Karl Ludwig Kahlbaum's concept of catatonia.

Catatonia is a neuropsychiatric syndrome described by Karl Ludwig Kahlbaum in 1874. Based on Kahlbaum's own description and Carl Wernicke's hypothesis about the mechanism of catatonia, we describe two types of catatonic domain: the akinetic motality psychosis, which is characterized by rigid immobility, fixed gaze, lack of blink, and cogwheel rigidity, and catatonia sensu strictu, which is characterized by spasms, iterations and verbigerations. The loss of motility allows the 'hypobulic levels' described by Kretschmer in 1920, which consist of aggressive acts, furious shouting, hyperactivity and orality, to break through.

[A neurobiological model of mind].

An essential difference is established between the dorsal, and ventral regions of the cerebral cortex: While dorsal cortex--linked to archicortex or hippocampal allocortex--elaborates acts, and objects used in, or by, acts, ventral cortex--linked to paleocortex or olfactory allocortex, builds up preventive values favoring the inhibition of acts whenever the use of objects may become dangerous. Such a distinction between the dorsal and ventral regions of the cerebral cortex is founded mainly on disinhibition syndromes appearing in patients with ventral lesions--besides, the said distinction can explain some disinhibition demonstrations included in the schizophrenic clinical pictures.

[Ideational apraxia in confusional psychosis].

Traditionally, Pick's ideational apraxia has been considered a neurologist's realm since it is one of the permanent manifestations of brain lesions located in the left hemisphere posterior territory. Besides, however, the ideational apraxia is likely to appear--altogether with misidentifications and spatial disorientation--as a part of the transient manifestations of confusional psychosis. It is thus quite possible that a reversible alteration of the posterior brain mechanisms could be the basis for the confusional psychosis.

[The frontal lobe and psychoses].

Manic-depressive illness may be explained as an alteration of the normally existing equilibrium to be found between two antagonist brain mechanisms located in the prefrontal isocortex area. Each mechanism, located in the middle frontal area, deriving from the hippocampal allocortex, is responsible for tendencies to change. Its predominance leads to clinical patterns of mania.

[The clinical position of catatonia].

Revising the principal historical and clinical data available allows catatonia to be considered a kind of brain reaction unrelated to schizophrenia in restricted sense--i.e. to dementia praecox.