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B Brichet

Publications and source records attributed to B Brichet.

At least 19 recordsLinked to original sources

[Significance of abnormally high somatosensory evoked potentials (SEV)].

Data found in the literature and our own observations prompted us to consider the possibility that abnormally enlarged Somatosensory Evoked Potentials (SEPs) may have a diagnostic and physiopathological significance, particularly in a group of diseases which include common clinical features of encephalopathy with stimuli-sensitive myoclonus and epilepsy, whatever their etiology may be (degenerative or storage disease, metabolic, toxic or post-hypoxic encephalopathy...). We discuss the amplitude, morphology, diagnostic and therapeutic contribution of these 'giant' SEPs and pathogenic assumptions with reference to 'cortical reflex myoclonus'. Studies of back-averaged encephalogram, SEPs and long-loop reflexes allow some illustration of a functional hyperreactivity of the sensori-motor cortex, but no conclusive demonstration of its origin.

Adolescent

[Changes in somatosensory evoked potentials during EEG activation by bemegride in man].

The use of evoked potentials for the evaluation of neuronal mechanisms by which convulsant drugs activate epilepsy and produce seizure has been reported by many authors. Electrophysiological effects of bemegride with augmented responsivity of brain structure to sensory stimulation is well known, especially in experiments performed with implanted electrodes in animals. After recording evoked activity from parietal scalp following median nerve stimulation before and during 12 human EEG activations by bemegride, the authors find an increase in amplitude of cortical somatosensory evoked potentials. Changes in amplitude after diazepam administration are analysed, as well as morphological changes preceding and following grand mal seizures induced by bemegride administration. This variation in amplitude of evoked responses is compared with those recorded in animals with several convulsant drugs and in man affected with progressive myoclonic encephalopathies. A common action of these agents, beyond their effects on specific neurotransmitters (perhaps mediated by a blockade of neurotransmitter-induced chloride conductance increases), is discussed.

Adolescent