Biomedical subjects

A Morel-Maroger

Publications and source records attributed to A Morel-Maroger.

At least 19 recordsLinked to original sources

PubMed1986

Postmortem studies on posthypoxic and post-methyl bromide intoxication: case reports.

In two cases of action myoclonus following hypoxic or shock encephalopathy, neuropathological examination disclosed mild or moderate scattered changes involving thalamus, griseum centrale mesencephali, and nucleus centralis superior. Other areas were affected only in one of these cases (striatum, nucleus subthalamicus or hippocampus, nuclei pontis, and cerebellar cortex). In another case (an alcoholic patient), the changes, which involved only corpus mamillare and thalamus, were those of Wernicke-Korsakoff encephalopathy. In one case of oscillatory myoclonus following septic shock, there were marked cerebellar changes involving deep nuclei and mild abnormalities in the thalamus and inferior olive. The last case of action myoclonus following acute methyl bromide intoxication was characterized by marked changes in the inferior colliculi and moderate or mild abnormalities of thalamus, griseum centrale mesencephali, nucleus centralis superior, nucleus reticularis tegmenti pontis, nuclei pontis, and dentatus. The findings are compared with the data of seven previously reported neuropathological examinations in action myoclonus following hypoxic encephalopathy.

Adult↗

PubMed1985

Dopaminergic and cholinergic lesions in progressive supranuclear palsy.

In 9 patients with progressive supranuclear palsy and in 27 controls, dopamine and homovanillic acid concentrations, choline acetyltransferase (CAT) activity, and the number of [3H]spiperone and [3H]quinuclidinyl benzilate binding sites were measured post mortem in the striatum (caudate nucleus, putamen, and nucleus accumbens), substantia innominata, and frontal cortex. Dopamine and homovanillic acid concentrations were reduced in the caudate nucleus and putamen but not in the nucleus accumbens or frontal cortex, indicating that the nigrostriatal dopaminergic system is lesioned in patients with progressive supranuclear palsy (as in those with Parkinson's disease) but not the mesocortical and mesolimbic dopaminergic systems, which are lesioned in parkinsonian patients. CAT activity and [3H]spiperone binding decreased in parallel fashion in all the structures. In the striatum, this suggests that the cholinergic neurons, which are target cells of the nigrostriatal system, also degenerate in this disease. This might explain the decrease in the number of dopamine receptors as well as the inefficacy of levodopa or anticholinergic therapy in these patients. The decrease in CAT activity in the substantia innominata and the frontal cortex indicates that the innominatocortical cholinergic system is lesioned in patients with progressive supranuclear palsy and may play a role in the intellectual deterioration observed. This lesion is also found in demented patients with Alzheimer's and Parkinson's diseases.

Aged↗

PubMed1983

[Paralysis of vertical gaze as a sequela of Wernicke's encephalopathy].

In the acute phase of Wernicke's encephalopathy the treatment with thiamine results quickly in a normal ocular motor function. In a patient with severe and long-time alcoholism, and poor nutrition, an acute Wernicke's disease is reported in which a complete gaze palsy was associated with cerebellar symptoms, desorientation and anterograde amnesia. The treatment by thiamine, pyridoxine and folic acid resulted in the disappearance, in 1 week, of the extra-ocular symptoms. Lateral gaze palsy disappeared in 3 weeks, but vertical gaze palsy was unchanged after 8 months. Eye movement disorders rarely persist more than 1 week in well-treated patients. In this case, clinical signs and course, computed tomography have excluded another disease of the midbrain (i.e.: tumor, infarct, centro-pontine myelinolysis.) Hypotheses are considered to account for this fact: first, subclinical lesions persisting after a similar episode three years before; second, an abnormality of the transcetolase enzyme system: third, the association of the thiamine deficiency with a possible toxicity of very odd fooding habits. This patient, since several months, ate nothing but spoiled food with an admixture of strong alcoholic beverages.

Drug Therapy, Combination↗

PubMed1982

[Non-lethal brain stem hematomas in hypertensive patients].

Brain stem hemorrhages (peduncular, pontine, medullary) were demonstrated by CT scan in hypertensive patients, the outcome being favorable without surgical intervention. Such lesions are considered as being usually massive and fatal. A review of the literature show that hemorrhages in the brain stem represent 5 to 9 p. cent of intraparenchymatous hemorrhages, and are usually located in the pons. A favorable course was known to occur before the use of computed tomography: the rare cases described were often related to subacute hematomas in young normotensive subjects which could be treated by surgery with or without ventricular shunting. Clinical diagnosis is based on the rapid progressive course of the disorder and the location of the lesion. Computed tomography provides an immediate correlation between anatomical and clinical findings, and allows a better evaluation of semiological and prognostic features that were previously considered well established. A major element appears to be the degree to which the hematoma is tolerated. As far as possible neurosurgical procedures should be avoided in hypertensive patients.

Aged↗

PubMed1978

[Positive effects of L-dopa on a "marginal" symptomatology observed in parkinsonians].

In some patients with parkinsonism, we have found and, often, cured by L-DOPA: 1) An unfrequent symptomatology (oculomotor, sensory, syncinesias, "Babinski" sign), not included in the classic rating scales. 2) A symptomatology "attributable to frontal lesion": grasping; inability to reproduce a serie of three gestures; inability to react to an audio-visual stimulus by a definited opposite gesture. In such patients, the improvement is in total contrast with the lack of effect of L-DOPA in several patients with frontal lesions, but without parkinsonism. It is possible that the last constatation may contribute: a) to localize more exactly the topography of dopaminergic pathways, b) to approach the respective parts of the cortical and subcortical structures in the programming of the movement.

Aged↗

PubMed1977