methods reducing hospital readmission in depression and schizophrenia shows (24), patients with schizophrenia or mood disorders often fail to continue treatment after hospital discharge, with as many as one third to one half of hospitalized patients with schizophrenia or related disorders missing their first scheduled outpatient appointment after hospital discharge.

In Israel, however, information on the risk factors for rehospitalization and for continuity of care is limited, whereas such information is very necessary for correct allocation of resources for psychiatric services (25). The aim of the present study was therefore to examine in Israel a) the association between continuing care and time to rehospitalization; and b) the predictors of time to first outpatient contact after discharge from psychiatric hospital.

Patients and Methods Research setting

The setting for this study was a state psychiatric hospital in Tirat Carmel, Israel. The mental health center has 228

beds: 24 for adolescents, 144 for acute patients and 60 for long-stay patients. All patients are referred, after discharge, to the hospital-affiliated clinics or to one of the public mental health clinics of the Health Maintenance Organization (HMOs). The hospital serves a catchment area with a mixed lower and middle income population of about 600,000.

Database and study population

The data on all hospitalizations of patients aged 18 years and above discharged from the Tirat Carmel psychiatric hospital between January 1, 2006, and December 31, 2006 (N=908) were extracted from the hospital records. For each hospitalization, demographic, clinical and administrative data were extracted. A 6-month follow-up since the first discharge during this period (â&#x20AC;&#x153;key dischargeâ&#x20AC;?) was performed individually for each patient for psychiatric rehospitalization (data from the National Register of Psychiatric Hospitalizations) and/ or outpatient aftercare. Data on outpatient visits were extracted from the administrative databases of all psychiatric clinics in the catchment area (not including private psychiatrists). The Institutional Review Board approved the study protocol.

Study variables

The main outcome measures were time to rehospitalization and time to first visit in mental health clinics within 180 days of key discharge. Predictor variables included age at key discharge, gender, primary diagnosis at key discharge, duration of the key hospitalization, total number of psychiatric hospitalizations until the key hospitalization, key discharge after daycare or not and making or not an outpatient visit within 180 days of key discharge. The diagnoses according to ICD-10 were: organic brain disorder (F0-F9), drug and alcohol dependence {F10-F19), schizophrenia or other psychosis (F20-F29), affective disorder (F30F39), neurotic disorders (F40-F48) and personality disorders (F60-F69).

Statistical analysis

A Cox regression allowed constructing a multi-factorial prediction model for time to readmission and time to outpatient first visit within 180 days from key discharge, controlling for various independent variables, which were entered simultaneously in the analysis.

Data analyses were performed using SPSS/PC version 15.0 (SPSS Inc, Chicago, IL).

263

Post-discharge Contact with Mental Health Clinics and Psychiatric Readmission

Results

Table 1. Cox regression results for predictor variables of readmission within 180 days from discharge

Patient characteristics

The analysis was carried out on the sample of 908 patients, 60% males. The most common diagnostic category was schizophrenia or other psychosis (589 patients; 68%), followed by organic brain disorder (92 patients; 11%), and affective disorder (72 patients; 8%). The remaining diagnostic groups - neurotic disorders, personality disorders and drug and alcohol dependence – altogether comprised 115 patients (13%). A relatively large percentage of patients (40%) had a history of four and more psychiatric hospitalizations prior to the key discharge. The proportion of discharges after a key hospitalization of more than one year was 1.5%. The duration of the key hospitalization was less than 40 days for 61 % of the patients and the median was 29 days; 29% of the patients were discharged after a daycare period.

Within 180 days of their key discharge, 267 patients (29%) were rehospitalized. There were significantly fewer readmissions among those who visited a clinic (22%) than among those who did not (40%) (χ2 = 37.42, df = 1, p=.000). Over the same period 535 patients (59%) made contact with an aftercare mental health clinic. The percentage was higher (66%) among patients with schizophrenia or affective disorders than among others. Only 35.8% of those who did not make contact with the clinic had a history of four or more hospitalizations.

Figure 1. Time to readmission within 180 day of key discharge (Cox regression) according to use (yes or no) of mental health clinics during the follow-up* % of patients remaining in the cummunity after discharge

1.0

N

p 0.179

Age

Up to 25 years

125

1.25

0.85 - 1.83 0.257

26 to 45 years

364 1.00

45 to 65 years

269 0.93

0.69 - 1.24

0.622

66 years or more

110

0.66

0.40 - 1.10

0.111

Gender

0.378

Male

519

1.13

0.86 - 1.47

Female

349 1.00

Diagnosis

Schizophrenia or other psychosis

589 1.00

0.473

Affective Disorder

72

0.69

0.38 - 1.25

Neurotic Disorder

38

0.73

0.33 - 1.59 0.430

0.223

Personality Disorder

24

0.92

0.40 - 2.09 0.837

Drugs and Alcohol

53

1.12

0.68

Organic Disorder

92

1.38

0.84 - 2.27 0.209

Duration of key hospitalization (days)

1 - 40

532 1.02

41 +

336 1.00

1.85

0.77

- 1.36

Number of Previous Hospitalizations

0.659 0.873

0.000

0

227

1-3

285 1.88

1.00 1.23

- 2.87 0.004

4

356 3.97

2.64 - 5.98 0.000

Index Discharge after Daycare

+

0.845

No

616 1.03

0.76 - 1.40

Yes

252 1.00

Visit to Clinic after Index Discharge

0.9

95% Odds confidence ratio* interval

No

352 1.00

Yes

516

Total

868

0.40

0.31

- 0.51

0.000

0.8

* A value smaller than 1 indicates a longer time to rehospitalization

0.7

Predicting time to readmission

0.6

0.5

0

30

60 90 120 150 Time since discharge till next hospitalization

* Use (yes or no) of mental health clinics relates to at least one visit within 180 days of key discharge or till first readmission (if the patients were rehospitalized).

264

180

We then examined the predictors of time to readmission while controlling simultaneously for the effect of each variable (Cox regression). The fact that a patient visited a mental health clinic after discharge was found to be related to longer time between key discharge and next hospitalization (p=0.000) (Figure 1). We did not relate to the number of visits to the clinic after discharge because patients with earlier rehospitalization have of course a smaller number of visits until rehospitalization

Alexander Grinshpoon et al.

Table 2. Cox regression results for predictor variables of visiting a clinic within 180 days from discharge 95% Odds confidence ratio* interval

p

0.165

Up to 25 years

125

0.90

0.69 - 1.18

26 to 45 years

364 1.00

N

Age

0.464

45 to 65 years

269 1.14

0.92 - 1.40 0.222

66 years or more

110

0.56 - 1.14

0.213 0.043

0.80

Gender

Male

519

1.21

1.01

- 1.46

Female

349 1.00

Diagnosis

0.000

Schizophrenia or other psychosis

589 1.00

Affective Disorder

72

1.09

0.79 - 1.49 0.609

Neurotic Disorder

38

0.66

0.40 - 1.09 0.103

Personality Disorder

24

0.74

0.42 - 1.29

0.288

Drugs and Alcohol

53

0.36

0.21

Organic Disorder

92

0.50

0.34 - 0.75 0.001

Duration of key hospitalization (days)

1 - 40

532 0.99

41 +

336 1.00

0.59 0.000

0.900

0.81 - 1.21

Number of Previous Hospitalizations

0.740

0

227

1-3

285 1.02

1.00 0.80 - 1.30

0.860

4

356 0.94

0.73 - 1.21

0.640

Index Discharge after Daycare

0.002

No

616 0.72

0.58 - 0.88

Yes

252 1.00

Total

868

+

period were significant predictors of time to first outpatient visit within 180 days of key discharge. Specifically, males visited outpatient clinics significantly earlier than female patients (Hazard ratio = 1.21, p=0.043). Compared to patients diagnosed with schizophrenia, patients having a diagnosis of drug or alcohol dependence (Hazard ratio = 0.36, p<0.0001) and those with a diagnosis of organic brain disorder (Hazard ratio = 0.50, p<0.001) visited a clinic significantly later during the follow-up period. Patients with a diagnosis of affective disorders were very similar to patients with schizophrenia. In addition, patients who were discharged from the hospital after a daycare period visited an outpatient clinic significantly later than those who were not in daycare (Hazard ratio = 0.72, p<0.002).

* A value smaller than 1 indicates a longer time to make contact with a clinic

and vice-versa. As shown in Table 1, another significant predictor of time to psychiatric readmission within 180 days of key discharge was the number of psychiatric hospitalizations prior to the key hospitalization, with time to readmission decreasing when the number of previous hospitalizations increased (p=0.000). In contrast, the remaining variables (age, gender, diagnostic category, duration of the key hospitalization, and discharge after a daycare period) were not significantly related to time to rehospitalization.

Predicting time to first outpatient post-discharge visit

The Cox regression results in Table 2 show that gender, diagnostic category and key discharge after a daycare

Discussion The present study shows that in Israel, like in other countries (24, 26), making contact with a mental health clinic after discharge from psychiatric hospitalization is related to later rehospitalization, i.e., continuity of mental health care enhances tenure of psychiatric patients in the community. Interventions enhancing such a contact could reduce the burdens and hazards of untreated mental disorder. A proposed solution is systems integration (27). The integration of inpatient and outpatient services could be a more cost-effective pathway of reintegration of psychiatric patients in the community than their standing separately (28).

Visiting an aftercare clinic earlier was found to be associated with male gender, while a diagnosis of organic disorder, drug or alcohol dependence was associated with later contact with aftercare clinic than a diagnosis of schizophrenia or affective disorders. One could thus have expected less rapid rehospitalization among patients with schizophrenia or affective disorders. On the other hand, one could have assumed a more rapid rehospitalization among these patients due to the severity of their disease.

The conjunction of these two factors may explain why no association was found between a diagnosis of schizophrenia or affective disorders and rehospitalization. It is worthwhile to point out that, even when the adherence to aftercare is the highest (among patients with schizophrenia or affective disorders), about one third does not reach an outpatient clinic within six months from discharge and thus an effort should be made to reach out to them.

As mentioned in the Introduction section, Thompson (7) discovered that referral to aftercare was found to be associated with a greater risk of rehospitalization. In his 265

Post-discharge Contact with Mental Health Clinics and Psychiatric Readmission

study, only 16% were offered aftercare within six months of discharge. This small referral rate may indicate that referral reflects severity of illness requiring continuity of treatment as determined by the referring specialist. In our study, on the contrary, practically all patients were referred to aftercare and what we examined was compliance to aftercare on the part of the patient, which may reflect cooperation and motivation for treatment, leading to continuity of treatment and thus to less rehospitalization.

Surprisingly, those who were discharged after daycare following hospitalization, in contrast to those discharged directly after the inpatient episode, had a greater probability of discontinuing contact. The possible explanation for this finding is that they might have mistakenly felt that they did not need any additional aftercare.

The obtained results may have important implications for policymakers in the context of the Mental Health Insurance Reform being currently conducted in Israel. Until now, the responsibility for treatment of mentally ill individuals was shared between the Government (Ministry of Health) and Health Maintenance Organizations (HMOs). The Reform aims to integrate all mental health services under the umbrella of one single organization, the HMOs. This transfer of responsibility for mental health treatment from the State to HMOs may improve service continuity and thus reduce rehospitalization, as shown in the present study. An underlying reason is that a single paymaster (the HMO) has the obvious financial interest to ensure continuity of care, i.e., savings from prevented or reduced rehospitalizations.

A limitation of this study is that we were unable to receive data on aftercare visits to private psychiatrists practicing in the area and, thus, the total number of postdischarge contacts with mental health professionals could be slightly underestimated. Another limitation is that the socio-economic status of the patients was not available in the databases we used, while it has been shown that it may affect rehospitalization and continuation of care (29, 30).

No data were available either about severity of disease or compulsory admission, which could be relevant factors.

In conclusion, our findings suggest that psychiatric rehospitalization is associated with discontinuity of contact with psychiatric services but not with diagnosis.

Acknowledgments Dr. A.M. Ponizovsky was supported in part by the Ministry of Immigrant Absorption of Israel. The authors wish to thank Mrs. Lily Cohen, Tirat Carmel Mental Health Center, and Mr. Yaakov Krayzman, Ministry of Health, Jerusalem, for their assistance with data collection.

266

References 1. Wierdsma A, Mulder C, de Vries S, Sytema S. Reconstructing continuity of care in mental health services: A multilevel conceptual framework. J Health Serv Res Policy 2009; 14:52-57.

2. Grossman LS, Harrow M, Rosen C, Faull R, Strauss GP. Sex differences in schizophrenia and other psychotic disorders: A 20-year longitudinal study of psychosis and recovery. Compr Psychiatry 2008;49:523-529.

3. Saarento O, Kastrup M, Lönnerberg O, Göstas G, Muus S, Sandlund M, et al. The Nordic Comparative Study on Sectorized Psychiatry: Patients who use only psychiatric in-patient care in comprehensive community-based services - a 1-year follow-up study. Acta Psychiatr Scand 1998;98:98-104.

4. Pfeiffer SI, O’Malley DS, Shott S. Factors associated with the outcome of adults treated in psychiatric hospitals: A synthesis of findings. Psychiatr Serv 1996;47:263-269.

5. Bruffaerts R, Sabbe M, Demyttenaere K. Effects of patient and healthsystem characteristics on community tenure of discharged psychiatric inpatients. Psychiatr Serv 2004;55:685-690.

6. Rabinowitz J, Lichtenberg P, Kaplan Z, Mark M, Nahon D, Davidson M. Rehospitalization rates of chronically ill schizophrenic patients discharged on a regimen of risperidone, olanzapine, or conventional antipsychotics. Am J Psychiatry 2001;158:266-269.

7. Thompson EE, Neighbors HW, Munday C, Trierweiler S. Length of stay, referral to aftercare, and rehospitalization among psychiatric inpatients.

Psychiatr Serv 2003;54:1271-1276.

8. Kolbasovsky A, Reich L, Futterman R. Predicting future hospital utilization for mental health conditions. J Behav Health Serv Res 2007;34:34-42.

9. Lin CH, Chen YS, Lin CH, Lin KS. Factors affecting time to rehospitalization for patients with major depressive disorder. Psychiatry Clin Neurosci 2007; 61:249-254.

10. Hamann J, Cohen R, Leucht S, Busch R, Kissling W. Shared decision making and long-term outcome in schizophrenia treatment. J Clin Psychiatry 2007;68:992-997.

11. Ginsberg G, Lerner Y, Mark M, Popper M. Prior hospitalization and age as predictors of mental health resource utilization in Israel. Soc Sci Med 1997; 44:623-633.

12. Solomon P, Davis J, Gordon B. Discharged state hospital patients’ characteristics and use of aftercare: Effect on community tenure. Am J Psychiatry 1984;141:1566-1570.

13. Patel NC, Crismon ML, Pondrom M. Rehospitalization rates of patients with bipolar disorder discharged on a mood stabilizer versus a mood stabilizer plus an atypical or typical antipsychotic. J Beh Health Serv Res 2005;32:438-445.

14. Lin CH, Chen CC, Wang SY, Lin SC, Chen MC, Lin CH. Factors affecting time to rehospitalization in Han Chinese patients with schizophrenic disorder in Taiwan. Kaohs J Med Sci 2008;24:408-414.

15. Wasylenki D, Goering P, Lancee W, Fischer L, Freeman SJ. Psychiatric aftercare in a metropolitan setting. Can J Psychiatry 1985;30:329-336.

16. Boydell KM, Malcolmson SA, Sikerbol K. Early rehospitalization. Can J Psychiatry 1991;36:743-745.

17. Mann NA, Tandon R, Butler J, Boyd M, Eisner WH, Lewis M. Psychosocial rehabilitation in schizophrenia: Beginnings in acute hospitalization. Arch Psychiatr Nurs 1993;7:154-162.

18. Klinkenberg WD, Calsyn RJ. Predictors of psychiatric hospitalization: A multivariate analysis. Adm Policy Ment Health 1998;25:403-410.

19. Dincin J, Wasmer D, Witheridge TF, Sobeck L, Cook J, Razzano L. Impact of assertive community treatment on the use of state hospital inpatient bed-days. Hosp Com Psychiatry 1993;44:833-838.

20. Eldon Taylor C, Lopiccolo CJ, Eisdorfer C, Clemence C. Best practices: Reducing rehospitalization with telephonic targeted care management in a managed health care plan. Psychiatr Serv 2005;56:652-654.

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21. Owen C, Rutherford V, Jones M, Tennant C, Smallman A. Psychiatric rehospitalization following hospital discharge. Community Ment Health J 1997;33:13-24.

22. Grinshpoon A, Ponizovsky AM. The relationships between need profiles, clinical symptoms, functioning and the well-being of inpatients with severe mental disorders. J Eval Clin Pract 2008;14:218-225.

23. Prince JD. Practices preventing rehospitalization of individuals with schizophrenia. J Nerv Ment Dis 2006;194:397-403.

24. Bridge JA, Barbe RP. Reducing hospital readmission in depression and schizophrenia: Current evidence. Curr Opin Psychiatry 2004;17:505-511.

25. Ginsberg G, Lerner Y, Mark M, Popper M. Prior hospitalization and age as predictors of mental health resource utilization in Israel. Soc Sci Med 1997;44:623-633.

26. Druss B, Rosenheck R. Evaluation of the HEDIS measure of behavioral

health care quality. Health Plan Employer Data and Information Set. Psychiatr Serv 1997;48:71-75.

27. Durbin J, Goering P, Streiner DL, Pink G. Does systems integration affect continuity of mental health care? Adm Policy Ment Health 2006;33:705-717.

28. Tyrer P. The future of specialist community teams in the care of those with severe mental illness. Epidemiol Psichiatr Soc 2007;16:225-230.

29. Levinson D, Lachman M, Lerner Y. The SES setting of psychiatric hospitalization in Israel. Soc Psychiatry Psychiatr Epidemiol 2006;41:364368.

30. Stahler GJ, Mennis J, Cotlar R, Baron DA. The influence of neighborhood environment on treatment continuity and rehospitalization in dually diagnosed patients discharged from acute inpatient care. Am J Psychiatry 2009;166:1258-1268.

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Isr J Psychiatry Relat Sci - Vol. 48 - No 4 (2011)

“Transferred to Another Institution”: Clinical Histories of Psychiatric Patients Murdered in the Nazi “Euthanasia” Killing Program Florian Steger, MD, PhD,1 Andreas Görgl, MD,2 Wolfgang Strube1, Hans-J. Winckelmann, PhD,3 and Thomas Becker, MD, PhD4 1

Institute for History and Ethics of Medicine, University of Halle-Wittenberg, MLU Halle-Wittenberg, Germany Clinic Silima, Riedering, Germany 3 Institute for History, Theory and Ethics of Medicine, University of Ulm, Germany 4 Department of Psychiatry II, University of Ulm, Bezirkskrankenhaus Günzburg, Germany 2

ABSTRACT This study aims to examine the practice of medical reporting in a totalitarian environment including systematic killing of people with mental illness in Nazi Germany. The historical analysis is based on patient documents and administrative files at today’s District Hospital, Günzburg, as well as on patient documents of inventory R 179 of the branch office of the Federal Archives (Bundesarchiv) in Berlin/Lichterfelde. The paper describes four patient histories and attempts to reconstruct some aspects of patients’ (mostly institutional) histories against the background of the Günzburg State Hospital serving as an assembly institution in the context of “Aktion T4.” There is no certainty regarding the places of death of the four patients whose medical documentation is reported. In the patient records examined, the practice of medical description and reporting was characterized by a mixture of medical terminology, ideological diction and common language. The type of medical description and documentation used is an expression of stigmatization and discrimination of patients and of traumatizing institutional practice, and it reflects institutional violence. It is an ethical responsibility to reconstruct and commemorate the individual histories of mentally ill patients who were victims of the program of organized mass killings of people with mental illness.

Places of death were camouflaged by the “Aktion T4,” and there is uncertainty for many patients regarding where they were killed.

Introduction The “euthanasia” project of National Socialism consisted of five distinct programs of systematic mass killing: 1. Child “euthanasia,” 2. the murder of psychiatric patients from the East Prussian Provinces and occupied areas of West Prussia by the SS (1939–1940), 3. the “T 4 Campaign” which refers to the decentralized murder of psychiatric patients by means of poison gas (1940–1941), 4. the “Special Treatment 14f13,” which refers to the gassing of concentration camp prisoners unable to work, organized by the members of the “T 4 Campaign” and the SS (1941-1943), and 5. the decentralized killing by intentional malnutrition and medical injections in long-term care institutions in the occupied eastern regions from summer 1942 until the end of the war (1). For political reasons, Adolf Hitler refused to initiate a euthanasia law and kept the mass killings secret under the code name “Aktion T4” both for Germany and occupied countries (and based on Hitler’s “euthanasia authorization” backdated to September 1st, 1939 in October). The “Aktion T4” (1939-1941) was used to organize the systematic killing of about 70,000 patients from psychiatric institutions (2).

This number corresponds to about one fifth of all patients who resided in psychiatric (mental) hospitals at the time.

