A Q&A WITH THE ORGANIZERS |
New Frontiers of Pain Research
WELCOME TO THE CAMPUS OF THE UNIVERSITY OF ALABAMA AT BIRMINGHAM Birmingham, Alabama How did the idea for the UAB Pain Symposium come about?
The conference started with discussions between the leadership of the School of Medicine and the College of Arts and Sciences. It was the first step in a larger initiative to develop UAB as the country’s largest and most comprehensive pain research and treatment center. This will be the largest pain conference ever held at UAB and its goal is to bring together all UAB faculty, staff, and students who have an interest in tackling the enormous worldwide problem of chronic pain.
What are some noteworthy issues so far in the 21st century that are impacting the field? Perhaps the biggest issue facing the field now is how to effectively manage pain given the recent strong recommendations by the CDC and FDA to drastically reduce reliance on opioid analgesics. It is essential that researchers develop new treatment options that are effective, safe, and non-addictive. Chronic pain is a rapidly growing medical issue and will become increasingly problematic as our population ages. The most promising lines of research need to be identified and followed so we can translate findings to therapeutic tools as quickly as possible.
How did you assemble the faculty? What were you looking for? The conference faculty was selected based on their novel lines of research and potential to greatly impact the field. Some of the speakers are established leaders in pain research and treatment, and some are new faculty members who are conducting cutting-edge research. We really intended this conference to be forward-looking, and for the speakers to address where the field goes from here and what advances they think will be made in the next few years.
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How does their breadth of experience impact the scope of the conference? The faculty members have a tremendously diverse set of perspectives and experiences in pain research and treatment. The speakers will involve both researchers and clinicians from psychology, anesthesiology, psychiatry, palliative care, physical medicine and rehabilitation, rheumatology, and physiology. Both basic scientists and physician scientists will present their new and upcoming work. Dr. John Kusiak from the National Institutes of Health will also discuss the federal initiatives to combat pain. The conference was designed to broadly represent the field and to be engaging for all attendees.
What can attendees expect to learn? This conference is focused on what exciting things will unfold in the near future. We expect to review several new approaches for treating pain and discuss plans for making UAB a key player in the global effort to eradicate unnecessary pain. While we are looking forward to all the local presentations, we are excited to have presentations from our visiting faculty members Drs. Jeffrey Mogil (McGill University), Jon Levine (UCSF), and Robert Edwards (Brigham & Williams Hospital, Harvard School of Medicine). We believe this conference will be an excellent showcase for all the work that UAB members do in the field of pain, and we hope the conference will bring together a strong network of individuals who are interested in the future of pain research and treatment.
2016 Target Audience This conference is designed for clinicians, researchers, students and trainees. Accreditation This activity has been planned and implemented in accordance with the Division of UAB Continuing Medical Education. UAB is accredited by the ACCME to provide continuing medical education to physicians, psychologists and nurses. Credit Designation The University Of Alabama School Of Medicine is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The University of Alabama School of Medicine designates this live activity for a maximum of 10.25 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. UAB EOE Statement UAB is an Equal Opportunity / Affirmative Action Employer committed to fostering a diverse, equitable and family-friendly environment in which all faculty and staff can excel and achieve work/life balance irrespective of ethnicity, gender, faith, gender identity and expression as well as sexual orientation. UAB also encourages applications from individuals with disabilities and veterans. Learning Objectives The symposium’s goal is to bring together pain scientists and clinicians, facilitate awareness and collaboration, and serve as an educational resource on basic science, clinical research, and treatment advances.
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AGENDA OVERVIEW |
New Frontiers of Pain Research
Friday, October 14th 7:45
8:30
Breakfast & Registration
*Note that all posters should be in place by 8:30AM
Opening Address
Richard Marchase, Ph.D.
Vice President For Research and Economic
Development, UAB 8:45
Welcome Remarks
Keith A. (Tony) Jones, M.D.
Alfred Habeeb Professor and Chair, Department of
Anesthesiology and Perioperative Medicine, UAB 9:00
KEYNOTE
Jon Levine, M.D., Ph.D.
Toward a Cell Biology of Chronic Pain
9:45 Talk Burel Goodin, Ph.D. Understanding the Mechanisms of Pain Disparities Within Disadvantaged Subgroups 10:15
Talk
10:45
Break
11:00
Talk
Jessica Merlin, M.D., M.B.A.
HIV and Chronic Pain: State of the Science
Michael Frölich, M.D., M.S.
New Approaches for Pain Imaging
11:30 Talk Shawn Hochman, Ph.D. Neuromodulation Based Control of Protean Primary Afferents 12:00
Lunch
1:00
KEYNOTE
Robert Edwards, Ph.D.
Psychosocial Contributions to Chronic Pain:
Implications for Precision Pain Medicine 1:45 Talk Beverly Thorn, Ph.D. Reducing the Cognitive Demands of Psychosocial Treatments for Chronic Pain: Clinical Research 2:15
Break
2:30
Talk
Timothy Ness, M.D., Ph.D.
Neuromodulation of Bladder Hypersensitivity
3:00
Talk
Jeff Curtis, M.D., M.S., M.P.H.
Using Mobile Health Information to Track Pain and
Patient Outcomes
3:30 Talk Candace Floyd, Ph.D. Sex Differences in Pain Response in a Porcine Model of Spinal Cord Injury 4:00
Break
4:15
KEYNOTE
John Kusiak, Ph.D.
Pain Research in the 21st Century: The View from
the National Institutes of Health 5:00 – 6:00
Posters, Cocktails, and Light Hors D’oeuvres
Networking
Saturday, October 15th 8:00
Breakfast
9:00
KEYNOTE
9:45 10:15
Jeffrey S. Mogil, Ph.D.
Pain in Mice and Man; Ironic Adventures in Translation
Talk
Robert Sorge, Ph.D.
Diet and Inflammation: Interactions and Interventions
Talk
Ursula Wesselmann,
Pain in the Context of Comorbid Conditions: Translational
M.D., Ph.D. 10:45
Break
11:00
Talk
Matthew Stoll,
Research Findings and Complex Clinical Implications Central and Inflammatory Pain in Arthritis: Is it
M.D., Ph.D., M.S.C.S.
Either/Or?
11:30
Talk
Precision Pain Medicine: A Path Forward
12:00
Lightning Talks
12:30
Awards/Conclusion
1:15
End of Conference
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Stephen Bruehl, Ph.D.
Detailed agenda available at: uab.edu/painsymposium
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GUEST SPEAKERS |
New Frontiers of Pain Research
Stephen Bruehl, Ph.D.
Professor Department of Anesthesiology Division of Research Vanderbilt University School of Medicine
Jeffrey R. Curtis, M.D., M.P.H.
Assistant Professor of Medicine Division of Clinical Immunology and Rheumatology University of Alabama School of Medicine
Robert Edwards, M.D.
