Methodology for studying spontaneous nystagmus. Checking tonogenic reactions
IN clinical practice In neurological patients, four types of nystagmus are distinguished:
Congenital nystagmus
Congenital nystagmus is characterized by long-term horizontal pendulum-like or jerky movements of the eyeballs. In some cases, congenital nystagmus is accompanied by damage to the visual pathway and deterioration of the patient’s vision. The mechanism and location of the lesion in congenital nystagmus are unknown.
Labyrinthine-vestibular nystagmus
Damage to the vestibular apparatus leads to the appearance of a slow smooth phase and a corrective fast phase, which together form a jerky saw-tooth nystagmus. Such unidirectional movement slow phase nystagmus reflects instability of the tonic neuronal activity of the vestibular nuclei. Damage to the semicircular canals of the inner ear leads to a slow deviation of the eyeball towards the lesion of the semicircular canal, followed by a rapid compensatory movement in the opposite direction.
Slow deviations of the eyeballs in the same direction are also pathological, however, according to the rules, the side of nystagmus is determined by the direction of the fast corrective impulse (fast phase of nystagmus). This instability of vestibular tone usually leads to systemic dizziness and oscillopsia (illusory movements of surrounding objects) in the patient.
Damage to the peripheral parts of the vestibular system is almost always accompanied by damage to several semicircular canals simultaneously. This leads to an imbalance between the signals entering the brain from the individual semicircular canals of the inner ear. In such a case, nystagmus is often mixed:
- with benign positional nystagmus, the patient usually develops mixed vertical-rotational nystagmus
- with unilateral destruction of the labyrinth, the patient experiences mixed horizontal-rotational nystagmus
Peripheral vestibular nystagmus decreases when the head is fixed and increases when its position changes (tilt, turn, rotation).
In cases of damage to the central vestibular connections, a central imbalance occurs between signals coming from various semicircular canals, and ascending vestibular or cerebellar-vestibular connections are also interrupted. Central vestibular nystagmus may visually resemble the nystagmus that develops with lesions of the semicircular canal, but bilateral vertical (up, down), rotational or horizontal nystagmus is more common. Central vestibular nystagmus decreases slightly when the patient's head is fixed and intensifies or is caused by a change in its position in space (tilt, turn, rotation).
Three types of labyrinthine-vestibular nystagmus are important for establishing the location of the lesion:
- Downward nystagmus is usually observed when looking straight ahead and increases when looking to the sides. Downward nystagmus is caused by anomalies of the posterior fossa, such as Arnold-Chiari malformation and platybasia, as well as multiple sclerosis, cerebellar atrophy, hydrocephalus, metabolic disorders, familial periodic ataxia; Downward nystagmus may also occur as a toxic reaction to administration anticonvulsants.
- Upward nystagmus is a consequence of damage to the anterior parts of the cerebellar vermis, as well as diffuse damage to the brain stem due to Wernicke encephalopathy, meningitis, or as a result side effect medications.
- Horizontal (left, right) nystagmus in the initial position (when the patient is looking straight), observed when affected peripheral part vestibular analyzer and only sometimes for tumors of the posterior cranial fossa or Arnold-Chiari malformation.
Nystagmus, which occurs during targeted eye movements, is detected when the eyeballs deviate from the center. The ability to hold the eyes in the desired position is weakened due to damage to the neuronal integrator in the brain stem. Asymmetrical but conjugate horizontal nystagmus during targeted movements of the eyeballs occurs in the case of unilateral cerebellar lesions and tumors of the cerebellar-pontine angle (acoustic neuroma or auditory neuroma). A common cause of horizontal nystagmus is also the use of sedatives and anticonvulsants. Horizontal nystagmus, in which the fast phase when the eyeball is brought inward occurs more slowly than when the eyeball is abducted outward (dissociated nystagmus) is characteristic feature internuclear ophthalmoplegia.
Converging (converging) pulsating nystagmus, intensifying when trying to raise the eyes upward, is characterized by pulsating saccadic movements of the eyeballs towards each other. As a rule, convergent pulsating nystagmus is accompanied by other symptoms of damage to the posterior parts of the midbrain (Parinaud syndrome).
Periodic alternating nystagmus
In the case of periodic alternating nystagmus, the patient experiences horizontal nystagmus when looking straight ahead, periodically (every 1-2 minutes) changing its direction, either to the right or to the left. Nystagmus that occurs with purposeful eye movements and downward nystagmus may also be noted. This form of the disease (periodic alternating nystagmus) can be hereditary and occurs in combination with craniovertebral anomalies, as well as with multiple sclerosis and poisoning with anticonvulsants. If the nature of periodic alternating nystagmus is non-hereditary, giving the patient baclofen has a positive effect.
Dissociated vertical nystagmus
In the case of dissociated vertical nystagmus, alternating movements of the eyeballs are observed: while one eyeball moves up and inward, the other moves down and outward. Dissociated vertical nystagmus indicates damage to the nuclei of the reticular formation of the midbrain, including the intermediate nucleus of Cajal. Dissociated vertical nystagmus occurs with tumors located above the area of the sella turcica (craniopharyngioma), head trauma, and less commonly with cerebral infarction. Dissociated vertical nystagmus is often combined with bitemporal hemianopsia.
Conditions resembling nystagmus
Nystagmus may resemble such movement disorders eye like:
- convulsive twitching of the eyeballs with a characteristic rectangular signal (small jerky movements away from the point of fixation and back)
- trembling of the eyeballs (horizontal pulsating vibrations)
- opsoclonus (frequent saccadic oscillations)
- myokymia of the superior oblique muscle (monocular rotatory-vertical movements)
- ocular bobbing (ocular bobbing - rapid deviation of the eyeballs down with a slow return to the top)
- periodic movements of the eyeballs in a horizontal direction with a change in the direction of deviation every few seconds
Visual disturbances and eye movements are a signal of danger, the recognition of which is to a large extent increases the knowledge of a neurologist and neurosurgeon. A neurologist or neurosurgeon who is alert to such visible signals that the eye can send will not only recognize and differentiate them from each other, but will also understand their clinical significance.
Nystagmus (nystagmus; Greek nystagmos drowsiness, from nystaz to doze, to bow one's head drowsily) is an involuntary rhythmic biphasic (with fast and slow phases) movements of the eyeballs.Nystagmus is detected by visually fixing the doctor’s finger, placed 20-30 cm away from the temple of the person being examined in turn on both sides.
