Methodology for studying spontaneous nystagmus. Checking tonogenic reactions

Nystagmus is a severe form of oculomotor disorders, manifested in spontaneous oscillatory eye movements and accompanied by a significant decrease in visual acuity - low vision.

Nystagmus is repeated involuntary pendulum-like oscillations of the eyes, which can be physiological or pathological. Thus, nystagmus that appears in response to rotation of the optokinetic drum or body in space is normal and serves to maintain good vision. Eye movements that fixate on an object are called foveating, and those that move the fovea away from the object are called defoving. With pathological nystagmus, each cycle of movement usually begins with an involuntary deviation of the eye from the object, followed by a reverse refixation saccadic movement. The direction of nystagmus can be horizontal, vertical, torsional or nonspecific. In terms of amplitude, nystagmus can be small-caliber or large-caliber (the amplitude of nystagmus is determined by the degree of eye deviation), and the frequency of nystagmus can be high, medium and low (determined by the frequency of eye oscillations).

ICD-10 code

H55 Nystagmus and other involuntary eye movements

What causes nystagmus?

The development of nystagmus can be caused by the influence of central or local factors.

Nystagmus usually occurs with congenital or early-onset vision loss due to various eye diseases (optical clouding, atrophy optic nerve, albinism, retinal dystrophy, etc.), as a result of which the mechanism of visual fixation is disrupted.

Physiological nystagmus

1. Installation nystagmus is a small, jerky nystagmus of low frequency with extreme gaze abduction. The fast phase is in the direction of gaze.
2. Optokinetic nystagmus is a jerky nystagmus caused by repeated movements of an object in the field of view. The slow phase is the tracking movement of the eyes behind the object; the fast phase is a saccadic movement in the opposite direction, so the eyes fixate the next object. If the optokinetic tape or drum was moved from right to left, the left parieto-occipital region controls the slow (pursuit) phase to the left, and the left frontal lobe controls the fast (saccalic) phase to the right. Optokinetic nystagmus is used to identify malingerers simulating blindness and to determine visual acuity in young children. It may also be useful in determining the cause of isolated homonymous hemianopia (see below).
3. Vestibular nystagmus is a jerky nystagmus caused by altered input from the vestibular nuclei to the centers of horizontal eye movements. The slow phase is initiated by the vestibular nuclei, and the fast phase by the brain stem and frontomesencephalic pathway. Rotatory nystagmus is usually associated with pathology of the vestibular system. Vestibular nystagmus can be induced by caloric stimulation:
   • When cold water is poured into right ear, a left-sided jerky nystagmus appears (i.e., a fast phase to the left).
   • When warm water is poured into the right ear, a right-sided jerky nystagmus (i.e., a fast phase to the right) appears. The mnemonic “COWS” (cold - opposite, warm - same) helps in remembering the direction of nystagmus, which translated means: cold - opposite, warm - same.
   • When cold water is poured into both ears at the same time, a jerky nystagmus appears with a rapid upward phase; warm water in both ears causes nystagmus with a rapid downward phase.

Motor imbalance nystagmus

Motor imbalance nystagmus occurs as a result of primary defects in efferent mechanisms.

Congenital nystagmus

Inheritance can be X-linked recessive or autosomal dominant.

Congenital nystagmus manifests itself 2-3 months after birth and persists throughout life.

Symptoms of congenital nystagmus

• Horizontal nystagmus, usually of a jerky type.
• May be weakened by convergence and not noted during sleep.
• There is usually a bullet point - the direction of gaze in which nystagmus is minimal.
• When setting the eyes at the zero point, an abnormal position of the head may be noted.

Nodule spasm

This is a rare condition between 3 and 18 months.

Symptoms

• • Unilateral or bilateral small-amplitude high-frequency horizontal nystagmus with head nodding.
  • Nystagmus is often asymmetrical, with an increase in amplitude with abduction.
  • Vertical and torsional components may be noted.

• Idiopathic sternocleidomastoid spasm resolves spontaneously by age 3 years.
• Glioma of the anterior optic pathway, empty sella syndrome and porencephalic cyst.

Latent nystagmus

Associated with infantile esotropia and not combined with vertical deviation. Characterized by the following:

• When both eyes are open, there is no nystagmus.
• Horizontal nystagmus occurs when one eye is closed or the amount of light entering the eye is reduced.
• Fast phase in the direction of the open fixating eye.
• Sometimes an element of latent nystagmus is superimposed on the manifest nystagmus, so if one eye is closed, the amplitude of the nystagmus increases (latent-manifest nystagmus).

Periodic alternating nystagmus

Symptoms

• Friendly horizontal jerky nystagmus, periodically taking the opposite direction.
• Each cycle can be divided into an active phase and a resting phase.
• During active phase amplitude, frequency and speed slow phase nystagmus first progressively increases, then decreases.
• Then there is a short, calm interlude, lasting 4-20 seconds, during which the eyes make low-amplitude, often pendulum-like movements.
• This is followed by a similar sequence of movements in the opposite direction, full cycle lasts 1-3 minutes.

Causes: cerebellar diseases, demyelination, ataxia-telangiectasia (Louis-Bar syndrome), medications, such as phenytoin.

Convergence-retraction nystagmus

Caused by simultaneous contraction of extraocular muscles, especially the medial rectus muscles.

