[4] The semicircular canals in the vestibule of the ear sense angular acceleration, and send signals to the nuclei for eye movement in the brain.

Nystagmus occurs when the semicircular canals are stimulated (e.g., by means of the caloric test, or by disease) while the head is stationary.

Previously considered untreatable, in recent years several drugs have been identified for treatment of nystagmus.

Some of the diseases that present nystagmus as a pathological sign or symptom are as follows: Sources of toxicity that could lead to nystagmus: Risk factors for thiamine deficiency, or beriberi, in turn include a diet of mostly white rice, as well as alcoholism, dialysis, chronic diarrhea, and taking high doses of diuretics.

[14][15] Rarely it may be due to a genetic condition that results in difficulties absorbing thiamine found in food.

Purely vertical nystagmus usually originates in the central nervous system, but it is also an adverse effect commonly seen in high phenytoin toxicity.

The simplest one is the caloric reflex test, in which one ear canal is irrigated with warm or cold water or air.

The resulting movement of the eyes may be recorded and quantified by a special device called an electronystagmograph (ENG), a form of electrooculography (an electrical method of measuring eye movements using external electrodes),[22] or an even less invasive device called a videonystagmograph (VNG),[23] a form of video-oculography (VOG) (a video-based method of measuring eye movements using external small cameras built into head masks), administered by an audiologist.

[24] Over the past forty years, objective eye-movement-recording techniques have been applied to the study of nystagmus, and the results have led to greater accuracy of measurement and understanding of the condition.

Orthoptists may also use an optokinetic drum, or electrooculography or Frenzel goggles to assess a patient's eye movements.

Pathological nystagmus is the result of damage to one or more components of the vestibular system, including the semicircular canals, otolith organs, and the vestibulocerebellum.

These descriptive names can be misleading, however, as many were assigned historically, solely on the basis of subjective clinical examination, which is not sufficient to determine the eyes' true trajectory.

[38] Several therapeutic approaches, such as contact lenses,[39] drugs, surgery, and low vision rehabilitation have also been proposed.

[40] Surgical treatment of congenital nystagmus is aimed at improving head posture, simulating artificial divergence, or weakening the horizontal recti muscles.

[45] A Cochrane Review on interventions for eye movement disorders due to acquired brain injury, updated in June 2017, identified three studies of pharmacological interventions for acquired nystagmus but concluded that these studies provided insufficient evidence to guide treatment choices.

[3] Authors of another study in the United Kingdom estimated an incidence of 24 in 10,000 (c. 0.240%), noting an apparently higher rate amongst white Europeans than in individuals of Asian origin.

Horizontal gaze nystagmus will show if a subject is under the influence of a central nervous system depressant, an inhalant, or a dissociative anesthetic.