Fibrositis syndrome and narcolepsy.

Fibrositis is often associated with sleep disturbances and with an alpha nREM abnormality on sleep electroencephalogram. We describe a case occurring during the course of a typical longstanding narcolepsy-cataplexy. Modafinil, that is an effective treatment of hypersomnia, did not alleviate the symptoms of fibrositis in the short term.

[Trigeminal neurotrophic ulcer and vascular disorders of the brain stem. A clinico-electrophysiological study]. / Ulcération neurotrophique trigéminée et accidents vasculaires du tronc cérébral. Etude clinique et électrophysiologique.

Torpid facial ulcerations may occur as a result of lesions involving the trigeminal fibers. These neurotrophic ulcerations have usually been observed after alcohol injection in the trigeminal ganglion. We report two cases associated with brainstem infarction. In both patients, the blink reflex was studied. The masseter inhibitory reflex was studied in one case. Analysis of these electrophysiological recordings can be of particular value in localizing the site of the lesion along the trigeminal pathway.

[Epilepsy and the female sex]. / Epilepsie et sexe féminin.

PIP: Treatment of epilepsy in fertile-aged women raises questions of the effect of epileptic episodes on the outcome of the pregnancy, the interaction between antiepileptics and oral contraceptive (OCs), and the possible teratogenic effects of antiepileptic agents. Many antiepileptic agents are enzyme inductors, stimulating the activity of microsomal hepatic enzymes and consequently accelerating the degradation of combined OCs, diminishing their serum levels and their efficacy. Enzyme inductors include phenobarbital, hydantoins, carbamazepine, and primidone. Valproate sodium and the benzodiazepines are not enzyme inductors. Low-dose combined and phasic OCs should be avoided when enzyme inductors are used and a formulation with at least 50 mcg of ethinyl estradiol or another method such as an IUD selected. If combined OCs are used, the appearance of metrorrhagia is a sign of insufficient hormonal blocking. During pregnancy, the frequency of epileptic crises is unchanged in about 1/2 of cases, increases in 1/4, and decreases in 1/4. The serum level on antiepileptic medications tends to decline during pregnancy and increase in the postpartum. The decline appears to be due to several factors: modification of binding to proteins, increased volume of distribution, and increases in metabolism of antiepileptics due to hormonal changes. Thus, in case of increased frequency of crises during pregnancy, the serum level of antiepileptic medications are associated with problems of hemostasis and increase the risk of neonatal hemorrhage. Coagulation problems can be prevented by administration of vitamin K to the mother at the end or pregnancy and to the newborn. Antiepileptic medications cross the placental barrier and can cause a withdrawal syndrome. The teratogenic risk of these drugs is very difficult to evaluate with assurance because of the many factors implicated in development of a malformation. All antiepileptics have a teratogenic risk, which increases with the number of drugs taken simultaneously. Phenobarbital, carbamazepine, and phyenytoin are basically responsible for facial and cardiovascular malformations, while valproate sodium is implicated in malformations of the nervous system. Malformations occur in the 1st 2 months of gestation. The teratogenic risk should be kept in mind, but there is also a risk to the fetus in repeated epileptic crises. Suppression of all treatment is often impossible, but limitation to 1 drug is desirable. Folic acid treatment should be prescribed 2-3 months before conception and during pregnancy. Surveillance is essentially sonographic, with amniocentesis if necessary.^ieng