Symptoms

• Jock nystagmus caused by downward movement of the OKN observation tape.
• The superior fixation saccade brings the eyes toward each other in a convergent movement.
• Combined with retraction of the eye into the orbit.

Causes: lesions of the pretectal area, such as pinealomas and vascular accidents.

Downward nystagmus

Symptoms: vertical nystagmus with a rapid phase. “hitting” down, i.e. which is more easily evoked when looking down.

• Pathologies of the craniocervical junction at the level of the foramen magnum, such as Aniold-Cliiari malformation and ringobulbia.
• Medicines (lithium compounds, phenytoin, carbamazepine and barbiturates).
• Wernicke encephalopathy, demyelination and hydrocephalus.

Nystagmus, "beating" upward

Symptoms: vertical nystagmus with a fast phase that “beats” upward.

Causes: pathology of the posterior cranial fossa, medications and Wernicke encephalopathy.

Maddox reciprocating nystagmus

Symptoms: pendulum-like nystagmus, in which one eye rises and turns inward, and the other eye at the same time lowers and turns outward; thus, the eyes turn in the opposite direction.

Causes: parasellar tumors, often causing bitemporal hemianopia, syringobulbia and brain stem stroke.

Ataxic nystagmus

Ataxic nystagmus is a horizontal nystagmus. occurring in the abducted eye of a patient with internuclear ophthalmoplegia (see below).

Sensory deprivation nystagmus

Sensory deprivation nystagmus (ocular) is a consequence of visual impairment. The severity of the condition is determined by the degree of vision loss. Horizontal and pendular nystagmus may decrease with convergence. To reduce the amplitude of nystagmus, the patient can take a forced head position. The cause of sensory deprivation nystagmus is a severe disorder central vision V early age(eg, congenital cataracts, macular hypoplasia). As a rule, nystagmus develops in children under 2 years of age with bilateral vision loss.

Symptoms of nystagmus

With some types of nystagmus, sufficiently high visual acuity is maintained; in such cases, the reason for its development is disturbances in the regulation of the oculomotor system.

Depending on the direction of the oscillatory movements, horizontal (most often observed), vertical, diagonal and rotational nystagmus is distinguished; according to the nature of the movements - pendulum-shaped (with equal amplitude of oscillatory movements), jerk-like (with different amplitudes of oscillations: slow phase - in one direction and fast - to the other) mixed (either pendulum-like or jerk-like 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 an amplitude of less than 5°).

To determine the amplitude, frequency and nature of oscillatory nystagmoid movements, an objective research method is used - nystagmography. In the absence of a nystagmograph, the nature of the nystagmus amplitude can be determined by the degree of displacement of the light reflex from the ophthalmoscope on the cornea. If the light reflex during oscillatory movements of the eyes moves from the center of the cornea to the middle of the distance between the center and the edge of the pupil, they speak of small-caliber, small-scale nystagmus, if it goes beyond these limits - large-caliber. If the movements of both eyes are not the same, such nystagmus is called dissociated. It is observed extremely rarely.

Types of nystagmus

1. Jerky nystagmus with a slow defoving "drifting" movement and a fast corrective refloating jerking movement. The direction of nystagmus is indicated by the direction of the fast component, so jerk nystagmus can be right-sided, left-sided, superior, inferior, or rotatory. Jerky nystagmus can be divided into positional (vestibular) and gaze palsy nystagmus (slow and usually a sign of brain stem damage).
2. Pendulum-like nystagmus, in which both foveating and defoving movements are slow (the speed of nystagmus is the same in both directions).
   • Congenital pendular nystagmus is horizontal and tends to become jerky when viewed to the side.
   • Acquired pendular nystagmus has horizontal, vertical and torsional components.
   • If the horizontal and vertical components of pendulum nystagmus are in phase (i.e., occurring simultaneously), the perceived direction appears oblique.
   • If the horizontal and vertical components are out of phase, the direction appears elliptical or rotatory.

Mixed nystagmus includes pendulum nystagmus in the primary position and jerky nystagmus in lateral gaze.

Diagnosis of nystagmus

When examining patients with nystagmus, the results of electrophysiological studies (electroretinogram, visual evoked potentials, etc.) are important to clarify the diagnosis, determine the degree of organic lesions, the presence of amblyopia, and determine treatment tactics.

With nystagmus, the visual acuity of each eye is examined with and without glasses, with the head in a straight and forced position. In this position, the amplitude of the nystagmus usually decreases and visual acuity becomes higher. This criterion is used to decide whether it is advisable to perform surgery on the extraocular muscles. It is important to determine visual acuity with two eyes open (with and without glasses), since with binocular fixation the amplitude of nystagmus also decreases and visual acuity becomes higher.

Treatment of nystagmus

The system of measures to improve visual functions with nystagmus includes carefully selected optical correction for distance and near. In case of albinism, retinal dystrophy, partial atrophy of the optic nerves, it is advisable to select protective and visual acuity-enhancing color filters (neutral, yellow, orange, brown) of the density that provides the greatest visual acuity.

