The corticomotoneurone connection is normal in Parkinson's disease

Abstract

Voluntary movements in Parkinson's disease are initiated and executed slowly. It is assumed that the motor cortex and its output pathway are intact and that bradykinesia is due to abnormal motor commands delivered to a normal corticospinal system. We have tested this assumption using electrical stimulation of the motor cortex through the scalp in three patients with severe Parkinson's disease, studied during fluctuations from relatively normal mobility when receiving drugs (ON) to severe bradykinesia when not receiving drugs (OFF). Thresholds and latencies for motor cortex stimulation to excite thumb flexor muscles and the resulting fast mechanical responses were the same in both ON and OFF conditions, even though the patients were unable to execute fast thumb flexion movements voluntarily when OFF. We conclude that the excitability and conduction velocity of the corticospinal motor pathways are normal in Parkinson's disease.