18 research outputs found

    MĂ©ningo-EncĂ©phalite HerpĂ©tique CompliquĂ©e D’un Syndrome De KlĂŒver-Bucy: A Propos D’un Cas

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    Le syndrome de KlĂŒver-Bucy est un syndrome neuropsychologique trĂšs rare qui rĂ©sulte d’une atteinte temporale bilatĂ©rale et caractĂ©risĂ© par une hyperoralitĂ©, une hypersexualitĂ©, une placiditĂ© Ă©motionnelle, une agnosie visuelle, une hypermĂ©tamorphosie et un changement du comportement alimentaire. Les Ă©tiologies du syndrome de KlĂŒver-Bucy sont multiples parmi lesquelles les causes infectieuses notamment une mĂ©ningo-encĂ©phalite herpĂ©tique. Le pronostic fonctionnel est gĂ©nĂ©ralement sombre mĂȘme si un traitement adaptĂ© de la cause est effectuĂ© prĂ©cocement. Nous rapportons le cas d’un patient de 31 ans qui Ă©tait admis pour des cĂ©phalĂ©es inhabituelles fĂ©briles et une confusion de survenue aiguĂ« chez qui l’électroencĂ©phalogramme et l’IRM cĂ©rĂ©brale Ă©taient en faveur d’une mĂ©ningo-encĂ©phalite herpĂ©tique. Le PCR HSV1 Ă©tait positif dans le LCR. Dans les suites, il a prĂ©sentĂ© un tableau neuropsychologique compatible avec un syndrome de KlĂŒver-Bucy dont l’évolution restait sans grande amĂ©lioration malgrĂ© un traitement Ă©tiologique et symptomatique prĂ©coces et adĂ©quats. Le syndrome de KlĂŒver-Bucy compliquant une mĂ©ningo-encĂ©phalite herpĂ©tique est le plus souvent de mauvais pronostic fonctionnel mĂȘme si une prise en charge adĂ©quate de la mĂ©ningoencĂ©phalite herpĂ©tique est faite. KlĂŒver-Bucy syndrome is a very rare neuropsychological syndrome that results from bilateral temporal impairment and characterized by hyperorality, hypersexuality, emotional placidity, visual agnosia, hypermetamorphose and a change in dietary behaviour. The etiologies of KlĂŒver-Bucy syndrome are multiple, including infectious causes including herpetic meningo-encephalitis. The functional prognosis is generally bleak even if treatment of the cause is done early. We report the case of a 31-yearold patient who was admitted for febrile unusual headaches and acute occurrence confusion in whom electroencephalogram and brain MRI were in favor of herpetic meningo-encephalitis. PCR HSV1 was positive in the LCR. In the suites, he presented a neuropsychological picture compatible with KlĂŒver-Bucy whose evolution remained without much improvement despite an early and adequate etiological and symptomatic treatment. The syndrome of Kliver-Bucy complicating a herpetic meningo-encephalitis is most often of bad functional prognosis even if adequate management of herpetic meningoencephalitis is made