Within the organizational structure of the “Aktion T4” the Günzburg State Hospital was used as a so-called “assembly institution” (Sammelanstalt) to gather patients selected for the program of mass killings (3-5). The Günzburg State Hospital was opened in 1915 due to marked overoccupancy at the earliest Swabian district lunatic asylum in Kaufbeuren-Irsee. The asylum was built according to

Address for Correspondence: Prof. Dr. Florian Steger, MD, PhD, Institute for History and Ethics of Medicine, MLU Halle-Wittenberg, Magdeburger Straße 8, D-06112 Halle (Saale), Germany florian.steger@medizin-uni-halle.de

268

Florian Steger et al.

a pavilion scheme, and it was planned for a maximum number of 400 patients. Outside Germany, the name of the small town of Günzburg is associated with the name of the SS-medical officer Josef Mengele. The Swabian town was home to Mengele, and he found shelter in Günzburg during his flight from Allied forces (6).

The medical staff involved in the patient killing programs were protected from prosecution for their actions.

From the beginning of October 1939, the Reich Ministry of the Interior or provincial authorities sent “notification forms” comprising questionnaires regarding criteria for patient selection to all psychiatric institutions (1, 7, 8).

These forms were examined by three medical officers (in Berlin), and this panel made a decision on the transfer and killing of each individual patient. In total, about 200,000 notification forms were examined by reviewers during the course of “Aktion T4.” The selection criteria used in Günzburg have been presented elsewhere; overall duration of hospitalization, diagnosis, social compatibility and working capacity of patients were used (9, 10). The diagnostic classification scheme used was the Würzburg (diagnostic) code [abbreviated Ws*] (11).

Due to widespread resistance in the general population and to open protest from within the Church (defining euthanasia as murder), the “Aktion T4” was suspended in August 1941. However, in many psychiatric institutions killing of patients was continued by other methods (e.g., by medication or by medical or nursing neglect). Many patients incapable of working were starved using a fat-free and low-calory diet following the “starvation diet decree” of 1942 (4). Between 1933 and 1943, 366 patients were sterilized at the Günzburg State Hospital (12). Forced sterilization was based on the Gesetz zur Verhütung erbkranken Nachwuchses (Law for Prevention of Hereditarily Diseased Offspring).

Moreover, organs of patients who died at the Günzburg State Hospital were sent to the Kaiser-Wilhelm Institut München (German Institute for Psychiatric Research) for the purpose of neuropathological research (13).

Method: Selected Patient Histories The presentation of institutional records and medical histories of female and male patients from the Günzburg State Hospital is primarily based on a total of 394 medical files noted in the inventory R 179 of the branch office of the *In contemporary documents the abbreviation “Ws” for “Würzburger Schlüssel” is used.

Federal Archives (Bundesarchiv) in Berlin/Lichterfelde (9, 14). The letters “AZ” behind the abbreviated name indicate “Aktenzeichen” (reference file number), and they are followed by a number and information from the file “R 179”; this helps identifying the corresponding file at the Bundesarchiv Berlin/Lichterfelde. The documents held at the Bundesarchiv were found during the early 1990s at the central archive of the Ministry of State Security of the former German Democratic Republic (GDR). Apart from administrative files they contained the histories of about 30,000 patients who, in the course of “Aktion T4,” were transported to killing institutions from diverse mental hospitals and nursing homes and killed in 1940 to 1941 (15). Apart from the medical files additional information was retrieved in (medical) patient files and administrative files of the Bezirkskrankenhaus Günzburg (Günzburg District Hospital).

The selection of institutional records and medical histories presented in this paper was made according to criteria defined in advance. The central criterion was that some information on patients’ medical history, the clinical picture and course of disease should be available. Single case studies were chosen to reflect differences in age group, diagnosis, form and duration of hospitalization. The case histories presented concern patients with differences in clinical characteristics and life histories. The state of conservation of patient files was a limiting criterion. Information was obtained by historical reconstruction of selected patient histories from the branch office of the Federal Archives in Berlin and by describing medical reporting and documentation as practiced at the time. On this basis, we report the information that could be retrieved on the histories of four specific patients. Other case histories have been reported in a previous paper (14).

Places of Death of Patients Patients were transported to assembly institutions (Sammelanstalten) and aggregated into larger groups before being deported to killing institutions (Bernburg, Brandenburg, Grafeneck, Hadamar, Hartheim and Pirna-Sonnenstein). The actual places of killing were camouflaged. There are records on patient killings on 394 patients of the Günzburg State Hospital. There is incomplete information (from various sources) on transfer of patients to killing institutions: On July 5, 1940, 75 patients were transferred (as far as we know, 6 patients to Grafeneck, 1 patient to Pirna-Sonnenstein, 2 patients to 269

Clinical Histories of Psychiatric Patients Murdered in the Nazi “Euthanasia” Program

the neighboring Kaufbeuren state hospital, 12 patients to another state mental hospital in Zwiefalten); on October 9, 1940, 91 patients were transferred (as far as we know, 2 patients to the state hospital at Zwiefalten, 1 patient to Hartheim); on October 22, 1940, 49 patients were transferred (as far as we know, 2 patients to Grafeneck, 1 patient to Hartheim, and 1 patient to Zwiefalten); on November 22, 1940, 39 patients were transferred to other institutions (as far as we know, 1 patient to Grafeneck, 1 patient to Zwiefalten, 1 patient to Kaufbeuren); on July 1, 1941, 140 patients were transferred (as far as we know, 3 patients to Hartheim). According to the literature many patients from Bavarian institutions were transferred to Hartheim, other patients were transferred to Grafeneck which was followed by Hadamar, some patients were also transferred to Pirna-Sonnenstein (5); Aas (16, 17) reported the following data: July 5, 1940 – patient transport from Günzburg to Grafeneck: 74 patients (65 male, 9 female); October 9, 1940 – patient transport from Günzburg to Zwiefalten: 89 patients (all female); October 22, 1940 – patient transport from Günzburg to Hartheim: 48 patients (36 male, 12 female); November 22, 1940 – patient transport to Hartheim: 42 patients (all male); July 1, 1941 – patient transport from Günzburg to Hartheim: 140 patients (54 male, 86 female) with slight inconsistencies. As far as we know, from the “Aktion T4” memorial center at Pirna (e-mail correspondence, March 25, 2011), no patients from Günzburg were transferred to the Pirna-Sonnenstein killing institution. According to correspondence with the Grafeneck memorial center (e-mail correspondence, March 7, 2011), a total group of 47 patients (27 male, 20 female) were transferred from Günzburg to Grafeneck (patient transport dated October 9, 1940: 11 patients; patient transport dated October 22, 1940: 22 patients). According to the Zwiefalten hospital (e-mail correspondence, March 7/25, 2011) there were patient transports from Günzburg to Grafeneck via Zwiefalten (patient transport dated July 5, 1940: 66 patients transferred to Zwiefalten of whom 64 were transferred to Grafeneck; 1 patient died in Zwiefalten on July 13, 1940; patient transport from Günzburg to Zwiefalten dated October 9, 1940: 89 patients were transferred of whom 85 or 86 patients were transferred to Grafeneck on November 6, 1940; two patients died in Zwiefalten, one patient may have been transferred later [November 7, 1940]; patient transport on October 22, 1940: 36 patients were transferred from Günzburg to Zwiefalten all of whom were transferred to Grafeneck on November 13, 1940).

270

In summary, it is likely that of the four patients referred to below two were killed at the Grafeneck and two at the Hartheim killing institution (near Linz, Austria).

Patient Histories Patient J.M. (AZ 3131 R 179), “transferred to another institution” on October 22nd, 1940, at the age of 50.

J.M., male, was born on July 24th, 1890. On August st 1 , 1911, he was first admitted to the mental hospital at Kaufbeuren. Nine months later J.M. was discharged to the care of his father; he subsequently started his military service in Munich. Due to mental instability he was committed to the University Psychiatric Clinic in Munich. In February 1913, J.M. was transferred to Kaufbeuren, which was close to his home; hospital transfer was supervised by the police. The medical report attached to the police report states that “M. is mentally ill” (dementia praecox).

As there is a risk of periods of aggression during which he attacks other people he must be considered a danger to the public. He has to be transferred to an institution according to the regulations of Art. 83 II of the Penal Code of the Police [Polizeistrafgesetzbuch] (assessment in police report of February 27th, 1913). The medical report from the Kaufbeuren hospital records states that the patient suffered from delusions. “The food is poisoned, it has always been poisoned...” Apart from this, J.M. also believed that he was being held in prison in his home town. In September 1913, J.M. was discharged to his home following medical assessment. During the three years that followed he was repeatedly admitted (and committed) to the hospital at Kaufbeuren. Finally, in March 1916, he was arrested for reasons of public safety and taken to the Kaufbeuren mental hospital. In an expert report of the district doctor his mental condition is described as follows: “J.M. (…) is mentally ill and as he has a tendency to states of aggression during which he becomes violent, he has to be considered a danger to the public as well. He [says that he] is Christ, ‘the almighty God, if my father is going to treat me badly, a terrible punishment will come upon him’” (report of district doctor of March 11th, 1916, medical report of Kaufbeuren state hospital).

In a decision of the district administration of Wertingen of March 27th, 1916, the following statement is made: “He refuses food, no longer works, threatens his father with murder, looks for weapons and does other similar things.”

After that J.M. remained in long-term inpatient treatment.

In the care report of April 26th, 1940, his state of health is described with the following words: “mentally indifferent

Florian Steger et al.

(…) doesn’t react to communicative approaches, is gnawing on his fingers. Unclean with feces and urine. Has to be nursed completely. Unfit for any kind of labour” (medical report of Kaufbeuren state hospital, April 26th, 1940).

On May 17 th, 1940, J.M. was transferred to the Günzburg State Hospital together with three other patients. The state of the patient is described as follows in an entry of September 18th, 1940: “Patient is completely stupid, obtuse, and not responsive. Frequently unclean, day and night, can thus no longer be integrated into the working group and, due to his swollen legs, also stays in bed in the mornings.” A diagnosis of schizophrenia (Ws 14) was made. In the same report the following assertion is made: “Unfit for any kind of labour in Kaufbeuren already, dangerous to the public, needs to be interned in a closed institution” (medical report of Günzburg State Hospital, September 18th, 1940).

On October 22nd, 1940 – after 24 years of hospitalization – the medical report ends with the sentence “Is transferred to another institution today.” It is likely that he was first transported to the Zwiefalten state hospital and subsequently (November 13, 1940) taken to the Grafeneck killing institution.

Patient S.F. (AZ 21231 R 179), “transferred to another institution” on November 22nd, 1940, at the age of 22.

Patient S.F., male, was born on September 28th, 1918.

At the age of 11 years S.F. was put under guardianship on account of mental instability and with a diagnosis of mental disorder. He was admitted to the churchrun care home of Schweinspoint, which provided care for people with mental illness and mental handicap / learning disability. The ruling of the guardianship court (Vormundschaftsgericht) of October 1929 stated: “The boy is not capable of learning and therefore cannot be educated. S. is physically robust and healthy, but mentally he remains at the stage of an animal, cannot speak but, at times, cries like an animal, is permanently looking for food and he is unclean; he can, therefore, – and because he will not accept other clothing on his body – only be dressed with a shirt, or, at most, with a gown. (…) But presumably the father A.F. is guilty of neglecting his son.” (Ruling of the guardianship court of October 1929). In the medical file there is a record of an expert report of the public health officer from Schweinspoint. It is dated September 12th, 1934, and includes the following paragraph : “[The patient, F. St.] suffers from complete idiocy, is fully disoriented, very unclean and restless. He resides in a locked ward and requires permanent professional attention and

supervision 24 hours a day. He requires a high level of care from the nursing staff as he leaves an impression of destitution and disgust in every respect. There is no way the patient can live with mentally sane people. It was even difficult to make him share his daily routine with other patients/inmates, and he would substantially disturb tranquility by constant screaming. In summary, there are effects of an incurable, serious mental illness: complete idiocy. Signed Dr. Eichinger” (Institutional medical report of the sanatorium and nursing home of Schweinspoint, September 12th, 1934). Mental handicap (Ws 1a) was diagnosed, it was assumed that the patient was unable to work.

On November 13th, 1940, i.e., after 11 years in the Schweinspoint institute, the patient was transferred to the Günzburg State Hospital at the age of 22 together with 31 other fellow-residents (patients). The stay at Günzburg lasted only 9 days. On November 22th, 1940, S.F. was taken to a killing institution, probably to Hartheim/Linz. During the short stay at the Günzburg State Hospital no entries were made in the patient’s medical file. The only document to refer to S.F. is a notification in the patient file from the archive of today’s Günzburg District Hospital by Dr. Barth, a senior member of the medical staff, to the town registry office (Standesamt) of Günzburg dated January 14th, 1941. It refers to an enquiry of the registry office regarding the whereabouts of the patient, and the brief statement reads, literally: “place of residence and demise unknown” (notification to town registry of Günzburg, January 14, 1941, file Z, patient archive, Günzburg).

Patient G.S. (AZ 3157 R 179), “transferred to another institution” on July 1st, 1941, at the age of 32.

G.S., male, was born at Stettenhofen near Augsburg on October 1st, 1909. There are few hints concerning the circumstances of his life prior to his admission to a mental institution. Early in his life a “congenital mental deficiency” (Ws 1a) was diagnosed. A medical report of the local health authority (Gesundheitsamt) of Augsburg, dated June 15th, 1937, states that the relatives had “neither time nor understanding” for what was considered, in terms of diagnosis, to be congenital insanity, and family members considered him to be a “malicious and lazy man.” In the report on medical findings the general condition of G.S. was described as being in need of care, and he himself was described as “feeble and shrunk” (medical report of the health authority of Augsburg, June 15th, 1937). Therefore, the health authority of Augsburg ordered the admission to the sanatorium (mental health care insti271

Clinical Histories of Psychiatric Patients Murdered in the Nazi “Euthanasia” Program

tution) of Schweinspoint on the basis of a custodial order.

In the documents that are available there is no medical / nursing record concerning his admission. It can, however, be assumed that the patient was registered within the framework of the “Aktion-T4” and that the decision for deportation was made in Berlin. Although G.S. had been hospitalized for only three years, he was taken to the Günzburg State Hospital along with 21 other patients, both male and female (November 14th, 1940). During his stay in Günzburg short entries were made in the medical file (which includes the additional marking of “collective transport”). In the admission record at Günzburg the patient is described as “idiotic, obtuse” and “sometimes violent” (medical report of the sanatorium and nursing home, Günzburg, entry dated November 11th, 1940). In the last entry of July 1st, 1941, there is the short statement: “Transferred to another institution.” It is likely that he was transported to the Hartheim killing institution.

Patient H. D. (AZ 3726 R 179), “transferred to another institution” on July 1st, 1941, at the age of 68.

H.D., female, was born on October 20 th, 1871.

H.D. was Jewish. From March to September 1919, she had been hospitalized at the mental hospital of Klingenmünster. Her clinical appearance was described as follows: “Usually, her mental health state changes from day to day. Talking a lot one day and eating plenty when she is in a manic state, she may be depressed with a negative outlook the following day and may well refuse food and complain about her environment on a third day” (medical report of Klingenmünster state hospital, entry dated September 9th, 1939). H.D. was diagnosed with manic-depressive insanity (Ws 15a). Regarding the behavior of H.D. medical records state that she is “apathetic” and “violent.” There is no clear statement regarding the patient’s working ability but the description of her clinical presentation suggests that H.D. may have been in a position to work. The last entry from Klingenmünster is: “Was transferred to the sanatorium and nursing home in Günzburg as a refugee in view of the present wartime situation.” On September 10th, 1939, H.D. was transferred to the Günzburg State Hospital together with five other female patients. In the patient file there is also a response letter to an enquiry of the patient’s son, who lived in New York (by Dr. Wilhelm H. Leinisch, who was a member of the senior medical staff). His statement includes a brief description of the current mental state of the patient. The characteristics of H.D.’s pattern of disease were described in similar words as in previous medical reports.

272

On July 5th, 1940, after a total duration of hospitalization of 21 years, H.D. was transferred from Günzburg to the mental hospital of Zwiefalten (with 75 other female and male patients). On that day, no other entry was made; on July 30th, 1940, she was transferred to the Grafeneck killing institution. Even if no other hints can be found for the assumption that some patients may have been sent to a killing camp directly, the date of death of the patient, which is noted in the patient file, suggests this assumption. In the administrative file of the patient at today’s Günzburg District Hospital, correspondence between relatives of the patient and the medical director, Dr. Sighart, has been preserved. A female cousin living in Jerusalem and a family from Speyer asked for the whereabouts of the patient after her deportation. Dr. Sighart responded and informed the patient’s family of the transfer to the Zwiefalten institution. There are also enquiries of the British Red Cross dated July 1939 and of the United Restitution Office dated 1953 which asked for the whereabouts of the patient. Enquiries of this kind from relatives and administrative authorities can often be found in medical files of (female and male) Jewish patients who were deported within the “Aktion-T4.” Contrary to the widely held belief that “euthanasia” was only practiced on nonJewish citizens – many thousands of Jewish people with mental illness died in the “Aktion T4” (18).

Conclusion The medical records of patients analyzed and described above bear testimony to the fact that everyday language and medical terminology were mixed in the medical entries, especially in the descriptions of patient behavior.

Further consideration of this practice of medical reporting requires that medical records should be seen in their historical context: mentally ill people were considered to be a potential danger in everyday life, and the period was characterized by widespread views that exhibiting behavior beyond the obvious norm constituted a danger and threat to public order. Expressions of everyday and colloquial language can be found in the description of psychopathologic examination reports. In summary, stigmatizing, disdainful, pejorative and humiliating wording is used in the descriptions of medical conditions and behaviors of patients; examples for this include terms such as “idiotic,” “dull,” “silly,” “completely stupid,” “stupid grimaces” or “congenital idiocy.” From a historical perspective this finding may not be surprising as there has

Florian Steger et al.

been a significant development in medical psychiatric terminology (especially since 1945), and this has comprised a clear distinction of descriptive clinical terminology from everyday language (7). In the 1930s and 1940s there was no recognized operationalized psychiatric classification system and no established psychopathological descriptive inventory which would have supported a diagnostic routine striving for more objectivity.

Another finding to be considered is that entries in medical reports were made at widely irregular intervals.

Shortage of time among medical staff may have played a role. The transfer of large patient groups made continuity of treatment and the provision of individualized care more difficult. On the basis of the medical records scrutinized it must be assumed that individualized care was not practiced. Furthermore, there is a clear impression that the practice of listening to patients in order to understand and determine the basis or type of mental disorder was not part of the daily routine of clinical examination, diagnostic work-up and treatment practice. At an early stage, stigmatizing and discriminating terms and concepts were chosen which are likely to have led to multiple traumatization. It is difficult to reconstruct biographical trajectories or data on illness course from clinical records. It is only rare that biographical fragments and personal statements of patients were taken note of and documented. These findings are also due to the genre of “patient history,” because in the patient file a socially designed reality emerges as the final point of biological and social parameters (7, 14).

Under the conditions of the medical documentation routine found in the patient files it was difficult to obtain insight into the living circumstances and individual biographies of the patients (8, 19). What has been presented barely reflects the institutional itinerary or history of patients and is restricted to a narrow institutional perspective. In patient histories and medical documents we are confronted with views which were close to the ideological premises of the time saturated with experiences of violence. Some entries are an expression of medical discourse in a time of degeneration theory and eugenics, with the additional element of political-ideological radicalization in the Third Reich (20) which exacerbated the traumatization of patients.

Thus, the brief case histories taken from medical records highlight medical evaluation practice regarding patients with mental illness in a general environment of a clandestine killing program and dehumanizing institutional practice. In addition, the case studies reported attempt

to recall the persons killed in the “Aktion T4” in a dignified way by partially reconstructing the institutional aspects of their life stories and claiming a historical place of remembrance for them. The description of single patient histories can help us understand the collective fate of a whole group of people suffering from mental disorders. The full biographical reconstruction is pending, and any such attempt will have to search beyond the institutional records that are available. The futile attempt of biographical reconstruction of life stories of patient victims presented in this paper is but one attempt to remember the fate of people with mental illness who were killed in Nazi Germany. Finally, we have to take note that the current state of research provides no clarity concerning the circumstances of patients’ deaths. The program of systematic extermination of people with mental illness comprised the attempt to camouflage even the places of death of victims.

Acknowledgements We thank Boris Böhm, Gedenkstätte Pirna-Sonnenstein, Gerhard Fischer, director of nursing, District Hospital (BKH) Günzburg, Sebastian Koch, Gedenkstätte Grafeneck, Wilhelm Losert, former head of administration, BKH Günzburg and Bodo Rüdenburg, Südwürttembergische Zentren für Psychiatrie Zwiefalten, for their support in our research.

References 1. Süß W. Der “Volkskörper” im Krieg – Gesundheitspolitik, Gesundheitsverhältnisse und Krankenmord im nationalsozialistischen Deutschland 1939-1945 (Studien zur Zeitgeschichte 65). München: Oldenbourg, 2003.

2. Benzenhöfer U. Der gute Tod? – Euthanasie und Sterbehilfe in Geschichte und Gegenwart. München: C.H. Beck, 1999.

3. v. Cranach M, Schüttler H. Heil- und Pflegeanstalt Günzburg. In: v.

Cranach M, Siemen H, editors. Psychiatrie im Nationalsozialismus.

Die Bayerischen Heil und Pflegeanstalten zwischen 1933 und 1945.

München: Oldenbourg, 1999: pp. 249–264.

