Nystagmus is derived from Greek nustagmos (nodding, drowsiness), and nystazein (be sleepy or doze). It is a rhythmic, involuntary, rapid, oscillatory movement of the eyes. It may have a slow, fast, or a combination of both. It can be continuous, paroxysmal, with positional or gaze or head positioning triggers. It can be distinguished from saccades, oscillations, and other abnormal involuntary eye movements that are fast-acting and mimickers. These movements can reduce vision, affect depth perception, balance, and coordination. Often, nystagmus can be seen transiently, which may indicate some type of underlying pathology. Nystagmus can also be labeled as manifest (omnipresent), latent (when covering one eye), or both.[1]
The Classification Committee of the Bárány Society established the different classification of nystagmus for clinical and research purposes, with special emphasis on a common language for vestibular disorders worldwide. Pathologic nystagmus results from diseases affecting the cortex, anterior visual tracts, brainstem, cerebellum, and peripheral vestibular apparatus.
Physiological nystagmus- normal nystagmus variant of oculomotor function
Etiology
Nystagmus in some patients can be asymptomatic. However, in the majority, nystagmus causes vertigo, oscillopsia, blurred vision, or abnormal head positioning. Vertigo is the primary symptom and occurs most commonly with vestibular problems. Oscillopsia, which is a sensation of the environment moving back and forth, depends on the type of nystagmus present but can be continuous, intermittent, or gaze-evoked.[5] Blurred vision usually occurs due to the retinal image being affected by the motion. This blurred vision can lead to abnormal head positioning, which is when patients compensate for their vision changes by finding gaze positions that minimize their symptoms.
A major concern with finding pathological nystagmus is localizing the abnormal brain or ear apparatus structures that are affected and what is the underlying etiology. For instance, acquired nystagmus which develops later in adolescence or adulthood can indicate a central nervous system issue like multiple sclerosis, head injury, brain tumor, metabolic disorder, medication side effect, hyperventilation, or even alcohol or drug toxicity.[6][7][8][9][10] The differential diagnosis of nystagmus also includes oculogyric crises and ocular bobbing. Oculogyric crises are distinguishable from nystagmus by noting a lack of a specific rhythm or slow phase with the eye movements. This type of eye movement most commonly presents with phenothiazine intoxication. Ocular bobbing is more irregular than nystagmus and usually occurs in locked-in syndrome.
Pathological nystagmus- abnormal nystagmus from central or peripheral nervous system damage to the vestibular-oculocephalic and/or cortical areas affecting the oculomotor function
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