With nystagmus, accommodative ability is also impaired and relative amblyopia is noted, so pleoptic treatment and accommodation training exercises are prescribed. Lights through a red filter (on a monobinoscope), selectively stimulating the central zone of the retina, stimulation with contrast-frequency and color test objects (the “Illusion” device, computer exercises according to the “Zebra”, “Spider”, “Cross”, “EYE” programs) are useful. ). These exercises can be performed sequentially for each eye and with both eyes open. Binocular exercises and diploptic treatment (dissociation method, binarimetry) are very useful, also helping to reduce the amplitude of nystagmus and increase visual acuity.

Drug treatment of nystagmus is used to improve nutrition of the tissues of the eye and retina (vasodilators, vitamin complex).

Surgical treatment of nystagmus is performed to reduce oscillatory eye movements. With jerky nystagmus, when a forced rotation of the head is diagnosed with an increase in visual acuity and a decrease in the amplitude of the nystagmus in this position (“rest zone”), the goal of the operation is to move the “rest zone” to the middle position. To do this, weaken the stronger muscles (on the side of the slow phase) and strengthen the weaker muscles (on the side of the fast phase). As a result, the head position straightens, nystagmus decreases, and visual acuity increases.

is a pathology characterized by involuntary oscillatory eye movements. Clinical symptoms include rapid fluctuations eyeballs in a vertical, horizontal, less often - oblique or circular direction. Accommodative ability is impaired, which is manifested by visual dysfunction. For diagnosis, objective examination, microperimetry, electronystagmography, visometry, refractometry, CT scan brain. Conservative therapy is based on the use of anticonvulsants and antiepileptic drugs. Surgical correction of the position of the eyeball is less often indicated.

General information

Nystagmus is a widespread nosology in practical ophthalmology. According to statistics, among visually impaired children, a congenital form of pathology is diagnosed in 20-40% of patients. It is often possible to establish the etiology of involuntary oscillatory eye movements. The idiopathic type occurs with a frequency of 1:3000. Horizontal nystagmus is the most common, while oblique and rotational variants are extremely rare. In the general structure of damage to the organ of vision horizontal type occupies 18%. Geographical features of epidemiology are absent.

Causes of nystagmus

Congenital nystagmus occurs against the background of neurological disorders. The hereditary nature of the disease is evidenced by the appearance clinical symptoms against the background of Leber's congenital amaurosis or albinism. The main reasons for the development of the acquired form:

• Brain pathology. Nystagmus in mature age may be one of the symptoms of multiple sclerosis or malignant neoplasm. The sudden onset of symptoms may indicate a stroke.
• Traumatic brain injury. Involuntary eye fluctuations are associated with damage to the optic nerves or the occipital lobe of the cerebral cortex.
• Intoxication. The disease occurs due to the toxic effects of alcoholic beverages, overdose of anticonvulsants and sleeping pills.
• Damage to the vestibular apparatus. Clinical manifestations are preceded by damage to the central or peripheral parts of the vestibular analyzer. Often, the development of the acquired form provokes damage to the semicircular canals of the inner ear.
• Decreased visual acuity. Nystagmus may develop due to a marked decrease in visual acuity in patients with mature cataracts, traumatic injuries history of the organ of vision or complete blindness (amaurosis).

Pathogenesis

Spontaneous movements of the eyeballs are based on decompensation of the tone of the membranous part of the labyrinth of the inner ear. Normally, nerve impulses are generated simultaneously from both sides and are transmitted at the same speed, which allows the eyes to be at rest or to carry out cooperative movements. An increase in tone in the labyrinth on a certain side leads to the development of nystagmus. When the peripheral and central parts of the vestibular analyzer are damaged, the appearance or change in the severity of clinical manifestations is noted when changing position. This is due to the secondary involvement of the semicircular tubules in the pathological process. The molecular mechanism of development of congenital idiopathic nystagmus is not fully understood. Scientists believe that it is based on a mutation in the FRMD7 gene, which is inherited in an X-linked manner. However, cases of autosomal dominant and autosomal recessive inheritance have also been observed in clinical practice.

Classification

Depending on the time of onset of the first symptoms, congenital and acquired nystagmus are distinguished. TO congenital form refers to latent and manifest-latent types. The acquired variant is classified according to etiology into neurogenic and vestibular. From a clinical point of view, there are:

• Pendulum-shaped (undulating). It is characterized by phases of oscillation of the eyeballs that are identical in magnitude and speed.
• Jerky. It is distinguished by rhythmic eye movements, in which the eyeball is directed slowly in one direction and quickly in the other. If in the fast phase the eyes are directed to the left, then we're talking about about a left-sided form, movements to the right indicate a right-sided variant.
• Mixed. This variant of the disease combines jerky and undulating forms.
• Associate. The eyeballs move in a friendly manner with the same amplitude in a pendulum-like or jerk-like manner.
• Dissociated. The nature of the movements of one eye does not coincide in direction and amplitude with the other eyeball.

Symptoms of nystagmus

In most cases, the first manifestations of the disease occur early childhood or from the moment of birth. Symptoms of the acquired form develop immediately after the action of the etiological factor. Patients complain of repetitive oscillatory eye movements. The direction of vibrations can be horizontal, vertical, less often - oblique or circular. The patient is unable to focus on the object in question. The ability to adapt to changes in external conditions is impaired. The decrease in visual functions is caused not by pathology of clinical refraction, but by a reduced reserve of accommodation.

