Etude comparative des données histochimiques et de l'innervation motrice terminale du muscle strié dans la pathologie neuro-musculaire

Doctorat en sciences médicalesinfo:eu-repo/semantics/nonPublishe

L'histochimie des fibres musculaires normales

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Muscle fibre types in denervation

In a large proportion of chronic neuropathies and motor neurone disease, in biopsies taken from clinically little affected muscles, the fibre type grouping is not conspicuous, so that this pattern should not be considered as a hallmark of the morphologic diagnosis of denervation. In this respect, the increased terminal innervation ratio remains a much more reliable parameter. The high proportion of type III or intermediate fibres occurring preferentially in cases without obvious type grouping must be emphasized, with regard to the hypothesis that these fibres represent a transient stage of reinnervation through collateral branching of subterminal axons. The pattern of type I grouping with numeric and sometimes volumetric reduction of type II fibres occurring in obviously neuropathic conditions leads to a reappraisal of the so called type II atrophy observed in disuse atrophy and in some myopathies. A neural influence in these conditions should only be accepted when there are characteristic changes in the terminal motor innervation pattern. (Journal received: 22 Oct. 1974)SCOPUS: NotDefined.jinfo:eu-repo/semantics/publishe

Changes of motor innervation in myasthenic muscles in relation to age

The motor innervation in muscle biopsies from 45 myasthenic patients was studied by intravital staining with methylene blue. The enzymatic pattern and fibre type distribution was analysed in 12 cases. Quantitative data including the proportion of elongated motor endings and the terminal innervation ratio (TIR) of motor axons, were compared to histochemical data and to clinical data including age of patients. The incidence of elongated motor endings tends to be greater in younger patients, whereas an increased collateral ramification of motor axons occurs only after the age of 50. Small type III fibers suggesting denervation are also found in elderly patients only. The significance of these morphological differences in relation to age is discussed.info:eu-repo/semantics/publishe

Complications cerebro-vasculaires de l'hypertension

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Triparésie spastique "ammoniacale" réversible.

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Motor innervation in Type II atrophy of skeletal muscle

The histochemical changes in Type II atrophy were compared to the motor innervation pattern in biopsy specimens obtained from patients with or without clinical evidence of denervation.Several quantitative data of the muscle fibres were analyzed, namely AI and AII factors, Type I/II ratio, the proportion of Type III fibres and of small fibres of Type III (S F III), strongly reactive to both NADH diaphorase and ATP ase. The collateral ramification of motor axons was estimated by the measurement of the terminal innervation ratio (TIR).No significant histochemical changes were found in relation to clinical eviden ce of denervation. The only obvious morphological difference was an increased TIR in disorders of the lower motor neurone or peripheral nerves.The analysis of muscle fibre changes in relation to TIR led to the following conclusions:1.(1) A very marked volumetric and numerical reduction of Type II fibres (high value of AII factor and Type I/II ratio) is suggestive of a neural defect, but there is no statistical evidence of this correlation.2.(2) The only histochemical evidence that denervation is taking place in Type II atrophy is the presence of S F III. The angular shape of these fibres is not relevant in their identification.3.(3) The occurrence of Type II atrophy without an increased TIR nor S F III indicates that this change may occur without any neurogenic participation.info:eu-repo/semantics/publishe

Les polymyosites: Revue critique et étude de 32 cas personnels

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Les premiers stades de la régénération neuromusculaire après écrasement de nerf sciatique chez le rat. Etude électrophysiologique et histologique

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APERCU SUR LA PATHOGENIE ET LE TRAITEMENT DE L'OEDEME CEREBRAL

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