Slowness of movement in Parkinson's disease

Loss of the ability to move is the most characteristic and fundamental motor deficit in Parkinson’s disease. Parkinsonian patients exhibit akinesia (inability to initiate movement), hypokinesia (reduced movement), and bradykinesia (slowness of the movement itself). (All these phenomena will be subsumed under the title akinesia.) Rigid muscles may contribute to akinesia, but they are not the cause. This is evident from the effects of both stereotactic surgery and treatment with levodopa. Stereotactic thalamotomy is an effective means of abolishing contralateral rigidity (and tremor), but does not relieve akinesia, which progresses to cause increasing disability. Levodopa therapy, on the other hand, dramatically relieves akinesia, even in those who have undergone previous stereotactic surgery. The akinesia of Parkinson’s disease represents a major negative symptom and, as such, probably gives the best clue as to what goes wrong with basal ganglia function in that condition (1,2). However, analysis of the pathophysiology of akinesia has proved difficult. One is dealing with higher-order motor function in all its complexity. Normal Movement Two approaches have been employed to investigate events in the brain before the initiation of movement in Parkinson’s disease; (a) the study of reaction times, and (b) the investigation of the Bereitschaftspotential.