The patient cannot completely stop the manifestations of nystagmus, but the magnitude of the oscillations decreases somewhat when changing the direction of gaze, the position of the head, or maximum focusing of attention on a specific object. To reduce the severity of clinical symptoms, the patient takes a forced position with the lowest frequency of movements. Turning the head to the side or torticollis (tilting) is common. The choice of position is determined by the zone of relative rest, in which the amplitude of movements decreases and accommodative ability improves.

Symptoms are most noticeable under stressful conditions, anxiety or fatigue. The duration of manifestations is influenced by the nature of movements. With the pendulum type, the duration of nystagmus is longer than with the jerky variant of the disease. The properties of oscillatory movements can change. A change in manifestations is provoked by the appearance of an object in the field of view, a change in its size or brightness. A certain role is assigned to the factor of visual concentration and even mood. The form of the disease is determined by eye movements that dominate the clinical picture.

Complications

A common complication of nystagmus is secondary alternating convergent strabismus, which often develops in patients with the dissociated form. The characteristics of strabismus are determined by the course of the underlying disease. The pathology is accompanied by reversible visual dysfunction - amblyopia and mixed astigmatism. The acquired variant is complicated by a number of vestibular disorders (dizziness, lack of coordination, headache). Due to the need to often hold the head in a forced position, the development of compensatory torticollis is possible. Individuals with a history of vestibular nystagmus are prone to recurrent labyrinthitis.

Diagnostics

An objective examination of the patient is sufficient to make a diagnosis. During an external examination, it is possible to visualize involuntary eye movements. To determine the direction of nystagmus, the patient is asked to focus his gaze on a pen or a special pointer. The ophthalmologist moves the instrument up, down, right and left. The shape of the lesion is determined in the direction of the fast component. To study the etiology of the disease and select further management tactics, the following is used:

• Microperimetry. The technique allows you to determine the point of fixation on the inner shell of the eyeball, record the parameters of optical nystagmus and study the sensitivity of the retina. The method makes it possible to monitor the condition of patients to assess the effectiveness of treatment measures.
• Electronystagmography (ENG). The study is based on recording biopotentials that arise between the cornea and retina. In individuals with involuntary eye movements, the electrical axis shifts, which is accompanied by an increase in the difference in corneoretinal biopotential to 100-300 μV.
• • Conservative therapy. Used if clinical manifestations develop against the background of central vestibulopathy. The use of neurotropic drugs from the group of anticonvulsants and antiepileptic drugs is recommended.
  • Surgery. Target surgical treatment– formation of a position of relative rest of the eyes by restoring the physiological position. To do this, the structural characteristics of the extraocular muscles are changed.

  Symptomatic treatment is based on spectacle or contact correction of visual acuity. The use of contact lenses is recommended, since when the eye moves, the center of the lens moves with it, and visual dysfunction does not develop. In some cases, Botox injections are performed into the orbital cavity to limit small-scale eye movements.

  Prognosis and prevention

  The prognosis for life and visual functions with nystagmus is favorable. Correct therapy of the underlying disease allows you to completely eliminate the clinical manifestations of the pathology. Specific prevention not developed. Nonspecific preventive measures boil down to timely diagnosis and treatment of lesions of the brain, vestibular apparatus and organ of vision. When involuntary movements of the eyeballs are detected in patients taking anticonvulsants or sleeping pills, it is necessary to adjust the dosage of medications.

Research methods of the vestibular analyzer are used in relation to patients suffering from attacks of dizziness, imbalance, and also during professional selection.

Anamnesis

A carefully collected anamnesis in most cases allows you to choose the right direction in further examination of the patient and make the most likely hypothesis about the nature of vestibular dysfunction. When collecting anamnesis, pay attention to the following questions:

1) duration of the disease, frequency and duration of attacks, their dynamics: suddenness of onset, remitting course, gradual or abortive cessation of clinical manifestations;

2) characteristics of symptoms (dizziness, ataxia, nausea, etc.), the sequence of their occurrence, combination with symptoms of dysfunction of other organs and systems (cardiovascular, digestive, endocrine, sensory organs, musculoskeletal system, etc. .). When assessing subjective vestibular symptoms, their qualitative characteristics are determined, for example, the nature of dizziness (systemic, non-systemic), the reasons for its occurrence (spontaneously or with sudden movements of the head), etc.;

3) the presence of hearing disorders (hearing loss - unilateral, bilateral), their coincidence with vestibular disorders in time and side of the lesion; the presence of tinnitus, diplo- or hyperacusis, deterioration of speech intelligibility, etc. In all cases of vestibular dysfunction, tone threshold audiometry and, if indicated, other audiometric studies are performed.

Special vestibulometric examination

This examination is carried out on the basis of anamnesis and a preliminary otoneurological conclusion after a mandatory consultation

neurologist and other specialists (as indicated). As a rule, the examination begins with the most gentle vestibulometric tests, and methods from the following list can be used in the specified sequence.

I. Study of spontaneous pathological vestibular reactions and tests for coordination of movements:

1) spontaneous nystagmus;

2) positional nystagmus;

3) pressor nystagmus;

4) coordination of movements;

5) static equilibrium function;

6) dynamic equilibrium function;

7) indirect otolitometry.

II. Vestibulometry methods:

1) electronystagmography (ENG) and nystagmometry;

2) videonystagmography (VNG);

3) experimental tests:

a) rotational;

b) caloric;

c) optokinetic.

