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nystagmus

 
American Heritage Dictionary:

nys·tag·mus

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(nĭ-stăg'məs) pronunciation
n.
A rapid, involuntary, oscillatory motion of the eyeball.

[New Latin, from Greek nustagmos, drowsiness.]

nystagmic nys·tag'mic (-mĭk) adj.

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Oxford Companion to the Body:

nystagmus

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Nystagmus is a disorder of eye movements, when they show involuntary, rhythmic oscillations. The name is from the Greek, depicting the slow nodding of drowsiness accompanied by irregular, quick raising of the chin. Clinically, most nystagmus is horizontal in direction, but vertical and torsional forms can occur. It usually presents a diagnostic challenge and special tests are used to induce nystagmus and elucidate the neurological cause. Two major groups are recognized: jerk nystagmus, with oscillations that are faster in one direction than in the other, creating a jerky rhythm; and pendular nystagmus, with oscillations that are roughly equal in speed to either side.

Jerk nystagmus is named according to the direction of the fast phase, although the slower, return movement that regains and holds ocular fixation is more important functionally. Such movements are easily seen in someone looking out of a moving train who is trying to count the railway sleepers in the adjacent track. The fast phase is in the direction of travel of the train. Such opto-kinetic nystagmus (OKN) can be demonstrated by rotating a cylindrical drum painted with black vertical stripes in front of the subject: the eyes will move in the direction of drum rotation, followed by a quick return to fixate on the next moving stripe. The urge to follow these movements is so powerful that OKN can even be used to prove vision in someone claiming to be blind.

Jerk nystagmus can also result from stimulation of the semicircular canals of the vestibular system. There are two groups of three canals that lie in three planes at right angles to each other in either side of the skull. Stimulation of these canals by head movement causes ocular movements that maintain the eyes' positions in space and so stabilize the field of view. If the head movement causes the eyes to reach the limit of comfortable sideward gaze the eyes make a fast, compensatory movement to the central position. Careful testing with OKN and vestibular-induced nystagmus can be used to pinpoint the site of neurological defects in some disease conditions.

Pendular nystagmus is found with loss of central, detail vision, such as occurs with bilateral macular lesions present from birth in albinism, aniridia (absence of the iris), or total colour blindness. There are rapid, pendular eye movements in miners' nystagmus' and the condition was attributed to defective illumination in mines. This occupational nystagmus has now been effectively eliminated by adequate lighting underground.

Congenital nystagmus can occur without other defects. The nystagmus appears pendular in straight-ahead gaze and becomes jerky on side gaze. Although visual acuity in the distance is always reduced, and usually to levels below the legal requirements for driving, reading can be surprisingly good, provided that the patient is allowed to hold the book in the preferred position. This may be closer than normal and with the head turned to one side. Parents of a child with congenital nystagmus may gain some comfort from the descriptive term ‘dancing eyes’ and from the knowledge that, with understanding teachers, education at a normal school followed by university is achievable.

— Peter Fells

See also eyes; eye movements; vestibular system.

Gale Encyclopedia of Children's Health:

Nystagmus

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Definition

Nystagmus is a condition in which there is involuntary and rhythmic movement or oscillation of the eye. It is often caused by an underlying ocular or neurological disorder.

Description

The eye movements associated with nystagmus are varied. They can be either pendular, in which the oscillations are equal in all directions and or jerk, in which the movements may be faster in one direction than another. The frequency of the oscillation or movement and the amplitude of the oscillation also vary. The movements themselves may be vertical, horizontal, circular, or oblique in direction. Nystagmus can be sensory and develop as a result of poor vision, or it can be motor and develop as a result of a neurological problem.

Nystagmus may be congenital, or it may be acquired. Congenital, or infantile, nystagmus appears within the first few months of life. Congenital nystagmus is usually binocular and affects both eyes, is horizontal in direction, and does not occur while the child is sleeping. It decreases when the child's eyes converge or move inward. Most of these cases of nystagmus develop because of poor vision and do not have an underlying neurological cause.

