CATATONIA. – abulia (v.) characterized by inability to act, whether spontaneously or in response to a command, as though the subject’s will encountered insurmountable resistance in being translated into action or, for every impulse to act, a corresponding impulse to the contrary automatically arose, so that the action remained blocked at the outset or was impeded during its execution. When commanded, for example, to open his eyes, the catatonic does not carry out the order, while the motor apparatus appears inert or is seized by simultaneous contractions of the muscles responsible for the commanded movement (the levators of the eyelids) and of their antagonists (the orbicular muscles of the eyelids). In such conditions, the individual remains for a long time motionless in uncomfortable or ridiculous statuesque poses, in attitudes of prayer, ecstasy, threat, terror, etc. The apparent apathy of the catatonic conceals an intense tension which, when the volitional arrest subsides, may discharge itself in a sudden explosion of activity (“catatonic impulsivity”).
C. may occur together with alterations of the affective sphere (melancholia, mania) and is one of a series of pathological motor manifestations such as stupor, catalepsy (v.), negativism, stereotyped and repetitive attitudes, grimaces, mannerisms, hyperkinesias, etc. C. is very frequent and typical in dementia praecox or schizophrenic athymia (v. SCHIZO-FRENIA); it may also be observed in toxic infections, amentia (v.), epilepsy (v.), cerebral syphilis, dementia (v.), senile dementia, and affective psychoses.
As regards its mechanism of origin, a psychogenic theory and a neurogenic theory have been advanced. According to the former, the defect would lie in the representational phase of the voluntary act: the absence or simultaneity of opposing representations overflowing into antagonistic actions; the neurogenic theory rests on the function of the extrapyramidal system (v. EXTRAPIRAMIDALE, SISTEMA, SISTEMA) and on pathological manifestations similar to c. occurring in the clinical picture of the post-Parkinsonian syndrome secondary to epidemic encephalitis. A mixed origin is probable, connected with abnormal psychic factors unfolding within the sphere of an extrapyramidal system functionally or organically altered.
Certain pharmacological substances (bulbocapnine, mescaline, cannabin, harmine; Somnifon intravenously, acetylcholine and adrenaline in high doses) can produce a kind of experimental c. (first demonstrated by Baruk and Dejong in 1928), whose mechanism of action, however, is in reality different, since the injected substances produce the catatonic picture by acting on the muscular apparatus rather than on the nervous centres.