Associate Professor Brigham & Women’s Hospital Harvard School of Medicine
Candace Floyd, Ph.D.
Associate Professor Director of Research Department of Physical Medicine & Rehabilitation University of Alabama School of Medicine
Michael Frölich, M.D., M.S.
Professor of Anesthesiology Department of Anesthesiology and Perioperative Medicine University of Alabama School of Medicine
Burel Goodin, Ph.D.
Assistant Professor Department of Psychology University of Alabama College of Arts & Sciences
Shawn Hochman, Ph.D.
Professor and Deputy Chair Department of Physiology Emory University School of Medicine
John Kusiak, Ph.D.
Acting Deputy Director Office of the Director National Institute of Dental and Craniofacial Research National Institutes of Health
SESSION CHAIRS Friday Sessions Session 1 (8:30 – 10:45): Gu & Merlin Session 2 (11:00 – 12:00): Goodin Session 3 (1:00 – 2:15): Ness Session 4 (2:30-4:00): DeBerry & Floyd Session 5 (4:15-5:00): Gu
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Saturday Sessions Session 1 (8:30 – 10:45): Younger & Sorge Session 2 (11:00 – 1:15): Wesselmann & Younger Lightning Talks (12:00-12:30): Bruehl Awards/Conclusion (12:30-12:45): Younger
Last Session Q/A Panel for Future UAB Pain Research (12:50-1:30): Younger, DeBerry, Gu & every speaker
Jon Levine, M.D., Ph.D.
Professor of Medicine University of California, San Francisco
Jessica Merlin, M.D., M.B.A.
Assistant Professor Department of Medicine Divisions of Infectious Diseases and Gerontology, Geriatrics and Palliative Care University of Alabama School of Medicine
Jeffrey Mogil, Ph.D.
Professor of Psychology Canada Research Chair in Genetics of Pain E.P. Taylor Chair in Pain Studies McGill University
Timothy J. Ness, M.D., Ph.D.
Simon Gelman Endowed Professor of Anesthesiology Department of Anesthesiology and Perioperative Medicine University of Alabama School of Medicine
Robert Sorge, Ph.D.
Assistant Professor Department of Psychology College of Arts & Sciences University of Alabama at Birmingham
Matthew Stoll, M.D., Ph.D., M.S.C.S. Associate Professor of Pediatrics Department of Pediatrics Division of Pediatric Rheumatology University of Alabama School of Medicine
Beverly E. Thorn, Ph.D. Professor of Psychology Department of Psychology The University of Alabama
Ursula Wesselmann, M.D., Ph.D.
William A. Lell, M.D.–Paul N. Samuelson, M.D., Endowed Professor of Anesthesiology Professor of Anesthesiology, Neurology, and Psychology Department of Anesthesiology and Perioperative Medicine University of Alabama School of Medicine
SCIENTIFIC REVIEW JUDGES Leanne Cianfrini, Ph.D.
UAB Adjunct Assistant Professor Department of Psychology
Timothy Ness, M.D.
UAB Professor of Anesthesiology Department of Anesthesiology and Perioperative Medicine
Alan Randich, Ph.D.
UAB Professor Emeritus Department of Anesthesiology and Perioperative Medicine Former Program Director, Behavioral Neuroscience Doctoral Program UAB Department of Psychology
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ABSTRACTS |
New Frontiers of Pain Research
QUANTITATIVE REGIONAL CEREBRAL BLOOD FLOW ASSOCIATED WITH PAIN IN INTERSTITIAL CYSTITIS PATIENTS WITH & WITHOUT COMORBIDITIES: A CASL MRI STUDY
Georg Deutsch (1), Hrishikesh Deshpande (1), Demet Gurler(1), Michael Froelich (2), Timothy J Ness (2) (1) Department of Radiology, (2) Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham
We have previously demonstrated changes in quantitative regional cerebral blood flow (rCBF) in interstitial cystitis (IC) patients due to bladder filling. The present study sought to examine the activation patterns when patients’ data were stratified according to the presence or absence of the co-morbidity of fibromyalgia (FM) as well as other co-morbidities and symptomatology. Participants were part of the NIDDK TransMAPP project. rCBF was measured using continuous arterial spin labeling (CASL) conducted on a 3T MRI (Philips Achieva) during rest and with a full bladder. CASL data was transferred for rCBF computations using custom software written in MATLAB. Analysis was performed two ways: as absolute rCBF values in 38 regions of interest (ROI) defined by the Wake Forest Pick Atlas and using FSL & SPM analysis of within group rCBF distribution changes from rest baseline. When subdividing the IC patients into those with and those w/o FM co-morbidity, it was noted that those with FM show exaggerated increases in both the left and right thalamus, the right amygdala and in the left and right insula. Other stratification schema utilizing other co-morbidities (e.g., IBS) and polysyndromic polysymptomatic criteria came up with similar results. The relatively striking results observed when examining the data of IC patients with FM indicates that the presence of FM may add strong effects to CNS activation during both the “natural” pain associated with IC and to more experimental pain manipulations. These co-morbidity factors need to be further evaluated as they suggest an underlying difference in CNS processing in different pain populations.
EFFECTS OF INTRATHECAL BACLOFEN ON BLADDER-EVOKED REFLEX RESPONSES IN THE RAT Cary DeWitte, Timothy Ness and Alan Randich Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham Sponsored by a contract from Medtronic, Inc.
Chronic pelvic pain associated with bladder symptoms is common, debilitating, difficult-to-treat and often involves pelvic floor hypertonia. Intrathecal baclofen (ITB) is effective for severe spasticity and pain (neuropathic and reflex-related). ITB effects on bladder distension evoked visceromotor responses were investigated in a rat model of bladder hypersensitivity. Intravesical zymosan (1%) or anesthesia-only was administered to anesthetized female Sprague-Dawley pups at age P14-16. At age 12-16 weeks, zymosan pretreatment or anesthesia-only was repeated one day before testing. Intrathecal catheters were introduced into the cisterna magna and advanced to the lumbar enlargement. Electrodes were inserted into external oblique or pubococcygeus muscles to measure electromyographic (EMG) visceromotor responses to 20-sec urinary bladder distensions (UBD) under isoflurane-urethane anesthesia. Responses to cumulative ITB doses or i.t. saline were determined to graded UBDs (10-60 mm Hg). Duration of ITB-induced pain inhibition was assessed; the effect of the GABAB antagonist, CGP35348, was evaluated as a pretreatment before ITB. ITB resulted in dose-dependent inhibition of visceromotor responses in all groups; IT saline had no effect on visceromotor responses. The ED50 baclofen dose produced a prolonged (2-hour) inhibition of UBDevoked superior oblique EMG responses and robust, rapid inhibition of the pubococcygeus EMG responses. CGP35348 pretreatment antagonized ITB effects. In summary, ITB dose-dependently attenuated pain in a rat model of bladder hypersensitivity via a GABAB mechanism. Clinical success of ITB for spasticity and encouraging results in this rat model suggest clinical research of ITB for bladder-associated pelvic pain is warranted.