4. Faulstich H. Hungersterben in der Psychiatrie 1914-1949. Mit einer Topographie der NS-Psychiatrie. Freiburg im Breisgau: Lambertus, 1998.

5. Siemen H. Die bayerischen Heil- und Pflegeanstalten während des Nationalsozialismus. In: v. Cranach M, Siemen H, editors. Psychiatrie im Nationalsozialismus. Die Bayerischen Heil und Pflegeanstalten zwischen 1933 und 1945. München: Oldenbourg, 1999: pp. 417-74.

6. Keller S. Günzburg und der Fall Josef Mengele. Die Heimatstadt und die Jagd nach dem NS-Verbrecher. München: Oldenbourg, 2003.

7. Fuchs P, Rotzoll M, Müller U, Richter P, Hohendorf G. Das Vergessen der Vernichtung ist Teil der Vernichtung selbst. Lebensgeschichten von Opfern der nationalsozialistischen “Euthanasie.“ Göttingen: Wallstein, 2007.

8. Schmuhl HW. Rassenhygiene, Nationalsozialismus, Euthanasie. Von der Verhütung zur Vernichtung “lebensunwerten Lebens,” 1890-1945.

2nd ed. Göttingen: Vandenhoeck & Ruprecht, 1992.

9. Görgl A. Die “Aktion T4” und die Rolle der Heil- und Pflegeanstalt Günzburg. Medizinische Dissertation. Ulm, 2008.

10. Steger F, Görgl A, Strube W, Winckelmann HJ, Becker T. Die “Aktion-T4” und die Rolle der Heil- und Pflegeanstalt Günzburg. Psychiatrische Praxis 2010;37:300-305.

273

Clinical Histories of Psychiatric Patients Murdered in the Nazi “Euthanasia” Program

11. Dörries A, Vollmann J. Medizinische und ethische Probleme der Klassifikation psychischer Störungen. Dargestellt am Beispiel des Würzburger Schlüssel von 1933. Fortschritte der Neurologie, Psychiatrie 1997;65:550-554.

12. Steger F, Schmer B, Strube W, Becker T. Zwangssterilisationen nach dem Gesetz zur Verhütung erbkranken Nachwuchses. Die Rolle der Heil- und Pflegeanstalt Günzburg. Nervenarzt 2011. DOI 10.1007/ s00115-011-3253-3.

13. Steger F, Strube W, Becker T. Neuropathologische Forschung an Organen von Patienten der Heil- und Pflegeanstalt Günzburg. MMWFortschritte der Medizin Originalien I/2011; 153; 6-9.

14. Steger F, Görgl A, Strube W, Winckelmann HJ, Becker T. Die “Aktion-T4.”

Erinnerung an Patientenopfer aus der Heil- und Pflegeanstalt Günzburg.

Nervenarzt 2010: DOI: 10.1007|s-00115-010-3031-7.

15. Sandner P. Die Euthanasie-Akten im Bundesarchiv. Zur Geschichte eines lange verschollenen Bestandes. Vierteljahreshefte für Zeitgeschichte

274

1999;47:385-400.

16. Aas N. Von der Logistik des Todes. Die Verlegung von bayerischen Anstaltskranken nach Schloss Hartheim (August 1940 bis August 1941). In: Kepplinger B, Marckhgott G, Reese H, editors. Tötungsanstalt Hartheim. 2nd ed. Linz: OÖLA, 2008: pp. 261-317.

17. Aas, N. Kalendarium der “T4”-Transporte aus bayerischen Heil- und Pflegeanstalten. In: Kepplinger B, Marckhgott G, Reese H, editors.

Tötungsanstalt Hartheim. 2nd ed. Linz: OÖLA, 2008: pp. 319-323.

18. Strous R. Examination of the Jewish mentally-ill during the Nazi era – “the doubly cursed.” Isr J Psychiatry Relat Sci 2008;45:247-256.

19. Jüdisches Museum Berlin, editor. Tödliche Medizin. Rassenwahn im Nationalsozialismus. Göttingen: Wallstein, 2009.

20. Roelcke V. Zeitgeist und Erbgesundheitsgesetzgebung im Europa der 1930er Jahre. Eugenik, Genetik und Politik im historischen Kontext.

Nervenarzt 2002;73:1019-1030.

Isr J Psychiatry Relat Sci - Vol. 48 - No 4 (2011)

Yaron Gilat et al.

Anti-ribosomal P antibody in schizophrenia Yaron Gilat, MD,1 Yehuda Shoenfeld, MD,2,4 Moshe Kotler, MD,3,4 and Iulian Iancu, MD 3,4 1

Brill Mental Health Community Center, Ramat Chen, Tel Aviv, Israel Department of Internal Medicine B and Center for Autoimmune Diseases, Sheba Medical Center, Tel Hashomer, Israel 3 Be'er-Yaakov and Ness Ziona Mental Health Center, Israel 4 Sackler Faculty of Medicine, Tel Aviv University, Ramat Aviv, Israel 2

ABSTRACT Background: A series of epidemiological, clinical and laboratory findings suggest an autoimmune process in schizophrenia and include, among others, high titers of various autoantibodies in the sera of patients. Antiribosomal P antibody is known to exist in systemic lupus erythematosus (SLE) patients with a psychiatric presentation, including psychosis, rationalizing the examination of its existence in patients with schizophrenia.

Methods: Sera of 59 patients, 48 diagnosed with schizophrenia and 11 diagnosed with a schizoaffective disorder, were examined for the presence of antiribosomal P antibody titers using ELISA. The control group consisted of 94 healthy subjects with similar age and gender distribution.

Results: Anti-ribosomal P antibody titers were below cut-off level in 58 patients and borderline in one patient, similar to the low titers of the control group.

Conclusions: Previous investigations have demonstrated high specificity for anti-ribosomal P antibody in SLE patients with psychosis. In view of the results of this study, however, anti-ribosomal P antibody is not a biological marker for schizophrenia.

Introduction Anti-ribosomal P antibodies (anti-P-R) are a unique group of autoantibodies found in the sera of systemic lupus erythematosus (SLE) patients. Anti-P-R target P0, P1 and P2 proteins are located on the eukaryotic ribosomal * This work was performed in partial fulfillment of the MD thesis requirements of the Sackler Faculty of Medicine, Tel Aviv University.

Address for Correspondence:

sub-unit and are capable of penetrating cells and inducing apoptotic changes, which lead to inhibition of specific cytokine secretion (1-8). Various reports have established anti-P-R as highly specific for SLE with a prevalence of 6-46%, while they only rarely appear in other autoimmune disorders (4, 9-13). Nonetheless, their major importance is related to the strong correlation between their presence and central nervous system (CNS) involvement in SLE patients (10, 14-23) and to their high sensitivity for SLE psychosis (4, 13, 21, 24). Animal studies have demonstrated that anti-P-R can bind to the limbic area of the mouse brain and penetrate into neuronal cells in vitro.

Furthermore, intra-cerebro-ventricular injection of these antibodies induces experimental depression-like models in naive mice (25, 26).

CNS involvement in SLE, often termed neuropsychiatric SLE (NPSLE), is prevalent in 50-90% of SLE patients (27, 28). Despite the fact that out of the eleven criteria established by the American College of Rheumatology for the diagnosis of SLE, only one relates to CNS involvement and refers to seizures and psychosis, a large variety of neuropsychiatric manifestations is mentioned in the SLE literature (24, 27-32). Pure psychiatric disorders are present in 15-75% of all SLE patients (32, 33), mainly adjustment disorder, anxiety disorders, mood disorders and psychosis (27, 29, 30, 32). In a minority of cases, the first presentation of SLE involves CNS symptoms and only few patients present solely with psychiatric symptoms (30, 34-37). Lim et al. (30) found that in patients with psychiatric presentation, depression was the most common symptom, while the rarest was psychosis.

The most common disorder presenting with psychosis in the general population is schizophrenia. This is a destructive and debilitating mental illness, affecting 1% of the population (38-41), in which no laboratory or imaging finding is pathognomonic, nor does any single symptom exist in all patients (40, 41). Several hypotheses relate

Dr. Iulian Iancu, Yavne Mental Health Center, 4 Dekel Street, Yavne 81000, Israel

â&#x20AC;&#x2020; iulian1@bezeqint.net

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Anti-ribosomal P antibody in schizophrenia

to the pathophysiological process underlying schizophrenia, mainly the hyper-dopaminergic hypothesis, but also the neuro-developmental hypothesis, the psychosocial hypothesis, the viral hypothesis and the immune hypothesis, the latter including the autoimmune hypothesis (38, 39, 41). Various epidemiological, clinical and laboratory reports show strong support for the autoimmune hypothesis in schizophrenia (42-52). Among these, repeated efforts have demonstrated a relatively high prevalence of autoantibodies in schizophrenic patients, including anti-dsDNA antibodies (Ab’s), anti-ssDNA Ab’s, anticardiolipin Ab’s, antinuclear Ab’s, anti-histone Ab’s, and anti-cardiolipin Ab’s, some of which have evidently been found in a range of presumably autoimmune disorders, including SLE (42-47). Even though antipsychotic medications may induce the appearance of autoantibodies (4853), several reports have demonstrated the existence of autoantibodies, including anti-cardiolipin Ab’s, anti-DNA Ab’s and anti-Sm Ab’s and others, in drug-naive patients (53-56), excluding the possibility that all autoantibody findings are drug related.

In view of the correlation between anti-P-R and psychosis in SLE patients, and in view of the autoantibodies often found in schizophrenia patients, we examined anti-P-R titers in patients with schizophrenia and schizoaffective disorder.

Methods The study was approved by our local Helsinki committee.

Forty-eight schizophrenia and 11 schizoaffective disorder inpatients from the Be'er-Yaakov and Ness Ziona Center of Mental Health in Israel were diagnosed by a senior psychiatrist according to the DSM-IV-TR diagnostic criteria.

Patients were evaluated and examined in their wards, after signing an informed consent form approved by a local Helsinki committee. For psychiatric evaluation we used the Positive and Negative Syndrome Scale (PANSS).

Eighteen patients were women, 41 were men. Their mean age was 39.66 years (S.D. = 11.97). Among the schizo-

phrenia patients, 26 were diagnosed as suffering from the paranoid subtype, 10 from the disorganized subtype, six from the residual subtype and four from the undifferentiated subtype of schizophrenia. The sub-classification of two patients was difficult to establish at the time of the study.

None were diagnosed with the catatonic subtype.

The inclusion criteria were good Hebrew speaking skills, no prior or concurrent autoimmune or rheumatic disorder diagnosis and no cytotoxic-immunosuppressive treatment in the month prior to our examination. Accordingly, since one paranoid schizophrenia patient was treated for leukemia with Mercaptopurine and Methotrexate, he was excluded from the study.

Two patients had hypothyroidism and Celiac Disease, respectively, but were not excluded because no evidence was found in the medical literature correlating these diseases with anti-P-R. The age of the disease onset was determined as age of first hospital admission, in years.

Six patients were hospitalized for the first time during the study period, five of whom were already treated for 1–6 weeks prior to our examination. Since the evidence suggests that autoantibodies might appear in the sera of neuroleptic-treated patients after 3 to 13 months of drug treatment initiation (48, 49), these latter patients were considered as “not drug-treated,” solely for a classification purpose regarding autoantibodies induction.

One patient was examined 20 days after cessation of drug treatment, yet since neuroleptic-induced autoantibodies disappear from the sera eight weeks after drug cessation (50), this patient was considered as “drugtreated,” once more, for a classification purpose. We also recorded the country of birth, ethnic origin, cigarette smoking, suicidal thoughts and prior suicide attempts (data not elaborated in this paper). Table 1 summarizes some of the patients’ demographic data.

The control group included 94 healthy subjects with similar age and gender. This group comprised of 66 males and 28 females, and had a mean age of 41.5 years (SD=12.11). There were no significant differences between the two groups on age and gender. No subject in the con-

Table 1. Demographic data of patients Diagnosis

N

Patients

Mean age (SD)

Mean age of disease onset (years) (SD)

Male

Female

Male

Female

Total

Schizophrenia

48

33

15

38.46 (10.64)

24.48 (7.25)

24.93 (7.66)

24.63 (7.39)

11

Schizoaffective disorder

11

8

3

44.91 (15.51)

22 (4.77)

19.67 (5.44)

21.36 (5.07)

2

Total

59

41

18

39.66 (11.97)

24 (6.91)

24.06 (7.6)

24.02 (7.13)

13

Legend: N=Number of patients; SD=Standard deviation; NND=Number of “not drug-treated” patients.

276

NND

Yaron Gilat et al.

trol group was diagnosed with a psychiatric or an autoimmune disorder.

Ten milliliters of peripheral venous blood was drawn from each subject, centrifugated at 2800 rounds per minute for 15 minutes, after which the sera was vacuumed out and kept in Eppendorf tubes at -20°C temperature for a maximum period of two months before analysis.

ELISA was used for establishing anti-P-R titers according to the manufacturer’s instructions (AESKU.Diagnostics GMBH, Germany). The cutoff level was 15 U/ml, above which APA titers were considered “positive.”

Results The mean PANSS score was 82.97±12.6, ranging between 53 to 110. No positive anti-P-R results were found, either in the patients’ group or in the control group. One subject from the patients’ group demonstrated a borderline anti-P-R titer of 17.32 U/ml (we refer to this result as borderline as positive results are usually higher). She was a patient of Ethiopian origin in her first hospital admission and was also the youngest of all patients examined (21 years old). Two other patients of Ethiopian origin did not demonstrate above cutoff level anti-P-R titers. Resulting from the overall low anti-P-R titers, it was not possible to establish a correlation between demographic data, PANSS scores and anti-P-R titers. Table 2 summarizes the mean anti-P-R titer results in the study sample.

Discussion Our aim was to examine the presence of anti-ribosomal P antibodies in the sera of schizophrenia and schizoaffective patients, based on two prior findings. 1) Autoimmune antibodies, including specific autoantibodies such as antibrain Ab’s, have been repeatedly found in sera of schizophrenia patients (42-47). 2) Anti-P-R antibodies have been repeatedly found in sera of SLE patients in general Table 2. Mean anti-P-R titer results according to psychopathology Diagnosis

Number of subjects

Mean APA titer (U/ml) (SD)

Schizophrenia

48

4.31 (2.91)

Schizoaffective disorder

11

5.78 (4.46)

Total

59

4.58 (3.34)

Control group

94

4.24 (2.20)

SD=Standard deviation. U/ml=units per milliliter.

and in NPSLE patients in particular, including those with psychiatric symptoms (13-21, 57).

To our knowledge, after performing a Medline search, except in few very small control groups, anti-P-R antibodies were not directly investigated in schizophrenia spectrum disorders thus far. Bonfa et al. (16) examined anti-P-R in the sera of 20 psychotic SLE patients. The control group included 13 psychotic patients without SLE, among whom there were manic patients, depressive patients and schizophrenia patients. They demonstrated high anti-P-R titers in 18 of the 20 SLE patients while anti-P-R titers were low in all of the control patients, including the schizophrenia patients. Press et al. (18) examined anti-P-R in 79 SLE pediatric patients, out of which 13 had SLE-related psychosis. The control group included 12 children with primary psychosis, unrelated to SLE. High anti-P-R titers were demonstrated in 5 of 13 (38%) SLE psychotic patients, while all 12 control patients had low titers. As in these papers, we too failed to demonstrate high anti-P-R titers in schizophrenia and in schizoaffective disorder.

Three possible drawbacks should be considered. first, most of our patients were chronic and drug treated.

Nevertheless, we found low anti-P-R titers in the untreated group as well as in the drug-treated group. Second, since recruiting patients into the study required their informed consent, those with extreme paranoid ideations refused to give consent, practically excluding this important subpopulation from the study. Third, the patients examined in our study were all adults, relatively older, with a mean age of 40 years. Subjects’ age and the time course of their illness may both be important.

Mendelovic et al. (43) asserted that the immune system’s involvement in schizophrenia in general and antibodies involvement in schizophrenia in particular, is not adequately understood. Moreover, it is not clear whether the latter expresses a primary pathophysiological process or a secondary reaction to endogenous or exogenous antigen stimulation, including brain antigens. Strous and Shoenfeld (47) point to the possible role of maternal viral infection in the induction of an autoimmune process ultimately leading to schizophrenia. The hypothesis tying birth complications or a maternal viral infection to schizophrenia (38, 42) might also be crucial to the understanding of immunological phenomena in this disease. If indeed autoantibodies appearance is related to some earlylife pathological event or to a pathological event in close time proximity to disease onset, the immunopathological reactions may take place early and fade with time, after 277

Anti-ribosomal P antibody in schizophrenia

damage has already been done. In this respect, it is not unlikely that autoantibody assessment, such as anti-P-R analysis, will prove positive in a pediatric population with first episode schizophrenia symptoms, rather than in older chronically ill patients, like those examined in our study.

Conclusions Sera of schizophrenia and schizoaffective patients examined in our study did not contain high titers of anti-P-R. The specificity of this auto-antibody in NPSLE patients as opposed to its absence in psychotic patients of schizophrenia spectrum might very well point to a different mechanism underlying psychosis in different disorders.

In this view, we join other authors (21, 58) in considering anti-P-R as a biological marker for SLE, used as a diagnostic tool to exclude SLE psychosis in psychotic patients. Yet, in order to establish the possible role of this autoantibody in both schizophrenia and in SLE, further research is warranted.

References 1. Elkon KB, Parnassa AP, Foster CL. Lupus autoantibodies target ribosomal P proteins. J Exp Med 1985;162:459-71.

2. Francoeur AM, Peebles CL, Heckman KJ, Lee JC, Tan EM. Identification of ribosomal protein autoantigens. J Immunol 1985;135:2378-84.

3. Shoenfeld Y. The diversity of autoantibodies to P-ribosomal: The infectious-autoimmunity plot. J Mol Med 2007;85:907-909.

4. Zandman-Goddard G, Chapman J, Shoenfeld Y. Autoantibodies involved in neuropsychiatric SLE and antiphospholipid syndrome.

Semin Arthritis Rheum 2007;36:297-315.

5. Shoenfeld Y. To smell autoimmunity: Anti-P-Ribosomal autoantibodies, depression, and the olfactory system. J Autoimmunity 2007;28:165-169.

6. Mahler M, Kessenbrock K, Szmyrka M, Takasaki Y, Garcia-De La Torre I, Shoenfeld Y, et al. International multicenter evaluation of autoantibodies to ribosomal P proteins. Clinical Vaccine Immunol 2006;13:77-83.

7. Sun KH, Tang SJ, Chen CY, Lee TP, Feng CK, Yu CL, Sun GH. Monoclonal ribosomal P autoantibody inhibits the expression and release of IL12, TNF-alpha and iNOS in activated RAW macrophage cell line. J Autoimmun 2005;24:135-143.

8. Reichlin M. Cellular dysfunction induced by penetration of autoantibodies into living cells: Cellular damage and dysfunction mediated by antibodies to dsDNA and ribosomal P proteins. J Autoimmun 1998;11:557-561.

9. Sato T, Uchiumi T, Ozawa T, Kikuchi M, Nakano M, Kominami R, et al.

Autoantibodies against ribosomal proteins found with high frequency in patients with systemic lupus erythematosus with active disease. J Rheumatol 1991;18:1681-1684.

10. Bonfa E, Elkon KB. Clinical and serologic associations of the antiribosomal P protein antibody. Arthritis Rheum 1986;29:981-985.

11. Spezialetti R, Bluestein HG, Peter JB, Alexander EL. Neuropsychiatric disease in Sjogrenâ&#x20AC;&#x2122;s syndrome: Anti-ribosomal P and anti-neuronal antibodies. Am J Med 1993;95:153-160.

12. Shovman O, Zandman-Goddard G, Gilburd B, Blank M, Ehrenfeld M, Bardechevski S, et al. Restricted specificity of anti-ribosomal P antibodies to SLE patients in Israel. Clin Exp Rheumatol 2006;24:694-697.

13. Ebert T, Chapman J, Shoenfeld Y. Anti-ribosomal P-protein and its role in psychiatric manifestations of systemic lupus erythematosus: Myth or

278

reality? Lupus 2005;14:571-575.

14. Gerli R, Caponi L, Tincani A, Scorza R, Sabbadini MG, Danieli MG, et al. Clinical and serological associations of ribosomal P autoantibodies in systemic lupus erythematosus: Prospective evaluation in a large cohort of Italian patients. Rheumatology 2002;41:1357-1366.

15. Tzioufas AG, Tzortzakis NG, Panou-Pomonis E, Boki KA, SakarellosDaitsiotis M, Sakarellos C, et al. The clinical relevance of antibodies to ribosomal-P common epitope in two targeted systemic lupus erythematosus populations: A large cohort of consecutive patients and patients with active central nervous system disease. Ann Rheum Dis 2000; 59:99-104.

16. Bonfa E, Golombek SJ, Kaufman LD, Skelly S, Weissbach H, Brot N, et al. Association between lupus psychosis and anti-ribosomal P protein antibodies. N Engl J Med 1987;317:265-271.

17. Schneebaum AB, Singleton JD, West SG, Blodgett JK, Allen LG, Cheronis JC, et al. Association of psychiatric manifestations with antibodies to ribosomal P proteins in systemic lupus erythematosus.

Am J Med 1991;90:54-62.