    Opportunistes du VIH/SIDA en milieu hospitalier neurologique au Togo

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    IntroductionLa morbi-mortalitĂ© au cours du VIH/sida est souvent liĂ©e Ă  des infections opportunistes (IO)  neurologiques. L’objectif de cette Ă©tude est de dĂ©terminer en milieu hospitalier neurologique au Togo, les principales IO et celles qui sont liĂ©es Ă  un fort taux de lĂ©talitĂ©.MĂ©thodesIl s’agissait d’une Ă©tude descriptive transversale sur 12 mois rĂ©alisĂ©e dans le service de neurologie du CHU Campus de LomĂ© de janvier Ă  dĂ©cembre 2008. Les patients hospitalisĂ©s et prĂ©sentant une IO avec une sĂ©rologie VIH positive avaient Ă©tĂ© inclus. Le diagnostic des IO a Ă©tĂ© fondĂ© sur la clinique et/ou les examens disponibles. Les examens paracliniques tout comme les frais d’hospitalisation Ă©taient Ă  la charge des patients.RĂ©sultatsSur 940 patients hospitalisĂ©s, 360 (38%) ont bĂ©nĂ©ficiĂ© d’une sĂ©rologie au VIH et 68 Ă©taient positifs soit 7% des hospitalisĂ©s. Au sein des patients vivant avec le VIH (PVVIH), nous avons notĂ© 66 cas d’IO (97% des PVVIH) et un taux de dĂ©cĂšs de 41% (28/68). Le dĂ©ficit neurologique focal, les cĂ©phalĂ©es et les crises convulsives Ă©taient les motifs d’admission les plus frĂ©quents. La toxoplasmose cĂ©rĂ©brale et la cryptococcose neuromĂ©ningĂ©e (CNM) Ă©taient les IO les plus frĂ©quentes touchant respectivement 54% et 10% des patients vivant avec le VIH (PVVIH). Le taux de lĂ©talitĂ© Ă©tait de 33% pour la toxoplasmose cĂ©rĂ©brale et de 28% pour la CNM.ConclusionLa CNM et la toxoplasmose cĂ©rĂ©brale sont les IO Ă  Ă©voquer en cas d’atteinte du systĂšme nerveux central chez le PVVIH

    Wallenberg Syndrome secondary to bilateral vertebral artery dissection and thrombosis

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    The Wallenberg syndrome or lateral medullar syndrome (LMS) is also known as posterior inferior cerebellar artery syndrome. It‘s a  dangerous affection because of his gravity for vital prognostic by the paralysis of cranial nerves. Occlusion of these vessels may be due to stenosis from arteriosclerosis/emboli or arterial dissection. The artery dissection may be spontaneous or after trauma is an important and often treatable cause of the stroke in younger people. The Magnetic Resonance Imagine diffusion weighted inversion (MRI-DWI), the  Magnetic Resonance Angiography (MRA) sequence FAT/SAT and the computed tomography (CT) angiography of the brain allow quickly to the diagnosis. The antithrombotic treatment (antiplatelet drug) and low-molecular weight heparins allow to reduce the neurological  sequelea. So we report two cases of Wallenberg‘s syndrome caused by spontaneous bilateral vertebral dissection and vertebral thrombosis and their clinical, prognostic and therapeutic aspects. A 34-years-old woman, no cardiopathy factors only obesity, no trauma, admitted for acute vomiting, vertigo, neck pain and weakness earlier in themorning and MRA FAT/SAT showedbilateral vertebral artery dissections without an evident posterolateral medulla infarct on MRI-DWI. A 48-year-old man, cumulated cardiopathy factors risks,  admitted with sudden vertigo, disequilibrium and neck pain. The MRI-DWI showed an acute left posterolateral medulla infarct and the CT angiography revealed thesevere left vertebral artery thrombosis. They were treated by the antithrombotic drugs (antiplatelet drugs) and low-molecular weight heparins. In front of a sudden neck pain and vertigo, think about Wallenberg‘s syndrome and do quickly an imaging. French title: Syndrome de Wallenberg secondaire a une thrombose et une dissection vertebrale bilateral

    Delayed early primary visual pathway development in premature infants: high density electrophysiological evidence.

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    In the past decades, multiple studies have been interested in developmental patterns of the visual system in healthy infants. During the first year of life, differential maturational changes have been observed between the Magnocellular (P) and the Parvocellular (P) visual pathways. However, few studies investigated P and M system development in infants born prematurely. The aim of the present study was to characterize P and M system maturational differences between healthy preterm and fullterm infants through a critical period of visual maturation: the first year of life. Using a cross-sectional design, high-density electroencephalogram (EEG) was recorded in 31 healthy preterms and 41 fullterm infants of 3, 6, or 12 months (corrected age for premature babies). Three visual stimulations varying in contrast and spatial frequency were presented to stimulate preferentially the M pathway, the P pathway, or both systems simultaneously during EEG recordings. Results from early visual evoked potentials in response to the stimulation that activates simultaneously both systems revealed longer N1 latencies and smaller P1 amplitudes in preterm infants compared to fullterms. Moreover, preterms showed longer N1 and P1 latencies in response to stimuli assessing the M pathway at 3 months. No differences between preterms and fullterms were found when using the preferential P system stimulation. In order to identify the cerebral generator of each visual response, distributed source analyses were computed in 12-month-old infants using LORETA. Source analysis demonstrated an activation of the parietal dorsal region in fullterm infants, in response to the preferential M pathway, which was not seen in the preterms. Overall, these findings suggest that the Magnocellular pathway development is affected in premature infants. Although our VEP results suggest that premature children overcome, at least partially, the visual developmental delay with time, source analyses reveal abnormal brain activation of the Magnocellular pathway at 12 months of age