The method of electronystagmography is also used, based on a graphical recording of the biopotentials of the eyeball, changing with its movement.
Depending on the direction of the oscillatory movements, there are:
horizontal (most commonly seen)
vertical
diagonal
rotational nystagmus
By the nature of the movements:
pendulum-shaped (with equal amplitude of oscillatory movements),
jerky (with different amplitudes of oscillations: slow phase - in one direction and fast phase - in the other)
mixed (either pendulum-like or jerky movements appear).
Jerky nystagmus is called left- or right-sided depending on the direction of its fast phase. With jerky nystagmus, there is a forced rotation of the head towards the fast phase. With this rotation the patient compensates for weakness oculomotor muscles, and the amplitude of nystagmus decreases, therefore, if the head is turned to the right, the “right” muscles are considered weak: the external rectus of the right eye and the internal rectus of the left eye. This type of nystagmus is called right-sided.
Nystagmus can be:
large-caliber (with an amplitude of oscillatory eye movements of more than 15°)
medium-caliber (with an amplitude of 15-5°)
small-caliber (with amplitude less than 5°)
Also, to determine the severity of nystagmus, you can use the following criteria, which are simpler and more convenient when examining the patient:
nystagmus 1st degree – detected only when looking towards the fast component of nystagmus
nystagmus 2nd stage – detected when the patient looks straight ahead
nystagmus 3rd stage – the appearance of nystagmus when the patient looks towards the slow phase of nystagmus
Depending on the mechanism of occurrence, several types of nystagmus are distinguished, the most important of which in clinical practice are:
vestibular nystagmus caused by irritation of the receptors of the vestibular analyzer
optokinetic, caused by irritation of the optical apparatus of the eye.
Vestibular nystagmus consists of rhythmically alternating fast and slow phases, the time ratio of which in compensated processes and in healthy people is 1:3 - 1:5. It can occur spontaneously and be caused artificially.
Spontaneous nystagmus (N) is always a sign of a pathological process in the labyrinth of the inner ear or the brain. It can have horizontal, vertical or diagonal, rotational and convergent directions, which are determined by its fast phase.
By the direction of N. one can judge the level of damage.
I. horizontal N. indicates damage to the labyrinth, middle parts of the rhomboid fossa
II.vertical and diagonal - upper sections rhomboid fossa
III.rotational - lower sections rhomboid fossa
IV.converging N. is a symptom of damage to the midbrain
The amplitude of movements of the eyeballs during N. indicates the degree of damage to the vestibular analyzer.
A sharp predominance of horizontal N. in one direction indicates one-sidedness of the lesion of the labyrinth or central nervous system. (unilateral purulent labyrinthitis, labyrinthine artery thrombosis, pyramidal fissure temporal bone, tumor of the vestibulocochlear nerve).
The predominance of spontaneous N. in one eye indicates defeat brain stem, posterior longitudinal fasciculus, oculomotor or abducens nerve.
A sharp prolongation of the slow phase of the vestibular spontaneous N. in combination with floating movements of the eyeballs indicates a severe lesion in the area of the brain stem and is observed in acute period stroke, with traumatic hemorrhages in the brain, in acute stage meningoencephalitis, with brain tumors accompanied by a sharp increase intracranial pressure.
Artificially caused N. is usually observed in healthy people; With pathology, its parameters change.
The main types of artificial N. are
caloric,
rotational
post-rotational
pressor
I. Caloric N. observed when the labyrinth is warmed or cooled. To identify it, 100 ml of water at temperature 25° is poured into the external auditory canal for 10 s. If there is no effect, pour in water at temperature 19°. Each labyrinth is examined separately (the test is contraindicated in case of perforation of the eardrum, otitis media). Normally, caloric N. appears after 25-30 s. With pathology, it does not occur at all, or its duration and intensity increase, and other characteristics change. Thus, in a comatose state of any etiology, during a caloric test, the eyes “float away” towards the slow phase of N. and remain in this position for a long time (2-3 minutes), which is prognostic unfavorable symptom. In deep coma, caloric N. falls out.
II. Rotational and post-rotational N. occurs as a result of rotation in the Barany chair (the test is contraindicated during an attack of Meniere’s disease, labyrinthitis, stroke, in the acute period of traumatic brain injury, sharp increase intracranial pressure). Post-rotational nystagmus is often examined. Normally, it appears immediately after rotation and lasts 20-30 s. With pathology, the duration of N. increases to 50-55 s, with severe disorders (complete bilateral loss of vestibular function as a result of the use of ototoxic antibiotics or after meningitis, with damage to the subcortical parts of the brain, etc.) it may not be caused at all.
III. Pressorny N. occurs when pressure is applied to the tragus of the auricle in persons with destruction of the wall of the labyrinth due to chronic purulent otitis.
Optokinetic N. is caused artificially by rotating a special drum in front of the eyes of the subject. It also has slow and fast phases; changes in nystagmus parameters indicate a pathological process in the posterior cranial fossa or in the depths of the occipital lobe.
Other types of N. include:
professional (for example, trembling N. among miners)
congenital (due to underdevelopment of the vestibular system, often accompanies hereditary diseases nervous system)
fixation and installation (occurs with extreme aversion of gaze as a result of fatigue eye muscles)
voluntary (observed in individuals who have the ability to influence muscles that do not obey voluntary contraction).
Spasmodic involuntary eye movements may occur in healthy person when tired, if he tries to fix his gaze in any one direction. They are called nystagmoid jerks, but do not indicate that a person has this disease.
Below is a detailed phenomenological description of some forms of nystagmus.
Congenital nystagmus
It can occur together with refractive errors, color vision errors, hemeralopia, albinism, or congenital cataracts. In most of these patients, the retina is not damaged. The cause of congenital nystagmus apparently lies in disturbances in oculomotor function in the brainstem region. It is often detected with the development of binocular gaze fixation 6 weeks after birth. Its direction is usually horizontal; vertical eye movements are intact. Autosomal dominant hereditary horizontal nystagmus with a vertical component has also been described. The form of nystagmus in most cases is undulating, arched, with twitching, sawtooth; fixing it accentuates it. At closed eyes it is partially inhibited, and in this position a completely different type of nystagmus is often recorded than with the eyes open. People with this nystagmus usually find an eye position where the nystagmus is minimal; if the chosen position does not coincide with the midline, it is accompanied by torticollis ocularis. In approximately 50% of cases, an inversion of horizontal optokinetic nystagmus is observed, often bilateral, when the nystagmus is directed by the fast component not against, but in the direction of the moving stimulus.
