[Crural and lumbar plexus neuropathies under anticoagulant treatment]. / Neuropathies crurales et du plexus lombaire sous traitement anticoagulant.

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. Treatment of a case with 5-hydroxytryptophane and a decarboxylase inhibitor.

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.

Neuropathy, amyloidosis, and monoclonal gammopathy.

Three cases of neuropathy with monoclonal gammopathy and amyloid deposits in peripheral nerves are described. They appeared to present a benign gammopathy because of the duration of the neuropathy in the absence of any clinical or biological sign of myeloma or macroglobulinaemia. The pathological abnormality found in the sural nerves of the three patients was characterised by a marked loss of myelinated and unmyelinated nerve fibres because of active axonal degeneration with Wallerian degeneration. The most striking feature in all three cases was the finding of deposits identified as an accumulation of microfibrils.

Recurrent familial neuropathy with liability to pressure palsies: reports of two cases and ultrastructural nerve study.

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.

[Usefulness of the immunoglobulin-albumin ratio compared to electrophoresis in the diagnosis of multiple sclerosis]. / Utilité diagnostique du rapport immunoglobuline sur albumine comparée à celle de l'électrophorèse dans la sclérose en plaques.

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.

[Determination of antibodies against nicotinic acetylcholine receptor: clinico-immunological correlations in 30 patients with myasthenia gravis]. / Dosage des anticorps dirigés contre le récepteur nicotinique de l'acétylcholine: corrélations clinico-immunologiques chez 30 myasthéniques.

In 30 patients with myasthenia gravis, serum assays were performed for antibodies to human nicotinic acetylcholine receptor. 19 of 20 generalized forms which were symptomatic and 6 of 9 patients in remission at the time of blood sample had detectable amounts of antibodies. The six highest levels were found in benign courses. 2 patients had a five- and twofold drop in antibody level during rapid deterioration. Patients in remission after thymectomy may still have low to moderate levels, while symptomatic patients occasionally have no detectable antibody.

[Consequeces of the elimination of a combination drug. Transition from combination antisacer: attention]. / Les conséquences de l'élimination d'un médicament combiné.

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.

Cerebral coenurosis. Report of a case with arteritis.

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.

[Determination of plasma phenytoine and treatment of epileptics]. / Dosage de phénytoïne plasmatique et traitement des épileptiques

In the diagnosis of epilepsy the prior approach will be to decide whether it is an epileptic attack or not. If so, is the epilepsy the primary disease or the symptom of an evolving cerebral affection or of a toxic or metabolic disorder? The causes of failure with phenytoin treatment are discussed. They may be exogenous, i.e. prescribing too low a dosage (the average dose in the adult is 5 mg/kg/day) or lack of cooperation by the patient who either takes the drug irregularly or fails to take it at all. The endogenous causes are harder to determine. Plasma phenytoin determination (therapeutic values from [5] to 10 to 20 mug/ml) makes it possible to adapt the dosage to the individual metabolism and sometimes to detect a drug interaction which lowers, and in rarer cases raises, plasma DPH levels. Toxic levels are rarely asymptomatic. In this condition repeated determinations may help to decide when the treatment is to be resumed and thus to avoid recurrence of attacks during or shortly after DPH withdrawal. Finally, plasma determination makes clear the extreme difficulty of adapting the dosage in the rare patients who react to a minimal of dose by a shift in blood level from insufficient to toxic values, or vice versa.