Dario A. Yacovino

New therapeutic maneuver for anterior canal benign paroxysmal positional vertigo

This article describes the clinical features of anterior semicircular canal benign paroxysmal positional vertigo (AC-BPPV) and a new therapeutic maneuver for its management. Our study was a retrospective review of cases from an ambulatory tertiary referral center. Thirteen patients afflicted with positional paroxysmal vertigo exhibiting brief positional down-beating nystagmus in positional tests (Dix–Hallpike and head-hanging position) were treated with a maneuver comprised of the following movements: Sequential head positioning beginning supine with head hanging 30° dependent with respect to the body, then supine with head inclined 30° forward, and ending sitting with head 30° forward. All cases showed excellent therapeutic response to our repositioning procedure, i.e. relief of vertigo and elimination of nystagmus. The maneuver described is an option for AC-BPPV treatment.

Clinical Characteristics of Cervicogenic-Related Dizziness and Vertigo

Cervical vertigo has long been a controversial entity and its very existence as a medical entity has advocates and opponents. Supporters of cervical vertigo claim that its actual prevalence is underestimated due to the overestimation of other diagnostic categories in clinics. Furthermore, different pathophysiological mechanisms have been attributed to cervical vertigo. Here the authors discuss the clinical characteristics of rotational vertebral artery vertigo, postwhiplash vertigo, proprioceptive cervical vertigo, and cervicogenic vertigo of old age. A clinical entity named subclinical vertebrobasilar insufficiency appears in the context of cervical osteoarticular changes. Migraine-associated vertigo may explain why some patients suffering from cervical pain have vertigo while others do not.

Bilateral vestibular loss.

Bilateral vestibular loss is a rare cause of visual disturbance (oscillopsia) and imbalance. When severe, the most common cause is iatrogenic-gentamicin ototoxicity. Bilateral loss is easily diagnosed at the bedside with the dynamic illegible E test. If this test is omitted, it can easily be misdiagnosed as a cerebellar syndrome. Treatment is largely supportive. Care should be taken to avoid medications that suppress vestibular function, and to encourage activity.

Characteristics of vestibular corrective saccades in patients with slow visual saccades, vestibular disorders and controls: A descriptive analysis

Objective Our aim was to determine whether overt catch up saccades (OS) provoked by vestibular stimuli, as observed in the video head impulse test (vHIT), have comparable metrics as visually triggered horizontal saccades (VS), indicating a common saccadic brainstem generator. Methods Three groups of patients were studied: patients with neurological disorders causing slow saccades (group 1, n = 12), patients with peripheral vestibular lesions (group 2, n = 43), and normal controls (group 3, = 24). All patients underwent vHIT and Videooculographic testing. OS velocity, acceleration, amplitude and duration and VS velocity in this group was compared between the groups. Results There was significant reduction in the velocity of visually guided saccades in group 1, as expected from the patient selection constraints of this study. Group 1 also exhibited saccades which were longer in duration and of reduced acceleration when compared to subjects without saccadic slowing to visual targets (Group 2 and 3). There were significant positive correlations between OS acceleration and amplitude in both normal saccade groups (2 and 3) which was not observed in the slow saccade group (1). Conclusions The metrics of overt saccades measured by the vHIT in patients with slow saccades and normal controls are similar to visually guided saccades. This supports the hypothesis that overt saccades associated with vestibular stimuli and visually triggered saccades share common circuitry that controls metrics.

Fluctuating Vestibulo-Ocular Reflex in Ménière's Disease.

OBJECTIVES To describe the fluctuating high velocity vestibular ocular-reflex (VOR) during the Ménières attacks and correlate those features with pathophysiology. PATIENTS A patient with unilateral Ménières disease (MD) was evaluated closely during and after acute vertigo episodes. MAIN OUTCOME MEASURES The spontaneous nystagmus and the dynamic VOR changes were measured by the video head impulse test (VHIT) at different stages of the vertigo crisis and during the quiescent phase of the condition. RESULTS During the Ménières attack, the VOR gain showed large changes on the affected side; however, on recovery a return to the normal value was evident. The VOR gain also showed fluctuation on follow up, paralleling symptoms. The greatest reduction of the VOR was during the paralytic nystagmus phase. CONCLUSIONS The present case documents rapid vestibular fluctuation documented with VHIT testing in MD. The ionic-chemical perilymphatic intoxication and the endolymphatic space collapse due to membrane rupture could explain those features. VHIT fluctuation is a promising tool for diagnosis of patients with episodic vestibular symptoms.

Neuritis vestibular: eficacia de la prednisona en la recuperación funcional

Resumen Introduccion La neuritis vestibular es la causa mas frecuente de vertigo agudo sostenido y de hipofuncion vestibular unilateral. El origen inflamatorio viral agudo es la teoria mas aceptada para explicar los hallazgos clinicos, electrofisiologicos y epidemiologicos. El objetivo de este trabajo es evaluar el efecto a corto plazo de la prednisona en la recuperacion de la lesion vestibular (canal paresia [CP]). Pacientes y metodo Mediante un diseno de casos y controles seleccionamos a pacientes que cumplian los criterios clinicos para una falla vestibular unilateral aguda periferica (FVA) evaluados dentro de los primeros 7 dias del comienzo de los sintomas, que hayan sido sometidos a un registro confirmatorio videonistagmografico inicial y un control de la funcion vestibular mediante tests caloricos al mes de evolucion. Resultados Identificamos a 193 pacientes con FVA, de los que 32 cumplian criterios de inclusion; 17 recibieron prednisona (GP) y 15 fueron controles (GC). No hubo diferencias significativas respecto a edad, sexo, antecedentes de infeccion de vias aereas superiores, hipertension arterial, hipotiroidismo, migrana, hipercolesterolemia. Encontramos una mejoria estadisticamente significativa en los valores absolutos de CP en el GP frente al GC (p = 0,025). Cinco pacientes (GP) presentaron valores normales en los test caloricos (CP Conclusiones La prednisona oral administrada precozmente en la neuritis vestibular mejoro en forma estadisticamente significativa los valores de la lesion vestibular medidos al mes de inicio de los sintomas.

Acute Bilateral Superior Branch Vestibular Neuropathy

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.

Bilateral Vestibular Weakness

Bilateral vestibular weakness (BVW) is a rare cause of imbalance. Patients with BVW complain of oscillopsia. In approximately half of the patients with BVW, the cause remains undetermined; in the remainder, the most common etiology by far is gentamicin ototoxicity, followed by much rarer entities such as autoimmune inner ear disease, meningitis, bilateral Ménière’s disease, bilateral vestibular neuritis, and bilateral vestibular schwannomas. While a number of bedside tests may raise the suspicion of BVW, the diagnosis should be confirmed by rotatory chair testing. Treatment of BVW is largely supportive. Medications with the unintended effect of vestibular suppression should be avoided.

A Pragmatic Strategy for the Evaluation and Management of Anterior Canal Benign Positional Vertigo.

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