18. Press J, Palayew K, Laxer RM, Elkon K, Eddy A, Rakoff D, et al.

Antiribosomal P antibodies in pediatric patients with systemic lupus erythematosus and psychosis. Arthritis Rheum 1996;39:671-676.

19. Nojima Y, Minota S, Yamada A, Takaku F, Aotsuka S, Yokohari R. Correlation of antibodies to ribosomal P protein with psychosis in patients with systemic lupus erythematosus. Ann Rheum Dis 1992;51:1053-1055.

20. Agius MA, Chan JW, Chung S, Lee EK. Role of antiribosomal P protein antibodies in the diagnosis of lupus isolated to the central nervous system. Arch Neurol 1997;54:862-864.

21. Abdel-Nasser AM, Ghaleb RM, Mahmoud JA, Khairy W, Mahmoud RM. Association of anti-ribosomal P protein antibodies with neuropsychiatric and other manifestations of systemic lupus erythematosus. Clin Rheumatol 2008; May 15.

22. Toubi E, Shoenfeld Y. Clinical and Biological aspects of anti-P-ribosomal protein autoantibodies. Autoimmunity Rev 2007;6:119-125.

23. Muscal E, Myones BL. The role of autoantibodies in pediatric neuropsychiatric systemic lupus erythematosus. Autoimmun Rev 2007;6:215-217.

24. Strous R, Shoenfeld Y. Behavioral changes in systemic lupus erythematosus are of an autoimmune nature. Nat Clin Prac Rheum 2007;3:592-593.

25. Blank M, Beinglass I, Shoenfeld Y. The therapeutic potential of targeting anti-Ribosomal-P antibody in treating SLE patients with depression.

Expert Opin Biol Ther 2007;7:1283-1285.

26. Katzav A, Solodeev I, Brodsky O, Chapman J, Pick CG, Blank M, Zhang W, Reichlin M, Shoenfeld Y. Induction of autoimmune depression in mice by anti-ribosomal P antibodies via the limbic system. Arth Rheum 2007;56:938-948.

27. Brey RL, Holliday SL, Saklad AR, Navarrete MG, Hermosillo-Romo D, Stallworth CL, et al. Neuropsychiatric syndromes in lupus: Prevalence using standardized definitions. Neurology 2002;58:1214-1220.

28. Borchers AT, Aoki CA, Naguwa SM, Keen CL, Shoenfeld Y, Gershwin ME. Neuropsychiatric features of systemic lupus erythematosus.

Autoimmun Rev 2005;4:329-344.

29. Calabrese LV, Stern TA. Neuropsychiatric manifestations of systemic lupus erythematosus. Psychosomatics 1995;36:344-359.

30. Lim L, Ron MA, Ormerod IE, David J, Miller DH, Logsdail SJ, et al. Psychiatric and neurological manifestations in systemic lupus erythematosus. Q J Med 1988;66:27-38.

31. Jennekens FG, Kater L. The central nervous system in systemic lupus erythematosus. Part 1. Clinical syndromes: A literature investigation.

Rheumatology 2002;41:605-618.

32. Purandare KN, Wagle AC, Parker SR. Psychiatric morbidity in patients with systemic lupus erythematosus. QJM 1999;92:283-286.

33. Stojanovich L, Zandman-Goddard G, Pavlovich S, Sikanich N. Psychiatric manifestations in systemic lupus erythematosus. Autoimmun

Yaron Gilat et al.

Rev 2007;6:421-426.

34. Hernandez Rodriguez I, Moreno MJ, Morano LE, Benavente JL. Systemic lupus erythematosus presenting as pseudocyesis. Br J Rheumatol 1994;33:400-402.

35. Moorhead SR, Lee AS. ANA negative systemic lupus erythematosus. Br J Psychiatry 1994;164:682-683.

36. Khan S, Haddad P, Montague L, Summerton C. Systemic lupus erythematosus presenting as mania. Acta Psychiatr Scand 2000;101:406-408.

37. Zapor M, Murphy FT, Enzenauer R. Echolalia as a novel manifestation of neuropsychiatric systemic lupus erythematosus. South Med J 2001;94:70-72.

38. Carpenter WT, Buchman RW. Schizophrenia. N Engl J Med 1994;330 :681-690.

39. Sawa A, Snyder SH. Schizophrenia: Diverse approaches to a complex disease. Science 2002;296:692-695.

40. Andreasen NC. Symptoms, signs, and diagnosis of schizophrenia.

Lancet 1995;346:477-481.

41. Thaker GK, Carpenter WT Jr. Advances in schizophrenia. Nat Med 2001;7:667-671.

42. Gaughran F. Immunity and schizophrenia: Autoimmunity, cytokines, and immune responses. Int Rev Neurobiol 2002;52:275-302.

43. Mendelovic S, Doron A, Shoenfeld Y. Schizophrenia â&#x20AC;&#x201C; an autoimmune disease? Harefuah 1997;133:629-631 (Hebrew).

44. Amital-Teplizki H, Shoenfeld Y. Has schizophrenia an immunologic basis? Harefuah 1991;120:392-394 (Hebrew).

45. Sirota P. Is schizophrenia an autoimmune disease? Isr J Med Sci 1990; 26:694-697.

46. Amital H, Shoenfeld Y. Autoimmunity and schizophrenia: An epiphenomenon or an etiology? Isr J Med Sci 1993;29:593-597.

47. Strous RD, Shoenfeld Y. Revisiting old ghosts: Prenatal viral exposure

and schizophrenia. IMAJ 2005;7: 43-45.

48. Canoso RT, Sise HS. Chlorpromazine-induced lupus anticoagulant and associated immunologic abnormalities. Am J Hematol 1982; 13:121-129.

49. Sarzi-Puttini P, Atzeni F, Capsoni F, Lubrano E, Doria A. Drug-induced lupus erythematosus. Autoimmunity 2005; 38:507-518.

50. Dubois EL, Tallman E, Wonka RA. Chlorpromazine-induced systemic lupus erythematosus: Case report and review of the literature. JAMA 1972; 221: 595-596.

51. Strous RD, Shoenfeld Y. The mosaic of schizophrenia: Has the time arrived to monitor the illness with biomarkers? Clinical Biochemistry 2008;41:353-354.

52. Schwartz M, Silver H. Lymphocytes, autoantibodies and psychosis â&#x20AC;&#x201C; coincidence versus etiological factor: An update. Isr J Psychiatry Relat Sci 2000;37:32-36.

53. Chengappa KN, Ganguli R, Ulrich R, Rabin BS, Cochran J, Brar JS, et al. The prevalence of autoantibodies among right and left handed schizophrenic patients and control subjects. Biol Psychiatry 1992;32:803-811.

54. Firer M, Sirota P, Schild K, Elizur A, Slor H. Anticardiolipin antibodies are elevated in drug-free, multiply affected families with schizophrenia.

J Clin Immunol 1994;14:73-78.

55. Sirota P, Firer MA, Schild K, Tanay A, Elizur A, Meytes D, et al.

Autoanti-bodies to DNA in multicase families with schizophrenia. Biol Psychiatry 1993; 33:450-455.

56. Sirota P, Firer M, Schild K, Zurgil N, Barak Y, Elizur A, et al. Increased anti-Sm antibodies in schizophrenic patients and their families. Prog Neuropsycho-pharmacol Biol Psychiatry 1993;17:793-800.

57. Karassa FB, Ioannidis JP, Touloumi G, Boki KA, Moutsopoulos HM. Risk factors for central nervous system involvement in systemic lupus erythematosus. QJM 2000;93:169-174.

58. Kiss E, Shoenfeld Y. Are anti-ribosomal P protein antibodies relevant in systemic lupus erythematosus? Clin Rev Allergy Immunol 2007;32:37-46.

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Isr J Psychiatry Relat Sci - Vol. 48 - No 4 (2011)

Evidence-Based Treatment for Pediatric Obsessive-Compulsive Disorder Lindsay Brauer, MA,1 Adam B. Lewin, PhD,2 and Eric A. Storch, PhD2 1

Department of Psychology, University of South Florida, Tampa, Florida, U.S.A. Department of Pediatrics, University of South Florida, St. Petersburg, Florida, U.S.A.

2

ABSTRACT Obsessive-compulsive disorder (OCD) is marked by incessant distressing thoughts or images (obsessions) and/or overt or covert behaviors (or mental rituals) aimed to reduce anxiety (compulsions). The disorder affects 1-2% of children and adults, with up to 80% of adults reporting symptom onset prior to the age of 18 years. Without appropriate intervention, symptoms tend to run a chronic course from childhood into adulthood. Obsessive-compulsive disorder contributes to considerable impairment across multiple domains of functioning, and as a result calls for effective and efficient treatment. To date, both psychological and pharmacological interventions have shown efficacy for pediatric OCD although there are associated advantages and disadvantages that must be considered in treatment planning. The intent of this review is to discuss the current state of literature regarding treatment for pediatric OCD, highlight efficient and cost-effective means of reducing impairment, and conclude with directions for future study.

Author Note: Ms. Brauer has no financial disclosures to report. Dr. Lewin receives research funding from NARSAD, the International OCD Foundation, the Joseph Drown Foundation, and the Friends of the Semel Institute. He serves as a consultant for Prophase Inc. and Otsuka Pharmaceuticals. Dr. Storch receives research support from the National Institutes of Health, Centers for Disease Control, All Children’s Hospital Research Foundation, and Ortho-McNeil Janssen Pharmaceuticals. He receives royalties from Lawrence Erlbaum, Springer Publishers, and the American Psychological Association. He serves as a consultant for Prophase Inc., Otsuka Pharmaceuticals, and CroNos Inc.

Obsessive-compulsive disorder (OCD) is an impairing anxiety disorder which afflicts approximately1-2% of youth and adults worldwide (1-3). The disorder is marked by distressing and uncontrollable thoughts or images (obsessions) and/or overt (i.e., washing, ordering) or covert (i.e., praying, counting) behaviors aimed to reduce distress (compulsions). Obsessive-compulsive symptoms are chronic in nature, and when present during childhood interfere considerably with a child’s psychosocial development across social, family, and academic domains (4-7). If left inadequately treated, clinically significant obsessive-compulsive symptoms are likely to persist into adulthood and cause future impairment (8). Taken together, this information demonstrates the need for appropriate treatment for children with OCD to curtail the negative developmental trajectory that distinguishes OCD from other anxiety disorders (9).

Traditionally, many clinicians have conceptualized the etiology and treatment of adult and pediatric OCD through a psychodynamic perspective, viewing the obsession and compulsions as a complex set of neuroses arising from intrapsychic conflict (10, 11). Unfortunately, treatments based on this premise are not empirically supported in reducing obsessive-compulsive symptoms and have little face validity in understanding etiological factors or symptom maintenance. Due to the prevalence and precarious nature of OCD, mental health providers have begun to move towards evidence-based intervention modalities for the treatment of OCD, including serotonin reuptake inhibitors (SRI) and cognitive behavioral therapy (CBT) (10). Notably, the limited treatment dissemination may contribute to a number of risks (e.g., medication side effects) and in missing an opportunity to intervene during a developmentally critical time period (12). Many youth with OCD are being prescribed antipsychotic or benzodiazepine medications in the absence of efficacy data. Such

Address for Correspondence: Eric A. Storch, PhD, Guild Endowed Chair and Associate Professor, Department of Pediatrics, University of South Florida, 880 6th Street South 4th Floor, St. Petersburg, FL 33701, U.S.A. estorch@health.usf.edu.

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widespread prescription practices are conducted in the absence of supporting pediatric data and the possibility of significant adverse metabolic and cardiovascular effects.

Indeed, youth taking an atypical antipsychotic medication had an average weight increase of 8.5kg over 10 weeks (13).Thus, lower-risk alternatives should be considered prior to prescription of such medications in children (14).Second, inadequate treatment of OCD symptoms during childhood have been associated with numerous psychosocial sequelae, such as problematic family relations, social dysfunction, and academic distress (4-7), which together disrupt normative development. Third, unresolved OCD symptoms tend to be chronic in nature, result in higher rates of reported unemployment, interpersonal conflict, sleep problems, and chronic distress and impairment in adulthood when compared to nonOCD anxiety disorders (9).Thus, early effective intervention is crucial to improving a child’s quality of life and preventing future impairment. Although such treatments are available, information regarding their implementation is not widely disseminated. With these points in mind, the text that follows reviews evidence-based practice for the treatment of pediatric OCD, highlights the intricacies of tailoring treatment to address developmental needs and psychological comorbidity of children, and also discusses the future of treatment for this tenacious disorder.

Phenomenology of Pediatric Obsessive-Compulsive Disorder Like adults, youth with OCD experience obsessions that center upon themes of contamination, symmetry and precision, religiosity, lucky or unlucky numbers, and a marked preoccupation with inappropriate sexual or aggressive thoughts (15-17). Compulsions related to these common themes frequently present as cleaning or decontamination rituals, reassurance seeking, praying, touching or tapping, counting, behaviors that prevent the potential for a child to do harm to self or others, hoarding, or more general routinized behaviors.

Although symptoms presentation in children is generally similar to that of adults, developmental differences do exist. Such differences include children endorsing more vague obsessions (particularly in younger children, 18), simplified content of obsessions (e.g., sexual or aggressive obsessions), increased reassurance-seeking and family involvement in rituals (19, 20), and more rituals focused on achieving a “just right” feeling (21, 22). Unfortunately, it appears that children and adolescents, like many adults

(23), experience a significant delay between symptom onset and appropriate clinical assessment/intervention (22). This may be related to a lack of knowledge/awareness of the disorder by the parent, limited clinician expertise in OCD, and/or lack of available appropriate treatment resources, the latter two issues having been cited as particular issues in Israel (22). Without intervention, OCD is likely to run a chronic course (8), increasing risk for social, academic and overall functional impairment (4). Fortunately, available treatments yield robust effects, with less than half of those treated with psychotherapy, pharmacotherapy, or a combination of both meeting diagnostic threshold at treatment follow-up (4, 24).

Treatment Psychopharmacology. Serotonin reuptake inhibitors have been demonstrated to be effective for both pediatric and adult OCD (25-28). While numerous SRI medications have been examined in youth with OCD, the United States Food and Drug Administration has only given approvals for clomipramine (ages 10 up), sertraline (ages 6 and up), paroxetine (ages 6 and up), fluoxetine (ages 7 and up), and fluvoxamine (ages 8 and up). Clomipramine, sertraline, paroxetine, fluoxetine, and fluvoxamine have consistently demonstrated efficacy in attenuating OCD symptoms (26, 29-35)with case reports in children as young as 3.5 years of age (36). Clomipramine, once the first-line pharmacological treatment for OCD(37), has demonstrated superiority to placebo with statistical separation at 5-6 weeks (38).

Sertraline (26, 31) and fluoxetine (30), similarly, have demonstrated superior efficacy to placebo in reducing OCD symptoms and overall impairment. In addition, sertraline appears to have enhanced effects when used in combination with CBT (26) leading to the suggestion of combined CBT and SRI therapy for the most severe cases. Paroxetine has demonstrated superior treatment response rates compared to placebo (64.9% v. 41.2%), but is unfortunately associated with mild to moderate side effects resulting in treatment discontinuation (34) and the nonlinear pharmacokinetics can complicate dosing in children. Finally, fluvoxamine (32) appears to be only marginally more efficacious in symptom reduction than placebo.

Unfortunately, treatment with pharmacotherapy alone rarely achieves standards of clinical remission (8, 14, 26, 28).In fact, Geller et al. (29) showed that although statistically superior to placebo, the overall difference in reduction between active treatment and placebo in the Children’s Yale-Brown Obsessive Compulsive Scale (39)was marginal 281

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(only 6 points on the 40 point scale). In addition to the concern that many youth will remain symptomatic following an adequate medication course, many SRIs are associated with adverse events which may lead to treatment discontinuation (31, 34, 36) and some families do not find SRI therapy an acceptable intervention (40). In addition, there are few SRI maintenance trials and – overall – there is limited information regarding durability of treatment gains once medications are discontinued in children with OCD. Results from numerous controlled trials in adults do suggest, however, that it is in the best interest of individuals treated with pharmacological interventions alone not to discontinue treatment as recurrence of symptoms is likely (41). Finally, there is concern regarding the risk of “suicidality” (suicidal thoughts and behavior) and behavioral activation in children and adolescents during treatment with antidepressants (see 42 for a comprehensive review).

In sum, although pharmacotherapy presents as an efficacious and widely disseminated treatment for pediatric OCD, there are limitations including the presence of side effects (34), incomplete treatment response, potential for increased suicidality and behavioral activation (42), and recurrence of symptoms once active treatment ends (41).

Cognitive-behavioral therapy. Cognitive-behavioral therapy with exposure and response prevention is an empirically-supported treatment premised on classical and operant conditioning theories. In OCD, previously neutral stimuli become associated with aversive properties (i.e., anxiety, distress), which cause the individual to engage in compulsions to alleviate this distress.

Compulsions, however, only temporarily reduce distress, causing the individual to repetitively engage in ritualistic behaviors. Exposure and response prevention is a central component of CBT which requires the individual to confront the anxiety-inducing thought or stimulus without engaging in compulsions. Distress associated with the stimulus eventually habituates over time with repeated exposures without ritual engagement (43).

Pragmatically, CBT for OCD is a multi-component treatment conducted in a sequential manner. First, an individual is provided with psychoeducation regarding the nature of OCD, including the neurobiological, cognitive, and behavioral underpinnings, and the typical treatment course. Second, a rank-ordered hierarchy is created delineating the degree of distress exposure to anxiety-inducing stimuli without ritual engagement would elicit. Treatment begins with exposure to loweranxiety stimuli together with refraining from ritual engagement, and gradually progresses to exposure to 282

more anxiety-provoking stimuli. As previously described, the exposure involves having the individual confront the feared situation or focus on the anxiety-inducing thought, without engaging in compulsive behaviors. Individuals remain focused or engaged in the feared situation until habituation (i.e., reduction in anxiety to negligible levels) occurs. A single exposure is typically repeated until it no longer produces significant distress. Following successful completion of an exposure (or situation on the hierarchy), treatment progresses to more difficult exposures in a gradual manner through the hierarchy (44).

Based on available empirical data and consideration of the risk/benefit profile of SRI therapy, practice guidelines recommend CBT as the first line treatment for children and adolescents with mild to moderate obsessive-compulsive symptom severity. For those youngsters with more severe symptoms, practice parameters recommend CBT in conjunction with a trial of an SRI (38).

From an outcome standpoint, CBT has consistently shown impressive results in youth with OCD in both efficacy (i.e., controlled clinical trials) (45, 46) and effectiveness research (i.e., analysis of CBT approaches outside of clinical trials) (47, 48). Two separate meta-analyses of randomized-controlled trials comparing the efficacy of CBT to pharmacotherapy and/or control conditions indicated superiority of CBT to pharmacotherapy and control comparisons in reducing obsessive-compulsive symptom severity in youth (25, 49). A large multi-site study compared the efficacy of CBT alone, sertraline alone, CBT and sertraline combined, and pill placebo in the reduction of obsessive-compulsive symptom severity in youth with OCD. Although results suggest that combined treatment was superior to CBT alone, this difference was not statistically significant on some outcomes (e.g., remission). In addition, CBT alone showed a significantly larger treatment effect (overall effect d = .97; site effect d = .51-1.6) than sertraline alone (overall effect d = .67; site effect d = .53-.80). However, it is relevant to note that a site effect in terms of CBT efficacy was observed with one site performing significantly better than another (d= 1.6 versus .51) suggesting caution when interpreting study results.

In addition to these robust empirical findings, effectiveness of CBT outside of the research setting has been well-demonstrated. For example, two open trials of CBT suggest 79-80% response rates (and 45-54% symptom reduction) (47, 48). Similarly, a Norwegian outpatient clinic implementing a combination of individual and family-based CBT demonstrated a large treatment effect (d= 3.49), with youth experiencing an average of 60.6%

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reduction in symptom severity over the course of 12 sessions (51). These data corroborate the author’s clinical experiences at three specialty programs for cognitivebehavioral treatment of pediatric OCD. Rates of remission following CBT range from 40-85% (46), and have been maintained up to 7 years following treatment (45, 46). Although the utility of maintenance therapy has not been empirically evaluated, clinical experience suggests that some children will experience symptom relapse. Accordingly, booster sessions may be one method of reducing relapse and maintaining treatment gains.

Enhancing Treatment Outcomes Despite their efficacy (25, 49), a significant portion of children with OCD do not respond to pharmacotherapy (~50%;(51)) or CBT (30%) (5, 26) and partial response is common. Effects are likely to be enhanced when treatments are tailored to:1) fit the developmental needs of the child, 2) address the manner in which the family system may contribute to obsessive-compulsive symptoms, and 3) address comorbid conditions that may interfere with treatment (52). Next, we discuss the manner in which various treatment strategies have been developed to address these issues.

Family-based CBT. Many children lack the insight into the irrationality of their obsessions either due to their cognitive development level or as a function of the disorder (53-55). This lack of insight likely reduces motivation to engage in therapeutic tasks, attenuating treatment response (56, 57). In order to address this lack of insight and motivation, families are often included in the treatment of youth with OCD for multiple reasons. First, parents can help the child to generalize skills developed in session in real world settings. Second, a child’s parents can increase a child’s awareness of his/her OCD symptoms. Third, parents can help to motivate that child through contingencies to enhance the child’s effort to confront symptoms adaptively. Lastly, by involving a family in treatment for youth with OCD, the manner in which the family system maintains a child’s symptoms can be addressed (58).

