From a review of the anatomical relationships and single unit activity in the components of the basal ganglia related to limb movement, it is concluded that the major outflow from basal ganglia circuits is via the motor cortex (area 4). Recent results of recording from area 4 neurons revealed that they preferentially “encode” the higher derivatives of movement, i.e. acceleration and jerk. In the parkinsonian (PK) patient and in the monkeys treated with l-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP), EMG responses to imposed loads show a markedly increased gain of the “M2” component which depends upon the integrity of area 4 and which correlates with the severity of PK rigidity.The above observations are considered, along with those of others (demonstrating prolonged movement times, a decreased “repertoire” of voluntary movements fractionation of voluntary movements’, inability in tracking movements without visual input, and failure to improve performance in PK’s) in relation to a model of the interactions between sensory input and motor programs. Using this model, it is hypothesized that the above PK movement deficits, as well as rigidity, can be accounted for by abnormal processing of the mechanoreceptor sensory input utilized in the generation and execution of movements. The MPTP treated monkey is suggested as a model in which to directly test the hypothesis.
EMG responses to sudden displacement of the forelimb were studied in Cebus monkeys tranquilized with Atravet, a phenothiazine tranquilizer. The monkey's forearm was strapped firmly to a manipulandum handle. A torque motor attached at the pivot point of the handle, under servo control, provided reproducible limb displacements. In response to a sudden maintained displacement three periods of EMG activation in biceps muscle occurred with peak latencies of approximately 25, 45 and 85 msec. These correspond to the latencies of the M1, M2 and M3 responses in the alert animal. Similar responses were observed in 'naive' animals which had not previously been used in experimentation. All three responses increased in magnitude with increasing background activity and all appeared to be associated with suppression of EMG activity in the antagonist muscle. M1 and M2 responses were position dependent, M1 being greater in extension than in flexion and M2 the opposite. The position-dependence of the M2 response was produced by a depression of activity following the M1. This depression of activity lasted up to 30 msec following M1 and was directly dependent on the M1 magnitude.
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