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ABSTRACTS |
New Frontiers of Pain Research
CENTRAL NERVOUS SYSTEM SENSITIZATION IS ASSOCIATED WITH CHRONIC PAIN IN HIV
Michael A. Owens, BS, BA (1), Jessica S. Merlin, MD (2), (3), Rachael L. Rainey (1), Jennifer I. Okunbor (1), Dyan M. White, BS (1), Kaneisha A. Mushatt (1), Lindsey R. Yessick, BS (1), Sonya L. Heath, MD (3), Janet M. Turan, PhD, MPH (4), & Burel R. Goodin, PhD (1), (5) Affiliations: University of Alabama at Birmingham (UAB): (1) Department of Psychology, (2) Division of Gerontology, Geriatrics, and Palliative Care, (3) Division of Infectious Diseases, (4) Department of Healthcare Organization and Policy, & (5) Division of Pain Medicine
Background: Chronic pain is a common and disabling comorbidity among people living with HIV (PLWH). Chronic pain prevalence in PLWH ranges from 39-85%, higher than in the general population. Central sensitization is a condition of the nervous system associated with the development and maintenance of chronic pain through enhanced processing of painful stimuli (pain hypersensitivity). Animal studies suggest HIV envelope proteins such as GP120 are potent promotors of pain hypersensitivity. Therefore, the aim of the present study was to compare objective measures of central sensitization in PLWH with and without chronic pain. Methods: Participants were recruited from an urban HIV clinic in the Southeast. Chronic pain was defined as pain of at least moderate severity for ≼ 3 months. Study participants completed a battery of experimental pain testing procedures that assessed temporal summation of pain in response to heat and mechanical stimuli, a widely-used method that invokes neural mechanisms related to central sensitization. Analytical methods included repeated-measures models, adjusted for age, sex, race, and CD4/viral load. Results: Forty-six PLWH with chronic pain and 46 PLWH without chronic pain were enrolled. The sample was comprised mostly of African Americans (85%) and men (61%), with a mean age of 47.6 years. Mean CD4+ count was 690.5 and 13% had detectable viral loads (>200 copies/mL). Of PLWH with chronic pain, primary self-reported pain locations included: 44% back, 30% hips/knees, 9% neck, 9% widespread (3 or more sites), 4% shoulders/arms/hands, and 4% feet. PLWH with chronic pain demonstrated significantly greater magnitudes of temporal summation of heat pain at 460C (F4,340 = 7.72, p = .007) and 480C (F4,340 = 4.67, p = .012), as well as greater temporal summation of mechanical pain at the hand (F1,85 = 12.26, p = .001) and trapezius (F1,85 = 8.53, p = .004) compared to PLWH without chronic pain; see Figure for example. Conclusions: Temporal summation of heat and mechanical pain was greater in PLWH with chronic pain than PLWH without chronic pain. This suggests that central sensitization may be an important contributor to chronic pain in PLWH. This is consistent with previous research showing central sensitization to be a major driver of pain in other conditions such as non-specific low back pain and fibromyalgia. Future studies are needed to understand whether the experimental finding of central sensitization predicts development and maintenance of chronic pain in PLWH.
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ABSTRACTS |
New Frontiers of Pain Research
MODIFIABLE FACTORS THAT IMPACT LONG-TERM QUALITY OF LIFE AND DEVELOPMENT OF CHRONIC PAIN AFTER PULMONARY RESECTION (AN INTERIM ANALYSIS) Alexia Powers, BS, Roland Short, Ayesha Bryant
Purpose: Quality of life (QOL) may be compromised by the development of chronic post-operative pain. The objective of this study was to determine if modifiable patient factors are associated with long-term QOL and development of chronic pain after lung surgery. Methods: QOL was assessed using the SF-12 on a consecutive series of patients who underwent surgical resection for a benign or early stage pulmonary tumor. The physical (PCS) and mental (MCS) QOL scores were evaluated and compared to a national average score of 50. Pain was assessed using the Visual Analog Scale (VAS), Faces Pain Scale, and modified McGill Pain Questionnaire. Patients who received neo-adjuvant or adjuvant chemotherapy and/or radiation, had lymphovascular invasion and/or metastatic disease, and who underwent surgery for an infection were excluded. Results: Between 1/2010 and 12/2015, 803 patients underwent pulmonary resection; 580 met the inclusion criteria. This interim analysis provides results from 205 responders to date. Median follow-up was 2.9 years (0.5-6.7 years). The overall median PCS was 36.8, MCS was 54.6. Pre-operative opioid use and surgical approach were correlated with chronic pain score and long-term QOL: higher pain score was associated with pre-operative opioid use (p=0.04); patients who underwent minimally invasive surgery reported a significantly higher PCS compared to those who had a thoracotomy (38.2 vs. 31.1, respectively, p=0.004) and a lower pain score (p=0.04). Conclusions: This interim analysis shows that the median long-term physical QOL score was significantly lower in patients who underwent lung surgery compared to the average population; conversely, the mental QOL score was higher. Patients who did not use opioids pre-operatively and underwent robotic surgery reported a better physical QOL and lower pain scores (median 3 years post-operatively). These findings indicate that cessation of opioid use pre-operatively and/or a minimally invasive surgical approach may reduce the incidence of chronic pain and improve long-term QOL.
CURRENT FATIGUE SYMPTOMS IMPACT FUTURE ACTIVITY LEVELS IN CHRONIC FATIGUE PATIENTS Cooper Bailey, Skylar McMahan, Meredith Schertzinger, Kate Wesson-Sides, Jarred Younger, PhD.
Chronic Fatigue Syndrome (CFS) plagues over one million people, primarily women, in the United States. CFS manifests itself in many different ways; however, the most common symptom is severe fatigue. Pain, headache, and concentration and memory issues also commonly accompany a CFS diagnosis. Previous research has shown that having a higher body mass index (BMI) has a weak positive association with increased levels of CFS symptoms. It is commonly assumed that the individuals’ increased weight is a contributing factor to the increase of severity of symptoms. However, it is possible that the debilitating fatigue symptoms of CFS can lead to the increased BMI by way of facilitating a decrease in the levels of activity the person has throughout the day. As part of this study, participants with a diagnosis of CFS completed a questionnaire at night every day for the forty day duration of the study period. The daily measure assessed daily fatigue levels and various levels of physical activity and exertion before the participant went to sleep. Each participant also underwent a body composition exam using a Tanita Body Composition Analyzer. It was found that there was a significant negative association between the level of fatigue on one day and the level of activity on the following day by using a time-lapse model assessment. In particular, if the participant reported a high fatigue rating, they then reported a lower activity rating the following day. We concluded that higher levels of fatigue are associated with lower levels of activity, which could be a factor in increased BMI.
