Physiological nystagmus is a form of involuntary eye movement that is part of the vestibulo-ocular reflex (VOR), characterized by alternating smooth pursuit in one direction and saccadic movement in the other direction.

Pathological nystagmus is characterized by "excessive drifts of stationary retinal images that degrades vision and may produce illusory motion of the seen world: oscillopsia (an exception is congenital nystagmus)".

When nystagmus occurs without fulfilling its normal function, it is pathologic (deviating from the healthy or normal condition). 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.

Pathological nystagmus generally causes a degree of vision impairment, although the severity of such impairment varies widely. Also, many blind people have nystagmus, which is one reason that some wear dark glasses.

The optokinetic response is a combination of a slow-phase and fast-phase eye movements. It is seen when an individual follows a moving object with their eyes, which then moves out of the field of vision at which point their eye moves back to the position it was in when it first saw the object. The reflex develops at about 6 months of age.

Optokinetic nystagmus (OKN) is nystagmus that occurs in response to a rotation movement. It is present normally. The optokinetic response allows the eye to follow objects in motion when the head remains stationary (e.g., observing individual telephone poles on the side of the road as one travels by them in a car, or observing stationary objects while walking past them).

If an optokinetic drum is available, rotate the drum in front of the patient. Ask the patient to look at the drum as you rotate it slowly. If an optokinetic drum is not available, move a strip of paper with alternating 2-inch black and white strips across the patient's visual field. Pass it in front of the patient's eye at reading distance while instructing the patient to look at it as it rapidly moves by. With normal vision, a nystagmus develops in both adults and infants. The nystagmus consists of initial slow phases in the direction of the stimulus (smooth pursuits), followed by fast, corrective phases (saccade). Presence of nystagmus indicates an intact visual pathway.

Another effective method is to hold a mirror in front of the patient and slowly rotate the mirror to either side of the patient. The patient with an intact visual pathway will maintain eye contact with herself or himself. This compelling optokinetic stimulus forces reflex slow eye movements.

OKN can be used as a crude assessment of the visual system, particularly in infants. When factitious blindness or malingering is suspected, check for optokinetic nystagmus to determine whether there is an intact visual pathway.

Amaurotic nystagmus is defined as the nystagmus associated with blindness or the central vision defects. It is characterized by the pendular or jerky movements of the eyes in the patients who have visual impairement for a long period of time.

Oscillopsia is a visual disturbance in which objects in the visual field appear to oscillate. The severity of the effect may range from a mild blurring to rapid and periodic jumping. Oscillopsia is an incapacitating condition experienced by many patients with neurological disorders. It may be the result of ocular instability occurring after the oculomotor system is affected, no longer holding images steady on the retina. A change in the magnitude of the vestibulo-ocular reflex due to vestibular disease can also lead to oscillopsia during rapid head movements. Oscillopsia may also be caused by involuntary eye movements such as nystagmus, or impaired coordination in the visual cortex (especially due to toxins) and is one of the symptoms of superior canal dehiscence syndrome. Sufferers may experience dizziness and nausea. Oscillopsia can also be used as a quantitative test to document aminoglycoside toxicity. Permanent oscillopsia can arise from an impairment of the ocular system that serves to maintain ocular stability. Paroxysmal oscillopsia can be due to an abnormal hyperactivity in the peripheral ocular or vestibular system.

"Cross-fixation congenital esotropia", also called "Cianci's syndrome" is a particular type of large-angle infantile esotropia associated with tight medius rectus muscles. With the tight muscles, which hinder adduction, there is a constant inward eye turn. The patient cross-fixates, that is, to fixate objects on the left, the patient looks across the nose with the right eye, and vice versa. The patient tends to adopt a head turn, turning the head to the right to better see objects in the left visual field and turning the head to the left to see those in the right visual field. Binasal occlusion can be used to discourage cross-fixation. However, the management of cross-fixation congenital esotropia usually involves surgery.

