Background: Obstetrical analgesia remains a matter of controversy because of the fear of neurotoxicity of local anesthetics on demyelinated fibers or their potential relationship with subsequent relapses. Objective: To assess the impact of neuraxial analgesia on the risk of relapse during the first 3 months post-partum, with a focus on women who experienced relapses during pregnancy. Methods: We analyzed data of women followed-up prospectively during their pregnancies and at least 3 months post-partum, collected in the Pregnancy in Multiple Sclerosis (PRIMS) and Prevention of Post-Partum Relapses with Progestin and Estradiol in Multiple Sclerosis (POPARTMUS) studies between 1992–1995 and 2005–2012, respectively. The association of neuraxial analgesia with the occurrence of a post-partum relapse was estimated by logistic regression analysis. Results: A total of 389 women were included, 215 from PRIMS and 174 from POPARTMUS. In total, 156 women (40%) had neuraxial analgesia. Overall, 24% experienced a relapse during pregnancy and 25% in the 3 months post-partum. Women with a pregnancy relapse were more likely to have a post-partum relapse (odds ratio (OR) = 1.83, p = 0.02), independently of the use of neuraxial analgesia. There was no association between neuraxial analgesia and post-partum relapse (OR = 1.08, p = 0.78). Conclusion: Neuraxial analgesia was not associated with an increased risk of post-partum relapses, whatever multiple sclerosis (MS) activity during pregnancy.

CAROLE is a prospective survey of children and adults who experienced epileptic unprovoked seizure(s) diagnosed for the first time between May 1 1995 and June 30 1996 by 243 French neurologists and neuropediatricians. Case records forms at entry allowed to compare patients who had a single seizure or several seizures prior to diagnosis. In patients with recurrent seizures, the time elapsed between the onset of attacks and the diagnosis (diagnostic delay) was looked for.Half of the 1942 included individuals already experienced more than one seizure when diagnosed. Due to natural history of epilepsies, 13 p.100 of the patients did not come to medical attention after a single seizure. Time to diagnosis ranged from 0 day to 52 years. While the overall median delay was 6 days, it ranged from 0 day to 7-8 months according to the type of seizure and the epilepsy syndrome. Two thirds of generalized convulsive seizures were immediately diagnosed versus one third of partial seizures. One half of infantile spasms were identified within 2 weeks versus 6 weeks in complex partial seizures, 4 months in absence seizures, 6 months in simple partial seizures, and 7 months in myoclonic seizures. Three quarters of idiopathic partial epilepsies were diagnosed within 4 weeks versus 3 months in symptomatic generalized epilepsies, 8 months in symptomatic partial epilepsies, 15 months in idiopathic generalized epilepsies, 30 months in cryptogenic partial epilepsies, and 33 months in undetermined epilepsies.So, the time elapsed between a first epileptic event and its diagnosis is epilepsy-dependent seizure type and cause. Other reasons of diagnostic delay do exist: doctor and patient They will be addressed in another study.

Vigabatrin (VGB) has been shown through several studies to be safe and effective as add-on therapy, particularly for the treatment of partial seizures in patients with severe epilepsies followed for years in hospital-based clinics. We now report additional clinical experience with VGB arising from an open trial of add-on VGB therapy in patients with relatively few seizures followed by qualified neurologists in private practice (the French Neurologists Sabril(R) Study Group). VGB was administered to 397 patients aged 12-74 years (mean age = 37.5 +/- 13.8 years) who presented with no more than seven partial seizures of any type per month during a 3-month baseline period (mean number of seizures = 3.7 +/- 1.9/month).Simple partial seizures were reported in 121 (30.5%) patients, complex partial seizures in 282 (71.0%) and seizures with secondary generalization were reported in 111 (28.0%). The mean number of associated antiepileptic drugs (AEDs) was 1.9 +/- 0.9 and the mean dose of VGB was 2.21 +/- 0.64 g/day. Following introduction of VGB, 53 (13.4%) became seizure-free and remained so during the whole trial. During the fourth month of treatment, 158 patients (39.8%) had no seizures at all and a further 69 (17.4%) had their seizure frequency reduced by more than 50%. Secondary generalization was controlled during the whole period of treatment in 55 out of 97 patients (56.7%), 17 of which remained free of all types of partial seizures. VGB showed a good tolerability profile; adverse experiences more frequently reported were drowsiness and sleep disturbances. No action was necessary in the great majority of cases; the dose was reduced in 26 (6.5%) and VGB was discontinued in 32 (8%) patients.These data provide additional evidence that VGB can be used safely early on to treat patients with mild to moderate partial epilepsies. Secondary generalization was controlled in the majority of patients. Factors associated with the everyday clinical use of VGB, that resulted from a series of organized meetings with the investigators, are discussed.

Background In patients with acute ischemic stroke, early treatment with thrombolytic agents is thought to permit reperfusion of ischemic neurons and to promote recovery of function. The Multicenter Acute Stroke-Trial - Europe (MAST-E) was designed to assess the efficacy and safety of streptokinase in patients with acute ischemic stroke.Methods Patients with moderate-to-severe ischemia in the territory of the middle cerebral artery were randomly assigned to receive streptokinase (1.5 million units over a period of one hour) or placebo within six hours after the onset of stroke. The primary efficacy outcome was a binary criterion combining mortality and severe disability at six months, with severe disability defined as a score of 3 or higher on the Rankin scale. The primary safety outcomes were mortality at 10 days and cerebral hemorrhage.Results All randomized patients (156 in the streptokinase group and 154 in the placebo group) were evaluated at six months. The incidence of the primary efficacy outcome was similar in the two groups (124 patients in the streptokinase group and 126 in the placebo group died or had a Rankin score greater than or equal to 3). However, the mortality rate at 10 days was significantly higher in the streptokinase group than in the placebo group (34.0 percent vs. 18.2 percent, P=0.002). The higher rate in the streptokinase group was mainly due to the hemorrhagic transformation of ischemic cerebral infarcts. At six months, more deaths had occurred in the streptokinase group than in the placebo group (73 vs. 59, P=0.06).Conclusions In patients with acute ischemic stroke, treatment with streptokinase resulted in an increase in mortality. The routine use of streptokinase cannot be recommended in acute ischemic stroke. (C) 1996, Massachusetts Medical Society.

In addition to neurological deficits, headache, seizures, and intracranial hypertension, psychiatric disorders may occur as the first manifestation of intracranial tumor (13.6 % in the authors series). Seven cases with isolated or predominant psychiatric disorders at the time of diagnosis are reported. The pattern of psychiatric manifestations varied widely across patients and was not strongly related to the histological type or location of the tumor. An intracranial tumor should be looked for when isolated psychiatric disorders develop in the absence of a triggering factor in a patient with no history of psychiatric disease.

Seven patients with unilateral arterial carotid occlusion and contralateral arterial carotid stenosis in the neck are reported. Authors perform an extra-cranial to intra-cranial anastomosis on the occluded side prior to realize endarterectomy on the stenosed side. This policy obviates the need of an internal vascular shunt during temporary occlusion of I.C.A.

Authors point out three observations of spontaneous dissection of cervical internal carotid artery (I.C.A.) with various evolution. They emphasize on evolutivity of residual aneurysms and necessity to purpose a preventive treatment of secondary projections.

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.

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.

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.

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.

Deux cas s'apparentent a la dystrophie musculaire des ceintures mais en different par l'evolution. Un cas de dystrophie facioscapulohumerale se distinguant de la maladie de Landouzy Dejerine par son debut tardif et l'absence d'antecedents familiaux