[Mechanism of post-stroke reflex sympathetic dystrophy: study with needle electromyography].
OBJECTIVE
To explore the mechanism of post-stroke reflex sympathetic dystrophy (RSD) patients electromyographic abnormality and confirm its clinical value.


METHODS
Fifty patients with first-onset stroke, aged 33 - 78, including 30 with RSD and 20 without RSD, underwent needle electromyography (EMG) to test the nerve conduction velocity (NCV) and sensory nerve conduction velocity (SCV) of bilateral median nerves, and the number and position of spontaneous EMG activity of bilateral short abductor muscles of thumb and abductor muscles little finger.


RESULTS
The median nerve compound muscle action potential (CMAP) amplitude of the affected upper extremities of the RSD group was 8.6 mV +/- 2.9 mV, significantly lower than that of the non-RSD group (13.2 mV +/- 4.6 mV, P < 0.01). The incidence of spontaneous electrical potential of the RSD group was 100%; significantly higher than hat of the non-RSD group (65%, P < 0.001). The quantity of spontaneous EMG activity on the short abductor muscles of thumb and abductor muscles little finger was increased in the RSD group (P < 0.01). The motor nerve conduction velocity and electrophysiological presentation of sensory nerve of these 2 groups were all normal and without significant differences between them.


CONCLUSIONS
Partial axonal degeneration occurs on the distal motor never fibers of the affected upper extremity of the RSD patients, which may be related to subsequent peripheral nerve injury after central nerve system impairment.
Wang
Xiao-yan
XY
Department of Neurorehabilitation, China Rehabilitation Research Center, Beijing 100068, China.
Zhang
Tong
T
Li
Jing
J
D000328:Adult; D000368:Aged; D004576:Electromyography / Q000295:instrumentation / Q000379:methods; D019054:Evoked Potentials, Motor; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012019:Reflex Sympathetic Dystrophy / Q000209:etiology / Q000503:physiopathology*; D020521:Stroke / Q000150:complications / Q000503:physiopathology*