Work and Mental Illness Professor David Castle Chair of Psychiatry, St. Vincent’s Hospital Melbourne Dept. of Psychiatry, The University of Melbourne Email: david.castle@svhm.org.au
Work exclusion in Schizophrenia Australia “Low Prevalence” study (Jablensky et al,1997) 5.8% males, 6.1% females in full time employment 72% males, 62% females on DSP
Positives of work
Structured daily activities
Social opportunities
Feeling socially ‘useful’
Enhanced self esteem
Regular income (Mueser et al,1997)
Reasons for work exclusion in schizophrenia
Symptoms of mental illness
Side effects of psychiatric medications
Lack of access to vocational/educational training
Job design problems (Human Rights and Equal Opportunities Commission,1993)
“A Psychiatrist’s Perspective…”
Support and work with other services towards “an integration of vocational and clinical services at the level of service delivery” (Frost et al, 2002)
Optimistic symptom control and reduce side effect burden Examples:
Manage mood instability in bipolar Ameliorate effects of cognitive dysfunction in schizophrenia
Bipolar Affective Disorder: Psychosocial Treatments Professor David Castle Chair of Psychiatry, St.Vincent’s Hospital Melbourne and the University of Melbourne david.castle@svhm.org.au
Different Types of Bipolar Disorder Mood Profile (Castle & Bassett, 2009)
Type I BPAD
MANIC PHASE
DEPRESSE D PHASE
Type II BPAD
“Cyclothymia” Bipolar Spectrum Disorder
“Normal” Mood Variance
Longitudinal Course of Bipolar (an Example) (Castle & Bassett, 2009)
Presentation with Mania
Treatment Begins
ELEVATE D MOOD
Prodrome
Mania Following Treatment of Depression
DEPRESSE D MOOD
Prodrome
Depressed Phase Following Recovery From Mania
Depression
Walking the Black Dog
The Red Dragon
Prognostic Factors in Bipolar Psychosocial Factors Contribute 24-50% to outcome variables Negative life events Functional impairment Lower social support Conflictual family relationships
Bipolar Illness Variables Higher number of episodes More depressive episodes Psychotic symptoms Subsyndromal symptoms
Worse Prognosis Non- Adherence
Co-morbid Diagnosis
Range non-adherence from 20-66%, mean 41% Attitudes, beliefs important
Substance abuse Personality disorders
Johnson and Miller, J Abnorm Psychol 1997; 106: 449-457 Gitlin MJ , Hammen C Bipolar Disorder Golberg Jf, Harrow M (Eds) 1999 Keck P et al 1996 Jour. Clin. Psych. 1996;57:292-97 Miklowitz DJ. CNS Spectrum 1998;3:48 Post et al J Clin Psych 64:6 June 2003 Scott J, Br J Psychiatry 1995; 167: 581
Treatment Aims Understanding of illness Mood monitoring including early warning signs Control of illness rather than illness exerting control Symptom control Optimal pharmacotherapy Broader psychosocial parameters
What do we know about Psychosocial Interventions? Relapse rates high even if taking meds Different approaches: • Psychoeducation - individual/group (Colom et al, 2003) • • • • •
Family focused therapy
(Miklowitz et al, 2000)
CBT (Lam et al, 2003, 2005; Scott et al, 2006) IPSRT (Frank et al, 1999) Integrated models (Bauer et al, 2006; Simon et al, 2006) Collaborative Therapy (Berk, Berk & Castle, 2005) (Castle et al, 2007, 2010)
(Castle et al, 2007, 2010)
Translating Effective Psychosocial Interventions for Bipolar Disorder into Everyday Clinical Practice Carolynne Holdsworth Cath Bunton Frameworks for Health St.Vincent’s, Melbourne
Study Objectives Primary Goals:
To develop a group-based intervention and relapse prevention package to assist consumers to manage their bipolar disorder.