Children with congenital nystagmus usually have a point in their eye movement in which the intensity of the nystagmus is decreased. This is called the null point, and the child may adopt a head tilt or rotation to help maintain his or her eyes at this position. This point is usually not in straight ahead or in a primary gaze position. Children with nystagmus who have their the null point located at a position in which the eyes are positioned inward may develop an esotropia, a form of strabismus or eye turn.

One variant of congenital nystagmus is spasmus nutans, which appears as a triad with accompanying head nodding and torticollis (head turn or tilt), and is seen between four months and three-and-a-half years of age and usually resolves without treatment within one to two years of onset. Rarely does it persist past age five. Usually spasmus nutans appears bilaterally, and the nystagmus is in a horizontal direction. When the nystagmus of spasmus nutans is vertical or rotary, the child does not have a head tilt.

There are various types of nystagmus. Downbeat nystagmus is characterized by a nystagmus that is more pronounced when the child looks down, especially when looking to the side, or in lateral gaze. An accentuated oscillation when looking up is seen in upbeat nystagmus. Seesaw nystagmus is an unusual type of in which one eye moves in and down and the other out and up. A periodic alternating nystagmus (PAN) is observed in primary gaze when the patient is looking straight ahead and is characterized by eye movements that continuously change direction and speed. Peripheral vestibular nystagmus may be accompanied by vertigo, nausea, and tinnitus, or ringing in the ears. This type of nystagmus is not always apparent but can be seen by a doctor when he or she looks in the back of the eye with a direct ophthalmoscope.

Latent nystagmus appears only when one eye is covered. This is a congenital nystagmus caused by an ocular motor disturbance rather than visual deprivation. It is often accompanied by strabismus or an eye turn. A child with latent nystagmus will not see well when one eye is covered.

Gaze evoked nystagmus occurs only when one is looking to the side in extreme lateral gaze. This type of nystagmus can be caused by ethanol and recreational drug use, but is seen in myasthenia gravis and thyroid disease as well.

Some types of nystagmus are normal. If one looks at an object in extreme gaze for a long period of time, endpoint nystagmus may be noted. Optokinetic nystagmus (OKN) is a nystagmus that can be elicited involuntarily when a rapidly moving striped object is passed in front of an individual's eyes.

Transmission

Congenital nystagmus may be transmitted genetically, either as an autosomal recessive or dominant, or as an X-linked recessive trait. It can also be associated with other conditions that are genetically transmitted. For example, Leber's amaurosis is an autosomal dominant trait and albinism is X-linked.

Demographics

Congenital nystagmus occurs twice as frequently in males than in females. The prevalence of nystagmus in the pediatric population is .015 percent. Eighty percent of nystagmus is congenital, and the remaining 20 percent is acquired.

Causes and Symptoms

The eyes of an individual with nystagmus cannot remain still and oscillate in some position of gaze. Those with nystagmus usually have decreased vision and poor depth perception, although those born with nystagmus, may not realize that their vision is poor. Those with acquired nystagmus may experience double vision or oscillopsia, or that objects in their visual space appear to move. An acquired nystagmus may be accompanied by other symptoms such dizziness, difficulty with balance, hearing loss, poor coordination, and numbness. If an individual with nystagmus experiences oscillopsia, then the nystagmus is acquired.

The primary cause of congenital nystagmus is visual deprivation, and the causes of visual deprivation in an infant include cataracts, oculoalbinism, glaucoma, retinal detachments, Leber's amaurosis, developmental abnormalities of the optic nerve such as a coloboma, and achromatopsia, a condition in which the infant cannot see color.

Acquired nystagmus can be caused by demyelination of nerve fibers, such as occurs in multiple sclerosis, lesions or tumors of the vestibular or visual pathways, strokes of the central nervous system, and drug use, both recreational as well as a side effect of prescribed drugs, such as those used to treat seizures and depression. Other causes of acquired nystagmus are Arnold-Chiari malformations, vitamin deficiencies, syphilis, Wernicke's encephalopathy, Behcet's syndrome, and Meniere's disease.

