Transcallosal conduction in paroxysmal kinesigenic dyskinesia

Detecting whether a possible disequilibrium between the excitatory and inhibitory interhemispheric interactions in paroxysmal kinesigenic dyskinesia (PKD) exists.

This study assessed measures of motor threshold, motor evoked potential latency, the cortical silent period, the ipsilateral silent period and the transcallosal conduction time (TCT) in PKD patients. Data were compared between the clinically affected hemisphere (aH) and the fellow hemisphere (fH).

The transcallosal conduction time from the aH to the fH was 11.8 ms (range = 2.3-20.7) and 13.6 ms (range = 2.8-67.7) from the fH to the aH. The difference in TCT in the affected side was significant (p = .019).

The findings demonstrated that, although inhibitory interneurons act normally and symmetrically between the motor cortices and transcallosal inhibition was normal and symmetrical between both sides, the onset of transcallosal inhibition was asymmetrical. The affected hemisphere's inhibition toward the unaffected hemisphere is faster compared to the inhibition provided by the fellow hemisphere. These results are consistent with an inhibitory deficit in the level of interhemispheric interactions.

This study revealed a defect in inhibition of the motor axis could be responsible in the pathological mechanisms of kinesigenic dyskinesia.