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. Optokinetic (syn. opticokinetic) nystagmus: a nystagmus induced by looking at moving visual stimuli, such as moving horizontal or vertical lines, and/or stripes. For example, if one fixates on a stripe of a rotating drum with alternating black and white, the gaze retreats to fixate on a new stripe as the drum moves. This is first a rotation with the same angular velocity, then returns in a saccade in the opposite direction. The process proceeds indefinitely. This is optokinetic nystagmus, and is a source for understanding the fixation reflex. Postrotatory nystagmus: if one spins in a chair continuously and stops suddenly, the fast phase of nystagmus is in the opposite direction of rotation, known as the "post-rotatory nystagmus", while slow phase is in the direction of rotation. Treatment
Congenital nystagmus has long been viewed as untreatable, but medications have been discovered in recent years that show promise in some patients. In 1980, researchers discovered that a drug called baclofen could stop periodic alternating nystagmus. Subsequently, gabapentin, an anticonvulsant, led to improvement in about half the patients who took it. Other drugs found to be effective against nystagmus in some patients include memantine, levetiracetam, 3,4-diaminopyridine (available in the US to eligible patients with downbeat nystagmus at no cost under an expanded access program), 4-aminopyridine, and acetazolamide.
It also may be induced temporarily by disorientation (such as on roller coaster rides or when a person has been spinning in circles) or by some drugs (alcohol, lidocaine, and other central nervous system depressants, inhalant drugs, stimulants, psychedelics, and dissociative drugs). Early-onset nystagmus
Early-onset nystagmus occurs more frequently than acquired nystagmus. It can be insular or accompany other disorders (such as micro-ophthalmic anomalies or Down syndrome). Early-onset nystagmus itself is usually mild and non-progressive. The affected persons are usually unaware of their spontaneous eye movements, but vision can be impaired depending on the severity of the eye movements. Types of early-onset nystagmus include the following, along with some of their causes:

Infantile:
Albinism
Aniridia
Bilateral congenital cataract
Bilateral optic nerve hypoplasia
Idiopathic
Lebers congenital amaurosis
Optic nerve or macular disease
Persistent tunica vasculosa lentis
Rod monochromatism
Visual-motor syndrome of functional monophthalmus
Latent nystagmus
Noonan syndrome
Nystagmus blockage syndromeX-linked infantile nystagmus is associated with mutations of the gene FRMD7, which is located on the X chromosome.Infantile nystagmus is also associated with two X-linked eye diseases known as complete congenital stationary night blindness (CSNB) and incomplete CSNB (iCSNB or CSNB-2), which are caused by mutations of one of two genes located on the X chromosome. In CSNB, mutations are found in NYX (nyctalopin). CSNB-2 involves mutations of CACNA1F, a voltage-gated calcium channel that, when mutated, does not conduct ions. Acquired nystagmus
Nystagmus that occurs later in childhood or in adulthood is called acquired nystagmus. The cause is often unknown, or idiopathic, and thus referred to as idiopathic nystagmus.