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ICD-10 | H55 |
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ICD-9 | 794.14 |
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Nystagmus is involuntary eye movement can be part of the vestibulo-ocular reflex (VOR), with the eyes moving first in the direction of the lesioned side (slow phase) followed by a quick correction (fast phase) to the opposite side or away from the lesioned side.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). The oscillations may occur in the vertical, 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. Over the past forty years, however, 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.
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 eye movements, while nystagmus is characterised by the combination of a slow eye movement that usually act to take the eye off the point of regard, interspersed with the fast 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. Over forty types of nystagmus have been classified.
Diagnosis[]
Nystagmus is very noticeable but rarely 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),[1] or even less invasive devices called videonystagmograph (VNG),[2] 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.[3]
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.[4]
Induced nystagmus[]
An easy way of inducing nystagmus is by having the person close her or his eyes and spin around. After a few spins, there is a distinct jerking of the eyes from side to side when they are reopened: this is rotatory-induced nystagmus. The degree of nystagmus varies greatly between people and even in the same person at different times.
Another type of induced nystagmus is the optokinetic nystagmus (OKN). It can be elicited by presenting a moving pattern. The eyes tend to track the pattern, but snap back regularly. The nystagmus persists for a short while even after the cessation of the stimulus. This is called "opto-kinetic after-nystagmus" (OKAN).
Pathological nystagmus[]
- Main article: 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.[5]
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.[6]
Horizontal nystagmus[]
Horizontal nystagmus is also classified into three degrees as follows:
- First degree nystagmus is present only on lateral gaze, and has the fast phase in the direction of gaze;
- Second degree nystagmus is present in the primary (neutral) position of gaze;
- Third degree nystagmus is present in the same direction in all gaze positions
Such distinctions help to identify the anatomical source of the nystagmus. First degree nystagmus usually originates in the brainstem or cerebellum, while second and third degree nystagmus are usually vestibular in origin.
Other (extremely) rare pathologic nystagmuses are gaze paretic, rebound, fixation, congenital and dissociated nystagmus.
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.[7] 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.
Physiological nystagmus[]
- Main article: Physiologic nystagmus
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.
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,[8] 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.[9]
- 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.[9]
Diseases presenting nystagmus[]
Some of the diseases which present nystagmus as a pathological sign are:
- Head trauma (the most common cause in young people)
- Stroke (the most common cause in older people)
- Ménière’s disease and other balance disorders
- Multiple sclerosis
- Brain tumors
- Wernicke-Korsakoff syndrome
- Encephalopathy
- Lateral medullary syndrome
- Aniridia
- Optic nerve hypoplasia
- Albinism
- Noonan syndrome
- Pelizaeus-Merzbacher disease
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, stimulants, psychedelic drugs, 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 not normally aware of their spontaneous eye movements, but vision can be impaired depending on the severity of the movements.
Types of early-onset nystagmus include the following:
- Infantile:
- Albinism
- Aniridia
- Bilateral congenital cataract
- Bilateral optic nerve hypoplasia
- Idiopathic
- Leber's congenital amaurosis
- Optic nerve or macular disease
- Persistent tunica vasculosa lentis
- Rod monochromatism
- Visual-motor syndrome of functional monophthalmos
- Latent nystagmus
- Noonan syndrome
- Nystagmus blockage syndrome
X-linked infantile nystagmus is associated with mutations of the gene FRMD7, which is located on the X chromosome.[10][11]
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).[12][13] CSNB-2 involves mutations of CACNA1F, a voltage-gated calcium channel that, when mutated, does not conduct ions.[14]
Acquired nystagmus[]
It may be acquired from:
- Diseases. Some of the diseases that present nystagmus as a pathological sign:
- Aniridia
- Benign Paroxysmal Positional Vertigo [15]
- Brain tumors (Medulloblastoma, Astrocytoma, or other tumors in the posterior fossa.
- Head trauma
- Lateral medullary syndrome
- Ménière's disease and other balance disorders
- Multiple sclerosis
- Optic nerve hypoplasia
- Pelizaeus-Merzbacher disease
- Superior canal dehiscence syndrome
- Stroke (the most common cause in older people)
- Tullio phenomenon
- Wernicke-Korsakoff syndrome
- Whipple's disease
- Toxic/metabolic reasons could be the result of the following:
- Alcohol intoxication
- Amphetamines
- Barbiturates
- Benzodiazepines
- Ketamine
- Lithium
- Lysergic acid diethylamide (LSD)
- Methylenedioxymethamphetamine (MDMA)
- Methylenedioxyamphetamine (MDA)
- Other anticonvulsants or sedatives
- Phencyclidine (PCP)
- Phenytoin (Dilantin)
- Salicylates
- SSRIs
- Thiamine deficiency
- Wernicke's encephalopathy
- 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:
- Cerebellar ataxia
- Chiari Malformation
- Multiple sclerosis
- Stroke
- Thalamic hemorrhage
- Trauma
- Tumor
Other causes[]
- Non-physiological
- Trochlear nerve malfunction[16]
- Vestibular Pathology (Ménière's disease, SCDS (superior canal dehiscence syndrome), BPPV, Labyrinthitis)
Alcohol[]
- Main article: Positional alcohol nystagmus
In the United States, testing for horizontal gaze nystagmus is one of a battery of field sobriety tests used by police 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
- lack of smooth pursuit,
- distinct and sustained nystagmus at maximum deviation, and
- 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.[citation needed]
The horizontal gaze nystagmus test has been highly criticized and major errors in the testing methodology and analysis found.[17][18] 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 blood alcohol content than other standard field sobriety tests.[19]
==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,[20] levetiracetam, 3,4-diaminopyridine, 4-aminopyridine, and acetazolamide.[21] Several therapeutic approaches, such as contact lenses,[22] 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.Template:Medical citation needed
Acupuncture has also been shown in some studies to have beneficial effects on the symptoms of nystagmus. These benefits have been seen in treatments where acupuncture points of the neck were used, specifically points on the sternocleidomastoid muscle.[23][24] Benefits of acupuncture for treatment of nystagmus include a reduction in frequency and decreased slow phase velocities which led to an increase in foveation duration periods both during and after treatment.[24] By the standards of Evidence-based medicine, the quality of these studies can be considered poor (for example, Ishikawa has a study sample size of just six, is unblinded and without proper control), and given high quality studies showing that acupuncture has no effect beyond placebo, the results of these studies have to be considered clinically irrelevant until higher quality studies are produced.
