RESUMO
Acute cortical lesions rarely cause vertigo. We report a 51-year-old patient presenting with an acute vestibular syndrome including spontaneous vertigo and nystagmus, lateropulsion and nausea due to middle cerebral artery infarction. The central origin of the acute vestibular syndrome was revealed by a normal head impulse test. A comprehensive literature review on patients with hemispheric stroke manifesting with acute vertigo is provided. Typically, patients with an acute vestibular syndrome due to cortical stroke have involvement of the temporoparietal junction.
Assuntos
Acidente Vascular Cerebral/complicações , Acidente Vascular Cerebral/diagnóstico , Vertigem/diagnóstico , Vertigem/etiologia , Neuronite Vestibular/diagnóstico , Feminino , Humanos , Pessoa de Meia-Idade , Neuronite Vestibular/complicaçõesRESUMO
BACKGROUND: A 23 year-old female presented to a neurology department with a 3 year history of recurrent episodes involving hearing loss, encephalopathy, focal neurological deficits, and visual field deficits. In the 3 years before presentation, the patient had been treated with methylprednisolone for suspected acute demyelinating encephalomyelitis and peripheral otogenic dysfunction from which she made a complete recovery, and for a visual defect in both eyes caused by bilateral branch retinal arterial occlusion, from which she partially improved and commenced long-term treatment with acetylsalicylic acid. INVESTIGATIONS: Detailed history, clinical examination, extensive laboratory work-up, cerebrospinal fluid analysis, cerebral and spinal MRI, periventricular single-voxel (1)H magnetic resonance spectroscopy, retinal fluorescence angiography, optical coherence tomography, audiometry, neurophysiological work-up (EEG, evoked potentials). DIAGNOSIS: Susac syndrome, characterized by a combination of encephalopathy, branch retinal artery occlusions, and hearing loss. MANAGEMENT: Long-term immunosuppressive treatment with azathioprine (150 mg/day) and prednisolone (10 mg/day), and inhibition of thrombocyte function with acetylsalicylic acid (100 mg/day).
Assuntos
Transtornos da Percepção Auditiva/etiologia , Encéfalo/patologia , Perda Auditiva/etiologia , Síndrome de Susac/complicações , Transtornos da Visão/etiologia , Aspirina/uso terapêutico , Angiografia Cerebral/métodos , Diagnóstico Diferencial , Progressão da Doença , Feminino , Fibrinolíticos/uso terapêutico , Humanos , Imageamento por Ressonância Magnética/métodos , Síndrome de Susac/diagnóstico , Síndrome de Susac/tratamento farmacológico , Adulto JovemRESUMO
Migrainous vertigo (MV) is an increasingly recognized cause of episodic vertigo. However, the pathophysiology of MV is still a matter of speculation and it is not known to what extent the dysfunction is located in the central or peripheral vestibular system. The aim of this prospective study was to describe the clinical spectrum of acute MV and to clarify which structures of the vestibular system are involved. Testing of 20 patients with acute MV included neuro-otological examination, recording of spontaneous and positional nystagmus with 3D video-oculography, and audiometry. Pathological nystagmus was observed in 70% of patients during acute MV: six had isolated spontaneous nystagmus, five had isolated positional nystagmus and three had a combination of the two. Only a few patients showed additional ocular motor deficits. Imbalance was observed in all patients except one. Hearing was not affected in any patient during the attack. The findings during acute MV point to central-vestibular dysfunction in 10 patients (50%) and to peripheral vestibular dysfunction in three patients (15%). In the remaining seven patients (35%) the site of involvement could not be determined with certainty. MV should be considered in the differential diagnosis of vertigo with spontaneous and positional nystagmus and can present both as a central and a peripheral vestibular disorder.