Pathophysiology of Central Poststroke Pain

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.

The Experience of Post-Stroke Pain and The Impact on Quality of Life: An Integrative Review

“…Retaining physical capacity and independence was identified as an important aspect of QOL [36]. This is in line with Dysvik et al [10], who identified that each of the subscales of the SF-36 were lower where pain was present; the greatest effect was on physical role, referring to limitations in daily activities. Lack of independence can cause depression which can lower motivation to be physically active [58].…”

“…The overall experience of pain appeared to have a consistent and negative impact on QOL. Several studies support this finding [8][9][10]. Pain was reported to have no impact on QOL [28] when the BPI was used, an outcome measure that has not been validated for use in a stroke population.…”

“…Review evidence has identified negative associations between pain and quality of life [8][9][10]. However, there are several weaknesses of the current research including; evidence provided alongside other chronic conditions [8], limited focus on PSP within a broader review topic [9,10] or a lack of focus on qualitative evidence [8][9][10].…”

Alteration of White Matter in Patients with Central Post-Stroke Pain

“…First, for overcoming the relatively small sample size, we undertook the analyses by comparing three groups: CPSP, stroke control, and normal control. In addition, we enrolled the larger numbers of sample size compared to previous studies [ 16 , 20 , 21 ]. Thus, we drew out the alterations of white matter for CPSP.…”

“…The present study was an observational investigation of CPSP, so the exact sample size was not calculated beforehand. However, the sample sizes of previous studies varied from 2 to 14 [ 16 , 20 , 21 ]; thus, it was determined that the sample size for this study would be more than 14 subjects. Moreover, to increase the accuracy of our results, we decided to include a stroke control group 1.5 times the size of the CPSP group and a normal control group twice the size of the CPSP group.…”