Vértigo posicional paroxístico benigno: maniobras de provocación y liberación / Benign paroxysmal positional vertigo: provocation and freeing manoeuvres

El vértigo posicional paroxístico benigno (VPPB) se define como la aparición de episodios bruscos de vértigo de breve duración, provocados por cambios de posición, acompañados de nistagmo y que se reproducen al adoptar la posición desencadenante. La teoría fisiopatológica que mejor explica las características clínicas y del nistagmo en las maniobras de provocación del VPPB es la canalitiasis: partículas otolíticas desprendidas de la mácula del utrículo penetrarían en el interior de un conducto semicircular; su desplazamiento al realizar determinados movimientos en el plano de ese conducto produce una corriente endolinfática que estimularía la cúpula originando la aparición de vértigo y nistagmo. El diagnóstico se basa en una historia clínica típica, una exploración otoneurológica normal y una reproducción de la crisis con las maniobras de provocación. El tratamiento a través de las maniobras de reposición permite la resolución del cuadro de forma rápida y sencilla. Presentamos dos casos de mareo vistos en nuestro servicio de urgencias. La sospecha clínica y la realización de la maniobra de Dix-Hallpike confirmaron el diagnóstico de VPPB. La maniobra de Epley resolvió el cuadro de manera rápida y definitiva

The benign paroxystic positional vertigo (BPPV) is defined by brief episodic vertigo attacks and accompanied by a rotary-linear nystagmus, triggered by head position changes and is always produced in that position. The theory that better explains the BPPV is canalithiasis: free-floating particles leave the utricular macula and enter one of the semicircular canals, producing an endolymphatic movement that stimulates the cupula and produces vertigo and nystagmus. The diagnosis is based on a typical clinical history, normal ear and neurological examination and provocation maneuvers, such as the Dix-Hallpike test, reproduce the vertigo attacks. The treatments are the liberatory maneuvers, such as the Epley maneuver which makes the vertigo disappear. We present two cases of vertigo with a compatible clinic history of BPPV, where the Dix-Hallpike maneuver confirmed the diagnosis. The treatment in both cases was the Epley maneuver

Eye movements of the murine P/Q calcium channel mutant rocker, and the impact of aging.

Mutations in the gene encoding the ion pore of the P/Q voltage-activated calcium channel (CACNA1A) are predicted to alter synaptic transmission and dendritic excitability within cerebellar granule and Purkinje cells. Determining the relationships between these alterations, neuronal activity, and behavior may yield insight into the relationship between neuronal intrinsic properties and signal processing within the ocular motor system. Toward this end, we compared ocular motor performance in the CACNA1A mutant rocker and C57BL/6 controls. Average vertical eye position was abnormally elevated in the mutants, a finding that may be analogous to downbeat nystagmus seen in human cerebellar disorders. Fast phases of vestibular nystagmus were slowed by approximately 18% of control values. The angular vestibuloocular reflex (VOR) in darkness and light (visual VOR, or VVOR), assessed at 0.1-1.6 Hz, exhibited subnormal gains at the highest stimulus frequencies and increased phase leads at the lowest stimulus frequencies. Horizontal optokinetic responses to constant velocity drum rotation of +/-2.5-40 degrees/s exhibited minimally reduced gains. Attempts to increase VOR gain by concomitant optokinetic and vestibular stimulation were confounded by the tendency of the mice to habituate to repetitive vestibular stimulation, but attempts to induce coupling of vertical eye movements to horizontal vestibular stimulation (cross-axis adaptation) generated rapid plastic changes in controls and little effect in mutants. With the notable exceptions of the vertical elevation and optokinetic gains, the ocular motor abnormalities were stable over a broad range of animal age, a result compatible with the abnormalities arising as direct consequences of the inborn alteration in calcium channel biophysics.

Genetics of familial episodic vertigo and ataxia.

The familial episodic ataxias are prototypical inherited channelopathies that result in episodes of vertigo and ataxia triggered by stress and exercise. Episodic ataxia type 1 (EA-1) is caused by missense mutations in the potassium channel gene KCNA1, whereas episodic ataxia type 2 (EA-2) is caused by missense and nonsense mutations in the calcium channel gene CACNA1A. These ion channels are crucial for both central and peripheral neurotransmission. Within the last few years, the genetic mechanisms underlying these relatively rare familial episodic ataxia syndromes have been worked out. They provide a model for understanding the mechanisms of more common recurrent vertigo and ataxia syndromes, particularly those associated with migraine. Migraine affects as many as 15-20% of the general population, and it has been estimated that about 25% of patients with migraine experience spontaneous attacks of vertigo and ataxia. We identified 24 families with migraine and benign recurrent vertigo inherited in an autosomal dominant fashion. These families have numerous features in common with EA-1 and EA-2 (particularly EA-2), suggesting that benign recurrent vertigo may be an inherited channelopathy. An ion channel mutation shared by brain and inner ear could explain the combined central and peripheral features of the syndrome.