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Background and Purpose: We aimed at comparing the long-term benefit-risk balance of carotid stenting versus endarterectomy for symptomatic carotid stenosis., Methods: Long-term follow-up study of patients included in Endarterectomy Versus Angioplasty in Patients With Symptomatic Severe Carotid Stenosis (EVA-3S), a randomized, controlled trial of carotid stenting versus endarterectomy in 527 patients with recently symptomatic severe carotid stenosis, conducted in 30 centers in France. The main end point was a composite of any ipsilateral stroke after randomization or any procedural stroke or death., Results: During a median follow-up of 7.1 years (interquartile range, 5.1-8.8 years; maximum 12.4 years), the primary end point occurred in 30 patients in the stenting group compared with 18 patients in the endarterectomy group. Cumulative probabilities of this outcome were 11.0% (95% confidence interval, 7.9-15.2) versus 6.3% (4.0-9.8) in the endarterectomy group at the 5-year follow-up (hazard ratio, 1.85; 1.00-3.40; P=0.04) and 11.5% (8.2-15.9) versus 7.6% (4.9-11.8; hazard ratio, 1.70; 0.95-3.06; P=0.07) at the 10-year follow-up. No difference was observed between treatment groups in the rates of ipsilateral stroke beyond the procedural period, severe carotid restenosis (≥70%) or occlusion, death, myocardial infarction, and revascularization procedures., Conclusions: The long-term benefit-risk balance of carotid stenting versus endarterectomy for symptomatic carotid stenosis favored endarterectomy, a difference driven by a lower risk of procedural stroke after endarterectomy. Both techniques were associated with low and similar long-term risks of recurrent ipsilateral stroke beyond the procedural period., Clinical Trial Registration Url: http://www.clinicaltrials.gov. Unique identifier: NCT00190398., (© 2014 American Heart Association, Inc.)

Purpose: Ischemic stroke is a frequent pathology with high rate of recurrence and significant morbidity and mortality. There are several causes of stroke, affecting prognosis, outcomes, and management, but in many cases, the etiology remains undetermined. We hypothesized that atrial fibrillation was involved in this pathology but underdiagnosed by standard methods. The aim of the study was to determine the incidence of atrial fibrillation in cryptogenic ischemic stroke by using continuous monitoring of the heart rate over several months. The secondary objective was to test the value of atrial vulnerability assessment in predicting spontaneous atrial fibrillation., Methods and Results: We prospectively enrolled 24 patients under 75 years of age, 15 men and 9 women of mean age 49 years, who within the last 4 months had experienced cryptogenic stroke diagnosed by clinical presentation and brain imaging and presumed to be of cardioembolic mechanism. All causes of stroke were excluded by normal 12-lead ECG, 24-h Holter monitoring, echocardiography, cervical Doppler, hematological, and inflammatory tests. All patients underwent electrophysiological study. Of the patients, 37.5% had latent atrial vulnerability, and 33.3% had inducible sustained arrhythmia. Patients were secondarily implanted with an implantable loop recorder to look for spontaneous atrial fibrillation over a mean follow-up interval of 14.5 months. No sustained arrhythmia was found. Only one patient had non-significant episodes of atrial fibrillation., Conclusion: In this study, symptomatic atrial fibrillation or AF with fast ventricular rate has not been demonstrated by the implantable loop recorder in patients under 75 years with unexplained cerebral ischemia. The use of this device should not be generalized in the systematic evaluation of these patients. In addition, this study attests that the assessment of atrial vulnerability is poor at predicting spontaneous arrhythmia in such patients.

A nucleotide 807T variant of the glycoprotein Ia gene that correlates with increased platelet surface levels of the platelet collagen receptor alpha2beta1 was recently found to be associated with an increased risk of ischaemic stroke in younger patients. We report the history of twins who developed ischaemic strokes and were shown to be homozygous for the alpha2 807T allele. The twins developed ischaemic strokes at the ages of 23 and 33 years, one of them with recurrent events. They had no conventional risk factors. Cardiac and vascular investigations were normal and no aetiology could be found. There was a family history of cerebrovascular disease. Genotyping of glycoprotein alpha2 C807 T was performed and both twins were found to be homozygous for the 807T allele. This allele probably contributed to the occurrence of strokes in these young men. Further prospective studies are needed to evaluate whether screening for this polymorphism should be considered in young patients with unexplained stroke, particularly when a positive family history was found., (Copyright 2003 Lippincott Williams & Wilkins)

