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Biomedical subjects

G Lyon

Publications and source records attributed to G Lyon.

At least 91 records · Page 5Linked to original sources
PubMedDate not supplied

Considerations on the significance attributed to unusual cerebral histological findings recently described in eight patients with primary generalized epilepsy.

The authors, although they express appreciation of the importance of publishing careful anatomical reports in cases of epilepsy, express some doubts concerning the pathological nature of the histological features reported by Meencke and Janz in the brains of eight patients suffering from primary generalized epilepsy. As illustrated and described, most of the histological findings considered abnormal are commonly seen in neurologically normal controls. Also, true "minor dysgenetic changes" have been observed in individuals free of cerebral disorders. Furthermore, the hypothesis drawn from the neuropathological observations to explain the etiopathogenesis of this category of epilepsy and the physiopathogenesis of the seizures does not seem acceptable to the authors.

Brain↗
PubMedDate not supplied

[Familial syndrome combining short small intestine, intestinal malrotation, pyloric hypertrophy and brain malformation. 3 anatomoclinical case reports].

Anatomoclinical study of 3 cases of an exceptional malformative condition characterized by: --extreme shortness of the small intestine, --mesenterium commune, --hypertrophic pylorus, --malformation of the central nervous system (heterotopia, absence of operculum temporale). Clinically this malformative condition is characterized by failure and inertia of the intestinal peristalsis producing at intervals of 10-15 days episodes of subocclusion, the repetition of which causes death. The syndrome is familial and seems to be of autosomal recessive inheritance. The absence of mechanical obstruction, the repeated failure of colostomy and ileostomy, the normal aspect of the myenteric plexuses verified by cytoenzymatic and silver stains allow to individualize this anatomoclinical syndrome and to rule out the hypothesis of Hirschsprung's disease, Chagas' disease, idiopathic megacolon or hypoplasia of the myenteric plexuses. The association of cerebral malformations leads to consider the responsibility of a lack of synthesis of a same specific intermediate factor which is up to now poorly determined, implicated in the neuronal migration and neuromuscular transmission.

Abnormalities, Multiple↗
PubMedDate not supplied

[Intraventricular hemorrhage in utero].

A case of fetal intraventricular hemorrhage related to subependymal hemorrhage diagnosed by ultrasound scanning at 27 weeks of PMA is reported. No etiology was found. The outcome was favorable. This case suggests that some cases of neonatal idiopathic hydrocephalus may be explained by fetal subependymal/intraventricular hemorrhage.

Blood Coagulation Disorders↗
PubMedDate not supplied

[Early histogenesis in the cerebral cortex of the mouse: a Golgi analysis (author's transl)].

By the application of the rapid Golgi method to embryonic telencephalon, three stages can be distinguished in the early developmznt of the neocortex. Stage 1 is characterized by a neuroepithelium containing a continuously proliferating cell population. Stage 2 corresponds to the primordial cortical organization; the first neuronal (post-mitotic) cells appear in the external part of the neural tube and are differentiated in a predominantly horizontal pattern. Stage 3 begins when the cortical plate appears. This structure will give rise to the major part of the adult cortex. The cells of the cortical plate assume a typical radial orientation and their axons (afferent fibers) are well individualized. The afferent fibers however, are not easily analyzed by the technique employed. Those morphological findings are discussed in relation to various data from the literature in developmental neurology.

Animals↗
PubMedDate not supplied

[Progressive chronic rubella encephalitis. Report of a personal case (author's transl)].

This is a report on a now alive, 18 years old boy. He was affected by a progressive encephalitis which began between 7 and 12 years of age. The first signs were walking disorders and mental regression. The disease which developed during a few years led to a bed-ridden state and advanced mental deficiency. Strong biological arguments (analysis of the cerebrospinal fluid, virological study, brain biopsy) and comparison with several similar cases published before leading to the conclusion of rubella origin of this encephalopathy, despite of the absence of known history of congenital or acquired rubella in our case.

Adolescent↗
PubMedDate not supplied

Pontoneocerebellar hypoplasia--a probable consequence of prenatal destruction of the pontine nuclei and a possible role of phenytoin intoxication.

The autopsy findings of a 21/2-year-old microcephalic, mentally retarded girl, with tetraparesis, and dysmorphic features are reported. Neuropathologic findings, typical of the ponto-neocerebellar hypoplasia described by Brun [1917], suggest that this abnormality was the result of a prenatally acquired destruction of the pontine nuclei, with a secondary retrograde degeneration of the dentatopontine tract. The possible role of phenytoin, taken by the mother during pregnancy, is discussed.

Abnormalities, Drug-Induced↗