Pallidal dysfunction drives a cerebellothalamic circuit into Parkinson tremor

Abstract

Resting tremor may result from a pathological interaction between the basal ganglia and the cerebellothalamic circuit. The cerebellothalamic circuit, which controls tremor amplitude, appears to be driven into tremor generation when receiving transient signals from the dopamine-depleted basal ganglia. This may explain why basal ganglia dysfunction is required for developing resting tremor, although a cerebellothalamic circuit produces it. Our model also clarifies why neurosurgical interventions targeted at either the basal ganglia or the cerebellothalamic circuit can both suppress tremor.