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Biomedical subjects

S Brion

Publications and source records attributed to S Brion.

At least 73 records · Page 4Linked to original sources

A typical presenile dementia. Report of an anatomo-clinical case and review of the literature.

A clinico-pathological report is given of a case of dementia of frontal type with EEG changes, associated with a diffuse neuronal loss, subcortical gliosis and laminar spongiosis in the superficial part of the 2nd cortical layer. The authors discuss the cortical biopsy and the post-mortem findings in their case. They draw a comparison between their case an two conditions known as "progressive sub-cortical gliosis" and "Kraepelin's disease" which might be a single entity "atypical presenile dementia".

Adult↗

[Post-traumatic Korsakoff's syndrome: clinical and anatomical report].

Clinical and anatomical report of a post traumatic amnestic syndrome (Korsakoff's syndrome), associating anterograde amnesia persisting for fifteen years, with temporal disorientation, false recognitions, initially intense transitory confabulation and secondarily bursts of confabulation, intact remote memory and persistence of old learnings. Death after twelve years from mesenteric infarction. Anatomically, post-traumatic sequellae are limited to both cingulate gyri in their anterior part. This cingula involvement is easy to understand if one knows that post-traumatic Korsakoff's syndrome appears after severe cranial traumatisms, with at least three days of coma, and develops constantly, even if transitory, after long duration comas with 20 to 30 days of loss of consciousness. Anatomical explanation depends on the fact that Korsakoff's syndromes from various etiologies need, to be produced, a bilateral damage of the limbic circuit and that severe head traumatisms, when dying early in the evolution without possibility of a neuro-psychological investigation, have always a destruction of corpus callosum or cingulate gyri or both, resulting from crushing of these structures by the edge of the faulx cerebri. Consistent with these constatations, it is logical that a Korsakoff's syndrome develops after severe head traumas with bilateral lesions of the limbic circuit and especially of the cingulate gyri. But anatomical evidence remains rare, because early fatal evolution does not permit psychological evaluation and, reversely, long survivals who may die from another pathology would not have brain examination. We prefer the name of "Korsakoff's syndrome" rather than that of "amnesic syndrome" to denominate the anterograd amnesia (amnésie des faits récents) encountered in nutritional disorders due to B1 deficiency in true Korsakoff's disease, but also with other etiologies such as cerebral tumours, vascular cerebral disorders, post-commital anoxia, herpetic encephalopathy, head traumas, all of them developing amnesia for recent events, formerly classified under the title of "korsakowian syndrome" or "mental syndrome of Korsakoff" and more recently under the denomination of "amnesic syndrome". But whatever is the etiology of the memory disorder, the amnesic syndrome remains identical and the advanced small differences, such as euphoria in alcoholics or mood depression in tumours, are often fallacious, so that the only way of differentiation deals with accessory symptoms such as intracranial hypertension in tumours, sudden onset in vascular etiologies or polyneuritis in B1 deficiency. Post-traumatic Korsakoff's syndrome joins with this scheme, for its clinical aspect is so similar to that of nutritional disorders that it might be difficult to reach the exact diagnosis when an alcohol addict develops, after a head trauma, an amnesia which could be the consequence of the trauma but also of a nutritional disorder developed after the accident with inadequate parenteral treatment. Our case, which is the first well documented observation of this disease reported with long clinical survey and final pathological examination, was presented in 1981 at a joint meeting of the French and Dutch neurological societies. It gives the proof of the importance, in limbic circuit, of the cingulate gyri. A comparison is made with four other clinical cases of post traumatic amnestic syndrome with MNR procedures which show, for two of them, cingula lesions explaining the clinical features, for one of them a bilateral lesion of Ammon's homs and for the last one extra-limbic lesions, with destruction of the inferior part of both frontal lobes, associated with a possible deafferentation of the right cingula cortex.

Adult↗

[Perphenazine enanthate. Results of a 1-year open multicenter study].