Latent nystagmus
This is a form of congenital fixation nystagmus that has a familial pattern. Latent nystagmus can only be detected by interference with binocular fixation, such as closing one eye or using a biconvex lens separating the two visual fields. Nystagmus is always directed towards the fixed eye. It is constantly accompanied by concomitant strabispasm and can be caused in complete darkness in the absence of visual aference.
It is considered the result of damage to the brain stem (pons, tegmentum of the midbrain).
Free nystagmus
It is caused by tension in the extraocular muscles during fixation or convergence. It has a frequency of 10-17/s and undulates. A differential diagnosis should be made with myoclonus, which also manifests itself with the eyes closed, but not with convergence. It is also called hysterical nystagmus, or eye tremor. It does not affect saccades or the fast component of nystagmus.
Ocular myoclonus, opsoclonus, flutter, eyeball dance
Most often, horizontal eye movements are observed with a high frequency (13/s), sometimes grouped in series, occurring at irregular intervals, usually in the horizontal direction, both with closed and open eyes. He appears in acute phase brainstem encephalitis and dispersed disorders of the cerebellum of various etiologies. It disrupts the course of the provoked nystagmus reaction.
Myorhythmia soft palate and eye nystagmus
They appear simultaneously with disturbances in the area of the olive-toothed red triangle. Myorhythmia of the soft palate and uvula is often accompanied by nystagmus, characterized by the same frequency. Most of the examined patients had lesions of the dentate nucleus, and many had lesions of the olive. Myorhythmia does not stop during sleep; it is difficult to stop with medication.
Undulating nystagmus with spasnius nutans
It represents a special form of congenital nystagmus; appears at the age of one and a half years and has favorable course, lasts approximately 12 months. There are nodding or rotating movements of the head, accompanied by a gentle undulating nystagmus, often dissociated and even monoocular. There are also paroxysmal forms. Occurs with efforts related to fixation of gaze or when looking in a certain direction.
Nystagmus of the blind (eye movements in the blind)
It is observed in people who are blind from birth or with acquired blindness (very long-term). It is caused not by a lack of light stimuli, but by a lack of visual control over the position of the eyes. Excursions of the eyeballs are uncoordinated, sometimes dissociated, movements are mainly undulating, sometimes associated with deviation of the eyeballs; in a dream he is depressed.
Paroxysmal nystagmus
If a focus of irritation is simultaneously detected on the EEG, it is most likely of an epileptic nature.
Dissociated nystagmus during gaze fixation
It occurs with unilateral or bilateral anterior internuclear ophthalmoplegia (damage to the long medial fasciculus), has horizontal direction and is better expressed on the adducted eye than on the abducted eye. Sometimes monoocular horizontal nystagmus is subsequently detected only in the contralateral adducted eye. Anterior internuclear ophthalmoplegia can be unilateral with demyelination, tumors and vascular damage, or bilateral with demyelination or extensive tumors of the floor of the fourth ventricle of the brain.
Dissociated nystagmus Brunea-Stewart type
This nystagmus is more pronounced on the side of the damage localization, here it is rougher and has a larger amplitude (a mixture of central and peripheral vestibular nystagmus). It appears with unilateral damage to structures located in the posterior cranial fossa (abscess or tumor of the cerebellum, thrombophlebitis of the sinuses of the posterior fossa). This serves as an unmistakable diagnostic sign that can be identified by examining the movements of both eyes.
Alternative nystagmus
It is characterized by variable amplitude and change in direction of movement. The direction can change every minute with pauses of up to 20 seconds, during which the eyes are calm. Some authors consider this nystagmus to be congenital, others have recorded its occurrence in tumors, demyelination, and toxic lesions of the brain stem.
Nystagmus due to damage to the extraocular muscles
It is noted, for example, in myasthenia gravis. If only one eye is damaged, nystagmus occurs when closing healthy eye when the injured eye moves towards the paretic muscle. It should not be confused with paretic strabismus or gaze paresis. This nystagmus is transient, lasts several hours or days and stops after administration of proserin. It was not detected in progressive muscular dystrophy, myositis of the oculomotor muscles and in pseudomyasthenic syndrome in the case of hyperthyroidism.
Drug nystagmus
Most often it appears after the introduction of barbiturates and alcohol. This is usually a positional or fixed gaze nystagmus. Sometimes barbiturates cause only vertical gaze nystagmus and thereby stimulate disorders of the brainstem tegmentum. At large doses barbiturates, the fast component of nystagmus completely disappears, only the slow tonic deviation of the eyeballs remains. Anesthetic doses of barbiturates or deep coma can completely disrupt the vestibular response, then the eyes stop in a central position, which is reversible and depends on the depth of unconsciousness or anesthesia.
The diagnosis is vertical nystagmus. There is a tumor in the head, vision is deteriorating...
Publication date: 2018-02-09
Nystagmus is a pathological condition characterized by severe oculomotor disturbances associated with oscillatory involuntary twitching of the eyeballs. The patient cannot focus on any specific object, and due to constant vibrations of the eyeball, his vision also decreases. This disorder may occur as a result of watching an object move quickly or rotate rapidly. This normal reaction the body, arising to protect vision. In the case of pathological nystagmus, the eyeball involuntarily deviates from the object being examined and returns back. Nystagmus, like nystagmus, can occur in people of any gender and age, even in children.
Types of disease
Nystagmus has many classifications, depending on a number of circumstances. In accordance with the direction of vibration, pathology is divided into rotational, vertical and horizontal types. The vertical type of the disease is diagnosed when the eyeball involuntarily moves up and down. The horizontal type of the disease is characterized by spontaneous eye movements to the right and left. The rotational form of the pathology is characterized by circular eye movements. The disease is also classified according to the causes that caused it. The pathological form of the disease develops against the background of a number of pathologies affecting vestibular apparatus(responsible for balance) or the brain. And nystagmus of a physiological nature appears due to the excessively rapid flashing of various objects before the eyes and can normally occur in any person.