Empirical trials of family-based CBT for youth with OCD have demonstrated its superiority to relaxation training (56) and waitlist control. Group or individual formats have been associated with significant remission rates and maintenance of treatment gains at an 18-month follow-up (45). Similarly, intensive (daily for 3 weeks) and weekly (once per week for 14 weeks) family-based CBT have also revealed significant rates of remission;

75% of intensive and 50% of weekly participants achieved remission, and were able to maintain gains at a 3-month follow-up (57). Finally, it has been suggested as an efficacious treatment for youth who only partially-responded to trials of pharmacological interventions (47). As a result, family-based CBT presents as an effective intervention for youth with OCD which can be implemented in an efficient (group or intensive formats) manner.

Comorbidity. Similar to adults, approximately 75% of youth with OCD experience a comorbid psychiatric condition, with comorbid anxiety, depressive, and externalizing disorders among the most prevalent (27, 59-61). As the number of comorbid conditions increases, not only does response to CBT or SRI medication tend to decrease, but risk of relapse increases (27, 61). Disruptive behavior disorders (DBD) and Tourette Syndrome are disorders frequently diagnosed in children with OCD, and as a result their impact on OCD treatment has been widely examined.

Disruptive behavior disorders, such as oppositional defiant disorder and conduct disorder are among the most common comorbid disorders associated with pediatric OCD (62). Obsessive-compulsive disorder with a comorbid DBD is associated with greater OCD symptom severity and impairment, as well as greater overall anxiety and internalizing problems than those without a DBD (63). The presence of DBDs has been found to attenuate response to pharmacological (27) and psychosocial interventions (61). Anecdotally, the presence of rage or aggressive behaviors has been noted among youth with OCD. Unfortunately, “rage attacks” among youth with OCD are poorly studied. A recent study suggests that youth with OCD who present with rage attacks versus those without have increased OCD symptom severity and are more likely to report sexual, religious and aggressive obsessions and increased checking rituals (64). The presence of OCD may predispose some youth to have rage attacks, perhaps due to exposure to obsessional triggers or limited family accommodation of symptoms (19, 64). For these cases, parent-training approaches which introduce contingencies for non-compliance with therapeutic or parental commands have shown to reduce OCD-related impairment in youth (19, 46, 57).

Tics are common among youth with pediatric onset OCD (69, 70), with approximately 16% of children and adolescents with OCD exhibiting tics at some point (26, 27, 67). Similarly, 50% of children with Tourette Syndrome/ Chronic Tic Disorder (TS/CTD) meet diagnostic criteria for OCD at some point during their development (68).

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Given this significant overlap, OCD may have a different clinical presentation when TS/CTD is also present particularly in the presence of motoric compulsions and tics, complicating differential diagnosis (69). Some clinicians suggest that examining the relationship between the behavior and purpose (e.g., non-specific or anxiety-relieving) aids in this distinction. The presence of comorbid tics may attenuate pharmacological treatment response in pediatric OCD (67), but not CBT (67, 70). Notably, albeit a preliminary study, the presence of a tic disorder did not predispose youth with OCD to greater risk of rage attacks (64). Having a comorbid diagnosis of major depressive disorder (MDD) may attenuate treatment response as it may affect habituation to exposures (60, 71). For such cases, sequential treatment of MDD prior to OCD through the use of CBT or SRIs may enhance the effects of CBT for OCD. Attention-deficit hyperactivity disorder has also been found to attenuate CBT response, as this condition may interfere with a childâ&#x20AC;&#x2122;s ability to focus on therapeutic strategies, and execute exposures independently (59, 72).

Comorbid anxiety disorders have no impact on treatment response in OCD (67, 73).

Overall, comorbidity is a common feature in pediatric OCD, affecting up to 75% of children which may affect treatment outcome if not properly considered and addressed within the treatment plan (27, 59-61).

In addition to the psychosocial intervention strategies previously mentioned, there are pharmacological strategies to address comorbidities associated with pediatric OCD. As this is beyond the scope of the current review, however, we direct the reader to the following articles for more information on this topic (22, 27, 51, 74).

Flexible treatment modalities. Unfortunately, access to evidence-based psychotherapy for OCD is limited (75, 76), particularly for youth. In general, the dissemination of CBT for pediatric OCD is particularly problematic in Israel in that programs continue to train clinicians in psychodynamic approaches, rather than CBT, resulting in a shortage of available clinicians (76). In addition, there are many nuances involved in tailoring the treatment to match the clinical characteristics of the affected child. This predicament may be particularly relevant in Israel, as CBT has only recently begun to be recognized as an effective treatment for OCD (10, 77).As a result of limited training and treatment dissemination, many clinicians may rely on pharmacotherapy alone or with nonevidence-based psychotherapy given its accessibility.

Since treatment with pharmacotherapy does not have the same access issues as in psychotherapy (i.e., locat284

ing a CBT provider), a recent study in the United States examined the additive effects of CBT to ongoing pharmacotherapy (78). The study examined three modes of treatment: CBT provided by trained psychologists in conjunction with continued SRI treatment; a diluted from of CBT (encouraged the use of CBT strategies rather than implementing strategies in session) conducted by the prescribing psychiatrist with ongoing SRI treatment; and SRI treatment alone. Although results have yet to be published, this design highlights the potential of CBT dissemination through psychiatrists in a manner that decreases both time and financial burden on the family.

Intensive treatment. Intensive treatment serves as a treatment option which not only benefits more severe cases in which symptoms are pervasive and impairing, or when insight and motivation are low, but is also an option when typical treatment formats are not available (i.e., geographical barriers) (2, 79). Cognitive-behavioral therapy is quite flexible in terms of the frequency in which sessions are held. In standard CBT for OCD, 60-minute sessions are held once per week for 13-20 weeks (38). Intensive CBT, however, consists of sessions 3-5 times per week for typically 3-5 weeks. Numerous studies have demonstrated the efficacy of intensive CBT for children with OCD (47, 57, 80, 81).

Future Directions D-Cycloserine. Research on the neural circuitry underlying fear extinction has led to the examination of d-cycloserine (DCS), a partial agonist at the NMDA receptor in the amygdala, as a method of enhancing CBT outcome. Among adult OCD, preliminary results have supported the use of DCS to augment exposure therapy (e.g., 82, 83). Storch and colleagues (84) recently examined the impact of DCS administration in conjunction with weekly CBT compared to placebo augmentation in youth with OCD. Compared to the CBT+Placebo group, youth in the CBT+DCS arm showed small-tomoderate treatment effects (d=.31 to .47 on primary outcomes). DCS was safe and well tolerated.

Treatment augmentation. Unfortunately, many youth suffer from treatment resistant OCD. Treatment resistant OCD is defined as failing adequate trials of either CBT (which is typically defined as a minimum of 12 sessions of CBT, including psychoeducation, exposure and response prevention, and discussions of relapse prevention), or failure to respond to two different SRIs (a trial of an adequate dose for at least 10 weeks, depending on

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the medication) (85). For this subgroup of youth with OCD, use of an atypical antipsychotic has been used in an off-label fashion to augment SRI monotherapy (86, 87). Other medication augmentation strategies such as benzodiazepines and mood stabilizers have been used in an off-label manner but do not have empirical support in pediatric OCD (85). Psychotherapeutic strategies, such as tailoring treatments to address psychological comorbidity (as previously described), sequential treatment of comorbid disorders prior to OCD treatment, intensive treatment schedules, and home-based psychotherapies have also been suggested as means of augmenting treatment for treatment resistant pediatric OCD but also require empirical evaluation (85).

Telehealth. As discussed, CBT is a flexible treatment modality which can be tailored to address individual needs. A way in which this flexibility has been demonstrated and enhanced is its implementation via teletherapy. Teletherapy is a treatment conducted via webcam (either on a computer, tablet, or smartphone) in real time, in the contexts in which the symptoms occur. Theory suggests that treatment effects may be enhanced if treatment occurs in the same environment as the obsessional triggers. For many children, these triggers are present in less sterile environments than the clinic, such as at school or at home. Storch et al. (88) examined the efficacy of teletherapy for children and adolescents with OCD compared to 4-week waitlist control. Sessions were held for 60 minutes twice a week for 2 weeks, then weekly over the course of 10 weeks. A significant reduction in OCD symptoms was found at termination (56.1%), and gains were maintained over a 3-month follow-up. Although this mode of treatment may have limitations in regard to the types of exposures which can be conducted and negative impact on the therapeutic alliance, limitations may be balanced by the generalizability of skills from session to home, and the increased access to gold-standard treatment.

Conclusion Obsessive-compulsive disorder is associated with significant impairment in childhood which extends into adulthood without adequate treatment. Due to the critical nature of pediatric OCD, appropriate and timely intervention is necessary. Research to date has highlighted the intricacies of treating youth with OCD, and in response has developed effective and efficient modes of intervention. Pharmacological interventions demonstrate adequate results in reducing symptom impairment (25-28),yet it

is unclear if these gains remain once active treatment is discontinued (41). Similarly, alternative theoretical interventions have yet to demonstrate efficacy in randomized controlled trials. Cognitive-behavioral therapy, however, poses as an optimal treatment option as it has demonstrated robust effects in time-limited settings (25, 38, 49), and maintenance of gains following treatment discontinuation (45, 46). Further, innovative treatments (e.g., DCS, telehealth) not only help to enhance CBT efficacy, but also aid in the dissemination of the gold-standard treatment for youth with OCD (82, 84, 88). It is with great hope that the current review highlights evidence-based interventions for treating pediatric OCD to further disseminate information and improve child quality of life.

References 1. Douglass HM, Moffitt TE, Dar R, McGee R, Silva P. Obsessivecompulsive disorder in a birth cohort of 18-year-olds: Prevalence and predictors. J Am Acad Child Adolesc Psychiatry 1995;34:1424-1431.

2. Zohar AH. The epidemiology of obsessive-compulsive disorder in children and adolescents. Child Adolesc Psychiatr Clin North Am 1999; 8:445-460.

3. Zohar AH, Ratzoni G, Pauls DL, Apter A, Bleich A, Kron S, et al. An epidemiological study of obsessive-compulsive disorder and related disorders in Israeli adolescents. J Am Acad Child Adolesc Psychiatry 1992;31:1057-1061.

4. Stewart SE, Geller DA, Jenike MA, Pauls D, Shaw D, Faraone SV. Long-term outcome of pediatric obsessive compulsive disorder: A meta-analysis and qualitative review of literature. Acta Psychiat Scand 2004;110:4-13.

5. Piacentini J, Bergman RL, Keller M, McCracken J. Functional impairment in children and adolescents with obsessive-compulsive disorder. J Child Adolesc Psychopharmacology 2003;13: 61-69.

6. Storch EA, Ledley DR, Lewin AB, Murphy TK, Johns NB, Goodman WK, et al. Peer victimization in children with obsessive-compulsive disorder: Relations with symptoms of psychopathology. J Clin Child Adolesc Psychology 2006;35:446-455.

7. Rufer M, Hand I, Alsleben H, Braatz A, Ortmann J, Katenkamp B, et al.

Long-term course and outcome of obsessive-compulsive patients after cognitive-behavioral therapy in combination with either fluvoxamine or placebo: A 7-year follow-up of a randomized double-blind trial. Eur Arch Psy Clin N 2005;255:121-128.

8. Bloch MH, Craiglow BG, Landeros-Weisenberger A, Dombrowski PA, Panza KE, Peterson BS, et al. Predictors of early adult outcomes in pediatric-onset obsessive-compulsive disorder. Pediatrics 2009;124:10851093.

9. Barlow DH. Anxiety and its disorders: The nature and treatment of anxiety and panic. New York: Guilford, 2002.

10. Zohar J,. Hermesh H. Editorial: Obsessive-compulsive disorder. Isr J Psychiatry Relat Sci 2008;45:149-150.

11. Fenichel O. The psychoanalytic theory of neurosis. New York, N.Y.: WW Norton, 1945.

12. Piacentini J, Bergman RL, Keller M, McCracken J. Functional impairment in children and adolescents with obsessive-compulsive disorder. J Child Adolesc Psychopharmacol 2003;13 Suppl 1:S61-S69.

13. Correll CU, Manu P, Olshanskiy V, Napolitano B, Kane JM, Malhotra AK. Cardiometabolic risk of second-generation antipsychotic medications during first-time use in children and adolescents. JAMA 2009;302:1765-1773.

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14. Lewin AB, Storch EA, Storch HD. Risks from antipsychotic medications in children and adolescents. JAMA 2010;303:729-730.

15. Masi G, Millepiedi S, Mucci M, Bertini N, Milantoni L, Arcangeli F. A naturalistic study of referred children and adolescents with obsessivecompulsive disorder. J Am Acad Child Adolesc Psychiatry 2005;44: 673-681.

16. Swedo SE, Rapoport JL, Leonard H, Lenane M, Cheslow D. Obsessive-compulsive disorder in children and adolescents. Clinical phenomenology of 70 consecutive cases. Arch Gen Psychiatry 1989;46:335-341.

17. Gallant J, Storch EA, Merlo LJ, Ricketts ED, Geffken GR, Goodman WK, et al. Convergent and discriminant validity of the Childrenâ&#x20AC;&#x2122;s YaleBrown Obsessive Compulsive Scale-Symptom Checklist. J Anxiety Dis 2008 ;22:1369-1376.

18. Flessner CA, Allgair A, Garcia A, Freeman J, Sapyta J, Franklin ME, et al. The impact of neuropsychological functioning on treatment outcome in pediatric obsessive-compulsive disorder. Depress Anxiety 2009;27:365-371.

19. Storch EA, Geffken GR, Merlo LJ, Jacob ML, Murphy TK, Goodman WK, et al. Family accommodation in pediatric obsessive-compulsive disorder. J Clin Child Adolesc Psychology 2007;36:207-216.

20. Peris TS, Bergman RL, Langley A, Chang S, McCracken JT, Piacentini J. Correlates of accommodation of pediatric obsessive-compulsive disorder: Parent, child and family characteristics. J Am Acad Child Adolesc Psychiatry 2008;47:481-482.

21. Rettew D, Swedo S, Leonard H, Lenane M. Obsessions and compulsions across time in 79 children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry 1992;31:1050-1056.

22. Mancuso E, Faro A, Joshi G, Geller DA. Treatment of pediatric obsessivecompulsive disorder: A review. J Child Adolesc Psychopharmacology 2010;20:299-308.

23. Blanco C, Olfson M, Stein D, Simpson HB, Gameroff M, Narrow W. Treatment of obsessive-compulsive disorder by U.S. Psychiatrists. J Clin Psychiatry. 2006;67:946-951.

24. Micali N, Heyman I, Perez M, Hilton K, Nakatani E, Turner C, et al.

Long-term outcomes of obsessive-compulsive disorder: Follow-up of 142 children and adolescents. Br J Psychiat 2010;197:128-134.

25. Abramowitz JS, Whiteside SP, Deacon BJ. The effectiveness of treatment for pediatric obsessive-compulsive disorder: A meta-analysis. Behav Ther 2005;36:55-63.

26. Pediatric OcD Treatment Study (POTS) Team. Cognitive-behavior therapy, sertraline, and their combiniation for children and adolescents with obsessive-compulsive disorder: The Pediatric OCD Treatment Study (POTS) randomized controlled trial. JAMA 2004;292:1969-1976.

27. Geller DA, Biederman J, Stewart SE, Mullin B, Farrell C, Wagner KD, et al. Impact of comorbidity on treatment response to paroxetine in pediatric obsessive-compulsive disorder: Is the use of exclusion criteria empirically supported in randomized clinical trials? J Child Adolesc Psychopharmacology 2003;13 (Suppl 1):S19-S29.

28. Foa EB, Liebowitz MR, Kozak MJ, Davies S, Campeas R, Franklin ME, et al. Randomized, placebo-controlled trial of exposure and ritual prevention, clomipramine, and their combination in the treatment of obsessive-compulsive disorder. Am J Psychiatry 2005;162:151-161.

29. Geller DA, Hoog SL, Heiligenstein JH, Ricardi RK, Tamura R, Kluszynski S, et al. Fluoxetine treatment for obsessive-compulsive disorder in children and adolescents: A placebo-controlled clinical trial. J Am Acad Child Adolesc Psychiatry 2003;40:773-779.

30. Liebowitz MR, Turner SM, Piacentini J, Beidel DC, Clarvit SR, Davies SO, et al. Fluoxetine in children and adolescents with OCD: A placebocontrolled trial. J Acad Child Adolesc Psychiatry 2002;41:1431-1438.

31. March JS, Biederman J, Wolkow R, Safferman A, Mardekian J, Cook E, et al. Sertraline in children and adolescents with obsessivecompulsive disorder: A multicenter randomized controlled trial. JAMA 1998;280:1752-1756.

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32. Riddle MA, Reeve EA, Yaryura-Tobias JA, Yang HM, Claghorn JL, Gaffney G, et al. Fluvoxamine for children and adolescents with Obsessive-Compulsive Disorder: A randomized, controlled, multicenter trial. J Acad Child Adolesc Psychiatry 2001;40:222-229.

33. Masi G, Millepiedi S, Perugi G, Pfanner C, Berloffa S, Pari C, et al.

Pharmacotherapy in paediatric obsessive-compulsive disorder: A naturalistic, retrospective study. CNS Drugs 2009;23:241-252.

34. Geller DA, Wagner KD, Emslie G, Murphy T, Carpenter DJ, Wetherhold E, et al. Paroxetine treatment in children and adolescents with obsessive-compulsive disorder: A randomized, multicenter, doubleblind, placebo-controlled trial. J Am Acad Child Adolesc Psychiatry 2004;43:1387-1396.

35. Birmaher B, Axelson DA, Monk K, Kalas C, Clark DB, Ehmann M, et al. Fluoxetine for the treatment of childhood anxiety disorders. J Acad Child Adolesc Psychiatry 2003;42:415-423.

36. Coskun M, Zoroglu S. Efficacy and safety of fluoxetine in preschool children with obsessive-compulsive disorder. J Child Adolesc Psychopharmacology 2009;19:297-300.

37. March JS, Ollendick T. Integrated psychosocial and pharmacological treatment. Phobic and anxiety disorders in children and adolescents: A clinician's guide to effective psychosocial and pharmacological interventions. New York, N.Y.: Oxford University, 2004: pp. 141-172.

38. AACAP. Practice parameters for the assessment and treatment of children and adolescents with obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry 1998;37:27S-45S. 39. Scahill L, Riddle MA, McSwiggin-Hardin M, Ort SI, King RA, Goodman WK, et al. Children's Yale-Brown obsessive compulsive scale: Reliability and validity. J Acad Child Adolesc Psychiatry 1997;36:844-852.

40. Stevens J, Wang W, Fan L, Edwards MC, Campo JV, Gardner W. Parental attitudes toward children's use of antidepressants and psychotherapy. J Child Adolesc Psychopharmacol 2009;19:289-296.

41. Decloedt EH, Stein DJ. Current trends in drug treatment of obsessivecompulsive disorder. Neuropsychiatr Dis Treat 2010;6:233-242.

42. Reid JM, Storch EA, Murphy TK, Bodzin D, Mutch PJ, Lehmkuhl H, et al. Development and psychometric evaluation of the treatmentemergent activation and suicidality assessment profile. Child Youth Care Forum 2010;39:113-124.

43. Bouton ME. Context, time, and memory retrieval in the interference paradigms of Pavlovian learning. Psychol Bull 1993;114:80-99.

44. March JS, Franklin M, Nelson A, Foa E. Cognitive-behavioral psychotherapy for pediatric obsessive-compulsive disorder. J Clin Child Psychol 2001;30:8-18.

45. O'Leary EM, Barrett P, Fjermestad KW. Cognitive-behavioral family treatment for childhood obsessive-compulsive disorder: A 7-year follow-up study. J Anxiety Dis 2009;23:973-978.

46. Barrett P, Healy-Farrell L, March JS. Cognitive-behavioral family treatment of childhood obsessive-compulsive disorder: Long-term follow-up and predictors of outcome. J Am Acad Child Adolesc Psychiatry 2004;43:46-62.

47. Storch EA, Lehmkuhl HD, Ricketts E, Geffken GR, Marien W, Murphy TK. An open trial of intensive family based cognitive-behavioral therapy in youth with obsessive-compulsive disorder who are medication partial responders or nonresponders. J Clin Child Adolesc Psychol 2010;39:260-268.

48. Piacentini J, Bergman RL, Jacobs C, McCracken JT, Kretchman J. Open trial of cognitive behavior therapy for childhood obsessive-compulsive disorder. J Anxiety Dis 2002;16:207-219.

49. Watson HJ, Rees CS. Meta-analysis of randomized, controlled treatment trials for pediatric obsessive-compulsive disorder. J Child Psychol Psychiatry 2008;49:489-498.

50. Valderhaug R, Larsson B, Gotestam KG, Piacentini J. An open clinical trial of cognitive-behaviour therapy in children and adolescents with obsessive-compulsive disorder administered in regular outpatient clinics. Behav Res Ther 2007;45:577-589.

Lindsay Brauer et al.

51. Geller DA, Biederman J, Stewart SE, Mullin B, Martin A, Spencer T, et al. Which SSRI? A meta-analysis of pharmacotherapy trials in pediatric obsessive-compulsive disorder. Am J Psychiatry 2003;160:1919-1928.