The results of a one-year, open multicenter trial of perphenazine enanthate, a sustained-release neuroleptic drug, are reported. 240 patients (62% suffering from schizophrenia) were included in the study and 144 were followed during the 12-month period. The usual adverse reactions associated with sustained-release neuroleptic drugs were observed. Total and partial BPRS ratings showed that improvement (expressed as a percentage) after 12 months' treatment was similar for systematized chronic delusions, paranoid schizophrenia and hebephrenia. However, the onset of therapeutic activity was different in these three groups of patients. Maximum therapeutic activity, as defined by the BPRS rating, was obtained within 4 months in chronic delusions whereas schizophrenia improved more progressively. Such patients therefore require prolonged treatment before the therapeutic activity of a sustained-release neuroleptic drug can be assessed.

Adult↗

[Interaction between cotrimoxazole and antidepressive agents].

The association cotrimoxazole-tricyclic antidepressants seems to involve a rapid relapse of the depressive states continuously treated with the latter drugs. Five cases are reported. Mechanisms of this unknown drug interaction are discussed. The hypothesis of an enzymatic induction is not the most probable. A central inhibition of the tricyclic antidepressants seems to be possible but needs to be supported by further evidence.

Anti-Infective Agents↗

[Anxiolytic efficacy and tolerance of tetrabamate in anxious patients abusing alcohol. Multicenter double-blind versus placebo study].

The anxiolytic efficacy of tetrabamate was evaluated in 68 out-patients presenting an anxiety state with alcohol abuse according to DSM III criteria. The study followed a double-blind placebo-controlled design with parallel groups and lasted for 21 days. Anxiety was evaluated by the Hamilton anxiety scale, Norris visual analog scales, and the Hopkins Symptom Check List, along with the investigator's assessment. Safety was evaluated in terms of somatic symptoms (CHESS 84) and the physician's overall evaluation. The anxiolytic activity of tetrabamate (three 300 mg tablets/day) was significantly greater than that of placebo from seventh day on. There were no statistically significant differences in safety profile between tetrabamate and placebo. Moreover, in the tetrabamate group the significantly greater improvement in the scores of somatic symptoms indicates that the compound caused no notable adverse effects and its activity on somatic complaints (psychopathologic and/or toxic).

Alcoholism↗

[Lesions of the motor cortex in amyotrophic lateral sclerosis].

The lesions of the spinal cord and the medulla in ALS, have been known for a long time. However the existence of cortical lesions in this disease, and their description, remain debated questions. This study deals with ten anatomical cases of ALS, with a special attention to the precentral gyrus. Three kinds of lesions are described in most cases: a disappearance of Betz cells with shrinkage and ghost cells of some other neurons; principally a subcortical gliosis, and also a laminar spongiosis located in the second cortical layer. The value and the signification of these lesions, which are strictly located in the motor cortex, are discussed. This could be compared to diffuse cortical lesions which are described in some cases of ALS with dementia state.

Amyotrophic Lateral Sclerosis↗

[Alzheimer's disease and Meynert's nucleus basalis. An anatomo- clinical point of view].

The existence of a lesion in the nucleus basalis (NbM), in Alzheimer's disease, which has been brought up again by Whitehouse et al. (1981), is not doubted anymore. The lesion is correlated with the disease's cholinergic deficit. The histology of the lesion isn't much described, and its importance not very clear. This study compares ten cases of Alzheimer's disease, and six cases of "senile dementia". A cellular count and a histologic observation of the NbM are done on slides imbedded in paraffin. The cortex is studied in the classical way. There are neuro-fibrillary tangles "en boules" in the NbM of the two types of dementia, but more frequently in Alzheimer's disease. No senile plaques are observed. The neuronal loss appears much more important in the group of Alzheimer's disease than in the senile dementias. But a typical clinical and histological case of Alzheimer's disease did not show neuronal loss in the NbM. The final results invite to further discussions concerning the present knowledge of Alzheimer's disease and senile dementia.

Aged↗