We present a comprehensive review of sleep studies performed in patients with brain lesions complemented by 16 additional personal selected cases and by discussion of the corresponding animal data. The reader is cautioned about the risk of establishing an erroneous correlation between abnormal sleep and a given disorder due to the important inter and intra variability of sleep parameters among individuals. Salient points are stressed: the high frequency of post-stroke sleep breathing disorders is becoming increasingly recognised and may, in the near future, change the way this condition is managed. Meso-diencephalic bilateral infarcts induce a variable degree of damage to both waking and non-REM sleep networks producing and abnormal waking and sometimes a stage 1 hypersomnia reduced by modafinil or bromocriptine, which can be considered as a syndrome of cathecholaminergic deficiency. Central pontine lesions induce REM and non-REM sleep insomnia with bilateral lateral gaze paralysis. Bulbar stroke leads to frequent sleep breathing disorders. Polysomnography can help define the extent of involvement of various degenerative diseases. Fragmented sleep in Parkinson's disease may be preceded by REM sleep behavioural disorders. Multiple system atrophies are characterised by important sleep disorganization. Sleep waking disorganization and a specific ocular REM pattern are often seen in supra-nuclear ophtalmoplegia. In Alzheimer patients, sleep perturbations parallel the mental deterioration and are possibly related to cholinergic deficiency. Fronto-temporal dementia may be associated with an important decrease in REM sleep. Few narcoleptic syndromes are reported to be associated with a tumour of the third ventricle or a multiple sclerosis or to follow a brain trauma; all these cases raise the question whether this is a simple coincidence, a revelation of a latent narcolepsy or, as in non-DR16/DQ5 patients, a genuine symptomatic narcolepsy. Trypanosomiasis and the abnormal prion protein precociously after sleep patterns. Polysomnography is a precious tool for evaluating brain function provided it is realised under optimal conditions in stable patients and interpreted with caution. Several unpublished cases are presented: one case of pseudohypersomnia due to a bilateral thalamic infarct and corrected by modafinil, four probable late-onset autosomal recessive cerebellar ataxias without sleep pattern anomalies, six cases of fronto-temporal dementia with strong reduction in total sleep time and REMS percentage on the first polysomnographic night, one case of periodic hypersomnia associated with a Rathke's cleft cyst and four cases of suspected symptomatic narcolepsy with a DR16-DQ5 haplotype, three of which were post-traumatic without MRI anomalies, and one associated with multiple sclerosis exhibiting pontine hyper signals on MRI.

A 62-year-old woman was admitted for a disorder of color vision. This cerebral achromatopsia was isolated, without prosopagnosia, alexia, object agnosia. MRI showed bilateral temporo-occipital infarcts, including lingual and fusiform gyrus. Neuropsychological examination and topographic hypotheses are discussed.

Sleep decreases considerably the abnormal movements seen during waking in the degenerative extra-pyramidal diseases. However, the electrophysiologic recordings reveal that muscular contractions are not completely abolished. This decrease parallels the reduction of the waking system which act likely as a non-specific system of amplification. One can notice that sleep modifies the characteristics of the parkinsonian tremor and that some palatal myoclonias persist during sleep.

A 64-year-old woman was repeatedly hospitalized for various recurrent clinical signs of central nervous system involvement. The diagnosis of primary Sjögren's syndrome was established 3 years 6 months after the onset of the disease. Sicca symptoms, as well as inflammatory biological abnormalities were absent. Moreover, both lacrymal and salivary gland secretions were affected. A high level of antinuclear antibodies to SSA and SSB was associated with inflammatory lesions in minor salivary glands biopsy samples consistent with the diagnosis of Sjögren's syndrome.

Two exceptional cases of mesencephalic lacunar infarcts located both in the anterior vascular territory are reported. In patient 1, the infarct selectively involved the red nucleus, thus resulting in a Claude's syndrome. In patient 2, the lesion was limited to the external 2/3 of the cerebral peduncle, and was responsible for a pure motor hemiplegia (PMH). CT scan easily demonstrated the lesion in both cases. Claude's syndrome is very unusual, and PMH has only been reported once before in a mesencephalic infarct. The reasons why these lesions are so uncommon are discussed.

