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Biomedical subjects

F Cohadon

Publications and source records attributed to F Cohadon.

At least 73 records · Page 4Linked to original sources
PubMed1984

Modifications of synaptosomal Na+ -K+ -ATPase activity during vasogenic brain edema in the rabbit.

This study investigates the functioning of synaptosomal ouabain-sensitive Na+ -K+ -ATPase in cold-induced edema. During vasogenic brain edema development, the enzyme affinities for Na+ and K+ are progressively decreased paralleling the increase in the tissue water content, whereas maximal velocity of the reaction is not changed. On the basis of these data, it is likely that Na+ -K+ -ATPase impairment accounts for the intracellular uptake of water in this model of edema.

Animals↗
PubMed1984

[Role of interstitial radiation in the treatment of glioma].

Therapy of glioma is a function of numerous factors: their histology, localization and size, but also the age and functional state of the patient. Interstitial radiation by temporary implantation of Iridium 192 needles is recommended only under certain precise conditions: for tumors surgically inaccessible because of their deep localization or their site in a highly functional region, and for those with diameters of less than 35 mm. This restricts the number of cases that can be treated (45 in the present series). Numerous adverse reactions developed, either in the short (initial deficit and edematous reactions), medium (epilepsy) or long term (radionecrosis). However, many were regressive and the treatment is satisfactorily tolerated in view of the localization of these tumors in highly functional regions.

Adult↗
PubMed1984

[Cell membrane alterations during situations of acute stress to the cerebral parenchyma. Mechanisms, consequences and therapeutic perspectives].

Marked alterations to phospholipid structures of the different cell membranes can be clearly demonstrated on experimental models during acute or subacute cerebral aggression . Tissues surrounding hematomas, traumatic lesions, infective zones and certain tumors undergo autocatalytic peroxidation which attacks fatty acid chains that include double bonds. Intracellular invasion of ischemic foci by calcium, related to the energy deficit, activates phospholipases which liberate the same fatty acids. These lipidic disorders greatly alter membrane functions, particularly inactivating protein enzymes essential for maintenance of ionic gradients. Certain degradation products liberated disorganize other cell functions. The edema and microcirculation disorders that are characteristic of these focal lesions and are responsible for their invasive nature appear finally to be the consequences of membrane damage. The extent of membrane injury can be limited by various treatments, each possessing their time constant and specificity of biochemical action: the barbiturates could "protect", the corticoids "stabilize" and the metabolic precursors of the phospholipids "restore" membranes attacked in this way.

Acute Disease↗
PubMed1984

[Partial epilepsies of adolescence with computer tomography abnormalities, localized astrocytic reaction and spontaneously remitting course].

Four teenagers with partial epileptic seizures presented focal cortical enhanced CT scan images. Angiographies were normal. Stereotactic biopsies revealed astrocytic proliferation. CT scan abnormalities diminished or vanished in some months. On long-term follow-up seizures were either less frequent or disappeared. None of the possible aetiologic hypotheses (astrocytoma, encephalitis, sarcoidosis, multiple sclerosis, vascular malformation) was fully satisfying. Nevertheless, a regressive evolution observed in these four patients demonstrates that acquired epileptogenic lesions during adolescence are not always of poor prognosis.

Adolescent↗
PubMed1983

[Malignant astrocytoma and glioblastoma. Therapeutic results].

Statistical analysis of therapeutic results in malignant gliomas is impeded by the discrepancies between the various classifications. We have distinguished glioblastomas from malignant astrocytomas. The latter are defined as malignant gliomas other than glioblastomas with CT scan enhancement after IV contrast. The discrimination between these two types of tumor is justified by the very different actuarial survival curves. Total survival was not prolonged by chemotherapy in randomized studies. Systematic sequential treatment of glioblastomas with VM26-CCNU is questionable.

Astrocytoma↗
PubMed1983

[Course and outcome of severe traumatic coma].

This study will consider the course and final outcome of severe traumatic coma (Glasgow coma scale score 5-3 at admission). Intensive rehabilitation programs aimed at functional recovery must be undertaken from the very beginning. The importance of retraining of axial motricity is stressed. Successive stages of evolution and various neurological syndromes disclosed during the awakening period are described. Even in the case of these very severe brain injuries, a considerable amount of recovery is possible and leads to a normal socio-economic status in 62% of the cases. 22% however will remain bound to some type of sheltered life. Functional outcome is not related to the depth of initial coma but rather to the length of comatose period. It can be safely predicted only at the awakening phase, the neurological status reached at this time reflecting rather well the overall extent and severity of brain lesions. Neurophysiological mechanisms likely to support the functional recovery after this type of trauma are discussed.

Adult↗
PubMed1982

[A precursor of phospholipids in the treatment of severe traumatic comas].

CDP Choline, a metabolic precursor of phospholipids, has been tested against placebo in a controlled randomized double blind study concerning 60 cases of severe head injuries (wide-spread cerebral contusions and/or severe concussion). In the treated group, a shortening of the comatose period and an acceleration of neurological deficits recovery have been observed. These results are tentatively attributed to an effect of the drug against brain edema, already documented on experimental models.

Adult↗
PubMed1981

[The diagnosis and therapeutic malignant gliomas management (author's transl)].

3 principles lead, in our opinion, the malignant gliomas management: to place surgery in first position, to take prognostic factors into account, to require a convincing histological evidence before deciding on radiotherapy and chemotherapy. 111 cases are studied: in 8% of cases stereotax biopsies allow correction of CT scan diagnosis. The survival curves could be carefully interpreted according to patient and tumor features.

Biopsy↗
PubMed1981

[Principal fields of research into the pathogenesis of gliomas (author's transl)].

Our hypotheses concerning the pathogenesis of gliomas are based upon the study of numerous animal models. Malignant transformation is probably related to changes in the genome of somatic cells, caused either by chemical or physical agents or by the addition of viral material. Promotion of the tumor, which results in its clinical expression, would involve the failure of a hypothetical immune mechanism of surveillance. At the present time, we have no direct proof of the intervention of such various initiation or tumor-promotion factors in the pathogenesis of human gliomas.

Animals↗
PubMed1980

[Study on a mock cerebro-spinal fluid (author's transl)].

The work presented was initiated in order to evaluate the biological and clinical tolerance of the isotonic saline solution (9 p. mille) usually used in neuro-surgery directly in contact with the nervous tissue in comparison with a new solution proposed as a a mock cerebrospinal fluid. Clinically, two patient' populations including 75 patients each, were compared during dynamic investigation of intracranial pressure with intra-ventricular injections of different solutions. The effects of prolonged intra-ventricular perfusion with each solution were studied in animal models by: --electrophysiological analysis of EEG activity during perfusion --morphological observation: electronic microscopy of different cerebral structures after the perfusion. The biological tolerance was analyzed by the use of routine tissue culture of CNS tissue exposed to the two solutions. The results obtained show the toxicity of isotonic saline solution (9 p. mille) and the perfect tolerance of S.21.001 solution as a mock cerebro-spinal fluid.

Animals↗
PubMed1979

[Vasogenic cerebral oedema. Changes in membrane ATPases. Correction by a phospholipid precursor (author's transl)].

In vasogenic cerebral oedema, there is progressive quantitative and qualitative impairment of mitochondrial ATPase and of Na/K/ATPase. This impairment, which reflects the intracellular component of cerebral oedema, would appear to be related to changes in the phospholipid environment of the cell membrane enzymes. CDP choline, a metabolic phospholipid precursor, is to a certain extent capable of correcting this disturbed activity and at the same time reduce oedema.

Adenosine Triphosphatases↗