Objective:
The underlying neurophysiologic mechanism responsible for secondary paroxysmal kinesigenic
dyskinesia (PKD) is still unclear. Here, we study the pathogenesis of PKD in two patients with a
demyelinating lesion in the spinal cord.
Methods:
Electromyogram recordings from affected arms of
two patients with spinal cord lesions presenting PKD were compared with our laboratory standards.
The cutaneous silent period (CuSP), mixed nerve silent period (MnSP) and coincidence period (CiP), defined
as the common period between the CuSP and MnSP, were recorded.
Results:
A large decrease in the MnSP and disappearance
of the CiP were observed in our patients, which was secondary to simultaneous extinction of the third portion of the MnSP,
while the CuSP was normal. The MnSP and CiP were normal after recovery.
Conclusions:
Our results demonstrate that the third portion
of the MnSP and the CuSP do not correspond to the same physiologic process.
These findings suggest that PKD patients have abnormal spinal interneuron integration.
Cutaneous and Mixed Nerve Silent Period Recordings in Symptomatic Paroxysmal Kinesigenic Dyskinesia