52. Lewin AB, Piacentini J. Evidence-based assessment of child obsessive compulsive disorder: Recommendations for clinical practice and treatment research. Child Youth Care Forum 2010;39:73-89.

53. Lewin AB, Bergman RL, Peris TS, Chang S, McCracken JT, Piacentini J. Correlates of insight among youth with obsessive-compulsive disorder.

J Child Psychology Psychiatry 2010;51:603-611.

54. Lewin AB, Caporino N, Murphy TK, Geffken GR, Storch EA. Understudied clinical dimensions in pediatric obsessive compulsive disorder. Child Psychiatry Hum Dev 2010 ;41:675-691.

55. Storch EA, Milsom VA, Merlo LJ, Larson M, Geffken GR, Jacob ML, et al. Insight in pediatric obsessive-compulsive disorder: associations with clinical presentation. Psychiatry Res 2008;160:212-220.

56. Freeman JB, Garcia AM, Coyne L, Ale C, Przeworski A, Himle M, et al. Early childhood OCD: Preliminary findings from a family-based cognitive-behavioral approach. J Am Acad Child Adolesc Psychiatry 2008;47:593-602.

57. Storch EA, Geffken GR, Merlo LJ, Mann G, Duke D, Munson M, et al. Family-based cognitive-behavioral therapy for pediatric obsessivecompulsive disorder. J Am Acad Child Adolesc Psychiatry 2007;46:469478.

58. Merlo LJ, Lehmkuhl HD, Geffken GR, Storch EA. Decreased family accomodation associated with improved therapy outcome in pediatric obsessive-compulsive disorder. J Consult Clinical Psychology 2009;77:355-360.

59. Rapee RM. The influence of comorbidity on treatment outcome for children and adolescents with anxiety disorders. Behav Res Ther 2003;41:105-112.

60. Steketee G. Effects of axis I and II comorbidity on behavior therapy outcome for obsessive-compulsive disorder and agoraphobia. Compr Psychiat 2001;42:76-86.

61. Storch EA, Merlo LJ, Larson MJ, Geffken GR, Lehmkuhl HD, Jacob ML, et al. Impact of comorbidity on cognitive-behavioral therapy response in pediatric obsessive-compulsive disorder. J Am Acad Child Adolesc Psychiatry 2008;47:583-592.

62. Geller DA, Biederman J, Griffin S, Jones J, Lefkowitz TR. Comorbidity of juvenile obsessive-compulsive disorder with disruptive behavior disorders. J Acad Child Adolesc Psychiatry 1996;35:1637-1646.

63. Storch EA, Lewin AB, Geffken GR, Morgan JR, Murphy TK. The role of comorbid disruptive behavior in the clinical expression of pediatric obsessive-compulsive disorder. Behav Res Ther 2010; 48: 1204-1210.

64. Storch EA, Jones A, Lewin AB, Mutch J, Murphy TK. Rage and obsessivecompulsive disorder. Minerva Psichiatrica 2011;52:89-95.

65. Geller D, Biederman J, Jones J, Park K, Schwartz S, Shapiro S, et al. Is juvenile obsessive-compulsive disorder a developmental subtype of the disorder? A review of the pediatric literature. J Acad Child Adolesc Psychiatry 1998;37:420-427.

66. Geller DA, Biederman J, Faraone S, Agranat A, Cradock K, Hagermoser L, et al. Developmental aspects of obsessive compulsive disorder: findings in children, adolescents, and adults. J Nervous Mental Disease 2001;189:471-477.

67. March JS, Franklin ME, Leonard H, Garcia A, Moore P, Freeman J, et al. Tics moderate treatment outcome with sertraline but not cognitivebehavior therapy in pediatric obsessive-compulsive disorder. Biol Psychiatry 2007;61:344-347.

68. Leckman JF, Grice DE, Barr LC, de Vries AL, Martin C, Cohen DJ, et al.

Tic-related vs. non-tic-related obsessive compulsive disorder. Anxiety 1994;1:208-215.

69. Goodman WK, Storch EA, Geffken GR, Murphy TK. Obsessivecompulsive disorder in Tourette syndrome. J Child Neurology 2006;21:704-714.

70. Himle JA, Fischer DJ, Van Etten ML, Janeck AS, Hanna GL. Group

behavioral therapy for adolescents with tic-related and non-tic-related obsessive-compulsive disorder. Depress Anxiety 2003;17:73-77.

71. Abramowitz JS. Treatment of obsessive-compulsive disorder in patients who have comorbid major depression. J Clin Psychol 2004;60:11331141.

72. Olley A, Malhi G, Sachdev P. Memory and executive functioning in obsessive-compulsive disorder: A selective review. J Affective Dis 2007;104:15-23.

73. Storch EA, Bjorgvinsson T, Riemann B, Lewin AB, Morales MJ, Murphy TK. Factors associated with poor response in cognitive-behavioral therapy for pediatric obsessive-compulsive disorder. Bulletin of the Menninger Clinic 2010;74:167-185.

74. Murphy TK, Bengtson MA, Soto O, Edge PJ, Sajid MW, Shapira N, et al. Case series on the use of aripiprazole for Tourette syndrome. Int J Neuropsychoph 2005;8:489-490.

75. Foa EB, Steketee G. Behavioral treatment of phobics and obsessivecompulsives. In: Jacobson NS, editor. Psychotherapists in clinical practice: Cognitive and behavioral perspectives. New York: Guilford, 1987: pp. 78-120.

76. Abramowitz MZ, Greenberg D, Levav I. Editorial: Treatment gap in mental health care. Isr J Psychiatry Relat Sci 2008;45:80-82.

77. Lev-Ran S. Points to ponder regarding contemporary psychiatric training in Israel. Isr J Psychiatry Relat Sci 2007;44:187-193.

78. Freeman JB, Choate-Summers ML, Garcia AM, Moore PS, Sapyta JJ, Khanna MS, et al. The Pediatric Obsessive-Compulsive Disorder Treatment Study II: Rationale, design and methods. Child Adolesc Psychiatry Mental Health 2009;3:4.

79. Lewin AB, Storch EA, Adkins J, Murphy TK, Geffken GR. Intensive cognitive behavioral therapy for pediatric obsessive compulsive disorder: A treatment protocol for mental health providers. Psychol Serv 2005;2:91-104.

80. Abramowitz JS, Foa EB, Franklin ME. Exposure and ritual prevention for obsessive-compulsive disorder: effects of intensive versus twiceweekly sessions. J Consult Clin Psychol 2003;71:394-398.

81. Bjorgvinsson TP, Wetterneck CTP, Powell DMP, Chasson GSM, Webb SAP, Hart JM, et al. Treatment outcome for adolescent obsessivecompulsive disorder in a specialized hospital setting. J Psychiatric Practice 2008;14:137-145.

82. Wilhelm S, Buhlmann U, Tolin DF, Meunier SA, Pearlson GD, Reese HE, et al. Augmentation of behavior therapy with D-cycloserine for obsessive-compulsive disorder. Am J Psychiatry 2008;165:335-341; quiz 409.

83. Kushner MG, Kim SW, Donahue C, Thuras P, Adson D, Kotlyar M, et al.

D-cycloserine augmented exposure therapy for obsessive-compulsive disorder. Biol Psychiatry 2007;62:835-838.

84. Storch EA, Murphy TK, Goodman WK, Geffken GR, Lewin AB, Henin A, et al. A preliminary study of D-cycloserine augmentation of cognitive-behavioral therapy in pediatric obsessive-compulsive disorder. Biol Psychiatry 2010; 68: 1073-1076.

85. Krebs G, Heyman I. Treatment-resistant obsessive-compulsive disorder in young people: Assessment and treatment strategies. Child Adolesc Mental Health 2010;15:2-11.

86. Storch EA, Lehmkuhl H, Geffken GR, Touchton A, Murphy TK. Aripiprazole augmentation of incomplete treatment response in an adolescent male with obsessive-compulsive disorder. Depress Anxiety 2008;25:172-174.

87. Masi G, Pfanner C, Millepiedi S, Berloffa S. Aripiprazole augmentation in 39 adolescents with medication-resistant obsessive-compulsive disorder.

J Clinical Psychopharmacology 2010;30:688-693.

88. Storch EA, Caporino N, Morgan JR, Lewin AB, Rojas A, Brauer L, et al. Preliminary efficacy of web-camera delivered cognitive-behavioral therapy for youth with obsessive-compulsive disorder. Psychiatry Res 2011; 189:407-412.

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Book reviews Breaking and Mending: A Hasidic Model for Clinical Psychology Baruch Kahane. Rubin Mass Publishing, 2010, 368 pages

K

abbalah is a discipline and school of thought concerned with the mystical aspects of Rabbinic Judaism. It is a set of esoteric teachings meant to explain the relationship between an eternal and mysterious creator and the mortal and finite universe (His creation).

Kabbalah seeks to define the nature of the universe and the human being, the nature and purpose of existence, and other ontological questions.

Modern psychology originally saw itself as an empiric science, unaffected by any religion or other dogmatic system. However, after the rise of the postmodern movement, many psychoanalysts abandoned the traditional metapsychological constructs and began to see psychoanalytical theories more as a narrative that can explain a certain life story. How does Hasidic psychology see itself? Is it simply a particular form of narrative life-story reasoning, one that helps treat and understand patients with a strong Jewish background and identity?

The author argues that it is not. According to the book, Hasidic psychology presents a comprehensive alternative to modern scientific explanatory motifs, believing that it is a framework that can explain and treat all psychological and behavioral phenomena.

In this interesting and challenging book, the concepts of clinical Hasidic psychology are explained. This psychology sees all of reality as a revelation of a hidden transcendental world, and the author claims that Western psychology as compared to the multidimensional Hasidic psychology is unidimensional and lacking spirituality. The Hasidic theories of psychopathology utilize their own lexicon, understanding mental distress with concepts such as breaking and mending (all of which are clearly explained in the book even for readers unfamiliar with Kabbalah). In the book there is explanation of various psychoanalytical theories according to Hasidic concepts. The author argues that the spiritual element is missing in all those theories. In the last part of the book there are several case reports that illustrate practical applications of the theoretical material. The case reports are analyzed according to several psychoanalytical theories (Kohut, Freud, Jung and others), and the author tries to add his unique understanding 288

and technique to explain and intervene in those cases.

I think some may find the Hasidic treatment concepts quite vague and not specific so that they can explain almost any mental phenomena.

This book is recommended for any mental health clinicians who wishes to widen his or her horizons with an authentic Jewish spiritual perspective, although in my opinion it is only psychotherapists with a strong Jewish background who will integrate this psychology into their clinical practice.

Assaf Shelef, MD Bat Yam

Challenging the stigma of mental illness: Lessons for therapists and advocates Patrick W Corrigan, David Roe, Hector WH Tsang Wiley-Blackwell, 2011, xxii + 231 pages ISBN: 9780470683606

T

his is a short, focused guide to stigma and how to change it. It is written for those actively engaged in work as advocates or for consumers, without distracting references or footnotes, and written using clearly labeled short sections. To my mind, the two main chapters of the book are compulsory reading for anyone who works with serious mental illness. They deal with social stigma and personal stigma, how to evaluate and change them, and both are written in a clear format, with scales for assessment and methods recommended for their change. The chapter on social stigma describes how to build programs and arrange contact meetings for the public with people with mental illness in order to challenge and change stigmatic beliefs. The book has many movingly related personal stories, including the authors’ personal experiences, and guides for speakers, handouts for audiences, advice for the chairman of such sessions, and addresses for sites for those who are seriously interested in helping. Similarly, the chapter on personal stigma is essentially practical, with a brief account of stigma-breaking methods, such as CBT, a nuanced discussion of the process of disclosure of one’s mental illness to others, telling your personal story to reveal your strengths, with six suggestions towards empowerment, including changing one’s relationship with one’s psychiatrist to one of collaboration, providing consumer evaluation (that is utilized), attending clubhouses and self-help groups, and becoming a consumer-provider.

The chapter on structural stigma is a succinct, practical and highly recommended account of “accommodation,” which is the reasonable lengths the law expects

Book Reviews

an employer to go in enabling an ill person, in this case mentally ill, to be a productive employee.

This book is about and for all of us. Mental health staff is far from being free of stigmatic beliefs, and dealing with these issues should begin at home, inviting people with mental illness to speak to staff about their lives, their struggles and their achievements, to understand that we all dream and we all have the right to attempt to approach their fulfillment.

I was left wondering whether some of the goals have a broader agenda that are not appropriate to all cultures.

They advise using a “Freedom in society” scale that includes four statements for evaluation. Statement two is: A chance to pursue your dreams is: not important – important – very important, while Statement four is: Respect and admiration for your accomplishments is: not important – important – very important. I wonder whether these values are very Western and less suited to more traditional societies. When I measured my own values, it seems I have more stigmatic beliefs about freedom in society than about freedom and mental illness!

The reference to side-effects of anti-psychotics seems outdated, discussing “nasty” tremor, with no initial mention of obesity and diabetes, although this is corrected in a later chapter. The book has a significant number of typos, most minor, some substantial: the most unfortunate is that the terms odd and even are reversed in the instructions for evaluating two scales: public versus self stigma in the self stigma assessment scale on pages 120-121 and empowerment of one’s self versus one’s community in the personal empowerment self-assessment scale on page 136. Others are trivial but jar on this reader: we learn that stigma busting letters should contain relevant facts, and not be anonymous.

The example on page 108 refers to 8-10% of British people having serious mental illness, but the letter is addressed Illinois. In the exercise of cognitive restructuring on pages 123-4, the person first identifies a distressing feeling, and then the associated thought. In the table, these are erroneously reversed.

To the publisher: this book is not a long read and purposely compact for a wide non-academic audience.

The recommended price of £60 ($97, or 330 IS) will ensure it is a collector’s item.

These limitations, notwithstanding, Corrigan, Roe and Tsang have given us a wonderful enriching read, essential for all the mental health professions and those working to improve the lives of people with serious mental illness.

And finally, if you haven’t seen it yet – and I hadn’t before I read the book – type into Google “Change a mind about mental illness,” and click on the youtube.

David Greenberg Jerusalem

Mental Health, Psychotherapy and Judaism Seymour Hoffman, 2011, Golden Sky Books, 127 pages. $15:45

T

his slim volume is a potpourri of articles, on the interface of psychotherapy and Judaism. Nine of the ten articles were penned by the author and the last article is a reprint of an article that previously appeared in the Israel Journal of Psychiatry. The articles range from heavy, scholarly to light and entertaining. The book is the fourth (and the first in English) of a series sponsored by Nefesh Israel, “an organization of observant clinicians which recognizes the advantages of pulling together with men of the spirit, pooling resources and giving scope for members of both fields to cooperate, enrich each other, even while recognizing the differences in their orientation, purpose and methods.”

The book is dedicated to Dr. Judith Guedalia, the cofounder and co-chairperson of the organization that was founded over a decade ago.

The topics considered in this book are varied and relate to theoretical as well as practical issues. Thus for example, one can find in this book reports of effective therapeutic treatments involving rabbis and psychologists, markedly differing opinions of various rabbinic authorities regarding psychotherapy, detailed rich clinical case material illustrating treatment issues that have relevance in terms of Jewish law, treatment dilemmas arising from conflicts between Jewish law and aspects of psychotherapy as generally practiced, a report of the functioning of the first mental health clinic under haredi auspices, as well as entertaining and illuminating anecdotes of the strategic interventions of prominent rabbis, ancient and modern, in their attempts to aid people suffering from emotional and psychological stress and conflicts, and in effecting change in people.

The article by Greenberg and Shefler is of special interest as it clearly depicts the psychological insights and sophistication of two highly revered haredi rabbis’ insights into the psychopathology and treatment of obsessive-compulsive disorder of the religious type.

In reference to the latter points mentioned, the reader can begin to feel confused on the position of the author regarding the rabbi’s role in the therapeutic enterprise.

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Book Reviews

Should the rabbi always or sometimes take on the role of primary therapist? Readers may infer from some of the articles that the author may be endorsing rabbis taking on the role of primary therapists while in other articles, the author criticizes rabbis who refuse to refer patients to mental health professionals and see themselves as the best and most effective healers.

My impression is that the author does endorse the therapeutic involvement of rabbis who are sufficiently sophisticated, sensitive and knowledgeable of dynamics, psychopathology and psychotherapy, and who are able to differentiate between cases that require the intervention of a professional mental health practitioner and cases that can benefit from their counseling.

However, it is important that the spirit and conception of psychotherapy be respected in the clinic room and that the therapist as well as the patient have the freedom to raise, explore, discuss and deal with all issues that they deem relevant, pertinent and important; whereas, religious issues that seem to require halachic decisions will be dealt with by the patient’s religious authority.

Interspersed in the book are brief, pertinent and relevant comments on the issues being discussed by prominent mental health practitioners, researchers, rabbis, as well as by the author.

“In my opinion, there is no specific Jewish psychology or psychiatric treatment protocol, just as there is no specific Jewish way to treat pneumonia, or to surgically remove a gall bladder.” (Professor Werblowsky, page 4) “Appropriate therapeutic support can only be given by a therapist who understands that the religious prohibitions are givens, and the feelings and conflicts of

290

clients must be dealt within the context of the clients’ probable acceptance that the laws about sexual behavior are right, even if s/he does not find them easy or convenient.” (Professor Loewenthal, page 7) “It seems most judicious that rabbis should consult and refer religious patients to mental health practitioners who are religious or at least are sufficiently knowledgeable of Jewish law and customs and respect the values of their patients, and that the latter should consult with and refer their clients to rabbis who have a basic knowledge and understanding of psychopathology and psychotherapy, when there is a need for halachic and rabbinic guidance.” (Author, page 7) “The most important lesson we can learn from this article is that one should not present general questions to a rabbi (and the rabbi should not respond to general questions) but provide specific, relevant and pertinent information so that the rabbi can direct his response to the specific person and situation.” (Rabbi Bar Ilan, page 62) “Torah and mitsvot are not mental health treatments.

Torah study and strict adherence to the halacha does not automatically protect us from leading lives that are unbalanced, unhappy, and unfulfilled.” (Dr. Klafter, page 72) I found the book user-friendly, down-to-earth, yet infused with an interesting combination of psychological as well as Jewish concepts and ideas. Mental health practitioners, religious as well as secular, rabbis, and people interested in the interface between psychotherapy and Judaism, will find the book a worthwhile read.

Leah Rossman, PhD Rehovot

Correspondence Book Reviews

Correspondence Primary Delusional Parasitosis Treated Effectively with Paliperidone Dear Editor,

D

elusional parasitosis (DP) is a psychiatric disorder characterized by delusions about being infested with living organisms such as parasites. Patients usually complain of itching that they ascribe to cutaneous invasion. The belief of being infested is usually held with delusional intensity but the severity of the delusional belief can vary. DP is an uncommon condition with no reliable estimates of prevalence rates or treatment outcome. DP can occur as a monosymptomatic delusional disorder (primary DP) or it can be associated with other psychiatric and medical disorders (schizophrenia, depression), or substance use (cocaine, amphetamines).

DP is a non-specific psychotic syndrome rather than a single disorder (1). It is classified under delusional disorder, somatic type in DSMâ&#x20AC;&#x201C;IVâ&#x20AC;&#x201C;TR (2) and persistent delusional disorder in ICDâ&#x20AC;&#x201C;10 (3). Primary delusional parasitosis can be diagnosed only after underlying medical and other psychiatric disorders or an actual infection have been excluded, because it can be associated with several physical illnesses, psychiatric disorders or intoxications (1).

The clinical management of patients with delusional parasitosis is quite diffucult; patients are often reluctant to accept a psychiatric evaluation or treatment because of the belief that they are actually infested. Thus they commonly seek care from general practitioners and dermatologists but refuse psychiatric treatment or therapy.

Conventional and second generation antipsychotics are both recommended in the treatment of DP. The only available data was a case report in which paliperidone was reported to be effective in treating secondary DP (4). A case of primary DP that was treated effectively with paliperidone is presented in this report.

We report on a 60-year-old female patient whose symptoms had begun one month before her consultation to our outpatient clinic of psychiatry. The patient had a perception that something was crawling over her abdomen and shoulders and believed that her abdomen and shoulders were infested by parasites that she could see on the surface of her skin and sometimes on the walls of her room. The sense of crawling on the skin of abdomen and shoulders was quiet intense. She was admitted to the dermatology department where she

had an unremarkable physical examination before she was referred to the psychiatry department. She did not have any history of drug and alcohol use, and her past psychiatric and family history was unremarkable. In the psychiatric evaluation the patient had delusions of parasitosis (somatic delusions) and tactile and visual hallucinations. Brain magnetic resonance imaging (MRI) and encephalography (EEG) studies were normal. Laboratory investigations, including CBC, liver and renal function tests, TSH, B12, folic acid, and urine analysis, were all in the normal range. A diagnosis of delusional disorder-somatic type (delusional parasitosis) was made according to DSM-IV-TR (2), and paliperidone was started at a dose of 6 mg/day. After two weeks of treatment, visual hallucinations disappeared but tactile hallucinations and somatic delusions were partially improved. The dose of paliperidone was increased to 9 mg/day. We observed a remarkable improvement in all symptoms after three weeks. The patient was almost asymptomatic and the use of paliperidone was well tolerated with no adverse events. After a 6-month followup, the patient is still asymptomatic.