According to another classification, nystagmus is distinguished between acquired and congenital. Congenital form observed in patients from birth, while acquired develops under the influence of certain factors such as injuries, circulatory disorders, etc. The congenital type usually appears after birth in 2-2.5 months, persisting forever, and representing jerky horizontal vibrations of the eyes. Among the acquired forms, installation, optokinetic and vestibular nystagmus are separately distinguished. The vestibular type of the disease is characterized by slow movements of the eyeballs in one and then the opposite direction, resulting in nausea and dizziness.
Why does the disease occur?
The main factor provoking the development of the disease is dysfunction of the oculomotor system. Causes similar violations are central (general) or local in nature. Factors of local significance include visual disturbances due to eye pathologies such as strabismus or, myopia or astigmatism, or farsightedness, etc. Causes of a central nature are caused by brain damage due to diseases or injuries, infectious ear pathologies, drug poisoning, etc. In general, the development of nystagmus is promoted by causes such as various cerebrovascular accidents, brain tumors, craniocerebral malformations or injuries, hydrocephalus, multiple sclerosis, inflammatory pathologies of the inner ear, amblyopia or heredity.
Spontaneous nystagmus indicates the development of inflammation in the brain or inner ear. Moreover, experts judge the degree of damage by the direction of eye vibrations. Rotational movements indicate damage to the lower parts of the labyrinth of the rhomboid fossa, diagonal and vertical twitches indicate damage to the upper parts, and horizontal movements indicate damage to the middle parts. And the amplitude of oscillations indicates the level of vestibular analyzer lesions. The disease can develop as a result of nervous system overstrain against the background of disorientation that occurs after extreme attractions, etc. After normalization of spatial orientation, the oculomotor system is restored, and nystagmus goes away on its own.
In addition, the causes of the disease are determined by the results of the delay intrauterine development or birth complications. Multiple sclerosis or previous strokes, as well as frequent stressful conditions, can also lead to the development of pathology.
Clinical manifestations of pathology
Often patients do not feel the disease, but note sudden symptoms of frequent dizziness when the world revolves around the patient experiencing an unstable sensation. During examination, doctors note symptoms of involuntary eye oscillations in a certain direction. The patient is often bothered by nausea, which occurs due to fixation of the gaze on a certain object. In addition, symptoms of oscillopsia are observed, when the patient experiences continuous movement of surrounding objects.
Often, symptoms appear that are characteristic companions of nystagmus: unsteadiness when walking, impaired coordination, hearing loss and muscle tone, and squint. Patients also often experience increased sensitivity to light and a feeling of blurriness and constant displacement of the visual image.
Childhood nystagmus
Immediately after birth, the child’s gaze is not able to focus on a specific object; children’s eyes dart and squint. The bottom line is that newborn babies have different visual acuity low performance. But upon reaching the age of one month, children acquire the ability to focus their eyes on a bright toy and follow its movement. When this does not happen, you should consult a pediatrician, since nystagmus may be hidden behind such fluctuations in children's eyes. A more complete, comprehensive examination is carried out by an ophthalmologist and a neurologist.
Sometimes the causes of childhood nystagmus are caused by albinism, which can occur without external manifestations. Treatment must be started immediately, since constant fluctuations of the eyeball lead to decreased vision in children, which seriously affects the entire visual system. Practice shows that treatment in early childhood has the greatest effectiveness, which is explained by the constant development of the children's vision system.
Treatment options
A definitive cure for the pathological type is, unfortunately, impossible. Treatment of nystagmus begins with the main cause that caused the development of the pathology. If the etiology is caused by farsightedness or astigmatism, then treatment involves the use of hardware therapeutic techniques to eliminate the main symptoms of the disease and visual correction by wearing glasses. Applies also drug treatment in the form of taking vitamins and vasodilators, the purpose of which is to improve the nutrition of the retina and other eye tissues. To improve brain nutrition, treatment involves taking nootropic drugs. Specialized programs like “Cross”, “Spider”, etc. are often used.
If the course of the pathology becomes severe, then surgery nystagmus. The operation involves strengthening weakened oculomotor muscle tissues and weakening excessively strong ones, which leads to a decrease in the amplitude of ocular oscillations and an increase in visual function.
Nystagmus called repetitive, uncontrolled, oscillatory and rapid movement of the eyeballs. Its development may be due to the most various factors local or central genesis. It can appear in healthy people, for example, when rapidly rotating the body or when observing quickly moving objects; or be a symptom of a disease of the inner ear, visual system or brain damage of various origins.At various diseases this symptom is almost always accompanied by a significant deterioration in visual acuity.
Causes of nystagmus
The main cause of nystagmus is the unstable functioning of the oculomotor system. Many factors can cause such instability. These include:- hereditary predisposition;
- birth injuries;
- head injuries;
- retinal dystrophy;
- optic nerve atrophy;
- Meniere's disease;
- infectious ear inflammation;
- taking certain medications;
- albinism;
- tumors;
- stroke;
After orientation in space is restored, uncharacteristic movements of the eyeballs completely disappear. The appearance of nystagmus in calm state always indicates that the nervous system cannot recover on its own due to pathology.
Symptoms of nystagmus
Nystagmus almost always develops against the background of an underlying disease, and its symptoms run parallel to the signs of the underlying disease. The patient may notice the appearance of excessive photosensitivity, frequent dizziness, decreased visual acuity, and what he sees seems to blur or tremble. When examining the patient's eyes, uncharacteristic oscillatory movements of the eyeballs are observed, which can be different in direction.
Nystagmus in the direction of movement of the eyeballs can be:
- horizontal (most common) – left-right;
- vertical – down and up;
- diagonal - diagonally;
- rotational (rotatory) - in a circle.
- associated - identical movements of both eyes;
- dissociated – eyes move differently and in different directions;
- monocular - movements appear in only one eye.
- pendulum-shaped - the amplitude of movements is the same;
- jerky - the amplitude of movements is different (slow in one direction and fast in the other);
- mixed - the range of movements combines the characteristics of the previous types.
According to the intensity of oscillatory movements, nystagmus can be:
- small-caliber – range of motion less than 5 o;
- medium-caliber – range of motion 5-15 o;
- large-caliber – range of motion exceeds 15 o.
Each type of nystagmus has its own characteristic symptoms.
Types of nystagmus
Nystagmus is classified according to various parameters. He can be:- physiological – appears in adults and healthy people in response to various stimuli of the nervous system;
- pathological - caused pathological conditions and diseases.
