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The diagnosis of central positional vertigo (CPV) is challenging, mainly because symptoms overlap with the common variants of benign paroxysmal positional vertigo (BPPV). Recent correlations of imaging with neurotologic exams have improved our understanding of CPV and ability differentiate it from BPPV. Yet, there is still a need to develop better diagnostic algorithms to improve timely diagnosis and early intervention. Here we present a retrospective review of the clinical characteristics, neurotologic evaluation and imaging of CPV in a cohort of 27 patients and propose a diagnostic algorithm to be tested in future prospective fashion. Most patients had positional nystagmus (downbeat and apogeotropic horizontal), cerebellar ocular motor abnormalities and truncal ataxia indicative of a central lesion. 61.5% of our cohort had paroxysmal CPV, 30.5% had a non-paroxysmal CPV and 8% paroxysmal-evolving-to-non-paroxysmal CPV. The most common pattern of positional nystagmus evoked with maneuvers was positional downbeat nystagmus (pDBN, 69.2%), apogeotropic horizontal nystagmus (42.3%), geotropic (7.69%) and multiplanar (23.0%). Notably, 13 (50%) of patients had cerebral imaging prior to CPV being on the differential diagnosis, whereas another 50% of patients had CPV diagnosis preceding their work-up. Unilateral lesions on imaging were 4× less likely to exhibit nausea and vomiting, nearly 2× less likely to exhibit paroxysmal nystagmus, and 2× less likely to exhibit nystagmus with habituality. Findings of pDBN or apogeotropic nystagmus alone were enough to diagnose CPV in 50% of our patient cohort, underscoring the importance of clinical evaluation in a time when an "imaging-first" philosophy is gaining popularity in Neurology.

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OBJECTIVE: To evaluate the association between endothelial dysfunction and otoneurological symptoms and vaso-occlusive phenomena in children with sickle cell disease (SCD). METHODS: Cross-sectional study with 54 children, aged between 6 and19 years of age, of whom 28 had genotype SS and 26 apparently healthy (AA genotype) whose parents or guardians, or the children themselves, filled out a questionnaire designed to assess their otoneurological symptoms. All the individuals were submitted assessment of endothelial function by flow-mediated dilation (FMD) percentage with reactive hyperemia of brachial artery Doppler. RESULTS: Otoneurological symptoms (tinnitus and/or vertigo) predominated in the SCD group (46.4 vs. 15.4%; p = 0.006). A negative correlation was observed between FMD percentage and time of evolution of vertigo SCD (r = -0.432; p = 0.022) and the linear regression analysis demonstrated that for every reduction in FMD percentage there was an increase in time of evolution of vertigo of 1.79 months (ß = -1.79; p = 0.022). The positive correlation between episodes of painful crisis and time of evolution of vertigo (r = 0.3; p = 0.04). DISCUSSION: The presence of vascular endothelial damage in the labyrinthine artery in patients with SCD is capable of compromising the semicircular canals, shown by clinical expression of otoneurological symptoms, such as vertigo. In the present study, an association was observed between endothelial dysfunction with otoneurological symptoms and otoneurological symptoms and vaso-occlusive phenomena in SCD.

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Objetivo: La compresión de una estructura nerviosa por un vaso aberrante puede ser asintomática o producir importante sintomatología; en éste caso las imágenes suministran una relevante información clínica y prequirúrgica. Material y métodos: Se estudiaron entre enero de 1998 y marzo de 2001, 27 pacientes: 8 con neuralgia del trigémino, 7 con hemiespasmo del facial, 4 con vértigo y tinnitus pulsátil, 2 con hemiespasmo del facial, 4 con vértigo y tinnitus pulsátil, 2 con hemianopsias, 1 con neuralgia de la fosa amigdalina, 1 con voz bitonal, 1 con hemiatrofia lingual derecha con fasciculaciones, 2 con hipertensión esencial y 1 con cefalea. Todos ellos presentaron evaluación neurológica por 2 especialistas y los resultados fueron interpretados por 2 neurorradiólogos. Resultados: Las imágenes por TC y RM con secuencias especiales permitieron evidenciar las compresiones de los segmentos de entrada de las raíces de los pares craneales V, VII, VIII, IX, X, XII, del quiasma óptico y de la cara anterolateral izquierda del bulbo raquídeo en estrecha relación con el centro vasopresor. También se visualizó un vaso anómalo en el Acueducto de Silvio, impidiendo el flujo normal del LCR. Del total de los pacientes estudiados, el 37 por ciento tuvo confirmación quirúrgica. Conclusiones: La TC y especialmente la RM con secuencias para visualización de vasos demostraron ser métodos muy sensibles y específicos en la detección de la lesión de una estructura nerviosa intracraneal, producto de la compresión por un vaso (AU)

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