In patients with
drug-induced
parkinsonism and in healthy subjects the effect of stimulation of low-threshold skin fibres of sural nerve producing the polysynaptic flexion reflex of the short head of the biceps femoris muscle on the monosynaptic H reflex of calf muscles was studied before and after administration of
ethylbenzatropine. In healthy subjects stimulation of low-threshold skin nerve was followed by facilitation of H reflex in the time of 70 to 200 msec. from the conditioning stimulation to the test stimulation. After one single intramuscular dose of
ethylbenzatropine this late facilitating effect disappeared. In patients with
drug-induced
parkinsonism stimulation of afferent fibres of flexion reflex failed to cause late facilitation of H reflex and one dose of
ethylbenzatropine brought no changes. During systematic administration of the
drug an evident tendency for facilitation of H reflex was observed, similarly as in healthy subjects. The results obtained in healthy subjects and in patients with
drug-induced
parkinsonism are explained as evidence of inhibitory action of
noradrenaline in certain chains of spinal interneurons, since
noradrenaline release in the spinal cord is determined by the striatal equilibrium between the
cholinergic and dopaminergic systems. The corrective action of
ethylbenzatropine would depend on its central action on certain spinal chains of interneurons determining transmission of impulses from dermal afferent nerves to alpha motoneurons.