- congenital – abnormalities of visual motor skills manifest themselves soon after the birth of the child and persist throughout life; usually jerky and horizontal;
- acquired – visual motor disorders are caused by disorders of the central or peripheral nervous system; can appear at any age.
- optic– is a consequence of serious visual impairment and begins to manifest itself at 2-3 months of life; in most cases, pendulum-like and weakens with convergence (an attempt to focus the gaze on one object);
- latent– often occurs in children with amblyopia and strabismus, manifests itself only when one eye is closed with an eyelid, is jerky, and its fast phase is directed towards the open eye;
- sternocleidomastoid spasm – occurs very rarely at the age of 4-14 months, accompanied by torticollis, head nodding and nystagmus; in most cases, the nodding movements of the head do not coincide in speed, direction and frequency with the movements of the eyeballs, which can be different in direction.
Acquired nystagmus has the following varieties: - central– caused by diseases of the central nervous system (strokes, tumors, demyelination of the brain stem or cerebellum, etc.); symptoms are varied, may be accompanied by dizziness, change and appear constantly or periodically;
- peripheral– caused by lesions of the vestibular analyzer in its peripheral part (usually due to infections of the labyrinth or vestibulocochlear nerve, injuries or Meniere’s syndrome); movements of the eyeballs are horizontal, transient, occur abruptly and occur against the background of dizziness, last several days and then completely disappear; May be accompanied by hearing and balance problems.
Some types of nystagmus indicate the location of a particular lesion, while others indicate a specific disease.
Physiological nystagmus
Physiological nystagmus is observed in healthy people when exposed to various stimuli.It can manifest itself in several forms:
- installation nystagmus – low in frequency, small and jerky, in the fast phase it is directed in the direction of gaze, manifests itself at extreme abduction of gaze;
- vestibular– appears when rotating or performing a caloric test ( cold water flows into the left or both ears, warm water flows into the right or both ears), is jerk-like;
- optokinetic – in the slow phase, the eyes move behind the object, and in the fast phase, saccadic (jump-like) movements appear in the opposite direction; nystagmus is jerky, caused by repeated movement of an object in the field of view.
Pathological nystagmus
Pathological nystagmus is observed in lesions and diseases of various origins.It can manifest itself in the following forms:
- ocular (or fixation);
- professional;
- labyrinthine (or peripheral);
- neurogenic (or central).
Ocular nystagmus
This type of nystagmus develops with early acquired visual impairment or is congenital. Oscillatory movements of the eyeballs are caused by a disorder of the function of visual fixation or the mechanism that regulates this fixation.Movements of the eyeballs during ocular nystagmus different in their amplitude and character. Visual acuity in most cases is significantly reduced (0.3 or less). Sometimes the patient has a forced position of the head. Damage to the visual system occurs either from birth or during early age. Over the years, his character remains virtually unchanged. During examination, in the case of acquired nystagmus, opacities of the lens and cornea, albinism, and coloboma are revealed macular spot, pigmentary retinal degeneration or optic atrophy.
Professional nystagmus
This type of nystagmus is typical for mine workers with many years of work experience. It is caused by constant tension in the visual system, chronic intoxication with various gases (methane, carbon monoxide), poor lighting and ventilation of mines.The movements of the eyeballs in this nystagmus are rotatory or mixed, intensified when bending over, and may be accompanied by photophobia and trembling of the eyelids and head, narrowing of the visual fields and deterioration of adaptation. Usually, this type nystagmus progresses with increasing work experience in the mine and leads to significant deterioration of vision.
Labyrinthine nystagmus
This type of nystagmus develops against the background of damage to the inner ear. It is rotatory or horizontal, and its fast phase is directed towards the affected labyrinth. In most cases, movements of the eyeballs have a large-caliber (sweeping) amplitude. The eye vibrations are rhythmic and jerky. It does not last long - a few days or weeks.Neurogenic nystagmus
Develops when the vestibular oculomotor reflex is impaired. Neurogenic nystagmus can be caused by trauma various departments central nervous system; inflammatory, tumor or degenerative pathologies.The severity of its manifestation depends on the nature of the lesion itself. Its typical varieties are:
- abduction nystagmus – jerky, observed when the eyeball moves to the temple, characteristic of internuclear ophthalmoplegia;
- Jeroens nystagmus– jerky, horizontal; its low amplitude is observed when the eyeball moves in the opposite direction, and its high amplitude is determined when looking towards the side with the lesion; characteristic of tumors of the cerebellopontine ganglion.
Nystagmus in children
Nystagmus in children is manifested by the fact that the child is not able to fix his gaze, and his eyes constantly make oscillatory movements of an involuntary nature (as if “running”). The cause of pathological nystagmus in childhood may be various disorders congenital or acquired nature. The most common reasons may be:
- birth injury;
- disorders in the central nervous system;
- albinism.
Characteristics nystagmus is observed with such a hereditary disease as albinism. It is manifested by a decrease or complete absence pigment in hair, skin and eyes. There is also an ocular form of albinism, in which pigment is absent only in the eyes. This leads to disruption of activity nerve cells retina and optic nerve. These changes cause nystagmus.
Nystagmus in newborns
Nystagmus in newborns does not appear immediately, because at birth their visual system is not fully developed: the eyes cannot fix the object, visual acuity is still low, and the eyes still “wander.” This condition cannot be classified as nystagmus. Already by the first month of life, a child can normally clearly fix an object and follow a toy. If this does not happen, the doctor may suspect the appearance of nystagmus.As a rule, nystagmus fully manifests itself at 2-3 months of a child’s life, and up to a year, doctors perceive it as a temporary deviation, cosmetic defect and a variant of the norm. In most cases, the appearance of nystagmus is associated with immaturity visual apparatus which can take up to a year to resolve naturally and does not require treatment. Such children are observed by a neurologist and ophthalmologist for up to a year. Treatment is prescribed only if a pathology is identified that can cause pathological nystagmus.
Diagnostics
Diagnosis of nystagmus is always versatile. During an ophthalmological examination, the doctor evaluates the characteristics of nystagmus. A number of additional studies are carried out below: - visual acuity (with and without glasses, with normal and forced head position);
- condition of the fundus, retina, optic nerve and oculomotor system;
- state of the optical media of the eye;
- visual evoked potentials;
- electroretinogram.