Clinically Infantile esotropia must be distinguished from:

1. VIth Cranial nerve or abducens palsy

2. Nystagmus Blockage Syndrome

3. Esotropia arising secondary to central nervous system abnormalities (in cerebral palsy for example)

4. Primary Constant esotropia

5. Duane's Syndrome

Bruns nystagmus is an unusual type of bilateral nystagmus most commonly occurring in patients with cerebellopontine angle tumours. It is caused by the combination of slow, large amplitude nystagmus (gaze paretic nystagmus) when looking towards the side of the lesion, and rapid, small amplitude nystagmus (vestibular nystagmus) when looking away from the side of the lesion. It occurs in 11% of patients with vestibular schwannoma, and occurs mainly in patients with larger tumours (67% of patients with tumours over 3.5 cm diameter). Bruns nystagmus is also associated with an increased incidence of balance disturbance in patients with vestibular schwannoma. It may be caused by the compression of both flocculi, the vestibular part of the cerebellum, and improvement in both the nystagmus and balance problems occur commonly after removal of the tumour.

Bruns nystagmus is named for Ludwig Bruns (1858 – 1915).

Alexanders law refers to spontaneous nystagmus that occurs after an acute unilateral vestibular loss. It was first described in 1912 and has three elements to explain how the vestibulo-ocular reflex responds to an acute vestibular insult. The first element says that spontaneous nystagmus after an acute vestibular impairment has the fast phase directed toward the healthy ear. The direction of the nystagmus, by convention, is named for the fast phase, so the spontaneous nystagmus is directed toward the healthy ear. The second element says nystagmus is greatest when gaze is directed toward the healthy ear, is attentuated at central gaze and may be absent when gaze is directed toward the impaired ear. The third element says that spontaneous nystagmus with central gaze is augmented when vision is denied. This became apparent with the implementation of electrographic testing.

Alexander's law states that in individuals with nystagmus, the amplitude of the nystagmus increases when the eye moves in the direction of the fast phase (saccade).

It is manifested during spontaneous nystagmus in a patient with a vestibular lesion. The nystagmus becomes more intense when the patient looks in the quick-phase than in the slow-phase direction.

The law was named after Gustav Alexander who described it in 1912.

Many patients will report a history of vertigo as a result of fast head movements. Many patients are also capable of describing the exact head movements that provoke their vertigo. Purely horizontal nystagmus and symptoms of vertigo lasting more than one minute can also indicate BPPV occurring in the horizontal semicircular canal.

Patients do not experience other neurological deficits such as numbness or weakness, and if these symptoms are present, a more serious etiology, such as posterior circulation stroke or ischemia, must be considered.

The spinning sensation experienced from BPPV is usually triggered by movement of the head, will have a sudden onset, and can last anywhere from a few seconds to several minutes. The most common movements patients report triggering a spinning sensation are tilting their heads upwards in order to look at something, and rolling over in bed.

Ocular stability is maintained by three different ocular motor systems

1. The fixation system and its deficit

2. The visuo-vestibular stabilizing systems and their deficits

3. The neural integrator and its deficit

The defining characteristic of BPT is a tilting of an infant’s head in recurrent episodes, for varying periods of time. Furthermore, the child’s trunk may bend in the same direction as the head, giving the baby an overall curved shape; this complaint is known as tortipelvis. In addition to this, the individual may also, but not necessarily, experience vomiting, pallor, ataxia, agitation, infantile migraine, unsteadiness of gait upon learning to walk, general malaise and nystagmus.

The periods in which the child’s head is tilted and other symptoms appear can last anywhere from a few minutes to a few weeks, with a frequency of anywhere from two per year to two per month.

Benign paroxysmal positional vertigo (BPPV) is a disorder arising from a problem in the inner ear. Symptoms are repeated, brief periods of vertigo with movement, that is, of a spinning sensation upon changes in the position of the head. This can occur with turning in bed or changing position. Each episode of vertigo typically lasts less than one minute. Nausea is commonly associated. BPPV is one of the most common causes of vertigo.

BPPV can result from a head injury or simply occur among those who are older. A specific cause is often not found. The underlying mechanism involves a small calcified otolith moving around loose in the inner ear. It is a type of balance disorder along with labyrinthitis and Ménière's disease. Diagnosis is typically made when the Dix–Hallpike test results in nystagmus (a specific movement pattern of the eyes) and other possible causes have been ruled out. In typical cases medical imaging is not needed.

