RESUMO
The bedside examination associated with their clinical history remains the most critical means to accurately diagnose the cause for most of the signs and symptoms related to pathology of the cerebellum and vestibular system in patients presenting with dizziness and imbalance. This paper focuses on those critical bedside examinations, suggests when laboratory testing might be useful to confirm the clinical suspicion, and considers the shared neural circuitry within the visual and vestibular systems to offer an algorithmic approach in conducting the clinical bedside examination.
Assuntos
Nistagmo Patológico , Vestíbulo do Labirinto , Algoritmos , Cerebelo , Movimentos Oculares , Humanos , Nistagmo Patológico/diagnóstico , Reflexo Vestíbulo-OcularRESUMO
OBJECTIVE: To examine the high frequency horizontal vestibular ocular-reflex (hVOR) during acute attacks of vertigo in Menière's disease (MD). STUDY DESIGN: Retrospective case series and literature review. SETTING: Tertiary academic medical center. PATIENTS: Patients with clinical diagnosis of unilateral "definite MD." INTERVENTION: Review of medical records. MAIN OUTCOME MEASURES: Spontaneous nystagmus and the dynamic hVOR gain change at different stages of an acute episode of MD attack. RESULTS: We studied 10 vertigo attacks during the unique stages of the episode. During the acme stage of the attack, lower hVOR gain was recorded on the affected side (mean 0.48â±â0.23), which was associated with a paralytic nystagmus (beating away from the affected ear). Additionally, the mean hVOR gain remained significantly (pâ<â0.05) reduced during each of the other stages of the attack as compared with the unaffected side and a control group. After the attack, mean hVOR gains normalized in the affected ear. Mean hVOR gain of the unaffected ear remained normal during all stages. CONCLUSION: Vestibular function during an attack of MD is a dynamic process associated with fluctuation of the dynamic (hVOR gain) and static (spontaneous nystagmus) processes, which exist in parallel with the perception of vertigo. Our data support vHIT monitoring during an episode to provide objective and accurate evidence of the ear with active disease. This would be particularly useful for those patients with MD presentations of unreliable hearing or assisting to identify the ear to be treated in the case of bilateral MD.
Assuntos
Doença de Meniere , Reflexo Vestíbulo-Ocular , Vestíbulo do Labirinto , Humanos , Estudos Retrospectivos , VertigemRESUMO
The rapid onset of a bilateral vestibular hypofunction (BVH) is often attributed to vestibular ototoxicity. However, without any prior exposure to ototoxins, the idiopathic form of BVH is most common. Although sequential bilateral vestibular neuritis (VN) is described as a cause of BVH, clinical evidence for simultaneous and acute onset bilateral VN is unknown. We describe a patient with an acute onset of severe gait ataxia and oscillopsia with features compatible with acute BVH putatively due to a bilateral VN, which we serially evaluated with clinical and laboratory vestibular function testing over the course of 1 year. Initially, bilateral superior and horizontal semicircular canals and bilateral utricles were impaired, consistent with damage to both superior branches of each vestibular nerve. Hearing was spared. Only modest results were obtained following 6 months of vestibular rehabilitation. At a 1-year follow-up, only the utricular function of one side recovered. This case is the first evidence supporting an acute presentation of bilateral VN as a cause for BVH, which would not have been observed without critical assessment of each of the 10 vestibular end organs.
RESUMO
Tilt suppression refers to both tilting the head away from an Earth vertical axis and a reduction of an induced horizontal nystagmus. This phenomenon of reducing an induced horizontal nystagmus involves a circuitry of neurons within the vestibular nuclei and the cerebellum (collectively referred to as velocity storage) and signals from the otolith end organs. Lesions involving this circuitry can disrupt tilt suppression of induced horizontal nystagmus. We investigated the clinical value of combining the horizontal head-shaking nystagmus test with tilt suppression in 28 patients with unilateral peripheral vestibular hypofunction and 11 patients with lesions affecting the central nervous system. Each of the subjects with peripheral vestibular lesions generated an appropriately directed horizontal nystagmus after head shaking that then suppressed the induced angular slow phase velocity on average 52 ± 17.6% following tilt down of the head. In contrast, patients with central lesions had very little ability to suppress post-head-shaking nystagmus (mean 3.4 ± 56%). We recommend tilting the head after head shaking as a useful clinical test to assist in the differential diagnosis of vertiginous patients. In the case of unilateral peripheral vestibular hypofunction, head tilt suppresses the induced nystagmus via influence of the otolith organ. In the case of central pathology, the inability to suppress the nystagmus is from lesions impairing the otolith mediation on the velocity storage circuitry.