- electrophysiological studies - electroencephalogram (EEG), echo-encephalography (Echo-EG);
- MRI of the brain.
Treatment
Treatment of nystagmus in most cases is complex, complex and lengthy. It is carried out against the background of treatment of the underlying disease or pathology.Optical vision correction
To improve visual acuity, careful optical correction is carried out - selection of glasses or contact lenses for near and distance.When detecting albinism, atrophy optic nerves and dystrophic changes in the retina, it is recommended to use glasses with special light filters (orange, neutral, yellow or brown) of a density that can provide the greatest visual acuity. In addition, light filters perform a protective function.
Pleoptic treatment
To normalize amblyopia and the accommodative abilities of the eye, which accompany nystagmus, pleoptic treatment (retinal stimulation) and special eye exercises are prescribed. The patient is recommended: 1. Lights on the monobinoscope through a red filter, which stimulates central part retina.
2. Stimulation with color and contrast-frequency tests (computer exercises “Cross”, “Zebra”, “Spider”, “EYE”, device “Illusion”).
The exercises are performed sequentially for the right and left eyes, and then with the eyes open.
Good results are obtained by using diploptic treatment (binarimetry or the “dissociation” method) and binocular exercises. They help improve vision and reduce the amplitude of nystagmus.
Drug therapy
Drug treatment of nystagmus is auxiliary. Usually, medications are used to improve the nutrition of eye tissue. May be assigned vasodilators(Cavinton, Trental, Angiotrophin, Theobromine, etc.) and multivitamins.Surgery
Surgical treatment of nystagmus is aimed at reducing the amplitude of oscillations of the eyeballs. To do this, perform special operations on the muscles of the eye. The surgeon weakens the stronger muscles on the slow phase side and strengthens the muscles on the fast phase side. This correction not only reduces nystagmus, but also straightens the forced position of the head, which helps improve visual acuity.Nystagmus in children: causes, types, symptoms, treatment - video
Before use, you should consult a specialist.Spontaneous nystagmus can be congenital or acquired, pendulum-like (swinging) or jerk-like. Identification of spontaneous nystagmus occurs during a routine neurological examination without additional effects on the vestibular apparatus of the subject necessary to induce experimental nystagmus. When studying spontaneous nystagmus, the doctor and the patient sit opposite each other, their eyes are approximately at the same level; The patient's eyes should be well lit. First, the patient is asked to fix his gaze on an object located in front of his face at a distance of approximately 30 cm, then the doctor moves this object to one side, then to the other, up and down, diagonally. At the same time, the patient follows the moving object with his gaze. During the examination, the doctor observes the changing position of the patient’s eyes and identifies possible manifestations nystagmus. To assess nystagmus, the direction, amplitude, speed, rhythm, nature of movements of the eyeballs, binocularity or mono-ocularity (in the latter case - dissociated nystagmus) are taken into account. Depending on the direction of gaze in which spontaneous jerky nystagmus appears, three degrees of nystagmus are distinguished (Blagoveshchenskaya N.S., 1990): 1st degree nystagmus appears only when looking towards its fast phase, 2nd degree nystagmus occurs already with direct gaze , nis-tagm III degree is also observed when looking towards its slow phase. When checking spontaneous nystagmus in a healthy person, at extreme abductions of the eyeballs, single small-scale twitching of the eyeballs may occur, which quickly stop. This phenomenon is an installation, fixation nystagmus and is usually designated by the term “nystagmoid,” which should not be classified as a pathology. Spontaneous horizontal nystagmus is more often observed. The trajectory of eye movements during horizontal nystagmus is directed in the horizontal plane in relation to the head, regardless of its inclination. Pendulum-shaped horizontal nystagmus is characterized by rhythmic, smooth, sinusoidal oscillations of the eyes. Both of its phases are identical in speed and duration, and the movements of the eyeballs resemble the swinging movements of a pendulum. Pendulum-like nystagmus is often congenital. Jerky horizontal nystagmus is more often acquired - the eyeballs make fast movements in one direction and slow movements in the other; in such cases, the direction of jerky horizontal nystagmus is usually determined by its fast component. However, with this form of nystagmus, slow eye movements are decisive; they provoke the occurrence and continuation of nystagmus. Rapid eye movements are only corrective. Jerky nystagmus can be clonic or tonic. A jerky spontaneous nystagmus with a frequent rhythm is recognized as clonic. It may be peripheral or central. Tonic nystagmus is characterized by a slow phase extended in time (the ratio of fast and slow phases is 1:10-1:30), while the nystagmus is slowed down, but its rhythm remains. Tonic nystagmus is a sign serious condition patient, it is usually central, occurs when the brain is damaged and indicates an acute pathological process (poor blood circulation in the brainstem, severe traumatic brain injury, stage of decompensation of intracranial hypertension, etc.). Physiological nystagmus can occur in a healthy person. So, if a person looks at objects quickly moving to the side, physiological optokinetic nystagmus appears. The movement of objects can be absolute or relative. The absolute movement of a train passing in front of you causes optokinetic nystagmus. The apparent movement of objects is recognized as relative, causing a similar nystagmus in a passenger looking out the window of a moving train (railway nystagmus). Pathological nystagmus occurs when the mechanisms that ensure gaze fixation are disrupted. In most cases, this is vestibular nystagmus, which is usually jerk-like, which is characterized by alternating an active slow phase and a corrective fast phase (the ratio of the duration of these phases is often 1:3-1:5). As already noted, the direction of jerky nystagmus is determined by its fast phase, since it is usually more clearly expressed. Optical nystagmus is caused by impaired gaze fixation due to low vision, it manifests itself from birth or early childhood. Possible with a high degree of myopia (6 diopters or more) and various diseases leading to a decrease in visual acuity. When visual acuity decreases in only one eye, optical nystagmus can be monoocular. Optical nystagmus is usually pendulum-like (swinging). Congenital nystagmus is usually horizontal, often pendulum-shaped (swinging) and manifests itself from the moment of birth. It can be optical, i.e. due to very low vision. However, congenital nystagmus can also manifest itself with relatively preserved visual acuity. There is an opinion (Kamyanov I.M. et al., 1989) that in such cases it may indicate a congenital deficiency of the structures of the nervous system that control gaze fixation, and then is often combined with minimal cerebral dysfunction, stuttering, psychopathy, bedwetting and etc. Congenital nystagmus is