RESUMO
: Cerebrovascular events associated with marijuana use have been reported previously. This association is plausible, but not well-established yet. A 14-year-old girl, long-term heavy cannabis user, presented with generalized tonic-clonic seizures and decreased level of consciousness a few hours after smoking cannabis. Brain magnetic resonance imaging showed multiple areas of acute, subacute and chronic ischemic lesions in the left frontal lobe, basal ganglia, and corpus callosum. History of other illicit drug use and other known causes of stroke were ruled out. Cannabis might cause stroke through direct effects on the cerebral blood circulation, orthostatic hypotension, vasculitis, vasospasm, and atrial fibrillation. Long-term daily use of marijuana in young people may cause serious damage to the cerebrovascular system.
Assuntos
Cannabis/efeitos adversos , Infarto Cerebral/induzido quimicamente , Infarto Cerebral/diagnóstico por imagem , Fumar Maconha/efeitos adversos , Convulsões/induzido quimicamente , Adolescente , Feminino , HumanosRESUMO
A 3-year-old boy with Kawasaki disease developed a cerebral infarction after high-dose intravenous immunoglobulin. Aspirin did not prevent the stroke. Based on the numerous reports of thrombosis due to high-dose immunoglobulin in older individuals, we conclude that it is necessary to be aware of this complication when treating children with Kawasaki disease.
Assuntos
Infarto Cerebral/induzido quimicamente , Imunoglobulinas Intravenosas/efeitos adversos , Síndrome de Linfonodos Mucocutâneos/tratamento farmacológico , Pré-Escolar , Relação Dose-Resposta a Droga , Humanos , Imunoglobulinas Intravenosas/administração & dosagem , MasculinoRESUMO
This study demonstrates that somatostatin (SRIF), an endogenous peptide in vestibular nuclei and cerebellum, can produce both a dose-dependent death of Purkinje cells in distinct sagittal regions of cerebellar cortex and vascular infarcts centered selectively in the inferior vestibular nucleus. Alert, adult male rats were given a 5 microliters intracerebroventricular (i.c.v.) bolus of either SRIF alone (20 or 40 micrograms) or a combined dose of SRIF plus either arginine-vasopressin (AVP, 1 micrograms) or an AVP V1 antagonist, (1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)-tyrosine)-arginine 8-vasopressin (mcAVP, 1 micrograms), through an implanted cannula. After a 4-5 day survival, the brains were stained with the cupric-silver selective degeneration method. Two types of dose-dependent lesions were observed in the cerebellar and vestibular nuclei of these animals: degeneration of Purkinje cell responses in the cerebellar cortex and vascular infarcts in vestibular nuclei. These toxic responses were unaffected by application of AVP or mcAVP; hence, they can be attributed to actions of SRIF. The distribution of Purkinje cell degeneration varied with the SRIF dose in different cerebellar regions. Purkinje cell responses in lobules I-III were equivalent at both SRIF doses, and degeneration in the copula pyramis, paraflocculus and paramedian lobule emerged at the higher SRIF dose. Purkinje cells in the medial aspect of lobules IX-X had an intermediate sensitivity to SRIF intoxication. Degenerating Purkinje cells tended to be arranged in parasagittal bands in each region, suggesting parasagittal zonal variations in susceptibility to SRIF intoxication. By contrast, infarctions in the vestibular nuclei only appeared at the higher SRIF dose. These infarcts could be unilateral or bilateral and always involved the inferior vestibular nucleus at the level of the caudal margin of the acoustic tubercle; they often extended into the medial and lateral vestibular nuclei. The infarcts had a necrotic core that was infiltrated by non-neuronal elements. Thus, they appear to reflect a direct or neurally-mediated vascular response to the peptide.