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OBJECTIVE:: To describe a rare case of a patient who developed psychotic symptoms after a right stroke that disappeared with antipsychotic treatment, but appears to need low-dose maintenance antipsychotic therapy. CASE DESCRIPTION:: A 65-year-old man presented at the psychiatric emergency service with a history of persistent delusional jealousy, visual illusions and agitation with onset about 1 month after a right posterior cerebral artery ischemic stroke. These symptoms only disappeared with therapeutic dosages of an antipsychotic drug (3 mg/day of risperidone). At 2-year follow-up, he no longer had delusional activity and the antipsychotic treatment was gradually discontinued over the following year. However, 1 week after full cessation, the patient once more became agitated and suspicious and was put back on risperidone at 0.25 mg/day, resulting in rapid clinical remission. One year after the return to low-dose risperidone, the patient's psychopathology is still under control and he is free from psychotic symptoms. COMMENTS:: Psychosis is a relatively rare complication after stroke. To our knowledge, no cases of post-stroke psychosis that apparently require continuous low-dose antipsychotic treatment have been reported to date. Our case suggests that low-dose maintenance antipsychotic therapy may be needed for certain patients with post-stroke psychosis, especially for those with risk factors and non-acute onset.

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Abstract Objective: To describe a rare case of a patient who developed psychotic symptoms after a right stroke that disappeared with antipsychotic treatment, but appears to need low-dose maintenance antipsychotic therapy. Case description: A 65-year-old man presented at the psychiatric emergency service with a history of persistent delusional jealousy, visual illusions and agitation with onset about 1 month after a right posterior cerebral artery ischemic stroke. These symptoms only disappeared with therapeutic dosages of an antipsychotic drug (3 mg/day of risperidone). At 2-year follow-up, he no longer had delusional activity and the antipsychotic treatment was gradually discontinued over the following year. However, 1 week after full cessation, the patient once more became agitated and suspicious and was put back on risperidone at 0.25 mg/day, resulting in rapid clinical remission. One year after the return to low-dose risperidone, the patient's psychopathology is still under control and he is free from psychotic symptoms. Comments: Psychosis is a relatively rare complication after stroke. To our knowledge, no cases of post-stroke psychosis that apparently require continuous low-dose antipsychotic treatment have been reported to date. Our case suggests that low-dose maintenance antipsychotic therapy may be needed for certain patients with post-stroke psychosis, especially for those with risk factors and non-acute onset.

Resumo Objetivo: Descrever o caso raro de um paciente que desenvolveu sintomas psicóticos após um acidente vascular cerebral (AVC) no nível do hemisfério direito que remitiram com tratamento antipsicótico, mas parece precisar de uma terapêutica de manutenção com antipsicótico em baixa dosagem. Descrição de caso: Um homem de 65 anos apresentou-se no serviço de urgência psiquiátrica por um quadro persistente de delírio de ciúmes, ilusões visuais e agitação com início cerca de 1 mês após AVC isquêmico no nível da artéria cerebral posterior direita. Esses sintomas só desapareceram com doses terapêuticas de antipsicótico (risperidona 3 mg/dia). Após 2 anos de seguimento, o paciente não mais apresentava atividade delirante, e o tratamento antipsicótico foi progressivamente descontinuado durante o ano seguinte. No entanto, 1 semana após a suspensão total, o paciente começou a ficar agitado e desconfiado, tendo-se reiniciado a risperidona 0,25 mg/dia, com rápida remissão clínica. O paciente está medicado com esta baixa dose de antipsicótico há um ano, permanecendo psicopatologicamente compensado e sem sintomas psicóticos. Comentários: A psicose é uma complicação relativamente rara após AVC. Segundo nosso conhecimento, não há casos descritos até ao momento de psicose após AVC que, aparentemente, requerem uma dose baixa contínua de antipsicótico. Nosso caso sugere que uma terapêutica de manutenção com antipsicótico em baixa dosagem pode ser necessária para determinados pacientes com psicose após AVC, especialmente para aqueles com fatores de risco e início não agudo dos sintomas.

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OBJECTIVE: To assess whether acute findings of cerebral arteriopathy, large infarct, and acutely elevated plasma D-dimer levels are independently prognostic of poor long-term neurologic outcome as measured at ≥ 1 year post-event in children with arterial ischemic stroke (AIS). STUDY DESIGN: Sixty-one patients with childhood-onset (ie, >28 days of life) AIS were enrolled in a single-institution cohort study at Children's Hospital Colorado between February 2006 and June 2011. Data on demographic and diagnostic characteristics, antithrombotic treatments, and outcomes were systematically collected. RESULTS: Cerebral arteriopathy and D-dimer levels >500 ng/mL (a measure of coagulation activation) were identified acutely in 41% and 31% of the cohort, respectively. Anticoagulation was administered in the acute period post-event in 40% of the children, in the subacute period in 43%, and in the chronic period in 28%. When not receiving anticoagulation, patients were routinely treated with aspirin 2-5 mg/kg once daily for a minimum of 1 year. Death, major bleeding (including intracranial hemorrhage), and recurrent AIS were infrequent. The Pediatric Stroke Outcome Measure at 1 year demonstrated poor outcome in 54% of the children. Acute cerebral arteriopathy and elevated D-dimer level were identified as putative prognostic factors for poor outcome; after adjustment for D-dimer, arteriopathy was an independent prognostic indicator (OR, 19.0; 95% CI, 1.6-229.8; P = .02). CONCLUSION: Arteriopathy and coagulation activation are highly prevalent in the acute period of childhood AIS. Although recurrent AIS and intracranial hemorrhage were infrequent in our cohort, one-half of children experienced a poor neurologic outcome at 1 year, the risk of which was increased by acute arteriopathy. Substantiation of these findings in multi-institutional cohort studies is warranted, toward risk stratification in childhood-onset AIS.

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Extensive narrowing of lumens of many cerebral arteries caused strokes with brain damage and chronic hemipareses in two children with Williams syndrome. Increased irritability, loss of consciousness, and seizures were initial signs. Arterial stenoses are not limited to the supravalvular aorta and pulmonary arteries in patients with Williams syndrome.

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Giant aneurysms have rarely been reported in association with intractable complex partial seizures (CPS). We report a 30-year-old man with intractable CPS since age 18 years. Seizure onset was electrically localized to right temporal lobe. Preoperative neuroimaging studies showed a partially thrombosed giant aneurysm of the right posterior cerebral artery. Selective amygdalohippocampectomy and occlusion of the posterior cerebral artery did not cause deficits. The patient has been seizure-free for 15 months after operation. We review the relevant literature on aneurysms as a cause of epilepsy.

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Three patients with unusual presentations of basilar artery ectasia are described: subarachnoid hemorrhage was manifest in one and autonomic dysfunction developed in the other two. Aneurysmal rupture was the cause in the first patient, while compression of the brainstem and/or of the baroreceptor afferences of the IXth and Xth cranial nerves is postulated to be responsible for the symptoms found in the other two. Basilar artery aneurysms should be considered in cases with subarachnoid hemorrhage or autonomic dysfunction, particularly when diagnostic procedures fail to disclose other possible etiologies.

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A 16-mo-old girl is described with acute hemiplegia associated with virologic and serologic evidence of Coxsackie A9 infection. Possibilities of pathogenesis are discussed. It is suggested that the present hemiplegia may have been the result of a focal vasculitis due to Coxsachie A9 viral infection in the region of the middle cerebral artery.

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