BPPV is often treated with a number of simple movements such as the Epley maneuver or Brandt–Daroff exercises. Medications may be used to help with nausea. There is tentative evidence that betahistine may help with the vertigo but its use is not generally needed. BPPV is not a serious condition. Typically it resolves in one to two weeks. It however may recur in some people.

The first medical description of the condition occurred in 1921 by Robert Barany. About 2.4% of people are affected at some point in time. Among those who live until their 80s, 10% have been affected. BPPV affects females twice as often as males. Onset is typically in the person's 50s to 70s.

The signs of vertiginous epilepsy often occur without a change in the subject’s consciousness so that they are still aware while experiencing the symptoms. It is often described as a sudden onset of feeling like one is turning in one direction, typically lasting several seconds. Although subjects are aware during an episode, they often cannot remember specific details due to disorientation, discomfort, and/or partial cognitive impairment. This sensation of rotational movement in the visual and auditory planes is also known as a vertiginous aura (symptom), which can precede a seizure or may constitute a seizure itself. Auras are a “portion of the seizure that occur before consciousness is lost and for which memory is retained afterwards.” Auras can be focused in different regions of the brain and can thus affect different functions. Some such symptoms that may accompany vertiginous epilepsy include:

- Auditory hallucination

- Cognitive impairment

- Motor activity

- Ictal behavior

- Limbic auras

Many people tend to mistake dizziness as vertigo, and although they sound similar, dizziness is not considered a symptom of vertiginous epilepsy. Dizziness is the sensation of imbalance or floating, impending loss of consciousness, and/or confusion. This is different from vertigo which is characterized by the illusion of rotational movement caused by the “conflict between the signals sent to the brain by balance- and position-sensing systems of the body”.

The syndrome is frequently noticed first in children around six months of age by their photophobic activity and/or their nystagmus. The nystagmus becomes less noticeable with age but the other symptoms of the syndrome become more relevant as school age approaches. Visual acuity and stability of the eye motions generally improve during the first 6–7 years of life (but remain near 20/200).

The congenital forms of the condition are considered stationary and do not worsen with age.

The five symptoms associated with achromatopsia/dyschromatopsia are:

- Achromatopsia

- Amblyopia (reduced visual acuity)

- Hemeralopia (with the subject exhibiting photophobia)

- Nystagmus

- Iris operating abnormalities

The syndrome of achromatopsia/dyschromatopsia is poorly described in current medical and neuro-ophthalmological texts. It became a common term following the popular book by the neuroscientist Oliver Sacks, ""The Island of the Colorblind"" in 1997. Up to that time most color-blind subjects were described as achromats or achromatopes. Those with a lesser degree of color perception abnormality were described as either protanopes, deuteranopes or tetartanopes (historically tritanopes).

Achromatopsia has also been called rod monochromacy and total congenital color blindness. Individuals with the congenital form of this condition show complete absence of cone cell activity via electroretinography at high light levels. There are at least four genetic causes of congenital ACHM, two of which involve cyclic nucleotide-gated ion channels (ACHM2/ACHM3), a third involves the cone photoreceptor transducin ("GNAT2", ACHM4), and the last remains unknown.

Positional alcohol nystagmus (PAN) is nystagmus (visible jerkiness in eye movement) produced when the head is placed in a sideways position. PAN occurs when the specific gravity of the membrane space of the semicircular canals in the ear differs from the specific gravity of the fluid in the canals because of the presence of alcohol.

Aside from a complete inability to see color, individuals with complete achromatopsia have a number of other ophthalmologic aberrations. Included among these aberrations are greatly decreased visual acuity (<0.1 or 20/200) in daylight, Hemeralopia, nystagmus, and severe photophobia. The fundus of the eye appears completely normal. Also see Pingelap.

Zonular cataract and nystagmus, also referred as Nystagmus with congenital zonular cataract is a rare congenital disease associated with Nystagmus and zonular cataract of the eye.