The authors report the retrospective study of a medico-surgical series of 161 patients with intracranial meningiomas, diagnosed over a period of 9 years, with a follow-up period varying from 18 months to 9 years. Out of 185 cases studied, 24 were excluded because information or perspective were inadequate. Of the 161 cases retained, 133 (82.6%) were given surgical treatment and 28 (17.4%) were given conservative treatment because the clinical state was poor or the location was deemed inoperable. The sex ratio was 3 women to 1 man. The average age was 58 years. The most frequent locations were the convexity (27.9%) and the sphenoid ridge (24.7%). Among the clinical signs, apart from the usual general seizures or pyramidal signs should be noted the importance of psychological disorders. The operative mortality rate was 14.3% with a very high peak in the sixth decade, reaching 27%, while it was only 9% in the seventh decade and 13% in those over seventy. The internal sphenoid ridge location had a mortality rate of 31.5%, which is significantly higher than for all the other locations. Quality of survival was identical for all age groups. Complications were mainly seizures, functional deficits and psychological disorders. Recurrences were relatively few (10%), but insufficient lapse of time and the presence of only one malignant meningioma explain the lowness of this figure. The use of scanner was not determinant in our series, neither on the earliness of diagnosis, nor on prognosis, comparison of figures before and since scanning showing no significant differences.

Atheroma of the carotid bifurcation can be held responsible for 15% of the 150 000 cases of cerebrovascular attack recorded annually in France. Most of these are caused by an embolus detached from the thrombus formed around the atheromatous lesions. The natural history of asymptomatic carotid stenosis is imperfectly known because the patients are very heterogeneous. However, published series suggest that the risk of ischaemic complication in cases with more than 50% stenosis is about 0.7% per annum. No medical treatment has been tested against this disease. On the other hand, several uncontrolled studies have highlighted the therapeutic value of endarterectomy. The tendency towards surgery may become more widespread as non-invasive detection by ultrasounds is increasingly used. A randomized therapeutic trial is required to determine the value of this operation and the maximum tolerable morbidity rate. In the case of transient ischaemic attacks, a joint study on extracranial arterial occlusion has demonstrated the value of successful endarterectomy and shown that the maximum tolerable morbidity from surgery is 3%. Slightly higher figures are probably acceptable for cases with tight stenosis. Such an approach cannot determine whether endarterectomy would be of value in completed stroke, because the pathological conditions involved are extremely variable. Reasoning by analogy with transient ischaemic attacks, it would seem that tight or ulcerated stenoses could benefit from the operation some time after a regressive stroke. Ultrasonic techniques and intravenous angiography have made examination of the cervical arteries considerably easier. The risk of wounding the left carotid artery should be carefully weighed. Preoperative cardiac assessment is necessary in view of the high incidence of heart disease in the follow-up of these patients. Thus, natural history data set high standards for surgical performance and less risk for pre-operative investigations.

The symptom described as muscle weakness corrected by exercise appears to be part of the recessive form of congenital myotonia, of which it can constitute the dominant clinical manifestation in some cases. This symptom coincides with decrements of the action of potentials to repetitive stimulations in the electromyogram, which may be particularly severe in these same cases. These observations contribute to the modification and precision of the description of the recessive form of Thomsen's disease, but their pathogenicity remains unclear.

SEPs are evoked by electrical stimulation of tibial nerve in the fossa poplitea. Surface electrodes, located in S1, L4, L2, T12 with a reference in T6, can record lumbar evoked potentials and calculate a peripheral sensitive velocity. Bipolar leads between electrodes located in T12, T9, T6, T3 and C7 record medullary potential and calculate a medullary transit velocity. The cortical potential is monitored between C'z and a non-cephalic reference. 25 controls and 10 paraplegic patients are studied. In controls, sensitive peripheral velocity is 59 m/sec. The lumbar potential is composed of two negative waves, respectively due to the activation of sensitive roots and to the medullary potential. The medullary transit velocity, measured by the increase of the latency of the culmination of this negative wave along the spine, is 60 m/sec. The cortical potential is composed of two stable waves P30 N38 which are observed in every control; these waves are followed by a succession of positive and negative waves. In the 10 paraplegic patients, complete anesthesia observed in 5 cases is associated with an absence of cortical potential, and the hypoesthesia observed in 5 cases is associated with a cortical potential with a reduced amplitude (2 cases) or an increased latency (3 cases). In these last 3 cases, the medullary potential allows to specify the location of slowing of the transit velocity.