Refers to a condition of involuntary (or voluntary, in rare cases) eye movement, acquired in infancy or later in life, that may result in reduced or limited vision.
Normally, the head rotates about any axis, distant visual images are sustained by rotating eyes in the opposite direction on the respective axis.
Nystagmus is a relatively common clinical condition, affecting one in several thousand people.
The semicircular canals sense angular acceleration, and send signals to the nuclei for eye movement in the brain: subsequently a signal is relayed to the extraocular muscles to allow one’s gaze to fixate on one object as the head moves.
Nystagmus also occurs when the semicircular canals are being stimulated while the head is not in motion.
The direction of ocular movement is related to the semicircular canal that is being stimulated.
Two key forms of nystagmus: pathological and physiological, with variations occur within each type.
May be caused by congenital disorders, acquired or central nervous system disorders, toxicity, pharmaceutical drugs, alcohol, or rotational movement.
Nystagmus is also occasionally associated with vertigo.
Nystagmus is clinically investigated by non-invasive standard tests,including the caloric reflex test.
In the caloric reflex test the ear canal is irrigated with warm or cold water or air.
The temperature gradient during the caloric test provokes the stimulation of the horizontal semicircular canal and the consequent nystagmus.
The resulting movement of the eyes can recorded and quantified by electronystagmography (ENG), a form of electrooculography
Electrooculography is an electrical method of measuring eye movements using external electrodes.
Eye movements can also be measured using external small cameras to form video-oculography, as. Well as the use of swinging chairs with electrical controls can to induce rotatory nystagmus.
Nystagmus can be caused by substance use.
Can be benign, or it can indicate an underlying visual or neurological problem.
Pathological nystagmus is characterized by drifts of stationary retinal images that degrades vision and may produce illusory motion of the seen world.
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.
Many blind people have nystagmus
Central nystagmus occurs as a result of processes not related to the vestibular organ.
Lesions of the midbrain or cerebellum can result in up- and down-beat nystagmus.
Gaze induced nystagmus occurs or is exacerbated by changing one’s gaze toward or away from a particular side which has an affected central apparatus.
Peripheral nystagmus are a result of either normal or diseased functional states of the vestibular system.
Peripheral nystagmus may combine a rotational component with vertical or horizontal eye movements and may be spontaneous, positional, or evoked.
Positional nystagmus occurs when a person’s head is in a specific position, such as occurs with 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 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.
The direction of nystagmus is defined by the direction of its quick phase.
Oscillations may occur in the vertical, horizontal or torsional planes, or in any combination.
It is often named as a gross description of the movement- downbeat, upbeat, seesaw or periodic alternating nystagmus..
Opticokinetic nystagmus refers to nystagmus induced by looking at moving visual stimuli, such as moving horizontal or vertical lines, and/or stripes.
Postrotatory nystagmus occurs as 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.
The cause for pathological nystagmus may be congenital, idiopathic, or secondary to a pre-existing neurological disorder.
Pathological nystagmus may be temporarily induced by disorientation or by certain drugs such as alcohol and other central nervous system depressants, inhalant drugs, stimulants, psychedelic drugs, and dissociative drugs
Early onset nystagmus occurs more frequently than acquired nystagmus, and is usually mild and non-progressive.
With early onset nystagmus patients are not normally aware of their spontaneous eye movements, but vision can be impaired.
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 monophthalmus
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.
Acquired nystagmus:
Aniridia
Benign paroxysmal positional vertigo
Brain tumors in the posterior fossa.
Head trauma.
Lateral medullary syndrome.
Ménière’s disease.
Multiple sclerosis.
Optic nerve hypoplasia.
Superior canal dehiscence syndrome.
Stroke which is the most common cause in older people.
Wernicke–Korsakoff syndrome.
Whipple’s disease.
Toxic or metabolic reasons could be;
Alcohol intoxication
Amphetamines
Barbiturates
Benzodiazepines
Ketamine
Lithium
Anticonvulsants or sedatives
Salicylates
SSRIs
Thiamine deficiency
Wernicke’s encephalopathy
Central nervous system 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.
CNS causes of nystagmus causes include:
Cerebellar ataxia
Chiari Malformation
Multiple sclerosis
Stroke
Thalamic hemorrhage
Trauma
Tumor
Non-physiological associations:
Trochlear nerve malfunction
Vestibular Pathology (Ménière’s disease, SCDS (superior canal dehiscence syndrome), BPPV, Labyrinthitis)
Testing for horizontal gaze nystagmus to determine whether someone is driving under the influence of alcohol.
The test involves observation of the suspect’s pupil as it follows a moving object, with lack of smooth pursuit, distinct and sustained nystagmus at maximum deviation, and the onset of nystagmus prior to 45 degrees.
Congenital nystagmus has traditionally been viewed as non-treatable, but baclofen and gabapentin, provide improvement in about half the patients.
Other drugs effective in some patients include memantine, levetiracetam, and acetazolamide.
Treatment of congenital nystagmus attempts to improve the abnormal head posture, simulating artificial divergence or weakening the horizontal recti muscles.
Surgery to treat nystagmus is known as tenotomy
Physical/Occupational therapy is also used to treat nystagmus, consists of learning compensatory strategies to take over for the impaired system.