    Prevalence hospitaliere et facteurs de risque de la thrombose veineuse cerebrale au Togo

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    Introduction: Les thromboses veineuses cĂ©rĂ©brales (TVC) sont des cas spĂ©cifiques d’accidents vasculaires cĂ©rĂ©braux. Elles prĂ©sentent une sĂ©miologie variable selon la topographie veineuse. Les situations Ă  risque sont nombreuses, dominĂ©es dans notre contexte par les causes infectieuses, hĂ©matologiques, post-opĂ©ratoires et le pĂ©ripartum.Objectif: DĂ©terminer la prĂ©valence hospitaliĂšre des TVC, les facteurs de risque et les variantes topographiques Ă  l’imagerie.MĂ©thodes d’étude: Il s’agissait d’une Ă©tude transversale rĂ©trospective entre le 12 juin 2015 et 11 juin 2016. Nous avons inclus dans cette Ă©tude les patients admis dans le service de neurologie et pour lesquels le scanner cĂ©rĂ©bral avait montrĂ© un infarctus ne correspondant pas Ă  un territoire artĂ©riel, proche d’un sinus veineux, lorsqu’il avait une composante hĂ©morragique, ou une hĂ©morragie intra-parenchymateuse atypique pour une origine hypertensive. Le diagnostic de TVC Ă©tait confirmĂ© par l’IRM. Nous avons exclu les patients dont le scanner cĂ©rĂ©bral montrait des lĂ©sions hypodenses avec une prise de contraste annulaire ou qui ne respectaient pas de territoire veineux ou situĂ©es Ă  distance de sinus veineux.RĂ©sultats: Durant la pĂ©riode d’étude, 1070 patients avaient Ă©tĂ© hospitalisĂ©s pour un accident vasculaire cĂ©rĂ©bral. Cinq cas de TVC avaient Ă©tĂ© diagnostiquĂ©s soit une prĂ©valence hospitaliĂšre de 0, 46 %. L’ñge moyen Ă©tait de 40 ans (sex-ratio 0,6) avec une prĂ©dominance fĂ©minine. Les facteurs de risque Ă©taient l’alcoolisme chronique, le VIH /SIDA. Les territoires veineux atteints Ă©taient principalement le sinus sagittal supĂ©rieur, le sinus droit, les sinus latĂ©raux. La TVC Ă©tait hĂ©morragique dans 60% des cas. La mortalitĂ© Ă©tait Ă©levĂ©e (60%). La durĂ©e moyenne d’évolution des symptĂŽmes avant l’admission en neurologie Ă©tait de 1 mois.Conclusion: La TVC est mal connue dans nos structures sanitaires et le diagnostic est souvent fait tardivement.Mots clĂ©s: Thrombose veineuse cĂ©rĂ©brale, prĂ©valence, facteurs de risqueEnglish Title: Hospital prevalence of cerebral venous thrombosis and risk factors in TogoEnglish AbstractObjective: To determine the hospital prevalence of CTVs, risk factors and topographic variants in imaging.Methods: This was a retrospective cross-sectional study between June 12, 2015 and June 11, 2016. The study included patients admitted in the neurology department.with a brain scan displaying an infarct not of an arterial origin, close to a venous sinus, sometimes with a haemorrhagic component, or an atypical intraparenchymal hemorrhage not for a hypertensive origin. The diagnosis of CVT was confirmed by MRI. We excluded patients with hypodense lesions with annular contrast, or without respecting venous topography or located far from the venous sinus.Results: During the study period, 1070 patients were admitted for stroke. Five cases of CVT were diagnosed. The CVT hospital prevalence was of 0.46%. The mean age was 40 years (sex ratio 0.6) with a female predominance. Risk factors were chronic alcoholism, HIV/AIDS infection. The affected venous territories were mainly the upper sagittal sinus, the straight sinus, the lateral sinuses. CVT was hemorrhagic in 60% of cases. Mortality was high (60%). The mean duration between the symptoms onset to the hospital admission was of 1 month.Conclusion: CVT is poorly described in our health facilities and the diagnosis is often delayed.Keywords: Cerebral venous thrombosis, prevalence, risk factor

