What is acquired nystagmus?

Updated: Oct 17, 2018
  • Author: Christopher M Bardorf, MD, MS; Chief Editor: Edsel Ing, MD, MPH, FRCSC  more...
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Answer

Nystagmus may be defined as a periodic rhythmic ocular oscillation of the eyes. The oscillations may be sinusoidal and of approximately equal amplitude and velocity (pendular nystagmus) or, more commonly, with a slow initiating phase and a fast corrective phase (jerk nystagmus). [1, 2]

Nystagmus may be unilateral or bilateral, but, when the nystagmus appears unilateral, it is more often asymmetric rather than truly unilateral. Nystagmus may be conjugate or disconjugate (dissociated). It may be horizontal, vertical, torsional (rotary), or any combination of these movements superimposed upon each other.

Nystagmus may be congenital or acquired. When acquired, it most often is caused by abnormalities of vestibular input. Congenital forms may be associated with afferent visual pathway abnormalities (sensory nystagmus). [3]

To understand the mechanisms by which nystagmus may occur, it is important to discuss the means by which the nervous system maintains position of the eyes. Foveal centration of an object of regard is necessary to obtain the highest level of visual acuity. Three mechanisms are involved in maintaining foveal centration of an object of interest: fixation, the vestibulo-ocular reflex, and the neural integrator.

Fixation in the primary position involves the visual system's ability to detect drift of a foveating image and signal an appropriate corrective eye movement to refoveate the image of regard. The vestibular system is intimately and complexly involved with the oculomotor system.

The vestibulo-ocular reflex is a complex system of neural interconnections that maintains foveation of an object during changes in head position. The proprioceptors of the vestibular system are the semicircular canals of the inner ear. Three semicircular canals are present on each side, anterior, posterior, and horizontal. The semicircular canals respond to changes in angular acceleration due to head rotation.

The third mechanism is the neural integrator. When the eye is turned in an extreme position in the orbit, the fascia and ligaments that suspend the eye exert an elastic force to return toward the primary position. To overcome this force, a tonic contraction of the extraocular muscles is required. A gaze-holding network called the neural integrator generates the signal. The cerebellum, ascending vestibular pathways, and oculomotor nuclei are important components of the neural integrator.


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