Study of spontaneous nystagmus

Spontaneous vestibular nystagmus refers to involuntary cyclic contractions of the oculomotor muscles caused by disease or damage to the ear labyrinth or the centers of the vestibular analyzer. Spontaneous nystagmus consists of two components - fast And slow. The examination is carried out visually when the patient's gaze is moved to the right and left by 30° or up and down (Fig. 1).

Rice. 1. Determination of the intensity of spontaneous nystagmus visually using magnifying glasses: I, II, III—positions of the visual reference when detecting spontaneous nystagmus of the corresponding degrees. The fast component is directed to the right

When the eyes are abducted, the presence or absence of nystagmus is recorded. To exclude the phenomenon of fixation suppression of nystagmus, the patient wears special glasses with +20 lenses diopter. Spontaneous vestibular nystagmus also recorded using electronystagmography and videonystagmography (see below). The direction of nystagmus, its degree (intensity and amplitude) are determined by the fast component. According to the direction, nystagmus is classified into horizontal, horizontal-rotatory, diagonal, vertical, and pulsating nystagmus. By intensity Nystagmus is divided into 3 degrees. At I degree nystagmus occurs only when the eyes are moved towards the fast component, and disappears when looking straight or towards the slow component; such nystagmus is assessed as the most weak; II degree- nystagmus appears when looking towards the fast component and directly and disappears when looking towards the slow component; such nystagmus is assessed as medium strength; III degree- nystagmus is observed in any position of the eyeballs, intensifies when looking towards the fast component, and can weaken when looking towards the slow component. By amplitude Spontaneous nystagmus is divided into small-, medium- and large-scale.

Study of positional nystagmus

Positional nystagmus occurs in some pathological conditions in cervical spine spine, accompanied by circulatory disorders in the vertebrobasilar arterial system and with tumors in the posterior cranial fossa. To provoke this nystagmus, tests are used with turning the head and changing the position of the head relative to the direction of the force of gravity. In the first case, create unfavourable conditions for blood circulation in vertebral arteries, which are the sources of blood supply to the ear labyrinth, in the second - conditions for exerting tumor pressure on the brain stem, where the vestibular nuclei are located.

Pressor nystagmus study. Pressor nystagmus occurs when there is a defect in bone tissue ear labyrinth, which forms part of the medial (labyrinthine) wall of the tympanic cavity (bone caries, labyrinthine fistula). The appearance of nystagmus with increased pressure in the external auditory canal with the indicated anatomical changes is called fistula symptom. Typically, a labyrinthine fistula is combined with a defect eardrum, therefore, this symptom is easily caused by increasing the pressure in the external auditory canal using an ear obturator and a Politzer balloon. Instead of testing with a Politzer balloon, you can press the tragus into the external auditory canal.

Movement coordination research

Dysfunction of the vestibular apparatus is often accompanied by harmonious loss of coordination of movements upper limbs. Several samples are used.

Test of outstretched arms is that when the function of the vestibular apparatus is impaired, the hands deviate in the direction opposite to dizziness, or in the direction of the slow component of spontaneous nystagmus.

Index test- finger-finger and finger-nose. If the function of the vestibular analyzer is impaired, the patient cannot, with his eyes closed, put his finger on the tip of his nose or on the finger of the examiner.

Writing test. Tests with objective recording of movement coordination disorders include tests of vertical and horizontal letter, proposed by the Japanese author Fukuda (Fucuda T., 1959). The subject, sitting at a table, is asked to write a series of numbers, first from top to bottom, then from left to right. First, the test is performed with open eyes, then on the same sheet of paper with eyes closed. The result is assessed by the angle of deviation of a column or series of numbers from a vertical or horizontal line.

Study of the static equilibrium function

Romberg test(1846) is the most common and accessible, and comes in several varieties. Romberg's simple position, which was proposed by the author himself, is that the patient stands with his feet closed and his eyes closed. His stability in this position is assessed. The test can be complicated by asking the subject to stretch his arms forward. An even greater complication of the test is achieved by placing the feet one behind the other in one line. A simple position can be complicated by throwing your head back or tilting it towards your shoulder.

With unilateral damage to the vestibular apparatus, deviation in the Romberg position always occurs only in one direction. In the presence of spontaneous nystagmus or dizziness, the deviation occurs in the direction of the slow component of vestibular nystagmus or in the direction opposite to the sensation of self-motion. At cerebellar ataxia the body deviates backwards. The reaction of falling during a hysterical attack is different in that the patient feels not only the fact of falling, but also consciously chooses where it is more convenient for him to fall, so as not to injure himself.

TO quantitative methods Studies of the static balance function include various tests in which head excursions are recorded in the Romberg position ( cephalography). IN last years the static equilibrium function is studied using the method stabilography(posturography), for which installations called stabilographs are used, which make it possible to register in graphical and numerical display the slightest fluctuations in the center of gravity of the body, the parameters of which (amplitude, direction, etc.) reflect the compensatory scanning of the static regulatory system within the support area (during normal operation of this system) or when leaving the specified area due to certain violations of the equilibrium function. Computer stabilography allows you to differentiate and synthesize the results obtained, identifying in them signs of disruption of certain physiological elements involved in the regulation of static balance.

Study of the dynamic equilibrium function

The dynamic balance function is understood as the ability to maintain an adequate body position while actively moving in space. For this purpose, various walking options are used, in which deviations from a given route are recorded.

