L’oscillopsie est la perception erronée d’une instabilité de la scène visuelle. Il s’agit d’un symptôme invalidant et source d’une dégradation de l’acuité visuelle, observé dans différentes circonstances pathologiques en neurologie. Le but de cet article de synthèse est d’une part, d’aider à reconnaître cliniquement les différents mécanismes physiopathologiques pouvant conduire à une oscillopsie, et d’autre part, d’approcher les différentes prises en charge thérapeutiques possibles. L’oscillopsie résulte le plus souvent d’une instabilité oculomotrice anormale, comme un nystagmus, un autre mouvement oculaire anormal ou une insuffisance du réflexe vestibulo-oculaire. Il est important de comprendre le mécanisme de ces anomalies oculomotrices, ce d’autant que les progrès de la recherche en pathologie oculomotrice ouvrent de nouvelles perspectives thérapeutiques notamment pharmacologiques. L’oscillopsie pourrait aussi théoriquement résulter d’un dysfonctionnement des systèmes d’intégration qui participent à l’élaboration de la constance spatiale lors des déplacements du regard. Les données cliniques dans ce deuxième cas sont méconnues. Cependant, il nous apparaît que certains symptômes visuo-perceptifs par lésion temporo-pariétale pourraient s’apparenter à des oscillopsies et résulter d’un déficit de l’élaboration de la constance spatiale.

Oscillopsia is an illusion of an unstable visual world. It is associated with poor visual acuity and is a disabling and stressful symptom reported by numerous patients with neurological disorders. The goal of this paper is to review the physiology of the systems subserving stable vision, the various pathophysiological mechanisms of oscillopsia and the different treatments available. Visual stability is conditioned by two factors. First, images of the seen world projected onto the retina have to be stable, a sine qua non condition for foveal discriminative function. Vestibulo-ocular and optokinetic reflexes act to stabilize the retinal images during head displacements; ocular fixation tends to limit the occurrence of micro ocular movements during gazing; a specific system also acts to maintain the eyes stable during eccentric gaze. Second, although we voluntary move our gaze (body, head and eye displacements), the visual world is normally perceived as stable, a phenomenon known as space constancy. Indeed, complex cognitive processes compensate for the two sensory consequences of gaze displacement, namely an oppositely-directed retinal drift and a change in the relationship between retinal and spatial (or subject-centered) coordinates of the visual scene. In patients, oscillopsia most often results from abnormal eye movements which cause excessive motion of images on the retina, such as nystagmus or saccadic intrusions or from an impaired vestibulo-ocular reflex. Understanding the exact mechanisms of impaired eye stability may lead to the different treatment options that have been documented in recent years. Oscillopsia could also result from an impairment of spatial constancy mechanisms that in normal condition compensate for gaze displacements, but clinical data in this case are scarce. However, we suggest that some visuo-perceptive deficits consecutive to temporo-parietal lesions resemble oscillopsia and could result from a deficit in elaborating spatial constancy.