Conventional and atypical antipsychotics are both considered in the treatment of DP. Studies demonstrate that partial and full remission rates vary between 60% and 100% with typical antipsychotics. Pimozide is recommended as the first line drug among conventional antipsychotics. Case reports and a small number of controlled studies supporting the efficacy of pimozide have demonstrated that partial or full recoveries can be found in up to 90% of patients. However, a high rate of side-effects such as sedation, extrapyramidal symptoms and depression were noted in the studies in which pimozide was used. Haloperidol, chlorpromazine, trifluoperazine, perphenazine and other conventional depot antipsychotics were also reported to be effective in the treatment of DP (5).

There are only a few systematic reviews that are based on case reports about the use of atypical antipsychotics. Thus, controlled or open trials are needed. Oral or intramuscular depot form of risperidone is the most frequently used atypical antipsychotic agent in DP. The reported daily dose of risperidone varied. There are also case reports in which DP is treated effectively with olanzapine, quetiapine or aripiprazole (5).

Paliperidone is the major active metabolite of the widely used atypical antipsychotic agent risperidone and it was approved in Turkey. It is a monoaminergic antagonist chemically classified in benzoxisoxazole 291

Correspondence Book Reviews

derivatives. Paliperidone has an antagonistic activity at dopamine-D2 and serotonin-5-HT2A receptors, predominantly at 5HT2A. Additionally, it displays antagonistic activity at alpha-1 and alpha-2 adrenergic receptors and H1-histaminergic receptors, which might explain side effects such as weight gain, orthostatic hypotension and sedation. It exhibits no affinity to cholinergic muscarinic receptors, predicting a low risk of anticholinergic side effects including cognitive dysfunction and constipation, and also has no significant affinity at beta-1 and beta-2 adrenergic receptors (6). It has an unique pharmacological profile such as single dosing, predominantly renal excretion, low drug interaction risk and it differs from risperidone in terms of mode of action and pharmacokinetics. High-level evidence supports that paliperidone is efficacious and safe in schizophrenia, schizoaffective disorder, and acute manic episodes. There is a lack of published studies about comparisons between paliperidone and risperidone. Low-level evidence demostrates a lower risk for hyperprolactinemia and higher patient satisfaction with paliperidone than with risperidone (7). Thus, paliperidone may be considered to be suitable especially in elderly patients with and without comorbid medical conditions. Freudenmann et al. reported on a patient with DP who benefited from paliperidone treatment (4). It was the first and only account in which paliperidone was reported to be effective in treatment of DP. Similarly, our patient became asymptomatic within a

292

short time period without any significant or distressing adverse events.

In conclusion, paliperidone should be kept in mind as an alternative treatment choice of DP especially in elderly patients.

References 1. Kenchaiah BK, Kumar S, Tharyan P. Atypical anti-psychotics in delusional parasitosis: A retrospective case series of 20 patients. Int J Dermatol 2010; 49: 95-100.

2. American Psychiatric Association. Diagnostic and statistical manual of mental disorders (4th ed). Text revision (DSM-IV-TR).Washington, DC: APA, 2000.

3. World Health Organization. The ICD-10 Classification of Mental and Behavioural Disorders. Diagnostic Criteria for Research: WHO, 1993.

4. Freudenmann RW, Kühnlein P, Lepping P, Schönfeldt-Lecuona C. Secondary delusional parasitosis treated with paliperidone. Clin Exp Dermatol 2009; 34: 375-377.

5. Freudenmann RW, Lepping P. Delusional infestation. Clin Microbiol Rev 2009; 22: 690-732.

6. Nussbaum AM, Stroup TS. Oral paliperidone for schizophrenia.

Cochrane Database Syst Rev 2008;2:CD006369.

7. Chwieduk CM, Keating GM. Paliperidone extended release: A review of its use in the management of schizophrenia. Drugs 2010; 70: 12951317.

Yakup Albayrak, MD,1 Okan Ekinci, MD,2 Sena Yenel Özbay1 Kırklareli State Hospital, Department of Psychiatry, Ankara, Turkey 2 Yozgat State Hospital, Department of Psychiatry, Yozgat, Turkey 1

Address for Correspondence: Dr. Yakup Albayrak, Kırklareli Devlet Hastanesi Psikiyatri Klinigi, 39001, Kırklareli, Turkey.

Email: dr.fuge@hotmail.com

Book Reviews

Obituaries Hugh Freeman (1929-2011)

P

rofessor Hugh Lionel Freeman was born in Salford, Manchester. From Altrincham Grammar School, he won an open scholarship to study modern history at St John’s College, Oxford. After his switch to medicine, he finished his national service as a Captain in the Royal Army Medical Corps. He then specialized in psychiatry at the Maudsley Hospital, London, returning to Salford as a consultant psychiatrist in 1961 at the remarkably young age of 31. He set up community mental health services devoted to reducing hospitalizations to improve the lives of his patients, and initiated the Salford Psychiatric Case Register. He was consultant at the University of Manchester and professor of psychiatry at the University of Salford, as well as receiving many international honors.

Hugh was the fourth editor of the British Journal of Psychiatry from 1983-93 during which time he firmly established the journal as a world leader. He also started Current Opinion in Psychiatry along with many other publishing and financial initiatives, Hugh’s writings were wise and measured. In his later years, the obituaries he wrote for the BJP made you laugh aloud as he recalled exactly the humor of his deceased colleagues, each one a gem, a brief essay full of content, wit and warmth.

In 1992, when I was considering editing the Israel Journal of Psychiatry, I mentioned to Shari, my wife, that Hugh was my ideal. “Write to him,” was her suggestion.

His reply soon arrived – a real letter, written by hand with a fountain pen, inviting me to lunch at his London club, the Oxford and Cambridge in Pall Mall. I still thrill to recall the excitement of that day, the grandeur of the surroundings and the warmth and kindness of my host. I was astonished to learn of Hugh’s deep attachment to Israel, and how much he wished to share his experience to help the IJP. He arranged that I should meet the editorial staff of the BJP to give me all possible help, and wanted us to meet again with our wives. Since then, Hugh became one of my staunchest supporters and sources of advice.

Hugh contributed reviews and a paper to the IJP, and to any issue I would show him, he responded with a careful reading and commentary. With Hugh and his wife Joan, at their home in a beautiful square in the center of London, we would talk early in the morning and I could raise any subject. They never missed an occasion when I spoke pub-

licly in the UK. I recall a difficult ethical issue of publishing, where I was helped by a joint consult by both of them, each giving of their own particular expertise. They visited Israel regularly, particularly because of Joan’s work.

Joan is a professor of Psychology who recently received a Lifetime Achievement Award for her work with gifted children. They were married for 54 years, and I have a photograph of Hugh in bed during his last hospitalization editing her writing. He died in her arms. He left Joan, four children and two grandsons. For me, Hugh was the editor’s editor.

David Greenberg, Jerusalem

Hans Keilson (1909-2011)

O

ne of the most prominent Jewish psychiatrists in the Netherlands, Hans Keilson, died in Holland on May 31, 2011, at the age of 102. Keilson was born in 1909 in a small city on the river Oder in eastern Germany. He managed to escape from Nazi Germany and immigrated in 1936 to the Netherlands, where he became a child and youth psychiatrist and psychoanalyst. Keilson was himself a Holocaust survivor. After World War II he became the chief psychiatric consultant of the “le Ezrat Hayeled” foundation in Amsterdam, the official guardian of all Jewish orphans who survived the Holocaust and returned to Holland. Almost every orphan was seen by him at least once. Keilson also supervised the social workers who treated and supported these children. Many of those children live at the present time here in Israel.

After many years he wrote a well-known book about his clinical-psychiatric work and experience, which was translated from the original German to English: Sequential Traumatisation in Children. A clinical and statistical follow-up study on the fate of the Jewish War Orphans in the Netherlands, published by Magnes Press, The Hebrew University (Jerusalem, 1992, ISBN 965-223-806-6). His main observation was that the age at which a child was separated from his or her parents was an important predictor of the psychopathological symptomatology and behavior which developed later. In addition to his psychiatric-psychoanalytic work, he published belletristic books: poems, stories and novels, in Dutch and German. Until his very old age, he remained a vital, clever and artistic person with a wonderful sense of humor.

Benyamin Maoz, Even Yehuda

293

List of reviewers for Israel Journal of Psychiatry, 2011 The Editors would like to thank the following for their contribution as reviewers of manuscripts during 2011 Henry Abramowich

Shmuel Fennig

Benjamin Lerer

Baruch Shapira

Moshe Abramowitz

Max Fink

Vladimir Lerner

Gaby Shefler

Alean Al-Krenawi

Allen Frances

Itzhak Levav

Gila Shen

Paul Appelbaum

Harald Freyberger

Pesach Lichtenberg

Gal Shoval

Alan Apter

Mary Fristad

Kate Loewenthal

Amit Shrira

Shosh Arbelle

Gilad Gal

Ido Luria

Henry Silver

Oren Asman

Marc Gelkopf

Dolores Malaspina

Eliane Sommerfeld

Yoram Barak

Elliot Gershon

William Marshall

Daniel Stein

Oran Baron-Epel

Eva Gilboa-Schechtman

Yuval Melamed

Rafael Strjyer

Haim Belmaker

Gaby Golan

Shlomo Mendlovic

Rael Strous

Oded Ben Arush

Pavel Golobtchik

Roberto Mester

Nathan Szajnberg

Menachem Ben-Ezra

Harvey Gordon

David Miklowitz

Francisco Torres-González

Itzhak Ben-Zion

Doron Gothelf

Norbert Muller

Bruce Turetsky

Anat Biegon

Jon Grant

Hanan Munitz

Carol Veneziano

Boris Birmaher

Lior Greenbaum

Ora Nakash

Lee Wachtel

Avi Bleich

Gerald Grob

Yamima Osher

Martin Weinberg

Aviva Bloch

David Guay

Yoav Palgi

Michael Weingarten

Rochelle Caplan

Gerrit Hohendorf

Kenneth Pargament

Nomi Werbeloff

Gabrielle Carlson

Martin Irwin

Hagit Peres

Shirli Werner

Lisa Cohen

Evgenia Ivanova

Alexander Ponizovsky

Eliezer Witztum

Rena Cooper

Alan Jotkowitz

Lucinda Rasmussen

Rafi Yungman

Herwig Czech

Martin Kafka

Ariel Rosler

Gil Zalsman

Rachel Dekel

Zeev Kaplan

Abraham Rudnick

Zvi Zemishlany

Melissa DelBello

Victor Karpyak

Ebru Salcioglu

Danny Derby

Shimon Katz

Lior Schapir

Milka Donchin

Semion Kertzman

Martin Schmucker

Richard Ebstein

Mooli Lahad

William Seidelmann

Angela Eastvold

Yoav Lavee

Martin Seligman

Reinhard Eher

Julian Leff

Michael Seto

David Elisha

Ellen Leibenluft

Simone Shamay-Tsoory

294

‫‬

‫סיכום ישיבת הוועד המרכזי של איגוד הפסיכיאטריה בישראל‬ ‫‪ 8‬בנובמבר ‪2011‬‬

‫‪1 .1‬דווח על הכנס ה־‪ 19‬של האיגוד האירופאי למתמחים‬ ‫בפסיכיאטריה‪ .‬בכנס זה השתתפה ישראל לראשונה‬ ‫כנציגה רשמית ובעלת זכות הצבעה‪ .‬נושא הכנס היה‬ ‫"עתיד הפסיכיאטריה וההכשרה בעידן האינטרנט‪ ,‬עתיד‬ ‫הפסיכותרפיה והפרמקולוגיה ושיפור המעקב באמצעות‬ ‫מסרונים"‪ .‬תכנית ההתמחות הישראלית נמצאת במקום‬ ‫טוב ביחס למדינות מערב אירופה‪ .‬ישראל היא בין‬ ‫המדינות המעטות הדורשות מהמתמחים לעסוק במחקר‬ ‫ובפסיכותרפיה במהלך ההתמחות‪.‬‬

‫בתחום זה ללא צורך באישורים או בהכשרות נוספות‪.‬‬ ‫‪7 .7‬תופעל ועדה משותפת לאיגוד ולפורום מנהלי המרכזים‬ ‫לבריאות הנפש‪ ,‬להמשך הטיפול בתנאי העבודה של‬ ‫הרופאים במסגרת ההסכם שאושר‪ .‬נציגי האיגוד בוועדה‬ ‫הם פרופ' משה קוטלר‪ ,‬פרופ' יובל מלמד‪ ,‬ד"ר מרנינה שוורץ‬ ‫ופרופ' צבי פישל‪.‬‬ ‫בברכה‪,‬‬ ‫פרופ' זאב קפלן‬ ‫יו"ר האיגוד הפסיכיאטרי‬

‫‪2 .2‬בקשה להוסיף אפשרות לרוטציה בפסיכיאטריה בהתמחות‬ ‫בראומטולוגיה הועברה לראש האיגוד הראומטולוגי‪.‬‬ ‫‪3 .3‬המסמך "מתן חוות דעת מטעם רופאים פסיכיאטרים עובדי‬ ‫מדינה בהליכים נגד המדינה" הועבר לאישור הגורמים‬ ‫המוסמכים במשרד הבריאות ובפרקליטות המדינה‪.‬‬ ‫‪4 .4‬תמונה ועדה בחירות ליו"ר האיגוד הנכנס ויפורסם קול קורא‬ ‫לגבי הגשת מועמדות והקריטריונים הנדרשים‪.‬‬ ‫‪5 .5‬אושרה ההצעה לפנות לחברות הנסיעות לשם קבלת הנחות‬ ‫לחברי האיגוד בנסיעות ובאירוח‪.‬‬ ‫‪6 .6‬עמדת האיגוד בנושא טיפול בעברייני מין על־ידי‬ ‫פסיכיאטרים היא שכל פסיכיאטר מומחה יוכל לעסוק‬

‫רשימת הכנסים הצפויים‪:‬‬ ‫"יחסי מטפל מטופל"‪ ,‬אילת‬

‫‪1-3/12/11‬‬

‫‪" 15-17/12/11‬הטיפול בהתמכרויות"‪ ,‬אחוזת אסיינדה‬ ‫‪24/12/11‬‬

‫"היבטים רפואיים ומשפטיים של גילוי עריות"‪ ,‬צפון‬

‫‪5-7/1/12‬‬

‫"פסיכיאטריה וכלכלה"‪ ,‬טבריה‬

‫‪16-18/2/12‬‬

‫"טיפול בהפרעות אפקטיביות"‪ ,‬ים המלח‬

‫‪15-17/5/12‬‬

‫כנס איגוד מרכזי‪ ,‬ת"א‬

‫איגוד הפסיכיאטריה בישראל ‪ -‬ההסתדרות הרפואית ‪ -‬המועצה המדעית‬ ‫‪Israeli Psychiatric Association‬‬

‫יו"ר‪ :‬פרופ' זאב קפלן ‪President: Prof. Z. Kaplan /‬‬ ‫‪Zeev.kaplan@pbsh.health.gov.il‬‬ ‫מזכיר‪ :‬ד"ר נמרוד גריסרו ‪Secretary: Dr. N. Grisaru /‬‬ ‫‪grisarun@gmail.com‬‬ ‫גזבר‪ :‬ד"ר בוריס נמץ ‪Treasurer: Dr. B. Nemets /‬‬ ‫‪nemetz@bgu.ac.il‬‬ ‫יו"ר נבחר‪ :‬פרופ' משה קוטלר ‪Elected President: Prof. M. Kotler /‬‬ ‫‪Moshe.kotler@beerness.health.gov.il‬‬

‫יו"ר יוצא ואחראי קשרי חו"ל‪ :‬פרופ' אבי בלייך ‪/‬‬ ‫‪President Emeritus and Foreign Affairs: Prof. A. Bleich‬‬ ‫‪lean@bgu.ac.il ,ableich@lev-hasharon.co.il‬‬

‫‪295‬‬

‫המרכז לבריאות הנפש באר שבע‬ ‫‪Beer-Sheva Mental Health Center‬‬

‫ טל'‪ ;08-6401606 :‬פקס‪08-6401621 :‬‬ ‫ רח' הצדיק מירושלים ‪ ,2‬באר שבע‪ ,‬ת"ד ‪ 4600‬‬ ‫ ‪Hazadik from Jerusalem St. P.O. Box 4600‬‬ ‫ ‪www.psychiatry.org.il‬‬

‫מטופלת אחת‪ .‬תוצאות דומות נצפו בקבוצת הביקורת‪.‬‬ ‫מסקנות‪ :‬עבודות קודמות הדגימו ספציפיות גבוהה של נוגדן‬ ‫לחלבון ‪ P‬ריבוזומלי בקרב חולי זאבת אדמנתית מערכתית‬ ‫הסובלים מפסיכוזה‪ ,‬אך נוכח הממצאים בעבודה שלנו‪ ,‬לא ניתן‬ ‫להשתמש בנוגדן זה כסמן ביולוגי של סכיזופרניה‪.‬‬ ‫טיפול מבוסס ראיות בהפרעה‬ ‫אובססיבית קומפולסיבית אצל ילדים‬ ‫ל‪ .‬ברואר‪ ,‬א‪.‬ד‪ .‬לוין וא‪.‬א‪ .‬סטורך‪ ,‬פלורידה‪ ,‬ארה"ב‬

‫הפרעה אובססיבית–קומפולסיבית )‪ (OCD‬מאופיינת‬ ‫במחשבות או בדמיוניות טורדניים ותמידיים (אובססיות)‬ ‫ו‪/‬או בהתנהגויות גלויות או סמויות (או טקסים למיניהם‬ ‫שהאדם עורך מול עצמו או מול אחרים) הנערכים במטרה‬

‫להפחית חרדה שמתעוררת כתוצאה מהמחשבות הטורדניות‬ ‫(קומפולסיות)‪.‬‬ ‫הפרעת זו שכיחה בקרב ‪ 2%-1%‬מהאוכלוסייה (ילדים‬ ‫ומבוגרים)‪ 80% .‬מהמבוגרים הסובלים מההפרעה מדווחים‬ ‫על כך שתסמיני ההפרעה הופיעו לפני גיל ‪ .18‬באופן מצער‪,‬‬ ‫בישראל ובעולם אין כיום התערבויות וטיפולים שיעילותם‬ ‫הוכחה‪ .‬הפרעה אובססיבית–קומפולסיבית גורמת לבעיות‬ ‫רבות בתחומי תפקוד רבים ולכן מצריכה טיפול יעיל‪ .‬כיום יש‬ ‫התערבויות פסיכולוגיות ותרופתיות שהדגימו יעילות מסוימת‬ ‫בטיפול בהפרעה אצל ילדים ובני נוער‪.‬‬ ‫מטרת מאמר סקירה זה היא לדון בספרות הקיימת ובממצאים‬ ‫הקיימים בנוגע לטיפול בהפרעה אובססיבית–קומפולסיבית‬ ‫ובהשלכותיה‪ ,‬ולהתייחס לכיווני מחקר עתידיים‪.‬‬

‫תוכנית תלת־שנתית ‪ -‬פסיכותרפיה בגישה האנליטית של יונג‬ ‫אוניברסיטת בר‪-‬אילן ‪ -‬ביה"ס לעבודה סוציאלית ע"ש לואיס וגבי וייספלד‪ ,‬היחידה ללימודי המשך‬

‫אוכלוסיית היעד‪ :‬עובדים סוציאליים בעלי תואר שני לפחות‪ ,‬פסיכולוגים‪ ,‬פסיכיאטרים‪ .‬מספר מקומות ישמרו‬ ‫למועמדים בעלי תואר שני בתחומי הטיפול‪ ,‬כגון טיפול ביצירה והבעה וקרימינולוגיה קלינית‪.‬‬ ‫מטרת התכנית‪ :‬התוכנית מיועדת להכשיר אנשי מקצוע למטפלים בפסיכותרפיה ע"פ הגישה האנליטית של יונג‪.‬‬ ‫התוכנית תקנה היכרות מעמיקה עם תורתו של יונג ודרך יישומה‪ :‬כולל הבנת נפש האדם המתפתחת בתהליך‬ ‫האינדיבידואציה שלו ובתוך סביבתו ושורשיו התרבותיים‪ ,‬החל מהילדות המוקדמת‪ ,‬הבגרות‪ ,‬אמצע החיים והזקנה‪.‬‬ ‫תלמד גם הגישה הסימבולית והטיפולית של הפסיכולוגיה היונגיאנית ואופן העבודה עם תכני הלא‪-‬מודע‪.‬‬ ‫ההוראה וההדרכה ינתנו ע"י מיטב האנליטיקאיים היונגיאניים בארץ‪.‬‬ ‫סגל ההוראה‪ :‬‬ ‫ ‬ ‫ ‬ ‫ ‬

‫ד"ר אברמוביץ יהודה ‪ -‬פסיכיאטר‪ ,‬מנהל מחלקה בבאר יעקב‪ ,‬אנליטיקאי יונגיאני בכיר‪.‬‬ ‫ד"ר באומן אבי ‪ -‬פסיכולוג קליני ואנליטיקאי יונגיאני בכיר‪.‬‬ ‫גב' פורת רינה ‪ -‬פסיכולוגית חינוכית וקלינית‪ ,‬אנליטיקאית יונגיאנית בכירה‪.‬‬ ‫ד"ר שליט אראל ‪ -‬פסיכולוג קליני ואנליטיקאי יונגיאני בכיר‪.‬‬