When to Call the Doctor

Since nystagmus can be caused by tumors, stroke, and trauma or neurological disorder, any type of nystagmus must be evaluated by a qualified practitioner. The nystagmus can be a sign of a serious problem. For example, a type of tumor called chiasmal glioma has signs and symptoms similar to spasmus nutans.

Diagnosis

Diagnosis of nystagmus is made primarily by patient history as reported by a parent, the age of onset, and observation of any accompanying signs such as a head turn, tilt or tremor, or oscillopsia. If possible, the infant or child's best visual acuity is determined. If the onset is acute, then usually the nystagmus is acquired.

The type of nystagmus can accurately be determined by eye movement recordings, which map direction, frequency, null point, and amplitude of the nystagmus. For the infant with congenital nystagmus, evoked response potential (EVR) and electroretinogram (ERG) give the doctor objective information about visual potential, and magnetic resonance imaging (MRI) can determine if and where a lesion is located. For the infant or young child, some of these tests may be done under anesthesia.

Treatment

The treatment for nystagmus, once the etiology is determined and treated, includes optical devices such as contact lenses and glasses, medication, and surgery.

For individuals with nystagmus correction of refractive error with glasses or contact lenses is the first step in treating the condition. For 85 percent of children with nystagmus, a spectacle prescription improves vision significantly. For those with congenital nystagmus, prism may be put in glasses to help position the eye at its null point or to help the eyes converge. For some people contact lenses are prescribed. Contact lenses slow down eye movements, and because the optical center of the prescription is always centered on the eye with the contact lens, vision improves. Low vision aids such as telescopes assist those whose vision cannot be fully corrected with spectacles and contact lenses alone. Tinting of the glasses or sunglasses may decrease the nystagmus of individuals with albinism. For the patient with oscillopsia, grinding prism into the spectacles may move the visual field to a point of decreased oscillopsia.

Congenital nystagmus, when due to a visual deprivation, is rarely improved by surgery. But when a head tilt or head turn accompanies nystagmus, surgery to correct a muscle imbalance may improve nystagmus and visual acuity. Surgery on the extraocular muscles of the eye may be helpful when the child's null point is in not in primary gaze but located at least 30 degrees from straight-ahead vision. When a tumor or stroke has caused an acquired nystagmus, then neurosurgery, if indicated for the underlying cause, may lead to resolution of the nystagmus. When surgery is considered, the risks of anesthesia must also be considered.

If oscillopsia is a co-existing symptom, then drugs can be given to reduce the ocular oscillations. Vestibular nystagmus can be treated by diazepam or scopolamine. Drugs called GABA agonists, such as baclofen and carbamazepine, are useful in treatment of seesaw nystagmus and PAN, if the nystagmus is acquired and not congenital. Baclofen cannot be given to children.

Botox (Botulinum toxin) injections can temporarily control the eye movements, but because of side effects such as double vision and ptosis or drooping of the eyelid, and because it is not a permanent solution, Botox is not used often.

If the nystagmus is due to drug toxicity, then reducing or discontinuing the drug eventually resolves the problem.

Alternative Treatment

Acupuncture and biofeedback and vision therapy have been successful for some patients.

Prognosis

Congenital nystagmus is usually a benign condition. It is not curable, but its symptoms can be diminished with spectacles or contact lenses. The best corrected vision for most individuals with congenital nystagmus is between 20/40 and 20/70, but correction to 20/20 is possible for some. Nystagmus associated with spasmus nutans resolves spontaneously before the child reaches school age.

The prognosis for an acquired nystagmus depends on its cause. If the condition is due to a side effect of a drug, then decreasing or changing the treatment drug eventually resolves the nystagmus.

Prevention

In general nystagmus cannot be prevented. Since the cause of acquired nystagmus can be due to a co-existing neurological condition, prompt attention to other neurological signs that may accompany nystagmus, such as dizziness, may prevent or decrease the severity of nystagmus itself. Careful monitor of dosage of those drugs with nystagmus as a side effect may prevent the condition.

Parental Concerns

Because nystagmus can be associated with many medical problems, the child with this condition must undergo a complete ocular and neurological evaluation.