Perception of nystagmus[]
Nystagmus is very noticeable, but little recognised.
In 2003, the Royal National Institute of the Blind issued a press release [5] criticising the impressionist Rory Bremner for his impersonation of David Blunkett, then British Home Secretary, including mimicry of his nystagmus. In a subsequent segment on the BBC radio programme "In Touch", a variance of opinion is documented.
A typical adjective used [6][7] [8] to describe the appearance of actor Pruitt Taylor Vince's nystagmus is "creepy".
See also[]
References[]
- ↑ (2007). Introduction to electronystagmography for END technologists. American Journal of Electroneurodiagnostic Technology 47 (3): 178–89.
- ↑ (2003). Benign positional paroxysmal vertigo: videonystagmographic study using rotatory test. Acta Otorhinolaryngologica Italica 23 (2): 67–72.
- ↑ (2007). Eye movement recordings: methods. Developments in Ophthalmology 40: 15–34.
- ↑ 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.
- ↑ 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).
- ↑ nystagmus. URL accessed on 2007-06-07.
- ↑ (2006). Positional nystagmus and vertigo due to a solitary brachium conjunctivum plaque. Journal of Neurology, Neurosurgery & Psychiatry 77 (6): 790–2.
- ↑ Pierrot-Deseilligny C, Milea D (June 2005). Vertical nystagmus: clinical facts and hypotheses. Brain 128 (Pt 6): 1237–46.
- ↑ 9.0 9.1 "Sensory Reception: Human Vision: Structure and function of the Human Eye" vol. 27, p. 179 Encyclopaedia Britannica, 1987
- ↑ (2007). A Review of the Molecular Genetics of Congenital Idiopathic Nystagmus (CIN). Ophthalmic Genetics 28 (4): 187–91.
- ↑ (2008). Five novel mutations of the FRMD7 gene in Chinese families with X-linked infantile nystagmus. Molecular vision 14: 733–8.
- ↑ (2005). Focus on Molecules: Nyctalopin. Experimental Eye Research 81 (6): 627–8.
- ↑ (2008). A common NYX mutation in Flemish patients with X linked CSNB. British Journal of Ophthalmology 93 (5): 692–6.
- ↑ (2007). Functional analysis of congenital stationary night blindness type-2 CACNA1F mutations F742C, G1007R, and R1049W. Neuroscience 150 (2): 335–45.
- ↑ (2005). É importante restringir a movimentação cefálica após a manobra de Epley?. Revista Brasileira de Otorrinolaringologia 71 (6): 769–75.
- ↑ Lindgren, Stefan (1993). Kliniska färdigheter: Informationsutbytet mellan patient och läkare (in Swedish), Lund: Studentlitteratur.Template:Page needed
- ↑ Booker JL (2004). The Horizontal Gaze Nystagmus test: fraudulent science in the American courts. Science & Justice 44 (3): 133–9.
- ↑ Booker JL (2001). End-position nystagmus as an indicator of ethanol intoxication. Science & Justice 41 (2): 113–6.
- ↑ McKnight AJ, Langston EA, McKnight AS, Lange JE (May 2002). Sobriety tests for low blood alcohol concentrations. Accident Analysis and Prevention 34 (3): 305–11.
- ↑ (2007). Memantine/Gabapentin for the treatment of congenital nystagmus. Current neurology and neuroscience reports 7 (5): 395–6.
- ↑ Groves, Nancy (March 15, 2006). Many options to treat nystagmus, more in development. Ophthalmology Times.
- ↑ (2004). The use of contact lenses to treat visually symptomatic congenital nystagmus. Journal of Neurology, Neurosurgery & Psychiatry 75 (2): 314–6.
- ↑ Ishikawa, S., et al. (1987). Treatment of nystagmus by acupuncture. Highlights in neuro-ophthalmology, 6th ed. pg 227–232.
- ↑ 24.0 24.1 Blekher, T. (1998). "Effect of acupuncture on foveation characteristics in congenital nystagmus". British Journal of Ophthamology. 82:115-120. Accessed May 6th, 2012: [1]
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