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ABSTRACTS |
New Frontiers of Pain Research
INTRAMUSCULAR VERSUS INTRAVESICAL RETROGRADE LABELING TECHNIQUES IDENTIFY ANATOMICALLY AND ELECTROPHYSIOLOGICALLY DISTINCT GROUPS OF MOUSE BLADDER LUMBOSACRAL PRIMARY AFFERENT NEURONS Hirosato Kanda, Buffie J. Clodfelder-Miller, Jianguo G. Gu, Timothy J. Ness, Jennifer J. DeBerry
Four functionally distinct classes of pelvic nerve mechanosensitive bladder afferents have been characterized and described as urothelial, muscular/mucosal, muscular, and serosal, but the actual anatomical location of their respective terminal endings is unknown. We utilized two strategies to retrogradely label lumbosacral (LS) bladder primary afferent neurons: intramuscular (IMus) consisted of microinjection of tracer into the bladder parenchyma (the current gold standard), and intravesical (IVes) consisted of transurethral infusion of tracer into the bladder lumen. IMus and IVes techniques labeled two distinct populations of bladder neurons that could be differentiated on the basis of labeling in the dorsal root ganglia (DRG), dye distribution within the bladder, and electrophysiological properties reflecting neuronal excitability. IMus- and IVes-labeled neurons accounted for 91.5% (378.3 ± 32.3) and 8% (33.0 ± 26.0) of all labeled neurons, respectively (p<0.01), with only 2.0 ± 1.2 neurons labeled by both techniques (total of 1240 labeled cells from 3 mice). IMus labeling resulted in distribution of tracer throughout the bladder wall but not in the urothelium; in contrast, only the urothelium and in some cases the adjacent submucosa was labeled by the IVes method. Whole mount patch-clamp recordings of labeled neurons in LS DRG revealed significant differences between IMus- and IVes-labeled neurons, with IVes neurons exhibiting lower rheobase and membrane capacitance, higher input resistance, and lower total K+ current density, suggesting increased excitability of IVes afferents. This study is the first to demonstrate that IVes labeling is a minimally invasive approach for retrograde labeling of bladder afferent neurons, and to selectively identify urothelial versus muscular bladder afferent soma in the DRG. An important consideration is whether the current findings change the interpretation of published studies that only used IMus labeling techniques.
ELECTROPHYSIOLOGICAL PROPERTIES OF NODES OF RANVIER REVEALED BY PATCH-CLAMP RECORDINGS FROM INTACT AFFERENT NERVE FIBERS OF MAMMALS Hirosato Kanda, Jianguo G.Gu
Dept. of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingaham
Electrophysiological properties of the nodes of Ranvier are important for saltatory conduction along myelinated nerve fibers and have pathological implications. Much of what we know about the electrophysiological properties of the nodes of Ranvier came from previous studies performed on large axons of the invertebrates, and due to technical challenge patch-clamp recordings have not been applied to the nodes of Ranvier in an intact nerve fiber. In the present study, we developed a whole-cell patch-clamp recording method to study electrophysiological properties of the nodes of Ranvier in intact rat trigeminal afferent nerve fibers. We observed two major currents at the nodes of Ranvier in responses to voltage steps, a large voltageactivated fast inward current and a large leak current. The fast inward current was mediated by voltagegated Na+ channels since it was completely blocked by TTX. Action potentials were not significantly altered when 135 mM Cs+ was included in the recording internal solution. In addition to the two major currents, we also determined the function of KV7.2 at the node of Ranvier. Linopirdine, a KCNQ channel blocker, reduced resting membrane potentials, action potential rhoebase, and action potential propagation at high frequency. Taken together, our results provide new information about electrophysiological properties of the nodes of Ranvier in mammalian primary afferent fibers.
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ABSTRACTS |
New Frontiers of Pain Research
INFLAMMATION CONVERTS MYELINATED BLADDER AFFERENTS FROM NON-NOCICEPTIVE TO NOCICEPTIVE Timothy J. Fernandez, Cary DeWitte, Jennifer J. DeBerry
Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham
The urinary bladder is innervated by a heterogenous population of sensory neurons with lightly myelinated (Aδ) or unmyelinated (C) afferent fibers. It is generally thought that Aδ fibers mediate micturition and C fibers mediate pain under normal conditions. However, individual contributions of anatomically or neurochemically different neuron types to bladder sensation cannot easily be assessed using only mechanical stimulation (the most physiologically relevant stimulus). Transgenic mice expressing channelrhodopsin-2 (ChR2), a light-gated ion channel, allow for depolarization of the peripheral terminals of neuron subtypes by light, independently of natural transduction mechanisms. We have previously shown that visceral nociceptive behavior is evoked and modulated by photostimulation of unmyelinated bladder afferents. The aim of this study was to characterize nociceptive responses to activation of myelinated bladder afferents. A ChR2-EYFP fusion gene was expressed in myelinated afferents using Crelox recombination under the mouse neurofilament-H (NFH) gene (Nefh) promoter. Visualization of ChR2EYFP under this promoter in NFH-ChR2 mice revealed its expression in the bladder, dorsal root ganglia, and spinal cord. Visceral nociceptive behavior, quantified as abdominal electromyograph (EMG) activity, was assessed in lightly anesthetized mice in response to photostimulation of the peripheral terminals of bladder primary afferents and to graded urinary bladder distension (UBD; 10-60 mmHg). In naive NFHChR2 mice, photostimulation of only NFH-ChR2+ bladder afferents failed to evoke EMG responses, which occurred in a graded fashion as a function of pressure during UBD. Following bladder inflammation, responses to photostimulation alone and to UBD alone were significantly increased relative to naive mice, but photostimulation did not significantly augment UBD-evoked responses. These data indicate that inflammation alters the intrinsic electrical properties of myelinated bladder afferents in a manner that contributes to pain. Elucidating the contributions of individual neuronal subtypes to pain versus organ dysfunction may increase therapeutic efficacy for the treatment of pathological changes in bladder sensation.