Children with nystagmus are not aware that they may have a visual deficiency and as they get older must be helped with the restrictions that nystagmus places on them. For instance, driving may be restricted or not permitted. Certain occupations for which good visual correction is a requirement may be not feasible. Every effort must be made to integrate the child with nystagmus into a normal school setting in order to prepare the child for adult life, even if cosmetic concerns may instinctively lead the parent to want to protect the child.

Support for families of those with nystagmus can be found through the American Nystagmus Network.

Resources

Books

Halmagyi, G. Michael, and Phillip D. Cremer. "Central Eye Movements Disorders." Chapter 283 in Principles and Practice of Ophthalmology , 2nd ed. Philadelphia: Saunders, 2000.

Wheeler, David T. "Nystagmus." In Current Ocular Therapy 5. Philadelphia: Saunders, 2000, p. 407.

Periodicals

Hensil, Jennifer, and Andrew S. Gurwood. "Understanding Nystagmus." Optometry 71 (July 2000): 439–48.

Hertle, Richard W. "Examination of the Refractive Management of Patients with Nystagmus." Survey of Ophthalmology 45 (November-December 2000): 215–22.

Moster, Mark L. "Nystagmus." Ophthalmology Clinics of North America 14 (March 2001): 205–15.

Web Sites

American Nystagmus Network. Available online at www.nystagmus.org/entry.html (accessed November 12, 2004).

Smith, Rodney J. "Solving the Diagnostic Puzzle of Congenital Nystagmus." Review of Optometry, June 1999 Case Report. Available online at www.revoptom.com/archive/issue/ro06f9.htm (accessed November 12, 2004).

[Article by: Martha Reilly, OD]


Saunders Veterinary Dictionary:

nystagmus

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A periodic, rhythmic, involuntary movement of both eyeballs in unison. There is a slow component in one direction and a quick return. The movement may be vertical, horizontal or rotary. Common causes are lesions of the cerebellum or the vestibular apparatus, or increased intracranial pressure.

  • aural n. — labyrinthine nystagmus.
  • cerebellar n. — one characterized by tremor, without fast and slow components.
  • Cheyne's n. — a peculiar rhythmical eye movement resembling Cheyne–Stokes respiration in rhythm.
  • congenital n. — may be a primary functional defect or secondary to lesions in the visual pathways, sometimes associated with albinism. Reported in cattle, cats (particularly Siamese), and dogs.
  • dissociated n. — that in which the movements in the two eyes are dissimilar.
  • gaze n. — nystagmus made apparent by looking to the right or to the left.
  • horizontal n. — that in which the eyes move from side to side with the fast component opposite to the side of the lesion; seen with central or unilateral peripheral vestibular disease.
  • jerk n. — vestibular nystagmus (see below).
  • labyrinthine n. — vestibular nystagmus due to labyrinthine disturbance.
  • latent n. — that occurring only when one eye is covered.
  • lateral n. — involuntary horizontal movement of the eyes.
  • ocular n. — wandering movement of the eyes as though searching for something. Associated with congenital blindness.
  • optokinetic n. — nystagmus induced by looking at objects moving across the field of vision.
  • oscillatory n. — pendular nystagmus.
  • pendular n. — that which consists of to-and-fro movements of equal velocity.
  • positional n. — that which occurs, or is altered in form or intensity, on assumption of certain positions of the head.
  • postrotatory n. — a normal finding after the animal has been rotated, with the fast phase away from the direction of rotation.
  • resting n. — that occurring while the head is stationary.
  • retraction n., n. retractorius — a spasmodic backward movement of the eyeball occurring on attempts to move the eye; a sign of midbrain disease.
  • rotatory n. — involuntary rotation of the eyes about the visual axis.
  • spontaneous n. — that occurring without specific stimulation of the vestibular system.
  • vertical n. — involuntary up-and-down movement of the eyes.
  • vestibular n. — nystagmus due to disturbance of the labyrinth or of the vestibular nuclei; the movements are usually jerky.
  • undulatory n. — an inherited disorder of Finnish Ayrshire cattle; there is a synchronous, tremor-like movement of the eyes but affected aninals are otherwise healthy.
Mosby's Dental Dictionary:

nystagmus

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(nīstag′mus)
n

The state of oscillatory movements of an organ or part, especially the eyeballs; irregular jerking movement of the eyes. Each movement of the cycle consists of a slow component in one direction and a rapid component in the opposite direction.

