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Rupinder K. Sekhon ; Franklyn Rocha Cabrero ; Jonathon P. Deibel .
Last Update: February 27, 2023 .
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 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
Physiologic end-point nystagmus- horizontal jerks nystagmus results from testing oculomotor movements too far laterally
Per-rotational nystagmus- horizontal jerk nystagmus that occurs with sustained head rotations, with fast phases ipsilateral to the rotation
Post-rotational nystagmus- reflexive horizontal nystagmus that occurs with a rapid brake to a unidirectional head rotation, with a contralateral fast phase and a subjective rocking boat sensation
Asymmetry is abnormal, and the lesion can localize to the parietal-occipital cortex.Optokinetic after-nystagmus- persisting ipsilateral optokinetic nystagmus after the visual stimulus has extincted, can persist for seconds and dissipates.
Vestibular ocular reflex- reflex controlled by semicircular canals in the inner ear, seen when the patient sees a fixed image, and a rapid head rotation is elicited bilaterally.
Cold stimulus-eyes will turn slowly towards the cold water stimulation with rapid nystagmus away. Absence may indicate brain death.
Warm stimulus- eyes will turn slowly away with rapid nystagmus toward the side of the stimulus. Absence may indicate brain death.
Magnetic vestibular stimulation-induced nystagmus-nystagmus that occurs while the patient is undergoing an MRI depends on the strength and direction of the field. It results from an interaction between the MRI field currents with the ionic currents in the endolymph fluid.
Infantile nystagmus usually develops by three months of age. It is characterized by a horizontal movement and has correlations with conditions such as albinism, congenital iris absence, underdeveloped optic nerves, or congenital cataract. Children aged 6 months to 3 years can have a form of nystagmus known as spasmus nutans.[3] This form usually improves without intervention between ages 2 through 8 years. Characteristically, children will often nod or tilt their heads with this type of nystagmus, and the eyes may move in any direction.[4]
Acquired causes of nystagmus require exploration if the eye movements develop later in life.Nystagmus, in some patients, can be asymptomatic. However, in most, 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 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
Spontaneous nystagmus- occurs consistently with fixed central gaze position stationary, upright, and neutral positions.