Indirect statolitometry

This method is based on the unconditioned tonic vestibular-oculomotor reflex of counter-rotation of the eyes, reflecting the functional state of the otolithic apparatus. The essence of the reflex is the synchronous rotation of the eyeballs around the visual axes in the direction opposite to the tilt of the head in the frontal plane. The biological significance of this reflex is to maintain, at least to an approximate extent, the location of the retinal coordinates adequate to the direction of the gravitational vertical, which is necessary for a more correct perception of space.

Evoked vestibular nystagmus study

In clinical practice, methods of provoking vestibular nystagmus by influencing the vestibular apparatus with rotational, caloric or electrical stimuli have become widespread. Clinical versions of the rotational and caloric tests were developed by R. Barani.

Rotational test

The rotation test according to Barany (1906) consisted of the subject, with his eyes closed, being rotated on a special chair at a speed of 10 revolutions per 20 s, then he was abruptly stopped and the duration was recorded post-rotational nystagmus. In this case, the examinee fixed the examiner's finger, pointed in the direction opposite to the rotation. Normally, the duration of such nystagmus did not exceed 10-15 s. The duration of the counter-rotation illusion was recorded in the same way, while the subject remained with his eyes closed and reported the cessation of dizziness. Usually the duration of this illusion also does not exceed 10-15 seconds.

All rotational tests involve rotation in both directions. Take a break of at least 5 minutes between rotations to the right and left. With the help of some rotational tests (cupulometry, pendulum test, threshold rotational test, etc.), a more accurate assessment of the functional state of the vestibular analyzer is possible, for example, identifying the phenomenon interlabyrinthine asymmetry.

Caloric test

The caloric test, in contrast to the rotational test, makes it possible to evaluate the functional state of each vestibular apparatus separately, since it first stimulates one ear labyrinth with heat or cold, then the other.

R. Barany (1906) was the first to use caloric stimulation of the ear labyrinth in clinical practice: the subject, in a sitting position with his head tilted back 60°, had 100 ml poured into the external auditory canal. cold» water (23-25 ​​°C) for 10 s; The latent period and duration of the resulting caloric nystagmus were recorded. Nystagmus was assessed visually when gaze deviated 30° to the side. opposite ear. Nystagmus with its fast component when irrigating the ear cold water always directed in the direction opposite to the irritated ear. To increase the efficiency of the sample, V.I. Voyachek proposed increasing the irrigation time to 20 s and lowering the water temperature to 20 °C, maintaining the same volume of 100 ml.

A caloric test conducted with water at 37 °C does not cause nystagmus, which confirms the convective origin of caloric nystagmus. Currently, the so-called bithermal caloric test, at which the temperature of the carrier (water or air) is equal to cold test 30 °C and thermal test- 44 °C.

Vestibulometric formula

To record the results of vestibulometry, different authors used different versions of the so-called vestibular passport. For this purpose, V.I. Voyachek in 1912 proposed the so-called vestibulometric formula(Table 1), including a number of tests.

Table 1. A sample of the vestibulometric formula according to V. I. Voyachek

This formula indicates the presence of dizziness to the left, spontaneous nystagmus is noted in the same direction (according to the fast component, an increase in the duration of post-rotational and caloric nystagmus, which together indicates irritation of the left vestibular apparatus, one of the causes of which may be Meniere’s disease or the initial stage of serous labyrinthitis .

Currently, electron stagmography (ENG) and videonystagmography (VNG) methods are used to record nystagmus.

Electronystagmography

To conduct ENG, special electronic biopotential amplifiers are used, equipped with recording devices that make it possible to obtain a graphical record of eye movements unfolded over time. ENG is based on recording changes spreading in the periocular tissues corneoretinal bioelectric potential, varying depending on the amplitude of eye movement. Electrodes that measure this potential are located at the outer corners of the eyes. In Fig. Figure 2 shows diagrams of caloric and post-rotational nystagmus in the dynamics of their development.

Rice. 2. Diagrams of the dynamics of nystagmus reactions during caloric (I) and acceleration (post-rotation; II) tests; III - time scale: a - latent period of caloric nystagmus; b — period of increasing intensity of nystagmus; c — the culmination period of caloric and post-rotational nystagmus; d — total duration of caloric nystagmus; d - the final part of the rotational nystagmus caused by angular acceleration at the beginning of rotation; e — duration of post-rotational nystagmus caused by negative angular acceleration (stop stimulus); g - period of culmination of post-rotatory nystagmus

To calculate the parameters of nystagmus, special computer programs have been developed, which are implemented in automatic mode with direct input of electrical nystagmus signals into the computer in current time mode. Parameters such as frequency (Hz), amplitude (in angular degrees), angular velocity of the fast and slow components (°/s), and total duration of the nystagmus reaction (s) are calculated. The ultimate goal is to establish the presence and extent interlabyrinthine asymmetry, assessment of the degree of excitability of each labyrinth separately, determination of the dynamics of ENG parameters characterizing the clinical course of the disease.

The following options for assessing the state of the vestibular apparatus according to ENG data are possible:

1. Normoreflexia. This state of the vestibular system is characteristic of otiatrically healthy individuals.

2. Hyperreflexia. It is characterized by an increase in the numerical values ​​of the primary parameters of nystagmus. Characteristic for excitation of the vestibular apparatus.