Random House Word Menu:

categories related to 'nystagmus'

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Random House Word Menu by Stephen Glazier
For a list of words related to nystagmus, see:
  • Defects and Disabilities - nystagmus: congenital or acquired, persistent, rapid, involuntary movement of eyeball, usu. from side to side

Wikipedia on Answers.com:

Nystagmus

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Nystagmus
Optokinetic nystagmus.gif

Horizontal optokinetic nystagmus, a normal (physiological) form of nystagmus
ICD-10 H55, H81.4
ICD-9 379.50, 794.14
DiseasesDB 23470
eMedicine article/1199177
MeSH D009759

Nystagmus /nɪˈstæɡməs/ is a condition of involuntary eye movement, acquired in infancy or later in life, that may result in reduced or limited vision.[1]

There are two key forms of Nystagmus: pathological and physiological, with variations within each type. Nystagmus may be caused by congenital disorders, acquired or central nervous system disorders, toxicity, pharmaceutical drugs or alcohol. Previously considered untreatable, in recent years several pharmaceutical drugs have been identified for treatment of Nystagmus.

Contents

Prevalence

Nystagmus is a relatively common clinical condition, affecting one in several thousand people. A survey conducted in Oxfordshire, United Kingdom found that by the age of two, one in every 670 children had manifested nystagmus.[1] Authors of another study in the United Kingdom estimated an incidence of 24 in 10,000 (~0.240 %), noting an apparently higher rate amongst white Europeans than in individuals of Asian origin.[2]

Diagnosis

Nystagmus is very noticeable but little recognized. Nystagmus can be clinically investigated by using a number of non-invasive standard tests. The simplest one is the caloric reflex test, in which one external auditory meatus is irrigated with warm or cold water or air. The temperature gradient provokes the stimulation of the horizontal semicircular canal and the consequent nystagmus.

The resulting movement of the eyes may be recorded and quantified by special devices called electronystagmograph (ENG), a form of electrooculography (an electrical method of measuring eye movements using external electrodes),[3] or even less invasive devices called videonystagmograph (VNG),[4] a form of video-oculography (VOG) (a video-based method of measuring eye movements using external small cameras built into head masks) by an audiologist. Special swinging chairs with electrical controls can be used to induce rotatory nystagmus.[5]

Over the past forty years objective eye movement recording techniques have been applied to the study of nystagmus, and the results have led to a greater accuracy and understanding of the condition.

Orthoptists may also use an optokinetic drum, or Electrooculography to assess their eye movements.

Nystagmus can be caused by subsequent foveation of moving objects, pathology, sustained rotation or substance use. Nystagmus is not to be confused with other superficially similar-appearing disorders of eye movements (saccadic oscillations) such as opsoclonus or ocular flutter that are composed purely of fast-phase (saccadic) eye movements, while nystagmus is characterised by the combination of a smooth pursuit, which usually acts to take the eye off the point of regard, interspersed with the saccadic movement that serves to bring the eye back on target. Without the use of objective recording techniques, it may be very difficult to distinguish between these conditions.

In medicine, the presence of nystagmus can be benign, or it can indicate an underlying visual or neurological problem.[6]

Pathologic nystagmus

Pathologic nystagmus is characterized by a biphasic ocular oscillation alternating a slow eye movement, or smooth pursuit, in one direction and a fast eye movement, or saccadic movement, in the other direction. The velocity of the slow phase eye velocity (SPEV) and the fast phase eye velocity (FPEV) are related to each other and can be considered as a measurement of the efficiency of the system stimulus/response.[7]

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.[8]

