Use of rivaroxaban in patients with stroke.

Rivaroxaban, an inhibitor of Factor Xa, is a direct oral anti-coagulant that has been found to be non-inferior to warfarin in preventing cerebral ischemia in patients with non-valvular atrial fibrillation and in the subgroup of patients with a history of the previous stroke or transient ischemic attack. Vascular neurologists in daily clinical practice may encounter patients taking rivaroxaban or patients who may benefit from its use. In this paper, we review the current clinical indications, contraindications, and clinical management guidelines for rivaroxaban while providing a special focus on neurological aspects and expert opinions on rivaroxaban therapy management in various situations that a neurologist may encounter when treating patients with an ischemic stroke (including those requiring intravenous or intra-arterial reperfusion therapy) and patients with an intracerebral hemorrhage. Since data from clinical trials and real-life data are missing in some clinical situations, strong recommendations are not always available. Nevertheless, practical guidelines should be adopted to maximize benefits from this oral anti-coagulant.

A case of Wernicke encephalopathy combined with disulfiram intoxication.

There have been several reports of disulfiram intoxication, but little evidence of neurologic conditions resulting from disulfiram-induced brain damage combined with Wernicke encephalopathy-associated lesions. We report a rare patient with both Wernicke encephalopathy and disulfiram intoxication. This 50-year-old woman, who was taking disulfiram for chronic alcohol abuse, presented with an acute confusional state, dysarthria, nystagmus, supranuclear ophthalmoplegia, and paraparesis. Biochemical serum and cerebrospinal fluid analyses were normal. An electromyogram detected a motor polyneuropathy. Cognitive assessment revealed severe impairment of memory, attention, and logical and executive abilities. Magnetic resonance imaging with gadolinium enhancement showed brain lesions consistent with Wernicke encephalopathy, but also symmetric hyperintensities on T2-weighted images in the globus pallidus. Stopping the disulfiram and treating with hydration, high-dose thiamine supplements, and benzodiazepines significantly improved the patient's consciousness and oculomotor function. A magnetic resonance imaging scan after 1 month of treatment showed complete disappearance of the brain lesions and the hyperintensities in the globus pallidus. After a further month of intensive neurorehabilitation, the patient was able to interact with the medical staff, and her neuropsychological tests showed only mild memory impairment. Patients with alcoholism who present at emergency departments are at high risk for misdiagnosis, especially because there is no specific routine laboratory test for detecting asymptomatic disulfiram intoxication. Although uncommon, the combination of Wernicke encephalopathy and disulfiram intoxication should be suspected in patients with alcoholism. The disorder can be detected through a careful history and prompt clinical evaluation, together with characteristic magnetic resonance imaging findings.