To integrate the intervention using the Collaborative Therapy Framework and implement the project in a range of service settings.
To evaluate the effectiveness of the intervention using a RCT.
Study Objectives Challenges: To develop an intervention that is effective for “real-world” patients To ensure the intervention is sustainable beyond the life of the research project.
Study Design Stages of Assessment 1. Baseline 2. Post-Group (3 month) 3. 12 month assessment
Phase 1 • Literature review • Focus groups to map needs • Develop treatment package & pilot content Phase 2 • Evaluate “MAPS group program” using a randomised control trial. Intervention
(12 weeks + 3 boosters)
1
2
Phase 3 • Follow-up maintenance (9 months)
3
12 months
MAPS Group Program The group program aims to: • Provide information and develop skills to assist people to effectively manage bipolar disorder. • Enable people with bipolar disorder to get the most out of life despite the disorder.
12 x weekly 1 ½ hour sessions + 3 x monthly boosters. Resources: Personal Workbook, Information Book, Collaborative Treatment Journal (CTJ)
MAPS Session Outline Session
Focus
Content
1-2
Education
Introduction bipolar disorder and triggers commonly associated with bipolar disorder
3-6
Core skills development
Monitoring & assessment of stress/triggers Preventing relapse using coping skills, eg problem solving, stress tolerance and SMART goal setting & medication management
7-9
Depression
Assessing and managing early warning signs of depression Developing relapse prevention plans for depression
10 - 12
Mania
Assessing and managing early warning signs of mania Developing relapse prevention plans for mania
Booster 1-3
Integrating and reinforcing skills
Consolidating skills into daily life
A Real-world Clinical Sample Sample size: Total N= 82 (control: n=39, treatment: n=35)
Gender: Female 76%, Male 24%
Age: mean = 42, SD = 11
Employment: Part time
37%
Unemployed
32%
Full time
15%
Student
1%
A Real-world Clinical Sample Diagnosis Bipolar 1 22% Bipolar I (with psychotic episode) 8% Bipolar II 45%
Co-morbidities Ave no per person 2.9 most common: anxiety, suicidality, alcohol & substance use, etc
Relapse Type Depression Mania Hypomania Mixed
Treatment 4 0 9 1
Control 14 6 6 1
All relapses: mean time in relapse over 9 months was 11 days for treatment and 27 days for control group, p=0.01
Any Relapse – time to first recurrence Kaplan-Meier survival estimates, by treat Any 1st relapse
Treatment
Control
.75 .5 .25 0
survivor function
1
Any 1st relapse
0
100
200
300 0
100
time (post treatment, days) Treatment Graphs by treat
Control
200
300
Depression Relapse
0.00
survivor function 0.25 0.50 0.75
1.00
Depression
0
100 200 time (post treatment, days) Treatment
Control
300
Mania/Mixed Relapse
0.00
survivor function 0.25 0.50 0.75
1.00
Mania and mixed
0
100 200 time (post treatment, days) Treatment
Control
300
Service Utilisation Mean - Treatment
Mean - Control
Pre
post
Pre
Post
Admissions 1.03
0.39
0.89
0.91
Weeks
2.84
1.32
2.54
1.83
CAT Crisis Visits
1.97
0.00
0.74
0.53
Item
Getting it Out There
Acknowledgements Project Team Chief Investigators: David Castle, Monica Gilbert, Michael Berk Isaac Schweitzer and Leon Piterman Program Developers: Lesley Berk and Sue Lauder Research Clinicians: Carolynne Holdsworth, Cath Bunton, Terence Chong and Cathy Carman.
Our project funding partners:
Our service partners: Pathways Support and Rehabilitation Services Barwon Health Healthscope (The Melbourne & Geelong Clinics) Dr Greg Murray and Swinburne University of Technology
www.moodswings.net.au Ms Sue Lauder Professor Michael Berk Professor David Castle Dr. Seetal Dodd Dr. Andrea Chester This project gratefully acknowledges the funding support of beyondblue the national depression initiative
Cognition in Schizophrenia: Can We Fix It?
