Lisa A Kilpatrick1, Jason J Kutch1, Kirsten Tillisch1, Bruce D Naliboff1, Jennifer S Labus1, Zhiguo Jiang1, Melissa A Farmer1, A Vania Apkarian1, Sean Mackey1, Katherine T Martucci1, Daniel J Clauw1, Richard E Harris1, Georg Deutsch1, Timothy J Ness1, Claire C Yang1, Kenneth Maravilla1, Chris Mullins1, Emeran A Mayer2. 1. Gail and Gerald Oppenheimer Family Center for Neurobiology of Stress, David Geffen School of Medicine, University of California-Los Angeles (LAK, KT, BDN, JSL, ZJ, EAM), Los Angeles, California; Division of Biokinesiology and Physical Therapy, University of Southern California, Los Angeles (JJK), California; Division of Pain Medicine, Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University Medical Center (SM, KTM), Stanford, California; Human Performance and Engineering Laboratory, Kessler Foundation Research Center, West Orange and Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, New Jersey (ZJ); Department of Physiology, Feinberg School of Medicine, Northwestern University (MAF, AVA), Chicago, Illinois; Department of Anesthesiology, Chronic Pain and Fatigue Research Center, University of Michigan (DJC, REH), Ann Arbor, Michigan; Departments of Radiology and Anesthesiology, University of Alabama, Birmingham Medical Center (GD, TJN), Birmingham, Alabama; Department of Urology (CCY), University of Washington, Seattle, Washington; Department of Radiology (KTM), University of Washington, Seattle, Washington; National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health (CM), Bethesda, Maryland. 2. Gail and Gerald Oppenheimer Family Center for Neurobiology of Stress, David Geffen School of Medicine, University of California-Los Angeles (LAK, KT, BDN, JSL, ZJ, EAM), Los Angeles, California; Division of Biokinesiology and Physical Therapy, University of Southern California, Los Angeles (JJK), California; Division of Pain Medicine, Department of Anesthesiology, Perioperative and Pain Medicine, Stanford University Medical Center (SM, KTM), Stanford, California; Human Performance and Engineering Laboratory, Kessler Foundation Research Center, West Orange and Department of Biomedical Engineering, New Jersey Institute of Technology, Newark, New Jersey (ZJ); Department of Physiology, Feinberg School of Medicine, Northwestern University (MAF, AVA), Chicago, Illinois; Department of Anesthesiology, Chronic Pain and Fatigue Research Center, University of Michigan (DJC, REH), Ann Arbor, Michigan; Departments of Radiology and Anesthesiology, University of Alabama, Birmingham Medical Center (GD, TJN), Birmingham, Alabama; Department of Urology (CCY), University of Washington, Seattle, Washington; Department of Radiology (KTM), University of Washington, Seattle, Washington; National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health (CM), Bethesda, Maryland. Electronic address: emayer@ucla.edu.
Abstract
PURPOSE: The pathophysiology of interstitial cystitis/painful bladder syndrome remains incompletely understood but is thought to involve central disturbance in the processing of pain and viscerosensory signals. We identified differences in brain activity and connectivity between female patients with interstitial cystitis/painful bladder syndrome and healthy controls to advance clinical phenotyping and treatment efforts for interstitial cystitis/painful bladder syndrome. MATERIALS AND METHODS: We examined oscillation dynamics of intrinsic brain activity in a large sample of well phenotyped female patients with interstitial cystitis/painful bladder syndrome and female healthy controls. Data were collected during 10-minute resting functional magnetic resonance imaging as part of the Multidisciplinary Approach to the Study of Chronic Pelvic Pain Research Network project. The blood oxygen level dependent signal was transformed to the frequency domain. Relative power was calculated for multiple frequency bands. RESULTS: Results demonstrated altered frequency distributions in viscerosensory (post insula), somatosensory (postcentral gyrus) and motor regions (anterior paracentral lobule, and medial and ventral supplementary motor areas) in patients with interstitial cystitis/painful bladder syndrome. Also, the anterior paracentral lobule, and medial and ventral supplementary motor areas showed increased functional connectivity to the midbrain (red nucleus) and cerebellum. This increased functional connectivity was greatest in patients who reported pain during bladder filling. CONCLUSIONS: Findings suggest that women with interstitial cystitis/painful bladder syndrome have a sensorimotor component to the pathological condition involving an alteration in intrinsic oscillations and connectivity in a cortico-cerebellar network previously associated with bladder function.
PURPOSE: The pathophysiology of interstitial cystitis/painful bladder syndrome remains incompletely understood but is thought to involve central disturbance in the processing of pain and viscerosensory signals. We identified differences in brain activity and connectivity between female patients with interstitial cystitis/painful bladder syndrome and healthy controls to advance clinical phenotyping and treatment efforts for interstitial cystitis/painful bladder syndrome. MATERIALS AND METHODS: We examined oscillation dynamics of intrinsic brain activity in a large sample of well phenotyped female patients with interstitial cystitis/painful bladder syndrome and female healthy controls. Data were collected during 10-minute resting functional magnetic resonance imaging as part of the Multidisciplinary Approach to the Study of Chronic Pelvic Pain Research Network project. The blood oxygen level dependent signal was transformed to the frequency domain. Relative power was calculated for multiple frequency bands. RESULTS: Results demonstrated altered frequency distributions in viscerosensory (post insula), somatosensory (postcentral gyrus) and motor regions (anterior paracentral lobule, and medial and ventral supplementary motor areas) in patients with interstitial cystitis/painful bladder syndrome. Also, the anterior paracentral lobule, and medial and ventral supplementary motor areas showed increased functional connectivity to the midbrain (red nucleus) and cerebellum. This increased functional connectivity was greatest in patients who reported pain during bladder filling. CONCLUSIONS: Findings suggest that women with interstitial cystitis/painful bladder syndrome have a sensorimotor component to the pathological condition involving an alteration in intrinsic oscillations and connectivity in a cortico-cerebellar network previously associated with bladder function.
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