usually noted from the moment of birth, it is constant, manifests itself when the gaze is directed forward, and when the gaze is turned to the sides, its amplitude usually increases. Congenital nystagmus can also be jerk-like, in which case it is usually large-scale. Despite the severity of oscillopsia, there is no sensation of vibration in the visible space with congenital nystagmus. Its pathogenesis and localization of the lesion usually remain unspecified. There is an opinion that the appearance of congenital nystagmus is due to the uneven activity of the mechanisms vestibular reflex, responsible for saccadic movements of the eyeballs. Louis-Bar symptom. If a patient with nystagmus follows a moving object, then in the case of acquired nystagmus the amplitude of its oscillation increases over time, and in congenital nystagmus it decreases. Described by the French doctor D. Louis-Bar. Congenital nystagmus can be hereditary. Hereditary forms congenital nystagmus is usually transmitted by a recessive type linked to the X chromosome, less often by an autosomal dominant type. In the clinic of nervous diseases, acquired, jerky, vestibular nystagmus is more common. It may be caused by damage to various levels of the vestibular system: semicircular canals, vestibular ganglion, vestibular part of the VIII cranial nerve, vestibular nuclei located in the tegmentum of the trunk at the bottom of the IV ventricle of the brain, and their connections through the structures of the reticular formation of the trunk and medial longitudinal fasciculus with the nuclei of the VI, IV and III cranial nerves in the brain stem, as well as with the cerebellum and structures of the spinal, intermediate and big brain. Caused by a dysfunction of the central nervous system structures, vestibular nystagmus is regarded as central, in other cases it is peripheral. When examining a patient, spontaneous nystagmus and experimental nystagmus can be detected. Vestibular nystagmus is caused by irritation or destruction of the structures of the vestibular analyzer. In accordance with Ewald's law (German physiologist J. Ewald, I855-1921), if nystagmus is caused by irritation of the receptor apparatus of the vestibular system, its slow phase is directed towards the semicircular canal of the labyrinth in which the lymph flow moves to the ampulla. Vestibular nystagmus is an essential component of the vestibular-ocular reflex. It is jerky, and the primary reaction in response to irritation is the slow phase of nystagmus, followed by a corrective fast phase directed in the opposite direction. Vestibular nystagmus can be peripheral and central, as well as spontaneous and experimental. Peripheral nystagmus occurs when the peripheral structures of the vestibular system are damaged. Peripheral nystagmus in direction can only be horizontal or horizontal-rotatory. It occurs due to pathology of the labyrinth or vestibular part of the VIII cranial nerve. May be a manifestation of labyrinthitis, Meniere's disease, perilymphatic fistula, labyrinth trauma (usually due to a temporal bone fracture), labyrinthine apoplexy, toxic damage labyrinth (when taking streptomycin, etc.), neuroma of the VIII cranial nerve, pressure of adjacent vessels on the proximal part of the root of the VIII cranial nerve. When the receptors of the labyrinth are stimulated, nystagmus (its fast phase) is directed in the opposite direction; when the labyrinth is destroyed, it is directed towards the lesion. With peripheral nystagmus, a latent period of 3-10 s is common, its duration is approximately 10 s, with pronounced attenuation, nausea and, less commonly, vomiting are possible. Positional nystagmus of peripheral origin is nystagmus that appears or changes with changes in body position. Usually appears 3-10 seconds after changing the position of the patient’s head (this is the time corresponding to the latent period of the reaction), often combined with dizziness and nausea, lasts about 10 seconds. This nystagmus usually subsides after several successive attempts to induce it. Central nystagmus is a consequence of damage to the structures of the central nervous system, most often the vestibular nuclei and their connections with the medial longitudinal fasciculus, the nuclei of the cranial nerves that provide eye movements, the cerebellum, and the cortex cerebral hemispheres. Unlike peripheral nystagmus, central nystagmus can be of different directions. It is more often horizontal when the middle part of the rhomboid fossa is affected (medial vestibular nucleus), vertical and diagonal when its upper part is affected (superior vestibular nucleus), rotatory nystagmus indicates irritation of the structures of its lower part. Positional nystagmus of central origin manifests itself in vascular insufficiency in the vertebrobasilar system, multiple sclerosis, cystic tumors of the cerebellum, moderate traumatic brain injury, drunkenness. Occurs immediately after a change in head position, persists for more than 10 seconds, without fading; may be accompanied by nausea and vomiting. Bonnier syndrome. Damage to the lateral part of the bulbopontine level of the brain stem is accompanied by a disorder of the functions of the lateral vestibular nucleus (Deiters nucleus) and adjacent structures. It is characterized by nystagmus, dizziness, nausea, hearing impairment, and sometimes strabismus due to weakness of the external rectus muscle of the eye and trigeminal pain, which can be paroxysmal. Described in 1903 by the French otorhinolaryngologist P. Bonnier (186I-1918). Multiple central nystagmus (a combination of its variants) is observed when the pathological process has a pronounced impact on the brain stem over a long period. Central nystagmus may be one of the manifestations of a pathological process in the subtentorial space (tumor, inflammatory processes, circulatory disorders in the vertebrobasilar system, demyelinating process). Rotational (rotatory) nystagmus is characterized by rotational movements of the eyeballs around their anteroposterior axes . Rotation with it is often combined with its horizontal or vertical components. Rotational nystagmus of small amplitude is observed with damage to the caudal part of the trunk. When the diencephalon is damaged, high-amplitude rotational nystagmus is possible, in such cases it can be the basis of sawtooth nystagmus. Circular nystagmus is a variant of pendular nystagmus, in which the eyeball oscillates in a circle; can be acquired and congenital. In contrast to rotational (rotatory) nystagmus, oscillatory movements with it are rather a summation of simultaneous horizontal and vertical oscillations, differing in phase by 90°, while the amplitudes of both components are equal. Possible in multiple sclerosis and then usually combined with ataxia. Elliptical nystagmus, similar to circular, is a consequence of the summation of simultaneous horizontal and vertical pendulum-shaped oscillations that have unequal amplitudes. Like circular nystagmus, it occurs mainly in multiple sclerosis and is usually combined with ataxia. Oblique, or diagonal, nystagmus can be pendulum-like or jerk-like. Usually refers to acquired forms of nystagmus. Sawtooth nystagmus is characterized by rapid pendulum-like, uncooperative eye movements in which one eyeball rises and rotates inward, while the other lowers and rotates outward. It