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.
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
- Optokinetic or pendular nystagmus- multi-direction (e.g.vertical, torsional, or horizontal) nystagmus in response to moving or rotating visual fields or objects, the slow phase is ipsilateral to the visual stimuli, and it does not have a fast phase. 
- 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.
- Caloric nystagmus- VOR reflex elicited by stimulating the tympanic membrane and horizontal semicircular canals with either warm or cold water.
- 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 age 6 months to 3 years can have a form of nystagmus known as spasmus nutans. 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.
- Acquired causes of nystagmus require exploration if the eye movements develop later in life.