    Case report: an area postrema syndrome revealing a neuromyelitis optica spectrum disorder associated with central nervous system tuberculosis in a young Togolese (black African) woman

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    Abstract Background Area postrema syndrome (APS) is considered to be one of the most specific clinical presentations of neuromyelitis optica spectrum disorders (NMOSDs). In sub-Saharan Africa, NMOSDs and even more so those revealed by an APS, are rarely reported. However, studies among mixed populations have shown that NMOSDs disproportionately affect black people with relatively more frequent encephalic involvement. We report a case of APS revealing an NMOSD associated with central nervous system (CNS) tuberculosis in a young Togolese woman residing in Togo (West Africa). Case presentation A 28-year-old Togolese woman was admitted for left hemibody sensory problems with ataxia. These problems were observed while the patient was hospitalized for a few days in the hepato-gastroenterology department for persistent vomiting, abdominal pain and hiccups lasting for about a month. The examination confirmed left hemibody ataxia with nystagmus when looking to the left, pronounced left osteotendinous reflexes, and left hemibody hypoesthesia up to the base of the neck. Encephalic magnetic resonance imaging (MRI) showed a hypersignal lesion in the bulbar more lateralized on the left in the fluid-attenuated inversion recovery sequence, not enhanced after a gadolinium injection. Biological assessment showed the presence of Mycobacterium tuberculosis deoxyribonucleic acid in the cerebrospinal fluid and a sedimentation rate of 120 mm in the 1st hour. The result of the anti-AQP4 antibody test was positive. Two months from the onset of digestive problems with Lhermitte’s sign and hand and foot contracture access without vesico-sphincter problems were established. Cervical medullary MRI showed an additional intramedullary hypersignal lesion in the T2 sequence at the C2 level, not enhanced after a gadolinium injection. A second course of intravenous corticosteroids was administered, and anti-tuberculosis treatment was continued. The outcome was favorable. After 8 months of anti-tuberculosis treatment, the patient started immunosuppressive therapy (azathioprine 50 mg twice daily) to limit the risk of recurrence of NMOSD. Conclusion The recognition of an APS is an additional challenge for the diagnosis of NMOSDs, especially in countries with limited resources. CNS tuberculosis must be tested when faced with an NMOSD because it seems to be a major cause

    Carotid Dissection and Isolated Paralysis of Ipsilateral Half Tongue: Clinical Cases

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    Objective. We report two cases of carotid dissection revealed by isolated paralysis of the ipsilateral half tongue. Observations. First patient, 52 years old, with no particular medical or surgical history, presented with isolated paralysis of the left half tongue preceded by two weeks of moderate-intensity cervicalgia and having been the subject to cervical manipulation. MRI revealed dissection of the left internal carotid artery in its prepetrous portion. The evolution after 6 weeks of platelet aggregating inhibitors treatment was favorable. The second patient, 74 years old, with no particular medical or chirurgical history, presented with a sudden onset of paralysis of the left half tongue preceded by unusual headaches associated with neck pain. Brain MRI showed aneurysmal ectasia of the left internal carotid with parietal irregularity suggestive of carotid dissection. The evolution after four weeks of treatment with anticoagulant was favorable. Conclusion. Carotid dissection revealed by isolated paralysis of the half tongue is rare. It is generally of good prognosis. However, in paralysis of half tongue, it must be urgently sought and treated to reduce the risk of a transient or constituted ischemic accident

    Demographic and clinical data.

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    <p>N  =  number of participants included in the analyses; mo  =  months; w  =  weeks; SD  =  standard deviation; g  =  grams.</p><p>Demographic and clinical data.</p
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