Variations

  • Central nystagmus occurs as a result of either normal or abnormal processes not related to the vestibular organ. For example, lesions of the midbrain or cerebellum can result in up- and down-beat nystagmus.
  • Peripheral nystagmus occurs as a result of either normal or diseased functional states of the vestibular system and may combine a rotational component with vertical or horizontal eye movements and may be spontaneous, positional, or evoked.
    • Gaze Induced nystagmus occurs or is exacerbated as a result of changing one's gaze toward or away from a particular side which has an affected vestibular apparatus.
    • Positional nystagmus occurs when a person's head is in a specific position.[9] An example of disease state in which this occurs is Benign paroxysmal positional vertigo (BPPV).
    • Post rotational nystagmus occurs after an imbalance is created between a normal side and a diseased side by stimulation of the vestibular system by rapid shaking or rotation of the head.
    • Spontaneous nystagmus is nystagmus that occurs randomly, regardless of the position of the patient's head.

Physiologic nystagmus

Physiologic 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.

Variations

The direction of nystagmus is defined by the direction of its quick phase (e.g. a right-beating nystagmus is characterized by a rightward-moving quick phase, and a left-beating nystagmus by a leftward-moving quick phase). The oscillations may occur in the vertical,[10] horizontal or torsional planes, or in any combination. The resulting nystagmus is often named as a gross description of the movement, e.g. downbeat nystagmus, upbeat nystagmus, seesaw nystagmus, periodic alternating nystagmus.

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.

  • 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.[11]
  • 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.[11]

Causes

The cause for pathological nystagmus may be congenital, idiopathic, or secondary to a pre-existing neurological disorder. It also may be induced temporarily by disorientation (such as on roller coaster rides) or by certain drugs (alcohol and other central nervous system depressants, inhalant drugs, and the dissociative anesthetics [PCP]).

Congenital nystagmus occurs more frequently than acquired nystagmus. It can be insular or accompany other disorders (such as micro-ophthalmic anomalies or Down Syndrome). Congenital nystagmus itself is usually mild and non-progressive. The affected persons are not normally aware of their spontaneous eye movements, but vision can be impaired depending on the severity of the movements.

Types of congenital nystagmus include the following:

X-linked infantile nystagmus is associated with mutations of the gene FRMD7, which is located on the X chromosome.[12][13]

Congenital 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).[14][15] CSNB-2 involves mutations of CACNA1F, a voltage-gated calcium channel that, when mutated, does not conduct ions.[16]

Acquired Nystagmus may be acquired from:

  • Diseases. Some of the diseases that present nystagmus as a pathological sign:
  • Toxic/metabolic reasons could be the result of the following:
  • Central nervous system (CNS) disorders, such as with a cerebellar problem, the nystagmus can be in any direction including horizontal. Purely vertical nystagmus is usually central in origin, but it is also a frequent adverse effect of high phenytoin toxicity. Causes include:
  • Other causes

Treatment

Congenital nystagmus has traditionally been viewed as non-treatable, but medications have been discovered in recent years that show promise in some patients. In 1980, researchers discovered that a drug called baclofen could effectively stop periodic alternating nystagmus. Subsequently, gabapentin, an anticonvulsant, was found to cause improvement in about half the patients who received it to relieve symptoms of nystagmus. Other drugs found to be effective against nystagmus in some patients include memantine,[19] levetiracetam, 3,4-diaminopyridine, 4-aminopyridine, and acetazolamide.[20] Several therapeutic approaches, such as contact lenses,[21] drugs, surgery, and low vision rehabilitation have also been proposed.

Clinical trials of a surgery to treat nystagmus (known as tenotomy) concluded in 2001. Tenotomy is being performed regularly at the University of Pittsburgh Children's Hospital and by a handful of surgeons around the world. The surgery developed by Louis F. Dell'Osso Ph.D. aims to reduce the eye shaking (oscillations), which in turn tends to improve visual acuity.[medical citation needed]

Nystagmus and alcohol

Main article: Positional alcohol nystagmus

In police work, testing for horizontal gaze nystagmus is one of a battery of field sobriety tests used by officers to determine whether a suspect is driving under the influence of alcohol. The test involves observation of the suspect's pupil as it follows a moving object, noting

  1. lack of smooth pursuit,
  2. distinct and sustained nystagmus at maximum deviation, and
  3. the onset of nystagmus prior to 45 degrees.

