Associative Motor Cortex Plasticity is Reduced on the Non-Affected Side in Focal Hand Dystonia

Maladaptive plasticity has been implicated in the pathophysiology of focal dystonia. In support of this, we have recently shown that associative motor cortical plasticity induced by an external stimulation protocol is greatly enhanced and its somatotopic organization lost on the affected side in patients with writer's cramp (WC). However, it remains unknown whether these abnormalities are related to the dystonic phenotype or to an underlying pathogenetic disposition. We therefore studied the non-affected side in nine WC patients. In addition, the non-dominant hand of nine healthy control subjects was examined. Data were compared with previously obtained results on the contralateral (affected or dominant) side. Paired associative stimulation (PAS) consisted in repetitive electrical stimulation (0.1Hz, 180 pulses) of the left median nerve paired with transcranial magnetic stimulation (TMS, interstimulus interval 21.5 ms) over the hot-spot for the abductor pollicis brevis muscle (APB) on the right hemisphere. Changes in excitability of the motor cortex were monitored by recording motor evoked potentials (MEP) of the APB and abductor digiti minimi muscle (ADM) for up to 85 minutes after intervention. In healthy controls, PAS targeting the non-dominant hemisphere led to an increase of cortical excitability (APB +6.6±s.e.m. 5.6%, ADM +21.5±9.6%) comparable to that found previously on the dominant side (APB +12.3±s.e.m. 8.7%, ADM +4.6±2.9s.e.m.%). However, because MEP size increased similarly in APB and ADM muscles, the somatotopical specificity of the excitability change, as found on the dominant side, was lost. Surprisingly, PAS did not induce any increase in cortical excitability on the non-affected side in WC patients (APB -0.8±s.e.m. 9.1%, ADM +0.5±9.7s.e.m.%). These findings suggest that in healthy subjects the somatopical specificity of PAS-induced plasticity may be related to skilful hand-usage. Furthermore, development of focal dystonia in WC patients is unlikely to be causally related to loss of somatotopy alone. By contrast,