Aspects clinico-neurophysiologiques des troubles du sommeil dans une population d'adultes jeunes entre 18-35 ans / Clinical-neurophysiological aspects of sleep disorders in a population of young adults aged 18-35 years

Contexte et objectifs : L'accès aux tests neurophysiologiques pour le diagnostic des Troubles du Sommeil (TS) est très limité dans les pays d'Afrique subsaharienne. La présente étude avait pour objectif de déterminer les caractéristiques épidémiologiques, cliniques et neurophysiologiques des (TS) dans un groupe de jeunes adultes. Méthodes : Il s'est agi d'une étude descriptive d'une série de cas, réalisée au centre de Médecine du sommeil et des maladies respiratoires de l'hôpital de la Croix-Rousse de Lyon du 1er janvier au 31 mars 2019. Les patients hospitalisés pendant cette période pour l'exploration d'un (TS) ont été sélectionnés. Etaient éligibles ceux dont l'âge était compris entre 18 et 35 ans, des deux sexes, ayant renseigné un questionnaire et ayant bénéficié au minimum d'une polysomnographie (PSG). Résultats : Quatre-vingt-onze patients étaient examinés. Les femmes étaient les plus affectées (59,3 %). Leur âge moyen était de 26,6 ± 5 ans. La PSG a incriminé le Syndrome d'Apnée Hypopnée Obstructive du sommeil (SAHOS) comme étiologie principale (66 %). Pour les patients sans SAHOS, 38,7 % avaient une PSG normale et la PSG avec d'autres tests de sommeil ont objectivé, pour le reste (61,3 %), d'autres types de (TS). La dépression (50,7 %) et la fatigue chronique (84,6 %) étaient très fréquentes. L'indice d'efficacité du sommeil était faible pour 70 % des patients avec SAHOS. Il y avait un déséquilibre de la durée des stades du sommeil, augmentée pour le sommeil lent léger et diminuée pour le sommeil lent profond dans la population avec SAHOS, tandis que la durée du sommeil paradoxal chez ceux sans SAHOS était augmentée. Conclusion Le SAHOS est fréquent dans cette formation hospitalière, avec des répercussions significatives à type de dépression et de fatigue chronique. Il est important que des mesures rendant accessible l'usage des tests d'exploration du sommeil particulièrement en Afrique au sud du Sahara, soient mises en place pour diagnostiquer ces troubles

Context and objective. Access to neurophysiological tests for diagnostic of sleep disorders (SD) is very limited in Sub-Saharan Africa countries. The objective was to determine the epidemiological, clinical and neurophysiological characteristics of SD in a young adult group. Methods. This was a descriptive serial cases study carried out at the Sleep Medicine and Respiratory Diseases Center of the CroixRousse hospital of Lyon between January 1st and March 31th, 2019. Patients hospitalized during this period with tests for SD were selected. Eligible were those aged between 18 and 35 years, both sexes, who completed a questionnaire and who received at least a polysomnography (PSG). Results. Ninety-one patients were involved. Women remained the most affected (59.3%). Mean age was 26.6±5 years. PSG incriminated obstructive sleep apnea (OSA) syndrome as the primary etiology (66%). For patients without OSA, 38.7% had normal PSG. For the remaining 61.3% of patients, other types of SD were found using PSG with various sleep tests. Depression (50.7%) was an important comorbidity, and chronic fatigue (84.6%) was the most frequent complaint. Sleep efficiency index was low for 70% of sleep apnea patients. There was an imbalance in the duration of sleep stages, with an increase in light slow-wave sleep in the OSA population and a decrease in their deep slow-wave sleep, while REM sleep duration in patients without OSA was increased. Conclusion: OSA was the primary etiology in our study, with significant repercussions like depression and chronic fatigue. Public health measures such as increasing access to the use of sleep exploration tests, especially in subSaharan Africa, should be put in place for the diagnosis of these sleep disorders and their consequences

Managing neurocysticercosis: challenges and solutions.

