Effect of a striatal spreading depression on the pharmacogenic catatonia

The results of earlier investigations pointed to a connection between a raised striatal excitability and the catatogenic effect of neuroleptic drugs. This paper describes experiments in which the caudate function in catatonic rats was blocked by means of local application of KCl solution.

It is demonstrated that a spreading depression (recorded electrographically) in the caudate nucleus inhibits the catatonic picture seen following neuroleptics (reserpine and SUM-3170, 2-chlor-11(4-methyl-1-piperazinyl)-dibenz[b,f][1,4]-oxazepine). During blockage of the caudate function (as seen in the EEG) the previously akinetic animals show an increased locomotor activity with snuffling and searching head movements; the rigor disappears and the animals show an intense desire to gnaw or lick. With return of the caudate activity (as seen in the EEG) the animals appear to freeze suddenly during movement; the typical catatonic position being resumed.

A cortical spreading depression is without effect on the catatonia arising after administration of neuroleptics. Only with the arrival of the inhibitory wave in the striatum, 4–5 min after induction of the spreading depression in the cortex, is the neuroleptic-induced catatonia inhibited. That is to say, blockage of the cortical afferent and efferent capsule fibres does not explain the effect of striatal spreading depression on the catatonia.