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Biomedical subjects

J C Goldar

Publications and source records attributed to J C Goldar.

10 recordsLinked to original sources
PubMed1991

[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. It seems also reasonable to include the ideational apraxia within the symptoms to be sought in those cycloid psychotic states including confusional psychosis. This is why it can safely be said that Pick's ideational apraxia is also a psychiatrist's realm.

Adult↗
PubMed1988

[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. Owing to the probabilities there are that malignant manifestations be developed, it is the author's opinion that it should be included into general medicine instead. Many cases including several catatonic attacks do not follow the usual course of dementia praecox. Moreover, true catatonic attacks frequency is quite low in chronic schizophrenia known as "catatonic schizophrenia". Thus, it seems necessary that relationships between catatonia, and spasmodic hysterical and epileptic symptoms be reevaluated accordingly. Electroconvulsive therapy is a very useful treatment, not only in simple catatonia attacks (which is a well-known application) but also on different malignant manifestations likely to arise during attacks.

Catatonia↗
PubMedDate not supplied

[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 other mechanism--located in the lateral orbital area, deriving from the olfactory allocortex, is responsible for tendencies to perseveration. Its predominance leads to clinical patterns of depression. Any alteration in the frontal lobe morphogenesis is likely to cause a permanent unbalance between both mechanisms. Consequently, an oscillation between opposite tendencies--i.e. a tendency to change, and a tendency to perseveration, may be expected which, clinically speaking, appears as mania, and depression phases. In this connection, the following points are discussed, namely (a) prefrontal functions, (b) peri-allocortex frontal zones participating in affective behaviors, (c) the problem of differences between brain hemispheres, and the probability of an anatomic basis for temperament. Eventually, features of a psychiatric science based on brain anatomy are enhanced.

Animals↗