‫רשימת המרצים והמדריכים המלאה תופיע בפירוט התוכנית באתר היחידה ללימודי המשך‪:‬‬ ‫‪.www.biu.ac.il/soc/sw/hemshech‬‬ ‫תעודה‪ :‬לעומדים בהצלחה בדרישות התכנית תוענק תעודה המאשרת סיום לימודי פסיכותרפיה בגישת‬ ‫הפסיכולוגיה האנליטית של יונג‪ ,‬מטעם היחידה ללימודי המשך של ביה"ס לעבודה סוציאלית‪ ,‬ע"ש לואיס וגבי‬ ‫וייספלד‪ ,‬אוניברסיטת בר‪-‬אילן‪.‬‬ ‫הלימודים יתקיימו במשך שלוש שנים במתכונת משולבת של קורסים תיאורטיים‪ ,‬סדנאות חווייתיות‪ ,‬סמינר‬ ‫קליני והדרכה קבוצתית‪ ,‬בימי שני‪ ,‬בין השעות ‪ 15:00-20:30‬בשנה הראשונה‪ ,‬ובין השעות ‪ 20:30-13:00‬בשנה‬ ‫השנייה ושלישית‪ .‬סה"כ ‪ 572‬שעות‪.‬‬ ‫פרטים נוספים‪ :‬לימודי המשך‬ ‫ביה"ס לעבודה סוציאלית ע"ש לואיס וגבי וייספלד אוניברסיטת בר‪-‬אילן‬ ‫טלפונים‪ ,03-5318211 ,03-5317265 :‬פקס‪03-7384043 :‬‬ ‫אתר היחידה‪www.biu.ac.il/soc/sw/hemshech :‬‬

‫‪296‬‬

‫יהודים ישראליים במשך חמש שנים (‪ 4,073‬משתתפים)‪.‬‬ ‫הממצאים נלקחו מסקרים שנתיים שנערכו בישראל בשנים‬ ‫‪ 2006-2010‬כחלק מהסקר העולמי על שם גאלופ‪.‬‬ ‫שיטות‪ :‬בניתוח הנתונים זוהו מנבאים דתיים לסולמות של‬ ‫חמישה פריטים לרווחה ולמצוקה‪ ,‬ונעשו התאמות להשפעות‬ ‫של משתנים שונים‪ ,‬כולל שביעות רצון מהבריאות‪ .‬ניתוחים‬ ‫נוספים בדקו הבדלי דת‪ ,‬תחושות רווחה ומצוקה והקשרים‬ ‫בקטגוריות של סוג הזהות הדתית ומידת הדתיות (חילוני‪,‬‬ ‫מסורתי‪ ,‬דתי וחרדי)‪.‬‬ ‫תוצאות‪ :‬רמות הדתיות ותחושת הרווחה עולות כשאתה זז‬ ‫"ימינה" בדתיות‪ ,‬כלומר נהיה דתי יותר‪ .‬הערכות עצמיות של‬ ‫חשיבות הדת ושל השתתפות דתית מותאמות באופן משמעותי‬ ‫לתחושות רווחה בכלל‪ ,‬והמדד של הרמוניה דתית מותאם גם‬ ‫לתחושת הרווחה (חיובי) והמצוקה (שלילי)‪ ,‬וגם לפריטים של‬ ‫מדדים אלה בכלל ושל השתתפות דתית‪.‬‬ ‫מסקנות‪ :‬מדדים דתיים הם מנבאים משמעותיים לתחושות‬ ‫רווחה פסיכולוגית ומצוקה פסיכולוגית בקרב יהודים ישראליים‪,‬‬ ‫ללא קשר להשתתפות דתית‪.‬‬ ‫יצירת קשר עם מרפאת בריאות הנפש‬ ‫ואשפוז חוזר אחרי שחרור מאשפוז פסיכיאטרי‬ ‫א‪ .‬גרינשפון‪ ,‬י‪ .‬לרנר‪ ,‬צ‪ .‬הורניק־לוריא וא‪ .‬פוניזובסקי‪ ,‬ירושלים‬

‫רקע‪ :‬המשכיות הטיפול הנפשי בקהילה היא נושא מרכזי בעידן‬ ‫האל–מיסוד‪ ,‬במיוחד בשל חשיבותה האפשרית כגורם התורם‬ ‫למניעת אשפוז חוזר‪.‬‬ ‫מטרות‪ :‬מחקר זה בחן את המתאם בין יצירת קשר עם מרפאת‬ ‫מעקב אחרי השחרור לבין הזמן עד לאשפוז החוזר‪ .‬כמו כן‬ ‫נבדקו מנבאים למשך הזמן בין השחרור מאשפוז ועד לביקור‬ ‫הראשון במרפאת מעקב‪.‬‬ ‫שיטה‪ :‬הנתונים נלקחו מקובץ האשפוזים של משרד הבריאות‬ ‫ומקובץ האשפוזים של בית החולים טירת–הכרמל עבור חולים‬ ‫שהשתחררו בתקופה ‪ .31.12.2006-1.1.2006‬נאספו נתונים גם‬ ‫מהמרפאות באזור עבור חולים אלה בתקופת מעקב של ‪ 180‬יום‬ ‫מהשחרור‪ .‬לשם ניבוי הזמן עד לאשפוז החוזר ולשם ניבוי הזמן‬ ‫עד לביקור הראשון במרפאת מעקב נעשה ניתוח רב–משתנים‬ ‫מסוג רגרסיה של ‪.Cox‬‬ ‫תוצאות‪ :‬מתוך ‪ 908‬חולים אשר שוחררו בתקופה הנ"ל‪ ,‬כ–‪29%‬‬ ‫אושפזו מחדש ו–‪ 59%‬מהם ביקרו במרפאות במהלך תקופת‬ ‫המעקב של ‪ 6‬חודשים‪ 22% .‬מבין אלה שביקרו במרפאה אושפזו‬ ‫מחדש לעומת ‪ 40%‬מבין אלה שלא ביקרו במרפאה‪ .‬הגורמים‬ ‫שנמצאו כמנבאים אשפוז חוזר היו אי–יצירת קשר עם מרפאת‬ ‫מעקב והיסטוריה של ‪ 4‬אשפוזים קודמים או יותר‪ .‬באשר‬ ‫למנבאים לביקור ראשון במרפאת מעקב‪ ,‬נמצא שגברים יצרו‬ ‫קשר ראשוני עם מרפאת המעקב מוקדם יותר מנשים; חולים‬ ‫שסבלו משסעת ומהפרעה אפקטיבית ביקרו במרפאה מוקדם‬ ‫יותר מחולים עם אבחנות אחרות; חולים שהשתחררו מאשפוז‬ ‫יום הגיעו למעקב ראשון לאחר תקופה ממושכת יותר מאלה‬ ‫‪297‬‬

‫שהשתחררו מאשפוז מלא‪.‬‬ ‫מסקנות‪ :‬אשפוז חוזר קשור להיעדר קשר עם מרפאת מעקב‪ ,‬אך‬ ‫איננו קשור לסוג האבחנה‪ .‬ייתכן שהגעתם של חולים הסובלים‬ ‫משסעת וממחלות אפקטיביות למרפאות מעקב תוך פרק זמן‬ ‫קצר יותר לאחר השחרור היא הסיבה לכך שחולים אלה לא‬ ‫חוזרים לאשפוז מהר יותר מחולים קלים יותר‪.‬‬ ‫"העברה למוסד אחר"‪ :‬היסטוריה קלינית‬ ‫של חולים פסיכיאטרים שנרצחו‬ ‫בתכנית "המתת חסד" של הנאצים‬ ‫פ‪ .‬סטגר‪ ,‬א‪ .‬גורגל‪ ,‬ו‪ .‬סטרובה‪ ,‬ה‪ .‬ווינקלמן וט‪ .‬בקר‪ ,‬מינכן‪ ,‬גרמניה‬

‫מחקר זה נועד לבחון את הנוהל של דיווח רפואי בסביבה‬ ‫טוטליטרית‪ ,‬כולל הרג שיטתי של אנשים הסובלים ממחלות‬ ‫נפש בגרמניה הנאצית‪ .‬הניתוח ההיסטורי מבוסס על מסמכי‬ ‫מטופל ועל קבצים מנהליים של בית החולים המחוזי שנקרא‬ ‫היום גונצבורג‪ ,‬כמו גם על מסמכי החולים ממלאי ‪ 179 R‬של‬ ‫משרד הארכיון הפדרלי (‪ )Bundesarchiv‬בברלין‪.Lichterfelde /‬‬ ‫העיתון מתאר את ההיסטוריה של ארבעה מטופלים ומנסה‬ ‫לשחזר היבטים מסוימים של החולים (בעיקר מוסדיים) על‬ ‫רקע היותו של בית החולים הממשלתי גונצבורג מוסד "אסיפה"‬ ‫בהקשר ל"אקציה ‪ ."T4‬אין כל ודאות לגבי מקומות המוות של‬ ‫ארבעת החולים האלו‪ .‬ברשומות החולים שנבדקו‪ ,‬הנוהג של‬ ‫דיווח רפואי אופיין בערבוב של מינוח רפואי‪ ,‬מינוח אידיאולוגי‬ ‫ושפה עממית‪ .‬סוג התיאור והתיעוד הרפואי שנעשה בהם‬ ‫שימוש מעידים על אפליה של חולים ועל התנהגות מוסדית‬ ‫יוצרת טראומה‪ ,‬והוא משקף אלימות מוסדית‪ .‬זוהי אחריות‬ ‫אתית לשחזר ולהנציח את ההיסטוריה האישית של חולי נפש‬ ‫שהיו קרבנות תכנית ההרג ההמוני המאורגן‪ .‬מקומות המוות‬ ‫הוסוו על ידי "האקציה ‪ ,"T4‬ואין ודאות לגבי מקום מותם של‬ ‫חולים רבים‪.‬‬ ‫נוגדנים לחלבון ‪ P‬ריבוזומלי בקרב חולי סכיזופרניה‬ ‫י‪ .‬גילת‪ ,‬י‪ .‬שינפלד‪ ,‬מ‪ .‬קוטלר וי‪ .‬יאנקו‪ ,‬תל אביב‬

‫רקע‪ :‬סדרה של ממצאים אפידמיולוגיים‪ ,‬ממצאי מעבדה‬ ‫וממצאים קליניים‪ ,‬מצביעים על תהליך אוטואימוני בקרב חולי‬ ‫סכיזופרניה‪ ,‬הכולל‪ ,‬בין השאר‪ ,‬כייל נוגדנים גבוה למרכיבי עצמי‬ ‫בסרום החולים‪ .‬מאידך‪ ,‬ידוע על הימצאותו של נוגדן לחלבון ‪P‬‬ ‫ריבוזומלי בקרב חולי זאבת אדמנתית מערכתית אשר מציגים‬ ‫הסתמנות פסיכיאטרית‪ ,‬כולל פסיכוזה‪ .‬נוכח זאת ביקשנו‬ ‫לבדוק את ההימצאות של נוגדן זה אצל חולי סכיזופרניה‪.‬‬ ‫שיטות‪ :‬נבדקה נוכחותו של נוגדן לחלבון ‪ P‬ריבוזומלי בסרום‬ ‫של ‪ 59‬מטופלים (‪ 48‬לוקים בסכיזופרניה ו–‪ 11‬לוקים בהפרעה‬ ‫סכיזו–אפקטיבית) בעזרת תבחין ‪ .ELISA‬קבוצת הביקורת כללה‬ ‫‪ 94‬נבדקים בעלי מאפייני גיל ומגדר דומים‪.‬‬ ‫תוצאות‪ :‬אצל ‪ 58‬מטופלים הכייל של הנוגדן לחלבון ‪P‬‬ ‫ריבוזומלי היה נמוך מהרמה הנחשבת לחיובית והיה גבולי אצל‬

‫כתב עת ישראלי‬ ‫לפסיכיאטריה‬ ‫תקצירים‬ ‫סיכון לתמותה בקרב אנשים עם‬ ‫היסטוריה של אשפוז פסיכיאטרי‬ ‫צ‪ .‬חקלאי‪ ,‬נ‪ .‬גולדברגר‪ ,‬א‪ .‬פוגצ'וב‪ ,‬נ‪ .‬שטיין וי‪ .‬לבב‪ ,‬ירושלים‬

‫רקע‪ :‬אנשים הסובלים מתחלואה פסיכיאטרית חמורה נמצאים‬ ‫בסיכון גבוה לתמותה בהשוואה לאוכלוסייה הכללית‪.‬‬ ‫מטרות‪ :‬לבדוק את שיעור התמותה וסיבות מוות נבחרות‪,‬‬ ‫טבעיות וחיצוניות‪ ,‬של אנשים בעלי היסטוריה של אשפוז‬ ‫פסיכיאטרי בהשוואה לאנשים ללא עבר דומה‪ ,‬לפי גיל‪ ,‬מין‬ ‫ומאפייני האשפוז הפסיכיאטרי‪.‬‬ ‫שיטות‪ :‬זהו מחקר קוהורט‪ ,‬הבודק את שיעור התמותה בקרב‬ ‫יהודים בני ‪ 18‬ומעלה שהיו באשפוז פסיכיאטרי בישראל‬ ‫עד שנת ‪ ,2006‬בהתאם לרישום במאגר המאושפזים במשרד‬ ‫הבריאות (‪ ,)PCR‬בהשוואה לאנשים שלא אושפזו כלל‪ .‬המחקר‬ ‫מתבסס על הקבלה בין קובץ סיבות המוות הלאומי בשנים‬ ‫‪ 2006-1981‬לבין קובץ המאושפזים‪.‬‬ ‫ניתוח‪ :‬חושבו שיעורי פטירה לפי גיל‪ ,‬מין ואבחנה פסיכיאטרית‪,‬‬ ‫שיעורי פטירה מתוקננים לגיל ויחס שיעורים (‪ )RR‬של אנשים‬ ‫שהיו באשפוז פסיכיאטרי בהשוואה לאנשים שלא אושפזו‬ ‫מעולם‪ .‬שיעורים אלו חושבו גם לפי תקופות כדי לבדוק‬ ‫אם קיים קשר בין המדיניות בטיפול הפסיכיאטרי לשיעורי‬ ‫הפטירה‪ .‬כן חושב הזמן שעבר מהשחרור מאשפוז פסיכיאטרי‬ ‫עד לפטירה‪.‬‬ ‫ממצאים עיקריים‪ :‬שיעור התמותה המתוקנן לגיל של אנשים‬ ‫עם היסטוריית אשפוז פסיכיאטרי היה כפול בהשוואה ללא‬ ‫מאושפזים (‪ ,)RR=1.98 ,95% CI 1.96-2.00‬יחס דומה נמצא‬ ‫לגברים ולנשים‪ .‬השיעור גבוה יותר בכל קבוצות הגיל עבור אנשים‬ ‫בעלי היסטוריית אשפוז פסיכיאטרי ובמיוחד עבור צעירים‪ .‬שיעור‬ ‫תמותה גבוה במיוחד נמצא מסיבות חיצוניות‪ ,‬בעיקר מהתאבדות‬ ‫(‪ ,)RR=16.34 ,95% CI 15.49-17.24‬אך גם ממרבית הסיבות‬ ‫הטבעיות‪ ,‬פרט לסרטן (‪ .)RR=1.13, 95% CI 1.10-1.16‬הסיכון‬ ‫הגבוה ביותר לתמותה נמצא בקרב מאושפזים שסבלו מהתמכרות‬ ‫לסמים ולאלכוהול‪ .‬שיעור תמותה דומה נמצא בקרב מאושפזים‬ ‫הסובלים מסכיזופרניה ומאבחנת דיכאון או ביפולאר‪ .‬לא נמצא‬ ‫שינוי ביחס השיעורים במשך השנים כתוצאה משינויים במדיניות‬ ‫האשפוז או מהכנסת תרופות מדור שני‪ .‬כשליש ממקרי הפטירה‬ ‫ו–‪ 62%‬מההתאבדויות של האנשים שהיו באשפוז פסיכיאטרי קרו‬ ‫לפני השחרור מהאשפוז או בתוך שנה מהשחרור‪.‬‬

‫‪israel journal of‬‬

‫‪psychiatry‬‬ ‫כרך ‪ ,48‬מס' ‪2011 ,4‬‬

‫מסקנות והמלצות‪ :‬מחקר זה מצביע על החשיבות בקידום‬ ‫תוכניות התערבות למניעה ועל חשיבות הטיפול הרפואי‬ ‫לאנשים שהיו באשפוז פסיכיאטרי‪.‬‬ ‫סכיזופרניה‪ :‬זה שבור ולא בר–תיקון‪ .‬ניתוח רעיוני‬ ‫לכבוד יובל המאה להפיכת "שיטיון הבחרות"‬ ‫(‪ )Dementia praecox‬לסכיזופרניה על–ידי בלוילר‬ ‫י‪.‬ד‪ .‬בלום וה‪.‬מ‪ .‬ואן פראג‪ ,‬דן האג‪ ,‬הולנד‬

‫רקע‪ :‬ב–‪ 1911‬קבע בלוילר כי סכיזופרניה אינה בהכרח מצב של‬ ‫שיטיון (כפי שניתן היה ללמוד משמה עד אז "שיטיון הבחרות"‬ ‫ ‪ .)Dementia praecox‬הוא ראה בסכיזופרניה קבוצה של ישויות‬‫נוסולוגיות המאופיינות בפירוק של תפקודי הנפש השונים‪ .‬כיום‪,‬‬ ‫מאה שנים לאחר קביעה חשובה זו של בלוילר‪ ,‬נראה כי החשיבה‬ ‫הראשונית שלו עודנה מתאימה במובנים מסוימים‪.‬‬ ‫שיטה‪ :‬לשם ניתוח רעיוני זה נערכה סקירת ספרות מקיפה במאגרי‬ ‫המידע הבאים‪ Embase ,PubMed :‬ו–‪.historical literature‬‬ ‫ממצאים‪ :‬המושג העדכני לסכיזופרניה‪ ,‬כפי שמופיע ב–‪DSM‬‬ ‫ובמגדירים פסיכיאטרים אחרים‪ ,‬קשור עדיין לתפישה‬ ‫הראשונית של בלוילר של מושגים ומצבים הקשורים‬ ‫בפסיכופתולוגיה‪ .‬על אף שתפישה זו מיושנת וארכאית‪,‬‬ ‫השפעותיה עדיין ניכרות גם כיום‪ ,‬מאה שנים לאחר מכן‪ ,‬ואינן‬ ‫מאפשרות לנו להתקדם בתפישתנו לגבי המחלה‪ .‬אנחנו עדיין‬ ‫רואים בסכיזופרניה מחלה אחת בעלת פנים רבות‪ ,‬תסמינים‬ ‫מגוונים ותוצאה לא חיובית אחת‪.‬‬ ‫מסקנות‪ :‬אם ברצוננו לחקור וללמוד את ההשפעות הביולוגיות‬ ‫שבבסיסם של תסמינים פסיכוטיים‪ ,‬עלינו להתחיל בראש‬ ‫ובראשונה מיצירת המשגה חדשה למושג "סכיזופרניה"‪ .‬במאמר‬ ‫זה שמנו דגש על מושג בשם "תפקוד" (‪,)functionalization‬‬ ‫המאפשר לנו לתפוש את מחלת הסכיזופרניה מפרספקטיבה‬ ‫אחרת‪.‬‬ ‫מגבלות‪" :‬תפקוד" (‪ )functionalization‬יצריך המשגה מדעית‬ ‫חדשה‪ ,‬שונה מאוד מההמשגה הנוסולוגית הקיימת כיום ושונה‬ ‫מאוד ממערכת האבחון וההערכה הנהוגה כיום במערכות‬ ‫הבריאות‪.‬‬ ‫דת ותחושות רווחה (‪ )wellbeing‬ומצוקה‬ ‫בקרב יהודים ישראליים‪ :‬תוצאות‬ ‫הסקר העולמי על שם גאלופ‬ ‫ג'‪ .‬לוין‪ ,‬וואקו‪ ,‬ארה"ב‬

‫רקע‪ :‬מחקר זה בחן את המנבאים הדתיים של רווחה‬ ‫פסיכולוגית ומצוקה פסיכולוגית במדגם סבירות ארצי של‬ ‫‪298‬‬

AMISULPRIDE

In schizophrenia, how do you get from here

to here?

XeplionÂŽ, a new once-monthly injectable schizophrenia therapy,1 significantly reduces relapse.2 With early onset of efficacy3,4 and good tolerability,1â&#x20AC;&#x201C;6 Xeplion can help your patients shape a future in a way that they wish.

Preventing relapse, enabling futures

For comprehensive information please refer to full Prescribing information as approved by the Israeli Health Authority.

References: 1. Xeplion prescribing information. 2. Hough D et al. Schiz Res 2010; 116: 107-117.

3. Pandina GJ et al. J Clin Psychopharmacol 2010; 30: 235-244. 4. Kramer M et al. Int J Neuropsychopharmacol 2010; 13: 635-647. 5. Gopal S et al. J Psychopharmacol Online First, published on July 8, 2010 as doi:10.1177/0269881110372817. 6. Hoy SM et al. CNS Drug Rev 2010; 24(3): 227-244.