3. Hyporeflexia. It is characterized by a decrease in the numerical values ​​of the primary parameters of nystagmus. Characteristic of depression of the vestibular apparatus.

4. Asymmetry— quantitative difference in the parameters of nystagmus caused by stimulation of the right and left labyrinths. This characteristic is the main sign of vestibular dysfunction and is manifested by a predominance of nystagmus in one direction.

5. Areflexia. Characterized by complete absence vestibular nystagmus when trying to provoke it. Areflexia can be unilateral or bilateral and reflects the shutdown of vestibular function. Unilateral areflexia is detected only with the help of a caloric test with separate stimulation of the labyrinths.

Videonystagmography

Videonystagmography (VNG) refers to modern methods registration of nystagmus and computer analysis of its parameters during various test research programs (Fig. 3). The VNG method is based on the principle of video telemetry of eyeball movements, followed by computer analysis and display of the results obtained in graphical and numerical (tabular) expression. The measurement accuracy is 1/4° with high stability of the video image of the eye.

Rice. 3. Videonystagmographic installation: 1 - TV screen on which optomotor tests are displayed (OKN, saccades, smooth pursuit, etc.); 2 — otocalorimeter for air stimulation of the ear labyrinth; 3 — system unit (computer); 4 - computer monitor; 5 - mask with a video camera built into it (for recording eye movements)

In Fig. 4, a variant of the result of studying caloric nystagmus using videonystagmography is presented. In this version, the numerical parameters of caloric nystagmus and their graphical relationship when conducting a bithermal caloric test are displayed.

Rice. 4.

Bithermal caloric test

The bithermal caloric test involves the sequential application of first cold, then warm calorization (water or air) to each ear. The criterion for assessing the results of the study is the duration of nystagmus, and with ENG or VNG - other parameters of nystagmus (angular velocity of the slow component, frequency, etc.).

Galvanic test

The galvanic test involves stimulation of the ear labyrinths with a constant or low-frequency electric current of weak strength (up to 5 mA).

When conducting a test, sensations arise that are similar in quality to those that occur during a rotational or caloric test. At the same time, so-called galvanic nystagmus may occur. The essence of the technique is that an active electrode with a diameter of 10 mm is fixed to the tragus of the ear under study using a special clip. The other electrode is significantly bigger size fixed on the skin of the forearm. When a weak direct current (1-5 mA) is applied, after a few seconds the subject experiences dizziness and spontaneous nystagmus, the direction of which is determined by the polarity of the electric current. If the cathode (-) is located on the tragus, the nystagmus is directed in the same direction; if the anode is located (+), the nystagmus is directed towards the opposite ear. If you smoothly change the polarity of the current, the subject will experience a sensation of rocking rotation with the frequency of the change in current polarity. With prolonged stimulation or increased current strength, subjects sensitive to motion sickness experience vegetative reactions characteristic of motion sickness.

Otorhinolaryngology. IN AND. Babiyak, M.I. Govorun, Ya.A. Nakatis, A.N. Pashchinin

Spontaneous nystagmus is a severe form of the disorder motor function eye. Its manifestation is observed in the form of involuntary eye movements with high frequency. The reasons for this can be both physiological and pathological. For example, if you observe an object that is moving very quickly, or the person himself is spinning in a drum, wheel or ball, such a phenomenon may occur as a protective mechanism to preserve vision.

To detect the presence of such a disease, it is enough to conduct a routine examination by an ophthalmologist, while the vestibular apparatus does not experience additional stress, as a result of which nystagmus can be caused experimentally.

The patient sits opposite the doctor so that their eyes are at approximately the same level. The patient must be under lighting so that the slightest movements of the eyeball can be seen. Opposite the patient, at a distance of about 30 cm, there is an object, which the doctor begins to move from side to side, from top to bottom and back, in a diagonal direction. The patient must carefully monitor the subject all this time, and the doctor must monitor the slightest manifestations of the disease. For this experienced doctor evaluates eye movements using various parameters.

When spontaneous nystagmus is checked in a person who is healthy in this regard, he normally experiences minor short-term twitching in the extreme positions of the eyeballs; this phenomenon is not considered pathological.

If such a syndrome is identified, then to determine the disease of which it serves as a symptom, the patient is referred to a neurologist to conduct more detailed studies of its electrophysiological nature.

Classification, causes of nystagmus

Depending on the direction of the oscillatory movements, spontaneous nystagmus can be vertical, horizontal, diagonal or rotational. The most common movement of the eyes is horizontal from side to side. The rarest is dissociated spontaneous nystagmus, for which there is no specific direction of movement.

The nature of the movements allows us to distinguish pendulum-like nystagmus, in which the eye movements are uniform, so they sway from one side to the other. Another type of this disease is jerky, in which the eyes move slowly to one side but return quickly. When there is no definite movement, you can observe first one type, then another, nystagmus in this case is mixed.

There may be a pronounced different amplitude of eye movement, depending on which several degrees of development of the disease are distinguished.

The main cause of this disease is the occurrence of instability in the operation of the eye movement control system. Such instability may be influenced by local factors such as various diseases from myopia and farsightedness to optic nerve atrophy. Common causes may include damage to the cerebral pons, cerebellum, pituitary gland, after a concussion, after drug poisoning, past infectious diseases, etc.