DIVERGENT ROLES OF THE LEFT AND RIGHT CENTRAL AMYGDALA IN VISCERAL PAIN MODULATION Katelyn E. Sadler and Benedict J. Kolber
Supraspinal control of visceral pain is poorly understood. Following established neuroanatomy, it is hypothesized that the left and right hemispheres are equally involved in processing sensory information from midline organs like the bladder. Recent reports however, suggest the left and right central amygdala (CeA) differentially modulate visceral pain. In these studies, we investigated contributions of the left and right CeA to bladder nociception using optogenetic and pharmacologic techniques. Optogenetic activation of the right CeA, but not the left, increased pain-like responses to noxious bladder distension. Lateralization was also observed following administration of pituitary adenylate cyclase-activating polypeptide (PACAP), a neurotransmitter released by parabrachial nucleus terminals in the CeA. When applied to the right CeA and not the left, PACAP increased pain-like responses to bladder distension. Collectively these data suggest a pro-nociceptive function of the right CeA, but failed to provide any functional significance for the left CeA in the context of visceral nociception. To address this issue, inhibitory optogenetics were employed. Interestingly, NpHR-mediated inhibition of the left CeA increased bladder nociception, suggesting an ongoing anti-nociceptive role for this nucleus. The divergent anti- and pro-nociceptive roles of the left and right CeA respectively were further confirmed by optogenetically activating each nucleus while measuring abdominal sensitivity in naïve mice and referred visceral pain in bladder sensitized awake-behaving animals. Overall, these data provide striking evidence for brain lateralization in the absence of peripheral anatomical asymmetries.
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ABSTRACTS |
New Frontiers of Pain Research
IMMUNE SYSTEM FUNCTION AND PAIN OUTCOMES IN WOMEN WITH FIBROMYALGIA
Merriwether EN, Rakel BA, Dailey DL, Zimmerman MB, Vance CGT, Darghosian L, Abdelhamid R, Frey-Law L, Allen L A, Crofford LJ, Sluka KA Purpose/Hypothesis: Fibromyalgia (FM) is a chronic pain condition characterized by elevated levels of circulating pro-inflammatory cytokines. Monocyte subsets are associated with different cytokine release profiles. Classical (CD14++/CD16-) and intermediate (CD14++/CD16+) monocytes are associated with pro-inflammatory cytokine release profile, while non-classical monocytes (CD14+/CD16++) have an antiinflammatory profile. We hypothesized that monocyte phenotype would be associated with select pain outcomes in women with FM. Number of subjects: 33 women with FM Materials/Methods: This study is an analysis of baseline data as part of a clinical trial (Mean±SD, Age=50.9±11.2 years; BMI=35.0±8.3 kg/m2). Pain measures included pain intensity using the Numeric Rating Scale (NRS), Brief Pain Inventory (BPI), conditioned pain modulation test (CPM), and pain psychological factors using the Tampa Scale of Kinesiophobia (TSK) and the pain catastrophizing scale (PCS). Monocyte subset classification was assessed using flow cytometry. Data from 21 women were analyzed for cytokine release measurement. Cytokine concentrations from supernatants of cultured monocytes incubated with lipopolysaccharide (LPS, 50 ng/ml, 24h) and phosphate-buffered saline (PBS) were analyzed using multiplex assays. Paired t-tests assessed cytokine release differences, and Pearson’s correlation coefficients evaluated relationships between monocyte subset classification, cytokine release profiles, and pain measures. Results: LPS significantly increased release of select cytokines compared to those stimulated with PBS. BPI-Severity was negatively correlated with LPS-evoked release of IL-1β (r=-0.66, p<0.01, Pearson’s) and IL-4 (r=-0.51, p<0.01), and with spontaneous release (PBS) of IL-4 (r=-0.77, p<0.01). CPM at the lumbar (r=-0.61, p=.02) and leg (r=-0.80, p<.01) sites were negatively correlated with spontaneous release of IL-4, and were positively correlated with the intermediate monocyte phenotype (r=.0.61, p<0.01). PCS negatively correlated with the non-classical monocyte phenotype (r=-0.41, p<.01). Conclusions: These data suggest that monocyte phenotype may influence pain outcomes in participants with FM. Understanding these mechanisms could inform the role of interventions like physical activity for treatment of chronic pain. Funded by NIH UM1 AR063381 and AR063381-S1.
BACLOFEN AND OPIOID SYNERGISM IN MICE Remy Y. Meir, Stacie K. Totsch, Aaron R. Landis, Tammie L. Quinn & Robert E. Sorge The overlapping expression of GABA and opioid receptors in the central nervous system suggests that the two systems are likely interrelated and can modify one another. The GABA B receptor agonist baclofen has been used as a treatment for spasticity and addiction, but there is evidence supporting its potential as a weak analgesic. We have been interested in the interaction between baclofen and opioid analgesics with respect to analgesic efficacy and abuse potential. Analgesic interactions were assessed in the hot plate test, whereas rewarding interactions were assessed via the place preference procedure with outbred CD1 mice. To date, we have tested the interactions between baclofen and the opioids morphine, oxycodone, buprenorphine and fentanyl using isobolographic analyses. All opioids tested with baclofen show synergism in analgesia and no significant interactions in place conditioning. This effect is also consistent in another common strain of mice (C57BL/6J) and in rats. The combination of baclofen and morphine, given repeatedly, showed less tolerance and constipation than an equipotent dose of morphine alone. Finally, acute administration of baclofen reduced the self- administration of morphine, suggesting a rewardreducing effect. Together these data support the use of baclofen coupled with opioids to enhance the analgesia, reduce the abuse liability and associated side effects of opioid drugs.
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ABSTRACTS |
New Frontiers of Pain Research
OPERANT TESTS ASSESSING RAT OROFACIAL MECHANICAL PAIN INDUCED BY SYSTEMIC ADMINISTRATION OF OXALIPLATIN AND LOCAL INJECTION OF COMPLETE FREUNDâ&#x20AC;&#x2122;S AADJUVANT INTO TEMPOROMANDIBULAR JOINTS Viacheslav Viatchenko-Karpinski*, Ferhat Erol, Jennifer Ling, Jianguo G. Gu
Department of Anesthesiology and Perioperative Medicine, School of Medicine, University of Alabama at Birmingham
Chronic orofacial pain conditions are important clinical problems that are poorly treated. Two main causes of chronic orofacial pain states are cranial nerve neuropathy and orofacial tissue inflammation. Common symptoms associated with these pathological conditions are mechanical allodynia and hyperalgesia. In the present study, the chemotherapy drug oxaliplatin, which is known to be able to induce peripheral neuropathy, was systemically administered to rats to induce neuropathic pain. Complete Freundâ&#x20AC;&#x2122;s Adjuvant (CFA) was locally injected into temporomandibular joints (TMJ) to induce inflammatory pain of TMJ. We assessed orofacial mechanical pain in these two animal models using the orofacial operant test. In both pathological pain models, the operant test showed significant changes in operant behaviors in the presence of mechanical stimulation, which indicated orofacial mechanical allodynia/hyperalgesia in these animals. We determined whether the hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels may be involved in the orofacial mechanical allodynia/hyperalgesia by testing ZD 7288, a blocker of HCN channels, on orofacial operant behaviors.
