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  4. Pathophysiology of central poststroke pain motor cortex disinhibition and its clinical and sensory correlates
 
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Pathophysiology of central poststroke pain motor cortex disinhibition and its clinical and sensory correlates

Journal Volume
50
Journal Issue
10
Pages
2851
Date Issued
2019-10-01
Author(s)
SUNG-CHUN TANG  
Lee, Lukas Jyuhn-Hsiarn
JIANN-SHING JENG  
SUNG-TSANG HSIEH  
Chiang, Ming-Chang
SHIN-JOE YEH  
HSUEH-WEN HSUEH  
CHI-CHAO CHAO  
DOI
10.1161/STROKEAHA.119.025692
URI
https://scholars.lib.ntu.edu.tw/handle/123456789/467854
Abstract
Background and Purpose—Central poststroke pain (CPSP) is a disabling condition in stroke patients, and evidence suggests that altered corticospinal and motor intracortical excitability occurs in neuropathic pain. The objective of this study was to investigate changes in motor cortex excitability and sensorimotor interaction and their correlates with clinical manifestations and alterations in somatosensory systems in CPSP patients. Methods—Fourteen patients with CPSP but no motor weakness were compared with age- and sex-matched healthy controls for motor cortex excitability and sensorimotor interaction assessed by transcranial magnetic stimulation to measure resting motor thresholds, short-interval intracortical inhibition, intracortical facilitation, and afferent inhibitions. The sensory pathway was evaluated by quantitative sensory testing, contact heat evoked potential, and somatosensory evoked potentials. Clinical pain and quality of life were assessed with validated tools. Results—The duration of CPSP was 3.3±3.0 years (ranging 0.5–10 years), and pain significantly impaired quality of life. Compared with the unaffected hemisphere, the stroke hemisphere had higher thermal thresholds, lower contact heat evoked potential amplitudes, and prolonged cortical somatosensory evoked potential latencies. There was no difference in resting motor thresholds between the stroke and unaffected hemisphere or between patients and controls. CPSP patients had a reduction in short-interval intracortical inhibition in the stroke hemisphere compared with that in the unaffected hemispheres of patients and controls. No changes were noted in afferent inhibitions between the stroke and unaffected hemispheres. The short-interval intracortical inhibition of the stroke hemisphere was negatively correlated with self-rated health on a visual analog scale and positively correlated with cortical somatosensory evoked potential latencies. Conclusions—CPSP patients with intact corticospinal tracts showed reduced motor intracortical inhibition in the stroke hemisphere, suggesting defective gamma-aminobutyric acid-ergic inhibition. This disinhibition was associated with impaired quality of life and was related to dorsal column–medial lemniscus pathway dysfunction. ? 2019 American Heart Association, Inc.
SDGs

[SDGs]SDG3

Other Subjects
clonazepam; duloxetine; imipramine; oxcarbazepine; pregabalin; adult; aged; Article; central poststroke pain; cerebrovascular accident; clinical article; controlled study; cortical excitability; facilitation; female; GABAergic system; hemisphere; human; latent period; male; medial lemniscus; motor cortex; motor evoked potential; pain; pathophysiology; priority journal; pyramidal tract; quality of life; quantitative analysis; sensorimotor cortex; sensory evaluation; somatosensory evoked potential; somatosensory system; stroke patient; transcranial magnetic stimulation; visual analog scale; cerebrovascular accident; complication; middle aged; motor cortex; nerve cell inhibition; neuralgia; pathophysiology; physiology; somatosensory cortex; Adult; Aged; Female; Humans; Male; Middle Aged; Motor Cortex; Neural Inhibition; Neuralgia; Pyramidal Tracts; Somatosensory Cortex; Stroke
Type
journal article

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