Professor David Castle Chair of Psychiatry, St. Vincent’s Hospital Melbourne The University of Melbourne david.castle@svhm.org.au
What are the Cognitive Deficits in Schizophrenia? (Wykes & Castle, 2003)
Mild
Moderate
Severe
Perceptual skills
Distractability
Executive functioning
Delayed recognition memory
Memory and working memory
Verbal fluency
Verbal and full scale IQ
Delayed recall
Motor speed
Do Medications Improve Cognitive Impairment? optimal treatment of positive symptoms important some older (typical) antipsychotics seem to make cognition worse benzodiazepines and anticholinergics can make cognition worse
Do Atypical Antipsychotics Help Cognition? early studies suggested “yes”, but confounded by effect of halting typicals (EPSE etc.) clozapine seems to improve attention and verbal fluency but has less effect on working memory
52 Week Trial of Olanzapine vs Risperidone vs Quetiapine (1) (Keefe et al, 2007)
400 patients < 5 yrs illness Random assignment to: - Olanzapine (mean 12mg) - Quetiapine (mean 500mg) - Risperidone (mean 2.5mg) 400 patients started; 221 completed assessment at 12 weeks; only 81 completed neuropsychology tests at 52 weeks
52 Week Trial of Olanzapine vs Risperidone vs Quetiapine (2) (Keefe et al, 2007)
52 Week Trial of Olanzapine vs Risperidone vs Quetiapine (3) (Keefe et al, 2007)
areas of improvement
verbal fluency (especially Quetiapine) letter-number sequencing digit symbol continuous performance task
improvements correlated modestly with vocational & social enhancement, but not significant after controlling for symptom improvement
Conclusions (Keefe et al, 2007) (Keefe et al, 2007)
Olanzapine, quetiapine, and risperidone all produced significant improvements in neurocognition in early psychosis patients. Although cognitive improvements were modest, their clinical importance was suggested by relationships with improvements in functional outcome. BUT not corrected for multiple comparisons similar effect size seen due to practice effects alone massive subject attrition correlates with functional outcomes very modest & disappear after controlling for symptom change
Conclusions (Michael F Green, 2007) (Michael F Green, 2007)
“meaningful cognitive improvements will probably not come from second-generation antipsychotics”
“there was no clear procognitive effect in this study”
“the findings leave us feeling a little smarter and a lot more humble”
Conclusions (Michael F Green, 2007) (Michael F Green, 2007)
So, Green (2007) suggests: (i)
We need to look at other potential cognitive enhancing drugs; and
(ii) we need to consider â&#x20AC;&#x153;new non-pharmacological interventions that specifically target cognitionâ&#x20AC;?
Does Cognitive Remediation Enhance Work Capacity? (McGurk et al, 2007)
44 people with SMI with past job failures randomised to: supported employment alone OR supported employment plus cognitive training
Does Cognitive Remediation Enhance Work Capacity? (McGurk et al, 2007)
Programme Components
cognitive assessment & job loss analysis 24 computer-based training sessions over 12wks review and discussion of gains made and planning regarding future work
ongoing consultation with an employment specialist
Does Cognitive Remediation Enhance Work Capacity? Intervention Group (n=21)
Control Group (n=23)
16 (70%)
3 (14%)
Total weeks worked
27.0
5.4
Total hours worked
848.6
94.6
Total $â&#x20AC;&#x2122;s earned
5320
530
No. who worked
Does Cognitive Remediation Enhance Work Capacity? (McGurk et al, 2007)
Conclusions (McGurk et al, 2007) (McGurk et al, 2007)
A cognitive enhancement package can assist work capacity in SMI Not clear what elements of the package help Still only around 6 months work in a 3 year period
If all else fails â&#x20AC;Ś.