EVALUATION OF THE PREVALENCE OF GULF WAR ILLNESS, MYALGIC ENCEPHALOMYELITIS/CHRONIC FATIGUE SYNDROME, AND FIBROMYALGIA IN GULF WAR VETERANS Emily K. Donovan, Rebecca L. Massey, and Jarred W. Younger
Background: Twenty-six years after the 1990-1991 Persian Gulf War, we still have a poor understanding of the fatigue, pain, and other symptoms that affect approximately 250,000 veterans. Just as in Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis (CFS/ME) and Fibromyalgia, the pathophysiological mechanism of Gulf War Illness (GWI) has not been identified, nor has an objective biological test been developed. Objective: To evaluate co-morbidity among three chronic illnesses with unclear etiologies. Methods: 25 male Gulf War veterans in the pre-screening period of a clinical trial have been evaluated for GWI, CFS/ME, and Fibromyalgia using the Kansas inclusion criteria (Steele, 2000), the CDC case definition (1994), and the ACR Criteria (2010), respectively. Results: Of the veterans evaluated, 68% (n=17) met inclusion criteria for GWI. Of those 17, 41.2% (n=7) also met criteria for both CFS/ME and Fibromyalgia, 23.5% (n=4) met criteria for GWI and Fibromyalgia only, 23.5% (n=4) met criteria for GWI and CFS/ME only, and 11.8% (n=2) met GWI criteria only. Of the veterans who did not meet inclusion for GWI (n=8), 25% (n=2) met criteria for both CFS/ME and Fibromyalgia, and 75% (n=6) did not meet any of the case definitions. Conclusion: The findings show considerable overlap in symptomatology among GWI, ME/CFS, and Fibromyalgia. This overlap may indicate a common underlying pathophysiological mechanism. Scientific results from one of these diseases might therefore help advance our understanding of the others. The clinical trial is ongoing, and data accrual for this project continues.
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New Frontiers of Pain Research
META-ANALYSIS OF COGNITIVE PERFORMANCE IN FIBROMYALGIA Tyler Reed Bell, Melissa Buelow, Zina Trost, Olivio Clay, Michael Crowe
Fibromyalgia is a disease that encompasses difficulties with pain, physical function, and emotion, but is also characterized by complaints of poor cognition. Over the last two decades, a vast amount of literature has tested for cognitive differences between individuals with and without fibromyalgia. The purpose of the current study was to conduct a quantitative synthesis on these differences across multiple cognitive domains. After a systematic search of eligible studies, random-effect meta-analyses were conducted on effect sizes (Hedges’ g) derived from 37 cross-sectional studies covering domains of processing speed, memory and executive function. Participants included persons with fibromyalgia (total n = 964) and participants from age-matched control groups without fibromyalgia (total n = 1,025). Results showed the large deficit on measures of inhibitory control (g = .66), moderate deficits on measures of short-term and long-term memory, working memory, and premorbid intelligence (gs range from .44 to .51) and small deficits were found on set-shifting (g = .30) and accessing ability (g = .38). These findings suggest that screening for cognitive dysfunction in fibromyalgia may be needed in addition to other symptoms.
FEASIBILITY OF TELEHEALTH EDUCATIONAL PROGRAM ON SELFMANAGEMENT OF PAIN AND FATIGUE IN ADULT CANCER PATIENTS
Karina I. Halilova, M.D., M.P.H. ¹, Courtney P. Williams, M.P.H. 2, Allyson L. Varley ³, Richard A. Taylor, D.N.P. 1,4, Edward E. Partridge, M.D. 1, Elizabeth E. Kvale, M.D.1,5, Gabrielle B. Rocque, M.D. 1,2 Author Institutional Affiliation: ¹Comprehensive Cancer Center, ²Division of Hematology and Oncology, ³Division of Preventive Medicine, 4School of Nursing, University of Alabama at Birmingham; 5Birmingham VA Medical Center.
Background: Pain and fatigue are common symptoms among cancer patients and often lead to substantial distress, disability, and decreased quality of life. Innovative self-management programs for pain and fatigue are needed. Methods: This is a prospective, non-randomized, pre-post evaluation study assessing feasibility of telehealth, a telephone-based pain and fatigue self-management educational program, delivered by Pack Health among adult cancer patients. Feasibility was defined as 50% of eligible patients choosing to participate and completing the intervention. The secondary objectives were to assess recruitment and retention of patients with baseline pain and fatigue based on 2 screening strategies: (1) navigator-collected, patient-reported pain or fatigue, or (2) physician-identified pain or fatigue. Patient demographics and patient-reported outcomes (PROs) including patient activation, distress, symptoms, and quality of life were collected at baseline and study completion. Differences in baseline characteristics and PROs were compared for each screening strategy and for patients who did vs. did not complete the program. Results: The program did not meet feasibility requirements due to 34% (40/119) of all eligible patients choosing to participate in education: 24% (24/102) navigated and 94% (16/17) physician-referred patients. However, 50% of all patients who started the program graduated. Differences in baseline characteristics were noted by recruitment strategy. At baseline, 27.3% of navigated patients were at the highest activation level compared to 7.1% in the physician- referred, non-navigated patients (p=0.005). Non-navigated patients were more likely to report informational (31% vs 0%, p=0.007) and psychosocial stressors (81% vs. 4%, p<0.001). Program graduates had higher baseline activation than those who did not graduate (15% vs. 9%; p = 0.003). Conclusion: This program may be better accepted among self-motivated cancer patients with high psychosocial and information needs. Additional studies are needed to assess the efficacy of telehealth programs and to identify strategies to target self-management interventions to patients likely to participate.
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New Frontiers of Pain Research
DEPRESSION AMONG INPATIENTS WITH LOW BACK PAIN: PATIENT CHARACTERISTICS AND OUTCOMES Sahil Gupta MD (1), Zina Trost, PhD (2)
(1)Department of Neurology, UAB; (2) Department of Psychology, UAB
Introduction: Low back pain (LBP) is one of the most common and expensive health conditions in the United States and depression is a frequent comorbidity among individuals with LBP [1]. Drawing from a large database of patients hospitalized with LBP, the current study provides a preliminary comparison of patients with and without depression in terms of key demographic, treatment, and cost variables. Methods: Analysis of National Inpatient Sample data (2003-2013) showed a total of 159,329 patients discharged with primary diagnosis of LBP, ICD-9 Code 724.2. Patients with depression were identified using Agency of Healthcare Research and Quality (AHRQ) criteria. We compared age, length of stay (LOS) and total hospital charges between patients with and without depression, as well as association between depression and patient race, sex, and discharge/disposition status. Results: Analyses revealed that 15.3% of the sample met criteria for depression. Depression was associated with younger age (mean age: 58.51 vs. 60.93 years), female gender (72.3% vs. 60.3%), longer LOS (3.71 vs 3.36 days), higher hospital charges ($20,866 vs $19,439), Caucasian race, and disposition other than home self-care (see Table 1; all pâ&#x20AC;&#x2122;s<0.001). Conclusion: Results support that depression is a significant comorbidity among patients with LBP. Current findings point to gender and race disparities in terms of depression and LBP, and indicated that depression is associated with increased length of stay, higher cost to patient, and disposition other than home care. Further prospective studies are required to evaluate the impact of depression on inpatients with low back pain. Sagheer MA, Khan MF, Sharif S. Association between chronic low back pain, anxiety anddepression in patients at a tertiary care centre. JPMA. The Journal of the Pakistan Medical Association 63(6), 688-690 (2013).
