IntroductionRecurrent hypersomnia (RH) is a rare disorder without established treatment.MethodsWe report 2 RH medication-responsive cases with typical characteristics of Kleine–Levin syndrome (KLS).Case-reportsA 10 y.o. girl and a 14 y.o. boy presented with sudden sleepiness for 3–9 days (every 2–3 weeks). Physical examination, brain images and blood tests were normal. Polysomnographic findings were heterogenous, including disrupted sleep architecture. MSLTs revealed 2–3 SOREMPs and short sleep latency. Carbamazepine rendered girl׳s sleep normalization, while risperidone normalized boy׳s sleep cycles.ConclusionsFacing the absence of clinical trials in RH, reports of responsive cases are the available therapeutic evidence.
Tuberculosis is a chronic bacterial infection caused by Mycobacterium tuberculosis.Despite advances in treatment, resistant strains and unusual sites of involvement have been diagnosed. We present a case of a 13-year-old patient in treatment for tuberculous meningitis who presented with progressive paraparesis. The MRI showed two intramedullary nodular lesions at T4-T6 levels, isointense with annular hyperintensity on T1W, hypointense on T2W, becoming hypointense with ring enhancement after contrast. These characteristics differ from those usually described for intramedullary tuberculomas. Surgical excision was performed, confirming the diagnosis of intramedullary tuberculoma. The formation of intramedullary tuberculomas is rare, with a ratio of two cases per thousand diagnosed with CNS tuberculosis, and the thoracic spine is most frequently affected. The clinical picture is of progressive subacute spinal cord compression, and it may lead to paraplegia. At MRI, the lesion in early stage appears as hypointense rings on T1W and hyperintense on T2W, with homogeneous enhancement after contrast. After the formation of the solid caseous granuloma, it becomes isointense on T1W and hypointense on T2W with homogeneous enhancement after contrast. When the center of the granuloma becomes liquefied, it shows hypointense sign on T1W and hyperintense with peripheral enhancement on T2W. The treatment of choice is medical, with the current protocol including rifampin, isoniazid, pyrazinamide, and ethambutol. Surgery is reserved for cases of progressive neurologic
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