Taenia solium neurocysticercosis (NCC) is a major cause of neurological morbidity in the world. Variability in the neuropathology and clinical presentation of NCC often make it difficult to diagnose and manage. Diagnosis of NCC can be challenging especially in endemic and resource-limited countries where laboratory and imaging techniques are often lacking. NCC management can also be challenging as current treatment options are limited and involve symptomatic agents, antiparasitic agents, or surgery. Although antiparasitic treatment probably reduces the number of active lesions and long-term seizure frequency, its efficacy is limited and strategies to improve treatment regimens are warranted. Treatment decisions should be individualized in relation to the type of NCC. Initial measures should focus on symptomatic management, with antiparasitic therapy only to be considered later on, when appropriate. Symptomatic treatment remains the cornerstone in NCC management which should not only focuses on epilepsy, but also on other manifestations that cause considerable burden (recurrent headaches, cognitive decline). Accurate patients' categorization, better antiparasitic regimens, and definition of new clinical outcomes for trials on NCC could improve management quality and prognosis of NCC. Prevention strategies targeting tapeworm carriers and infected pigs are yielding good results in local models. If local elimination of transmission is confirmed and replicated, this will open the door to cysticercosis eradication efforts worldwide.

Late onset epilepsy associated with marijuana abuse: a case report with MRI findings.

Marijuana is the most widely used illicit substance in the world. The relation between marijuana use and epileptic seizures is still controversial. We report a case of late onset epilepsy associated with marijuana abuse, with brain magnetic resonance imaging (MRI) findings. A 44-year-old patient was admitted for 03 isolated episodes of secondary generalized tonic-clonic seizures. He had a history of 26 years regular marijuana smoking. On admission, we found a tachycardia, psychomotor slowing, asymmetric hyperreflexia, bilateral Babinski sign without weakness. Laboratory work-up showed a high level of urine of Δ-9-tétrahydroxycannabinol. Electroencephalogram was normal. Brain MRI revealed abnormal signal intensities in the right frontal lobe and basal ganglia. Seizures cessation was obtained with anti-epileptic treatment. We suggest that marijuana abuse through vascular and toxic mechanisms could explain seizures in this case.

Cerebral neurocysticercosis mimicking or comorbid with episodic migraine?

BACKGROUND: Neurocysticercosis is a major cause of neurological symptoms in developing countries. We report a case of cerebral neurocysticercosis presenting as episodic migraine without aura, with clinico-radiological correlations and discuss the possible causal influence of neurocysticercosis on the pathomechanisms of migraine. CASE PRESENTATION: We report a 24 year-old male consulting for a one year history of recurrent headaches. He described bilateral frontal and/or temporal attacks of throbbing headache, moderate to severe in intensity, worsened by head movements and accompanied by nausea, photophobia and phonophobia. Attacks lasted between 12 and 60 hours if untreated. He never had symptoms suggestive of a migraine aura or an epileptic seizure. Headache attacks progressively increased in frequency to up to 5 to 7 severe attacks per month. On taking history, the patient reported having consumed undercooked porcine meat. Physical examination was unremarkable. A brain CT scan showed two contiguous occipital cystic lesions with ring enhancement and surrounding edema suggestive of cerebral neurocysticercosis. On laboratory work-up, blood serology for cysticercal antibodies was positive. Full blood count, erythrocyte sedimentation rate, c - reactive protein level, human immunodeficiency virus serology, liver and hepatic function were all normal. Albendazole (1000 mg/day) and prednisolone (60 mg/day) were prescribed for seven days. The patient was examined again two and six months after the end of his treatment and there was a significant reduction in headache severity and frequency. CONCLUSION: We propose that in our patient the occipital neurocysticercosis lesions cause migraine without aura-like attacks via inflammation in the surrounding brain parenchyma leading to sensitization of the trigemino-vascular system. We cannot rule out, however, the possibility that our patient has a genetic predisposition for migraine without aura and that the fortuitous association of neurocysticercosis is simply an aggravating factor of his migraine.