Structural brain changes in chronic pain reflect probably neither damage nor atrophy

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Structural brain changes in chronic pain reflect probably neither damage nor atrophy. / Rodriguez-Raecke, Rea; Niemeier, Andreas; Ihle, Kristin; Ruether, Wolfgang; May, Arne.

in: PLOS ONE, Jahrgang 8, Nr. 2, 01.01.2013, S. e54475.

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@article{2241d4948b0b4b6c84907fdae9f2ba49,
title = "Structural brain changes in chronic pain reflect probably neither damage nor atrophy",
abstract = "Chronic pain appears to be associated with brain gray matter reduction in areas ascribable to the transmission of pain. The morphological processes underlying these structural changes, probably following functional reorganisation and central plasticity in the brain, remain unclear. The pain in hip osteoarthritis is one of the few chronic pain syndromes which are principally curable. We investigated 20 patients with chronic pain due to unilateral coxarthrosis (mean age 63.25±9.46 (SD) years, 10 female) before hip joint endoprosthetic surgery (pain state) and monitored brain structural changes up to 1 year after surgery: 6-8 weeks, 12-18 weeks and 10-14 month when completely pain free. Patients with chronic pain due to unilateral coxarthrosis had significantly less gray matter compared to controls in the anterior cingulate cortex (ACC), insular cortex and operculum, dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex. These regions function as multi-integrative structures during the experience and the anticipation of pain. When the patients were pain free after recovery from endoprosthetic surgery, a gray matter increase in nearly the same areas was found. We also found a progressive increase of brain gray matter in the premotor cortex and the supplementary motor area (SMA). We conclude that gray matter abnormalities in chronic pain are not the cause, but secondary to the disease and are at least in part due to changes in motor function and bodily integration.",
keywords = "Atrophy, Behavior, Brain, Brain Mapping, Chronic Pain, Cross-Sectional Studies, Female, Humans, Longitudinal Studies, Male, Middle Aged, Motor Cortex, Osteoarthritis, Hip, Prefrontal Cortex",
author = "Rea Rodriguez-Raecke and Andreas Niemeier and Kristin Ihle and Wolfgang Ruether and Arne May",
year = "2013",
month = jan,
day = "1",
doi = "10.1371/journal.pone.0054475",
language = "English",
volume = "8",
pages = "e54475",
journal = "PLOS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "2",

}

RIS

TY - JOUR

T1 - Structural brain changes in chronic pain reflect probably neither damage nor atrophy

AU - Rodriguez-Raecke, Rea

AU - Niemeier, Andreas

AU - Ihle, Kristin

AU - Ruether, Wolfgang

AU - May, Arne

PY - 2013/1/1

Y1 - 2013/1/1

N2 - Chronic pain appears to be associated with brain gray matter reduction in areas ascribable to the transmission of pain. The morphological processes underlying these structural changes, probably following functional reorganisation and central plasticity in the brain, remain unclear. The pain in hip osteoarthritis is one of the few chronic pain syndromes which are principally curable. We investigated 20 patients with chronic pain due to unilateral coxarthrosis (mean age 63.25±9.46 (SD) years, 10 female) before hip joint endoprosthetic surgery (pain state) and monitored brain structural changes up to 1 year after surgery: 6-8 weeks, 12-18 weeks and 10-14 month when completely pain free. Patients with chronic pain due to unilateral coxarthrosis had significantly less gray matter compared to controls in the anterior cingulate cortex (ACC), insular cortex and operculum, dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex. These regions function as multi-integrative structures during the experience and the anticipation of pain. When the patients were pain free after recovery from endoprosthetic surgery, a gray matter increase in nearly the same areas was found. We also found a progressive increase of brain gray matter in the premotor cortex and the supplementary motor area (SMA). We conclude that gray matter abnormalities in chronic pain are not the cause, but secondary to the disease and are at least in part due to changes in motor function and bodily integration.

AB - Chronic pain appears to be associated with brain gray matter reduction in areas ascribable to the transmission of pain. The morphological processes underlying these structural changes, probably following functional reorganisation and central plasticity in the brain, remain unclear. The pain in hip osteoarthritis is one of the few chronic pain syndromes which are principally curable. We investigated 20 patients with chronic pain due to unilateral coxarthrosis (mean age 63.25±9.46 (SD) years, 10 female) before hip joint endoprosthetic surgery (pain state) and monitored brain structural changes up to 1 year after surgery: 6-8 weeks, 12-18 weeks and 10-14 month when completely pain free. Patients with chronic pain due to unilateral coxarthrosis had significantly less gray matter compared to controls in the anterior cingulate cortex (ACC), insular cortex and operculum, dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex. These regions function as multi-integrative structures during the experience and the anticipation of pain. When the patients were pain free after recovery from endoprosthetic surgery, a gray matter increase in nearly the same areas was found. We also found a progressive increase of brain gray matter in the premotor cortex and the supplementary motor area (SMA). We conclude that gray matter abnormalities in chronic pain are not the cause, but secondary to the disease and are at least in part due to changes in motor function and bodily integration.

KW - Atrophy

KW - Behavior

KW - Brain

KW - Brain Mapping

KW - Chronic Pain

KW - Cross-Sectional Studies

KW - Female

KW - Humans

KW - Longitudinal Studies

KW - Male

KW - Middle Aged

KW - Motor Cortex

KW - Osteoarthritis, Hip

KW - Prefrontal Cortex

U2 - 10.1371/journal.pone.0054475

DO - 10.1371/journal.pone.0054475

M3 - SCORING: Journal article

C2 - 23405082

VL - 8

SP - e54475

JO - PLOS ONE

JF - PLOS ONE

SN - 1932-6203

IS - 2

ER -