Hemorrhagic stroke after naphazoline exposition: case report Acidente vascular encefálico hemorrágico após exposição à nafazolina: relato de caso

Ten percent of all strokes are due to spontaneous cerebral hemorrhages. They are associated to drugs (licit and illicit) in 9.5% of all cases in young adults. This is a case report of a 44-year-old man, without previous morbidities, who presented a sudden onset headache and arterial hypertension 24 hours after use of naphazoline as nasal decongestant. Cranial tomography showed right thalamus hemorrhage. Cerebral angiography showed no aneurisms, vascular malformations or vasculitis. No other risk factors were found during investigation in this patient and the stroke was attributed to naphazoline exposition.<br>Dez por cento de todos os eventos vasculares encefálicos são devido às hemorragias intracerebrais espontâneas, associados a drogas (lícitas e ilícitas) em 9,5% de todos os casos em adultos jovens. Relatamos o caso de um homem de 44 anos de idade, sem doenças prévias, que apresentou cefaléia súbita e hipertensão arterial 24 horas após o uso de congestionante nasal contendo nafazolina. A tomografia de crânio evidenciou hemorragia talâmica. Durante a investigação não foram encontrados outros fatores de risco e a hemorragia foi atribuída à exposição à nafazolina

Drug screening in Scn1a zebrafish mutant identifies clemizole as a potential Dravet syndrome treatment

Dravet syndrome (DS) is a catastrophic pediatric epilepsy with severe intellectual disability, impaired social development and persistent drug-resistant seizures. One of its primary monogenic causes are mutations in Na(v)1.1 (SCN1A), a voltage-gated sodium channel. Here we characterise zebrafish Na(v)1.1 (scn1Lab) mutants originally identified in a chemical mutagenesis screen. Mutants exhibit spontaneous abnormal electrographic activity, hyperactivity and convulsive behaviors. Although scn1Lab expression is reduced, microarray analysis is remarkable for the small fraction of differentially expressed genes (~3%) and lack of compensatory expression changes in other scn subunits. Ketogenic diet, diazepam, valproate, potassium bromide and stiripentol attenuate mutant seizure activity; seven other antiepileptic drugs have no effect. A phenotype-based screen of 320 compounds identifies a US Food and Drug Administration-approved compound (clemizole) that inhibits convulsive behaviors and electrographic seizures. This approach represents a new direction in modeling pediatric epilepsy and could be used to identify novel therapeutics for any monogenic epilepsy disorder