S84 Subthalamic and GPI stimulation and cortical plasticity

Abstract

Objectives Review the effects of subthalamic (STN) and internal globus pallidus (GPi) stimulation on cortical plasticity. Methods Several relevant studies are reviewed. Results Using paired associative stimulation, most studies found decreased plasticity in Parkinson’s disease (PD). Dopaminergic medications restored plasticity in patients without levodopa-induced dyskinesia but not in patients with dyskinesia. Early, drug naive PD patients had decreased plasticity on the more affected side but had exaggerated plasticity on the less affected side. This asymmetry in plastsicity decreased over 12 months, which may reflect reduced compensation. In dyskinetic PD patients treated with STN deep brain stimulation (DBS), cortical plasticity was deficient in the off medication state but was restored in the medication on state with the stimulator turned on. STN DBS increases motor cortical excitability at about 3 ms likely through antidromic activation of the hyperdirect pathway, and at 23 ms likely through the indirect pathway. Repeated pairing STN DBS and cortical magnetic stimulation at these specific intervals induced motor cortical plasticity in PD patients. Similarly, repeated pairing of GPi stimulation and cortical magnetic stimulation at specific intervals induced cortical plasticity in dystonia patients. Discussion Cortical plasticity appears to be decreased in PD patients and is partially restored in some patients on medications while increased plasticity may be a compensatory mechanism in early PD. Cortical plasticity is strongly influenced by the basal ganglia. Conclusion DBS can modulate and induce cortical plasticity in PD and dystonia. Significance Modulation of cortical plasticity may be involved in mediating the effects of DBS.