MECHANOTRANSDUCTION OF MOUSE MERKEL CELLS IN WHISKER HAIR FOLLICLES AND EFFECT OF PACLITAXEL ON WHISKER AFFERENT SA1 RESPONSE Weipang Chang, Hirosato Kanda, Jianguo G. Gu
Somatosensory dysfunction is a common side effect of many chemotherapy drugs. Paclitaxel induced neuropathy, commonly includes sensory disorders including mechanical allodynia, tingling, numbness and loss of vibration sensation. The paclitaxel-induced sensory disorders are thought to be due to afferent demyelination induced by paclitaxel. It is currently unclear if non-neuronal cells may be involved in paclitaxel-induced sensory dysfunctions. In the epidermis of mammals, Merkel cells are located in mechanically sensitive spots and they are innervated by large diameter afferent fibers. We have recently shown that rat Merkel cells play a critical role in driving electrophysiological tactile responses manifested as slowly adapting type 1 (SA1) impulses. In the present study, we characterized mechanical sensitivity and membrane excitability of mouse Merkel cells. We further investigated effects of paclitaxel on whisker afferent SA1 responses. We found that short-term treatment of whisker hair follicle with paclitaxel significantly enhanced whisker SA1 responses. Our findings raise a possibility that paclitaxel may affect mechanical transduction and/or membrane excitability of Merkel cells, which subsequently affect electrophysiological tactile responses. Keywords: Chemotherapy; Mechanotransduction, Touch, Pain; Paclitaxel; Merkel cell.
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New Frontiers of Pain Research
THE ROLE OF PAIN-RELATED FEAR AND PAIN CATASTROPHIZING DURING ACUTE SPINAL CORD INJURY Sahil Gupta MD (1), Kimberly Monden PhD (2), Zina Trost, PhD (3)
(1) Department of Neurology, UAB; (2) Department of Psychology, Baylor University, (3) Department of Psychology, UAB
Introduction: Pain catastrophizing and pain-related fear (fear of pain and re/injury due to movement, or kinesiophobia) are associated with negative psychosocial and functional outcomes in musculoskeletal conditions. While many individuals with spinal cord injury (SCI) report significant pain experience, research on these pain-related constructs remains limited. Methods: Forty-six individuals (31 males; mean age = 48.41 years) with traumatic (n=36) and nontraumatic (n=10) SCI completed measures during inpatient rehabilitation; measures included the Pain Catastrophizing Scale [4], Tampa Scale of Kinesiophobia [1], Patient Health Questionnaire [2], Perceived Disability Index [5], and McGill Pain Questionnaire Present Pain Intensity Index [3]; 27 participants sustained cervical injury; 14 sustained thoracic injury; 2 sustained lumbar injury.Results: Bivariate analyses revealed significant positive associations between catastrophizing, pain-related fear, self-reported depression, and perceived disability. Catastrophizing was also positively associated with pain intensity (r =.32 - .65). In regression analyses, participants’ level of pain-related fear and catastrophizing significantly and uniquely accounted for variance in self-reported level of depression and perceived disability beyond demographic variables, injury-related factors (time since injury, level of injury), and current pain intensity. Controlling for demographic and injury-related variables, catastrophizing uniquely predicted participants’ self-reported current pain intensity. Conclusion: Pain and harm-related psychological variables uniquely predicted pain, perceived disability, and depression in an SCI sample. These results are consistent with evidence from non-SCI samples with a variety of pain conditions. Although current findings are preliminary, they suggest that interventions targeting catastrophizing and pain-related fear may be beneficial following SCI. References (1)Goubert L, Crombez G, Van Damme S, Vlaeyen JWS, Bijttebier P, Roelofs J. Confirmatory factor analysis of the Tampa Scale for Kinesiophobia: invariant two-factor model across low back pain patients and fibromyalgia patients. Clin J Pain 2004;20:103–110. (2)Kroenke K, Spitzer RL, Williams JB. The PHQ-9: validity of a brief depression severity measure. J Gen Intern Med 2001;16:606–13. (3)Melzack R. The McGill pain questionnaire: Major properties and scoring methods. Pain 1975;1:277–299. (4) Sullivan MJL, Bishop SR, Pivik J. The Pain Catastrophizing Scale: Development and validation. Psychological Assessment 1995;7:524–532. (5) Tait RC, Chibnall JT, Krause S. The Pain Disability Index: psychometric properties. Pain 1990;40:171–182.
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New Frontiers of Pain Research
OPTOGENETIC DISSECTION OF CENTRAL PAIN PATHWAYS Chiang MC, Ross, SE
Department of Neurobiology, University of Pittsburgh
Pathological pain is a widespread condition that affects one in four Americans. Although opioids have long been used for their analgesic effects in pain management, these drugs have severe adverse effects. An alternative approach with reduced adverse effects is delivering pain therapeutics to modulate neural circuitry within the brain responsible for contributing to the affective component of pain perception. Pain affect is believed to arise from the spino-parabrachial pathway via the lateral parabrachial nucleus (LPBN). However, the role of distinct projections from the LPBN in the pain response is poorly understood. Here we show that the LPBN projects to six major targets in the brain: the insular cortex, bed nucleus stria terminalis, central amygdala, hypothalamus, ventral thalamus, and periaquedutal gray. Using optogenetic approaches to target specific pathways, we find that the two amygdala targets (central amygdala and dorsolateral bed nucleus stria terminals) are highly aversive, as measured in a real time place preference assay. In contrast, projections from the LPBN to the ventromedial hypothalamus mediate changes in heart and respiratory rates. Finally, projections from the LBPN to the periaqueductal gray mediate the descending modulation of pain, as measured by response latency to heat stimuli. These findings suggest that different components of a pain response are encoded within distinct pathways arising from the LPBN. Interestingly, anatomical tracing of LPBN pathways indicate that distinct subpopulations of LPBN neurons differentially project to subsets of recipient brain regions, suggesting that certain LPBN subsets mediate different aspects of pain perception. Identifying these will provide insight in our understanding of how the brain integrates nociceptive stimuli to generate pain perception. Furthermore, this understanding can potentially contribute to the development of novel therapeutic agents that target a specific neural pathway mediating clinically relevant aspects of pain such as those neural pathways conveying the unpleasantness of pain.