Vertiginous epilepsy is infrequently the first symptom of a seizure, characterized by a feeling of vertigo. When it occurs there is a sensation of rotation or movement that lasts for a few seconds before full seizure activity. While the specific causes of this disease are speculative there are several methods for diagnosis, the most important being the patient's recall of episodes. Most times, those diagnosed with vertiginous seizures are left to self-manage their symptoms or are able to use anti-epileptic medication to dampen the severity of their symptoms. Vertiginous epilepsy has also been referred to as Epileptic vertigo, Vestibular epilepsy, Vestibular seizures, and Vestibulogenic seizures in different cases, but vertiginous epilepsy is the preferred term.

When balance is impaired, an individual has difficulty maintaining upright orientation. For example, an individual may not be able to walk without staggering, or may not even be able to stand. They may have falls or near-falls. The symptoms may be recurring or relatively constant. When symptoms exist, they may include:

- A sensation of dizziness or vertigo.

- Lightheadedness or feeling woozy.

- Problems reading and difficulty seeing.

- Disorientation.

Some individuals may also experience nausea and vomiting, diarrhea, faintness, changes in heart rate and blood pressure, fear, anxiety, or panic. Some reactions to the symptoms are fatigue, depression, and decreased concentration. The symptoms may appear and disappear over short time periods or may last for a longer period.

Cognitive dysfunction (disorientation) may occur with vestibular disorders. Cognitive deficits are not just spatial in nature, but also include non-spatial functions such as object recognition memory. Vestibular dysfunction has been shown to adversely affect processes of attention and increased demands of attention can worsen the postural sway associated with vestibular disorders. Recent MRI studies also show that humans with bilateral vestibular damage undergo atrophy of the hippocampus which correlates with their degree of impairment on spatial memory tasks.

Problems with balance can occur when there is a disruption in any of the vestibular, visual, or proprioceptive systems. Abnormalities in balance function may indicate a wide range of pathologies from causes like inner ear disorders, low blood pressure, brain tumors, and brain injury including stroke.

Many different terms are often used for dizziness, including lightheaded, floating, woozy, giddy, confused, helpless, or fuzzy. Vertigo, Disequilibrium and pre-syncope are the terms in use by most physicians and have more precise definitions.

Vertigo

Vertigo is the sensation of spinning or having the room spin about you. Most people find vertigo very disturbing and report associated nausea and vomiting.

Disequilibrium

Disequilibrium is the sensation of being off balance, and is most often characterized by frequent falls in a specific direction. This condition is not often associated with nausea or vomiting.

Presyncope

Pre-syncope is a feeling of lightheadedness or simply feeling faint. Syncope, by contrast, is actually fainting. A circulatory system deficiency, such as low blood pressure, can contribute to a feeling of dizziness when one suddenly stands up.

Problems in the skeletal or visual systems, such as arthritis or eye muscle imbalance, may also cause balance problems.

It has been suggested that the disease follows a x-linked pattern of inheritance though studies done on this particular disease are few.

The main symptom of labyrinthitis is severe vertigo. Rapid and undesired eye motion (nystagmus) often results from the improper indication of rotational motion. Nausea, anxiety, and a general ill feeling are common due to the distorted balance signals that the brain receives from the inner ear.

Vertigo is a sensation of spinning while stationary. It is commonly associated with nausea or vomiting, unsteadiness (postural instability), falls, changes to a person's thoughts, and difficulties in walking. Recurrent episodes in those with vertigo are common and frequently impair the quality of life. Blurred vision, difficulty in speaking, a lowered level of consciousness, and hearing loss may also occur. The signs and symptoms of vertigo can present as a persistent (insidious) onset or an episodic (sudden) onset.

Persistent onset vertigo is characterized by symptoms lasting for longer than one day and is caused by degenerative changes that affect balance as people age. Naturally, the nerve conduction slows with aging and a decreased vibratory sensation is common.

Additionally, there is a degeneration of the ampulla and otolith organs with an increase in age. Persistent onset is commonly paired with central vertigo signs and symptoms.

The characteristics of an episodic onset vertigo is indicated by symptoms lasting for a smaller, more memorable amount of time, typically lasting for only seconds to minutes. Typically, episodic vertigo is correlated with peripheral symptoms and can be the result of but not limited to diabetic neuropathy or autoimmune disease.