The field sobriety test studies published by the National Highway Traffic Safety Administration have never been peer reviewed and attempts to duplicate the study results have been unsuccessful.[22]

The horizontal gaze nystagmus test has been highly criticized and major errors in the testing methodology and analysis found.[23][24] However, the validity of the horizontal gaze nystagmus test for use as a field sobriety test for persons with a blood alcohol level between 0.04-0.08 is supported by peer reviewed studies and has been found to be a more accurate indication of BAC than other standard field sobriety tests.[25]

Research

[icon] This section requires expansion.

Several universities are researching nystagmus and are looking for volunteers to take part in research activities.

See also

References

  1. ^ a b "General Information about Nystagmus". American Nystagmus Network. February 21, 2002. http://www.nystagmus.org/aboutn.html. Retrieved 2011-11-09. 
  2. ^ Sarvananthan, N.; Surendran, M.; Roberts, E. O.; Jain, S.; Thomas, S.; Shah, N.; Proudlock, F. A.; Thompson, J. R. et al. (2009). "The Prevalence of Nystagmus: The Leicestershire Nystagmus Survey". Investigative Ophthalmology & Visual Science 50 (11): 5201–6. doi:10.1167/iovs.09-3486. PMID 19458336. 
  3. ^ Markley, BA (2007). "Introduction to electronystagmography for END technologists". American Journal of Electroneurodiagnostic Technology 47 (3): 178–89. PMID 17982846. 
  4. ^ Mosca, F; Sicignano, S; Leone, CA (2003). "Benign positional paroxysmal vertigo: videonystagmographic study using rotatory test". Acta Otorhinolaryngologica Italica 23 (2): 67–72. PMID 14526552. 
  5. ^ Eggert, T (2007). "Eye movement recordings: methods". Developments in Ophthalmology 40: 15–34. doi:10.1159/0000100347. PMID 17314477. 
  6. ^ Serra A, Leigh RJ (December 2002). "Diagnostic value of nystagmus: spontaneous and induced ocular oscillations". Journal of Neurology, Neurosurgery, and Psychiatry 73 (6): 615–8. doi:10.1136/jnnp.73.6.615. PMC 1757336. PMID 12438459. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1757336. 
  7. ^ Angelo Salami, Massimo Dellepiane, Edoardo Cervoni, Giancarlo Mascetti.Temporal analysis of the vestibular and optokinetic nystagmus. Volume 1240, October 2003, Pages 1333-1337. Oto-Rhino-Laryngology. Proceedings of the XVII World Congress of the International Federation of Oto-Rhino-Laryngological Societies (IFOS).
  8. ^ "nystagmus". http://www.drhull.com/EncyMaster/N/nystagmus.html. Retrieved 2007-06-07. 
  9. ^ Anagnostou, E (2006). "Positional nystagmus and vertigo due to a solitary brachium conjunctivum plaque". Journal of Neurology, Neurosurgery & Psychiatry 77 (6): 790–2. doi:10.1136/jnnp.2005.084624. 
  10. ^ Pierrot-Deseilligny C, Milea D (June 2005). "Vertical nystagmus: clinical facts and hypotheses". Brain 128 (Pt 6): 1237–46. doi:10.1093/brain/awh532. PMID 15872015. 
  11. ^ a b "Sensory Reception: Human Vision: Structure and function of the Human Eye" vol. 27, p. 179 Encyclopaedia Britannica, 1987
  12. ^ Self, James; Lotery, Andrew (2007). "A Review of the Molecular Genetics of Congenital Idiopathic Nystagmus (CIN)". Ophthalmic Genetics 28 (4): 187–91. doi:10.1080/13816810701651233. PMID 18161616. 
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External links

Look up Nystagmus in Wiktionary, the free dictionary.
Visual perception
Muscles of orbit
Tracking
Horizontal gaze
Vertical gaze
Pupillary reflex
Circadian rhythm

M: EYE

anat(g/a/p)/phys/devp/prot

proc, drug(S1A/1E/1F/1L)
Signs and symptoms
Diagnosis and evolution following
Investigation
Treatment
Borderline forms
Other

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