INFLAMMATION CONVERTS MYELINATED BLADDER AFFERENTS FROM NON-NOCICEPTIVE TO NOCICEPTIVE Timothy J. Fernandez, Cary DeWitte, Jennifer J. DeBerry
Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham
The urinary bladder is innervated by a heterogenous population of sensory neurons with lightly myelinated (Aδ) or unmyelinated (C) afferent fibers. It is generally thought that Aδ fibers mediate micturition and C fibers mediate pain under normal conditions. However, individual contributions of anatomically or neurochemically different neuron types to bladder sensation cannot easily be assessed using only mechanical stimulation (the most physiologically relevant stimulus). Transgenic mice expressing channelrhodopsin-2 (ChR2), a light-gated ion channel, allow for depolarization of the peripheral terminals of neuron subtypes by light, independently of natural transduction mechanisms. We have previously shown that visceral nociceptive behavior is evoked and modulated by photostimulation of unmyelinated bladder afferents. The aim of this study was to characterize nociceptive responses to activation of myelinated bladder afferents. A ChR2-EYFP fusion gene was expressed in myelinated afferents using Crelox recombination under the mouse neurofilament-H (NFH) gene (Nefh) promoter. Visualization of ChR2EYFP under this promoter in NFH-ChR2 mice revealed its expression in the bladder, dorsal root ganglia, and spinal cord. Visceral nociceptive behavior, quantified as abdominal electromyograph (EMG) activity, was assessed in lightly anesthetized mice in response to photostimulation of the peripheral terminals of bladder primary afferents and to graded urinary bladder distension (UBD; 10-60 mmHg). In naive NFHChR2 mice, photostimulation of only NFH-ChR2+ bladder afferents failed to evoke EMG responses, which occurred in a graded fashion as a function of pressure during UBD. Following bladder inflammation, responses to photostimulation alone and to UBD alone were significantly increased relative to naive mice, but photostimulation did not significantly augment UBD-evoked responses. These data indicate that inflammation alters the intrinsic electrical properties of myelinated bladder afferents in a manner that contributes to pain. Elucidating the contributions of individual neuronal subtypes to pain versus organ dysfunction may increase therapeutic efficacy for the treatment of pathological changes in bladder sensation.
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New Frontiers of Pain Research
A LOW CARBOHYDRATE DIET REDUCES PAIN IN OLDER KNEE OSTEOARTHRITIS PATIENTS
Catherine D. Jones, Alan P. George, Shannon Lukens, Shannon L. Morrison, Taraneh Soleymani, Julie L. Locher, Barbara A Gower & Robert E. Sorge Background: Obesity and chronic pain affect the lives of Americans and can both be impacted by poor quality diet. The objective of this study was to test the hypothesis that the low carbohydrate diet group would experience significantly lower pain ratings on both self-report and functional pain testing when compared to the low-fat and control diet groups. Methods: 21 adult men and women (65-75 years of age) with current knee osteoarthritis pain were recruited to take part in a 12-week diet intervention. Participants were asked to complete the Brief Pain Inventory, Knee Osteoarthritis Outcome Survey, and the Quick Inventory of Depressive Symptomology and to perform functional tests (Timed walk and repeated chair stands) in addition to having knee discomfort assessed by temporal summation. Following baseline assessment, participants were randomly assigned to one of three diet conditions: control (no change), low carbohydrate (Low-Carb), or calorie-reduced (Low-fat) diet. Participants completed food diaries, attended diet classes, and met regularly with a physician and dietitian. Blood was sampled every 6 weeks during the 12-week intervention. Results: Low-Carb and Low-Fat showed a reduction in weight over the course of the intervention. However, only the Low-Carb group showed a significant decrease in pain interference as measured by the BPI (P<0.05). The Low-Carb group showed a decrease in pain intensity ratings following both repeated chair stands and temporal summation. Neither the Low-Fat nor Control group showed significant changes in pain ratings in the functional tests Conclusion: These pilot data support the use of a low carbohydrate diet to reduce pain interference and pain following activity in older adults with knee osteoarthritis. Future work will probe mechanisms and seek to determine whether these findings can be generalized to other chronic pain conditions.
RACIAL DIFFERENCES IN APPRAISAL OF PHYSICAL ACTIVITY AMONG COMMUNITY-DWELLING ADULTS WITH CHRONIC LOW BACK PAIN
Demario Overstreet, M.S., Terence Penn, B.S., Wesley Browning, B.S., Zina Trost, Ph.D., Burel Goodin, Ph.D. Research indicates that individuals who identify as non-Hispanic Black or Hispanic tend to report more frequent, severe, and disabling pain compared to other racial groups, particularly non-Hispanic Whites. In the context of chronic low back pain (CLBP), appraisal of physical activity is significantly associated with pain and disability outcomes. To date, no studies have examined the relationship between race/ethnicity and physical activity appraisal in the context of CLBP. Accordingly, the current study examined appraisal of common physical activities in a diverse sample of community-dwelling individuals with CLBP, focusing specifically on differences between individuals who identified as White (37.2%), Black (31.4%), and Hispanic (31.4%). Participants assessed both the pain and difficulty of common physical activities using the Photograph of Daily Activities Scale (PHODA; 0-100 rating); additionally, participants reported expected and experienced pain and difficulty in response to performance of 3 standardized laboratory tasks (task ratings were provided using a 100-mm Visual Analog Scale). Disability due to back pain was assessed using the Roland Morris Disability Questionnaire. Analyses revealed that Black participants reported significantly greater disability in comparison to White and Hispanic counterparts (p <.001). On average, Black and Hispanic participants rated PHODA stimuli as more painful and more difficult in comparison to Whites (all pâ&#x20AC;&#x2122;s <.05). Black and Hispanic participants likewise reported significantly higher expected and experienced pain and difficulty (all pâ&#x20AC;&#x2122;s <.01). In line with previous studies, disability was significantly associated with all appraisal ratings. Results underscore the importance of continuing to examine ethnic differences in the experience of CLBP and highlight appraisal of physical activities as potential mechanisms underlying observed disparities.
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2016 Birmingham, AL
WWW.UAB.EDU/PAINSYMPOSIUM Thank you for joining us at UAB for this unique conference experience. Please tell us about your experience by emailing your comments and suggestions to painsymposium@uabmc.edu
CONFERENCE FACULTY HOSTS Jennifer DeBerry, Ph.D. Jianguo Gu, M.B., Ph.D. Jarred Younger, Ph.D. We want to especially thank the following individuals: Hal Cobb (Psychology), Melanie Martin (UAB Events Planning), Janet McDaniel (Anesthesiology and Perioperative Medicine), Julie Cole Miller (Anesthesiology and Perioperative Medicine), Kate Wesson Sides (Psychology), Toby Siegel (UAB Events Planning) and Mary Frances Thetford (Psychology)
EVENT SPONSORS UAB School of Medicine, Department of Anesthesiology & Perioperative Medicine UAB College of Arts & Sciences, Department of Psychology UAB Comprehensive Neuroscience Center