New insights into positional alcohol nystagmus using three-dimensional eye-movement analysis

Abstract

The semicircular canals selectively transduce angular velocity and are normally insensitive to gravity and linear acceleration. In acute alcohol intoxication, however, the cupula becomes lighter than the endolymph, rendering it sensitive to gravity (buoyancy hypothesis). This results in positional alcohol nystagmus (PAN) and rotatory vertigo. We evaluated PAN in 8 normal subjects by means of three‐dimensional eye‐movement analysis in an attempt to clarify if the buoyancy mechanism is sufficient to explain PAN. Forty minutes after intake of 0.8 g of alcohol/kg of body weight, the subjects were positioned such that the lateral canals were earth vertical. They were then rotated in the plane of the lateral canals about an earth‐horizontal axis to either 45° or 90°, right or left ear down, and eye movements were recorded for 40 seconds in each position. The spatial analysis of the responses showed that in addition to the nystagmus induced by the buoyancy of all six cupulae, alcohol intoxication also causes a vertical velocity offset (in all subjects, slow phase down) that is independent of the orientation of the subject in space. The offset may represent a toxic effect on central vestibular pathways, producing a tone imbalance of the vertical vestibulo‐ocular reflex. Ann Neurol 1999;45:216–223

The consequences of beer consumption in rats: acute anxiolytic and ataxic effects and withdrawal-induced anxiety

“…This is consistent with previous studies showing ataxia following intraperitoneal injection of ethanol (Drugan et al 1996;Larson and Siegel 1998;Brooks et al 2001). It has been suggested that ataxia results from ethanol absorption in the otoliths and is an indication of ethanol intoxication (Fetter et al 1999). The present results therefore suggest that rats will drink beer to the point of intoxication.…”

Vertigem de posicionamento paroxística benigna

“…Segundo a teoria da cupulolitíase, a cúpula, com partículas aderidas à sua superfície, seria defletida inclusive em situações estáticas de acordo com a força da gravidade, funcionando como um transdutor de aceleração linear (teoria da flutuação). Este mecanismo explica, por exemplo, o nistagmo posicional presente na intoxicação alcóolica, que se relaciona à posição da cabeça 7,8 , mas não explica os ataques de VPPB por diferentes razões. Na VPPB, se observa um nistagmo de posicionamento, provocado por movimentos rá-pidos, que cessa em alguns segundos.…”

Medical and Nonstroke Neurologic Causes of Acute, Continuous Vestibular Symptoms

“…9 Acute alcohol intoxication produces dizziness by both central and peripheral mechanisms. 6,10 The resultant nystagmus can therefore be of a mixed type but is most commonly a direction-changing, gaze-evoked horizontal nystagmus (ie, beats to the right when looking right, beats to the left when looking left), as with other brainstem and cerebellar intoxicants, that results from impairment of central gaze-holding pathways. Alcohol use can also cause dizziness via other mechanisms such as thiamine deficiency (discussed later) and chronic cerebellar degeneration, although the last two mechanisms generally lead to a more chronic presentation, unless there is intercurrent medical illness.…”