manifests itself more clearly when trying to fix vision. Sometimes observed in patients in a coma. It is a consequence of damage to the rostral parts of the midbrain or the walls of the posterior part of the third ventricle of the brain. It can be combined with changes in visual fields such as bitemporal hemianopia and decreased visual acuity. This pathology was described in 1963 by N. Lourie. Nystagmus acquired in early childhood may be due to progressive bilateral vision loss, in particular arising in connection with intracranial pathology. It is difficult to distinguish from congenital nystagmus, but should not be considered congenital unless it is confirmed by medical documentation. In rare cases, nystagmus may appear in a child after loss of vision in one eye. Acquired pathological nystagmus, manifested in adults, is often jerk-like, but can also be pendulum-like. Usually central, reflecting dysfunction of the brainstem and/or cerebellum. It may be a manifestation, in particular, of vascular and demyelinating brain lesions. Acquired pendular nystagmus is often horizontal, but can be multivector, sometimes accompanied by head trembling. It is possible that the severity of nystagmus in one and the other eye is not identical; in this case, the severity of nystagmus may not correspond to the state of visual acuity. Nystagmus induced by drugs and alcohol is often jerky, can be horizontal or horizontal-rotatory, less often vertical; sometimes symmetrical gaze-paretic nystagmus, in which the eyes turned to the side slowly return to the midline, followed by their rapid reverse movement. It can be induced by quinine, barbiturates, phenothiazines, tranquilizers, anticonvulsants, and alcohol. With a pronounced degree of intoxication, horizontal nystagmus sometimes acquires a pendulum-like character and appears when looking in front of yourself. Drug- and alcohol-induced nystagmus may be accompanied by other manifestations vestibular syndrome. The diagnosis is usually facilitated by anamnesis and screening tests for the presence of relevant toxins and medicines in blood. Converging nystagmus is a rare form of acquired, pendular, horizontal nystagmus. It manifests itself by alternating convergence and divergence of the eyeballs. It appears when the gaze is fixed on an object located at a short distance, or when the eyeballs converge. Converging nystagmus is usually a consequence of primary damage to the midbrain or its compression during tentorial cerebral hernias. Possible with progressive supranuclear palsy. Dissociated pendulum-like or jerk-like nystagmus has a pronounced asymmetry of amplitude or direction (in contrast to associated, in which the movements of the eyeballs are combined). Dissociated nystagmus often occurs when the eye is abducted (abduction nystagmus) in cases of internuclear ophthalmoplegia. Pendulum-like dissociated nystagmus can occur in patients with multiple sclerosis. It is more often observed in cases of subtentorial localization of the pathological process. Abduction nystagmus (Harris' ataxic nystagmus) is a dissociated, acquired form of jerk-like nystagmus with an abduction fast phase (fast horizontal saccadic movements of the eye outward) and a slow phase directed towards the midline. It usually occurs when the eye moves towards the temple, while the other eye remains motionless in the primary position. It is observed in patients with internuclear ophthalmoplegia and manifests itself on the side opposite to the affected medial longitudinal fasciculus. With bilateral internuclear ophthalmoplegia, abduction nystagmus will be observed with extreme abduction of the eyes in both directions, but jerky movements are observed only in the eye that turns outward. Vertical nystagmus is a nystagmus in which the eyeballs move in a vertical plane. Is a sign of damage to the upper parts of the brain stem or drug intoxication, often caused by taking excessive doses of barbiurates. Vertical dissociated nystagmus is a dissociated nystagmus in which one eyeball moves upward and inward, the other downward and outward. Indicates damage to the nuclei of the reticular formation of the midbrain and the intermediate nucleus of Cajal. Is possible sign tumors of the sellar region, in particular craniopharyngiomas, traumatic brain injury. Vertical dissociated nystagmus can be combined with bitemporal hemianopsia, caused by the involvement of the central part of the chiasm in the process. Bruns nystagmus is a horizontal dissociated jerk-like nystagmus, the direction of which depends on the ability to fixate the gaze. Characteristic for a tumor of the cerebellopontine angle. When looking towards the pathological process, the nystagmus becomes large-scale, while the direction of its fast phases coincides with the direction of the gaze, and slow phases are characterized by an exponential decrease in speed. When looking in the direction opposite to the pathological focus, low-amplitude nystagmus with slow and fast phases, the direction of which coincides with the direction of gaze, is noted. Bruns nystagmus is a variant of horizontal nystagmus caused by unilateral pressure of the pathological focus on the brain stem and suppression of vestibular functions on the side of compression of the stem structures. Centripetal nystagmus is a horizontal jerk-like nystagmus, the slow phase of which is characterized by a decrease in speed exponentially and is directed from the center, while its fast phase is directed towards the center. Centripetal nystagmus, unilateral or bilateral, most often occurs due to damage to the cerebellum. It may also be a sign of labyrinth dysfunction. Conducting differential diagnosis, it should be taken into account that when the labyrinth is damaged, the nystagmus is directed towards the affected labyrinth in all gaze positions, and slow stage its linear, whereas with damage to the cerebellum the speed of the slow phase of nystagmus decreases exponentially. Monocular nystagmus is isolated nystagmus of one eyeball. Rarely seen. It is a consequence of damage to the vestibulo-oculomotor connections in the system of the medial longitudinal fasciculus. Variants of central vertical nystagmus are downward-beating nystagmus and upward-beating nystagmus. Downward nystagmus is a unique form of vertical jerky nystagmus, characterized by periods of intermittent, spontaneous, usually friendly, rapid downward movements of the eyeballs followed by a slow return to their original position, reminiscent of the movements of a float during a fish “bite.” It is most pronounced when the gaze is deviated to the side and slightly below the horizontal plane. As a rule, it manifests itself with severe primary or secondary damage to the lower parts of the brain stem. It is a probable sign of a pathological process in the craniovertebral region, for example, with platybasia, Arnold-Chiari anomaly, with damage to the cerebellum (tumor, atrophic process, etc.), possible, in particular, with multiple sclerosis, may be a consequence of a toxic reaction to taking anticonvulsants. This pathology was described by the American neuropathologist SM. Fisher. Nystagmus, beating upward, when looking straight, can be a consequence of damage to the anterior parts of the cerebellar vermis, diffuse damage to the brain stem with Wernicke encephalopathy, meningitis, and general intoxication.
