title: Tremor: pathophysiology.
abstract: The precise way that tremors emerge is not well known, but there is some good information and hypotheses. This review will focus on the classic ("rest") tremor of Parkinson disease and essential tremor. Both have their genesis in central oscillators, which appear to be malfunctioning networks. With classic Parkinson tremor, there appears to be dysfunction of the basal ganglia network and the cerebello-thalamo-cortical network. There is evidence that the basal ganglia network triggers the onset of tremor and the cerebellar network is responsible for the amplitude. Since it is a tremor of stability, the beta activity of the basal ganglia may be the trigger. With essential tremor, the cerebello-thalamo-cortical network itself is dysfunctional and perhaps the inferior olive-cerebellar network as well. This is a tremor of action, and the associated ataxia suggests that delays in motor control processing may set up the oscillation.
authors.affiliation: Human Motor Control Section, NINDS, NIH, Bethesda, MD, USA. Electronic address: hallettm@ninds.nih.gov.
authors.forename: Mark
authors.initials: M
authors.lastname: Hallett
mesh_terms: D001921:Brain / Q000503:physiopathology*; D006801:Humans; D009434:Neural Pathways / Q000502:physiology; D014202:Tremor / Q000473:pathology / Q000503:physiopathology*
keywords: Ataxia; Basal ganglia; Beta activity; Brain networks; Cerebellum; Essential tremor; Inferior olive; Oscillators; Parkinson's disease; Tremor