[The role of thymectomy in the treatment of myasthenia gravis].
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Biomedical subjects
Publications and source records attributed to G de Crousaz.
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Thirteen cases of crural or, less often, lumbar plexus neuropathies are reported which were secondary to hematomas in patients under anticoagulant therapy. They are the most frequent peripheral neurological complications of anticoagulant therapy. The clinical symptoms, which often point directly to the diagnosis, are discussed and several additional investigations (conventional X-ray, transverse tomography, EMG, etc.) are presented. The criteria for prognosis and therapeutic problems, in particular the indication for surgical drainage of the hematoma or for neurolysis, are discussed. Finally, the pathogenic mechanisms of these neuropathies are outlined.
Postanoxic myoclonus was first accepted as being related to a dysfunction of the ventrolateral thalamic nucleus. Several stereotaxic studies have invalidated this hypothesis. The neurochemical approach, in particular the measure of 5-hydroxyindolacetic acid in the cerebrospinal fluid, has opened new theoretical and therapeutic possibilities involving serotoninergic pathways. A typical case is presented who improved markedly under a combined therapy with 5-hydroxytryptophan and a decarboxylase inhibitor. A review of the pathogenesis and therapeutic approach to postanoxic myoclonus is presented.
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Electrophysiological, histological and ultrastructural studies on two patients (one family) with familial neuropathy and a liability to pressure palsies are reported. There was slowing of nerve conduction velocities and increase of distal latencies of clinically affected and clinically non-affected nerves. These alterations were confirmed by biopsy of the sural nerive which had the characterized signs of the disease. Pathogenetically there seems to be an endogeneous metabolic defect of the Schwann cell to synthetize a normal myelin sheath, which is responsible for the particular susceptibility to mechanical damage.
The results obtained with gel electrophoresis on CSF samples of multiple sclerosis patients are compared with measurements of CSF IgG indexes (IgG/alb and IgG/total protein). The correlation between these parameters is good, provided the upper normal limit of the IgG/alb index is over 35% and an "overlapping" zone between 21 and 35% is introduced where the IgG/alb index has not the same diagnostic value.
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Antisacer compositum, a commonly prescribed speciality which associated phenobarbitone and phenytoin in a dose ratio of 1:4, was withdrawn after demonstration of a negative interaction of this formula. A retrospective analysis is presented of phenytoin plasma levels during bitherapy and after passage to monotherapy, in 13 adult epileptics followed as outpatients. Phenytoin plasma levels increased over twofold in 12 cases, of whom 5 continued to take the same doses, while 7 received higher doses on, and in one case two weeks after, the withdrawal of phenobarbitone. Plasma level decreased slightly in the thirteenth in spite of increased doses. Five phenytoin intoxications occurred after this change of prescription: one amongst the 5 cases with identical doses, and 4 amongst the 7 cases with increased doses. The initially high levels of phenytoin tend to decrease after several months. Physicians required to change the prescription should be aware of the risk of initial intoxication and later underdosage.
A case of the unusual clinical condition of cerebral coenurosis, the unique parasitic disease that is localized only in the CNS, is reported. The patient had repeated attacks of transient hemiparesis due to intracranial arteritis which was demonstrated by several angiographic studies. The CSF showed a discreet lymphocytosis and increased immunoglobulins. This inflammatory reaction which preceeded the manifestations of the intracranial mass can be explained by the parasitic foreign bodies, the liberation of somatic and metabolic parasitic toxins and the immunological reaction of the organism. The arteritis of the basal intracranial vessels was probably secondary to the inflammatory reaction of the leptomeninges. In presence of the rare association of meningovascular disease and an expanding intracranial lesion a parasitic condition due to a larval stage of Cestodes (Hydatidosis, Cysticercosis, Coenurosis) should be always considered.
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Plasma concentrations of diphenylhydantoin were determined by the method of Wallace (double extraction, spectrophotometry) in 150 samples taken from 121 epileptic patients. They correlated well with those determined by gas chromatography, were not dose-dependent and were often below 10 mul/ml. They were above 20 mul/ml in 6 patients with CNS intoxication. These determinations were also useful for detecting patients who did not take the drug as prescribed (14 suspected cases, 4 confirmed). However, blood levels did not seem to offer an accurate index of the effectiveness of diphenylhydantoin.
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