RESUMO
Viral encephalitis causes an altered level of consciousness, which may be associated with fever, seizures, focal deficits, CSF pleocytosis, and abnormal neuroimaging. Potential pathogens include HSV, VZV, enterovirus, and in some regions, arboviruses. Autoimmune (eg, anti-NMDA receptor) and paraneoplastic encephalitis are responsible for some cases where no pathogen is identified. Indications for ICU admission include coma, status epilepticus and respiratory failure. Timely initiation of anti-viral therapy is crucial while relevant molecular and serological test results are being performed. Supportive care should be directed at the prevention and treatment of cerebral edema and other physiological derangements which may contribute to secondary neurological injury.
Assuntos
Aciclovir/administração & dosagem , Antivirais/uso terapêutico , Encefalite Viral , Encefalomielite Aguda Disseminada/etiologia , Viremia/etiologia , Aciclovir/efeitos adversos , Aciclovir/uso terapêutico , Corticosteroides/administração & dosagem , Corticosteroides/efeitos adversos , Corticosteroides/uso terapêutico , Anticonvulsivantes/administração & dosagem , Anticonvulsivantes/uso terapêutico , Antivirais/administração & dosagem , Antivirais/efeitos adversos , Encefalopatias/tratamento farmacológico , Encefalopatias/etiologia , Edema Encefálico/etiologia , Edema Encefálico/prevenção & controle , Transtornos da Consciência/etiologia , Transtornos da Consciência/virologia , Encefalite , Encefalite Viral/complicações , Encefalite Viral/tratamento farmacológico , Encefalite Viral/epidemiologia , Encefalite Viral/virologia , Encefalomielite Aguda Disseminada/tratamento farmacológico , Encefalomielite Aguda Disseminada/virologia , Escala de Coma de Glasgow , Síndrome de Guillain-Barré/etiologia , Síndrome de Guillain-Barré/virologia , Doença de Hashimoto/tratamento farmacológico , Doença de Hashimoto/etiologia , Humanos , Unidades de Terapia Intensiva/estatística & dados numéricos , Síndromes Paraneoplásicas do Sistema Nervoso/tratamento farmacológico , Síndromes Paraneoplásicas do Sistema Nervoso/etiologia , Síndromes Paraneoplásicas do Sistema Nervoso/virologia , Convulsões/tratamento farmacológico , Convulsões/etiologia , Convulsões/virologia , Estado Epiléptico/tratamento farmacológico , Estado Epiléptico/etiologia , Estado Epiléptico/virologia , Viremia/virologiaAssuntos
Carcinoma Pulmonar de Células não Pequenas/complicações , Ataxia Cerebelar/virologia , Cerebelo/virologia , Síndromes Paraneoplásicas do Sistema Nervoso/virologia , Febre do Nilo Ocidental/complicações , Ataxia Cerebelar/diagnóstico , Ataxia Cerebelar/fisiopatologia , Cerebelo/patologia , Cerebelo/fisiopatologia , Diagnóstico Diferencial , Evolução Fatal , Febre/virologia , Humanos , Imunoglobulina M/sangue , Imunoglobulina M/imunologia , Masculino , Pessoa de Meia-Idade , Síndromes Paraneoplásicas do Sistema Nervoso/diagnóstico , Síndromes Paraneoplásicas do Sistema Nervoso/fisiopatologia , Febre do Nilo Ocidental/diagnóstico , Febre do Nilo Ocidental/fisiopatologia , Vírus do Nilo Ocidental/imunologiaRESUMO
BACKGROUND: Between August 25 and September 25, 2003 seven patients with West Nile virus neurological manifestations were identified through the hospital neurology consultation services in Calgary, Alberta, Canada. Three of the seven patients were treated with interferon alpha-2b (IFN alpha-2b). In this report we document the clinical characteristics of these seven cases. METHODS: Clinical and laboratory information was obtained from a retrospective review of patient hospital and clinic charts. Patients were included if they had serological evidence of West Nile virus infection and had clinical evidence of aseptic meningitis, encephalomyelitis, cerebellar syndrome or motor neuronopathy. Three patients received a treatment course of three million units IFN alpha-2b, administered by subcutaneous injection once per day for 14 days. RESULTS: Four patients had cerebellar signs without change in consciousness, two had both encephalitis and neuromuscular weakness, and one patient had focal lower motor neuron arm weakness. The mean age was 52 (range 24 - 73). All patients had flu-like illness and fever as presenting symptoms and six had severe headaches. Two patients were immunocompromised prior to infection. Two patients with cerebellar signs (one with opsoclonus-myoclonus) improved spontaneously and exhibited only mild residual deficits on discharge. The other two patients with cerebellar findings developed brainstem involvement, one coinciding with and one subsequent to the cerebellar symptoms. Within one week of treatment with IFN alpha-2b these latter two patients showed marked improvement. One patient with encephalitis and neuromuscular weakness, was treated with IFN alpha-2b and subsequently recovered. INTERPRETATION: In this case review of seven patients, multiple neurological symptoms occurred in each patient and the neurological presentation was varied. Four patients had predominant cerebellar findings and one patient had opsoclonus-myoclonus, not previously reported. The marked improvement in three patients who received IFN alpha-2b raises preliminary optimism towards this potential treatment.