RESUMO
A variety of toxins cause parkinsonism and the lesions are primarily in the pallidostriatum. It usually does not respond to levodopa. We experienced a patient whose parkinsonian features developed after accidental acetone ingestion. She had rigidity, bradykinesia, gait disturbance and her speech was sluggish. Brain MRI showed bilateral basal ganglionic lesions. She was treated with levodopa and her neurological symptoms improved. To our knowledge, there has not been any previous reports of acetone causing parkinsonism. Acetone may cause parkinsonism by damaging the basal ganglia.
Assuntos
Humanos , Acetona , Gânglios da Base , Encéfalo , Ingestão de Alimentos , Marcha , Cistos Glanglionares , Hipocinesia , Levodopa , Imageamento por Ressonância Magnética , Transtornos ParkinsonianosRESUMO
Candida species is an uncommon pathogen and usually causes meningitis as a nosocomial infection. We report a case where a ventriculoperitoneal shunt was placed in a 72-year-old woman with hydrocephalus. Three months later, the patient was referred to the department of neurology due to fever and drowsiness. Candida parapsilosis was cultured in the cerebrospinal fluid as the causative agent of meningitis. Candida species should be considered as a pathogen when meningitis is present in severely ill patients with ventriculoperitoneal shunts.
Assuntos
Idoso , Feminino , Humanos , Candida , Líquido Cefalorraquidiano , Infecção Hospitalar , Febre , Hidrocefalia , Meningite , Neurologia , Fases do Sono , Derivação VentriculoperitonealRESUMO
BACKGROUND: Previous studies suggest that impaired cerebral hemodynamics may play a relevant but unclear role in the occurrence of stroke in patients with carotid artery occlusion.. The purpose of the current study was to investigate the relationship between hemodynamic disturbances and cerebrovascular events in patients with major cerebral artery occlusions. METHODS: We examined hemodynamic disturbances as cerebrovascular reactivity (CVR) to acetazolamide (ACZ), judged with single-photon emission CT (SPECT) and an ACZ challenge in 21 patients with internal carotid artery or middle cerebral artery occlusions who had transient ischemic attacks/minor or asymptomatic infarctions. CVR was calculated by a regional cerebral blood flow (rCBF) ratio on pre-ACZ-SPECT minus the rCBF ratio on post-ACZSPECT. They were followed longer than 2 years and the mean follow-up duration was 36 months. We compared the hemodynamic disturbances and risk factors between the ipsilateral stroke recurrance group and a stable group. RESULTS: Eight patients had additional ischemic events during the follow-up period, and all but 2 events occurred ipsilaterally to the carotid artery occlusions. Two patients died of acute myocardial infarction and brainstem infarction, retrospectively. All patients with recurred stroke or death were noted to have symptomatic carotid artery occlusions. There was no significant difference of risk factors between the two groups. But the ipsilateral stroke recurrance group had worse CVR than the stable group (p<0.05). CONCLUSIONS: These data suggest impaired CVR was significantly associated with the risk of ischemic events in patients with carotid artery occlusions.