An arbitrary syndrome can also occur in a healthy person after exposure to the nervous system. An example of such a situation would be when riding on attractions, when the brain and its vestibular system are under severe stress, or with a minor concussion. A short recovery brings the system responsible for eye movement back to normal. Voluntary nystagmus quickly passes.

The occurrence of pathological spontaneous nystagmus is a symptom of changes in the labyrinth of the inner ear or brain. He says that there are some disturbances in the system that captures a person’s gaze. The degree of damage and its level can be judged by which direction predominates in eye movements.

Main symptoms, treatment

Uncontrolled eye movement is an example of a symptom of nystagmus, but it is not the only one. There is also a decrease in visual acuity, an increase in photosensitivity, viewing the outside world creates a feeling of blurriness of the picture, its displacement and trembling. In parallel with this, in some cases, dizziness and lack of stability when moving are observed. Most often this happens when the defect appears quite often and begins to cause some inconvenience that forces you to pay attention to it.

In some types of the syndrome, visual impairment does not occur to a significant extent.

Given the pathological nature of the disease, it is impossible to completely cure nystagmus. As therapy, the emphasis is on curing the disease that caused its occurrence and subsequent development.

Myopia, farsightedness and astigmatism are corrected with glasses with appropriate lenses. In addition, hardware treatment is performed, which can reduce the manifestations of nystagmus, after which visual acuity also increases.

To improve the nutrition that the retinal tissue receives, the use of drugs with vasodilating properties, as well as vitamin complexes, is used.

When especially severe forms when oscillatory movements cause great discomfort, it may be necessary surgical intervention. During the operation, the eye muscles are affected, some of them need to be made weaker, some stronger, in order to compensate for their influence. After this, a reduction in amplitude, improvement in visual acuity and other positive changes are observed.

Nystagmus (nystagmus; Greek nystagmos drowsiness) - rapidly repeating movements of the eyeballs (eye tremors). The following types of N. are distinguished: vestibular, which occurs when the receptors of the vestibular apparatus are irritated, and optokinetic, which appears when the visual analyzer is irritated (looking at uniformly moving objects). Other types of N. are relatively rare (professional, congenital, fixation and installation, voluntary) .

Vestibular nystagmus is important for topical diagnosis and reflects the dynamic changes occurring in the c. n. With. and on the periphery. N. can be examined in a patient regardless of the severity of the condition, even in a coma.

The anatomical structures with the help of which vestibular N. is carried out are the neuroepithelium of the ampullae of the semicircular canals, the vestibular node, the vestibular part of the vestibular-cochlear nerve, the vestibular nuclei at the bottom of the fourth ventricle, crossed (for horizontal N.) and uncrossed (for vertical N.) vestibuloculomotor tracts running in an ascending direction at the bottom of the IV ventricle to the nuclei of the oculomotor (VI) and abducens (III) nerves (Fig.). Through the weight-tibulo-oculomotor connections passing in the posterior longitudinal beam, vestibular impulses reach eye muscles. In the same way, reflex combined deviations of the eyes occur, as a result of which the direction of gaze does not change when the position of the head changes, N. and compensatory adjustment of the eyes is carried out. The mechanism of vestibular N. is closely related to the mechanism of movement of the eyeballs. This connection is carried out through a complex system of the posterior longitudinal fasciculus. Some of its fibers connect the system of vestibular nuclei with the nuclei of the oculomotor and abducens nerves.

Adequate stimulation of the vestibular analyzer is the movement of endolymph in the semicircular canals. In this case, a whole complex of vestibular reactions arises (see), including vestibular H.

Vestibular N. is divided into spontaneous, which is always a sign of patol, a process in any part of the reflex arc that carries out vestibular N., and artificially caused, or experimental, N., detected using a caloric test or rotation (see Vestibulometry). Artificially caused N. is usually present and normal; with pathology, its indicators change - duration and character; This type also includes pressor N., which occurs when air pressure in the external auditory canal increases.

Spontaneous vestibular nystagmus has the following characteristics: direction, amplitude, degree, binocularity and monocularity (dissociated N.), predominance in a certain direction, changing character, alternation of phases, rhythm.

The direction of spontaneous vestibular N. is judged by its fast phase. It can have different directions: horizontal, vertical, diagonal, rotatory, converging, mixed (horizontal-rotatory). Horizontal N. occurs most often and is observed when the middle parts of the rhomboid fossa are affected. Vertical N. is usually less pronounced, rarely isolated, and more often diagonal (horizontal and vertical). Vertical and diagonal N. occur when the upper parts of the rhomboid fossa are affected, and rotatory N. occurs when there is a violation in its lower sections. Converging N., in which the eyeballs move towards each other, is a symptom of damage to the midbrain.

Depending on the amplitude, N. is divided into small, medium and large-scale. With small N., the movements of the eyeballs are barely noticeable and the amplitude of their vibrations is 1 - 2 mm; the amplitude of large-scale N. can reach 8-10 mm; V in rare cases the eyeballs move during N. throughout palpebral fissure from external to internal commissure and back. Large-scale N. is characteristic of brainstem lesions.

Spontaneous vestibular N., depending on the direction of gaze, in which it appears, is divided into three degrees. First degree nystagmus appears only when looking towards the fast phase of H.; II degree occurs with direct gaze; III degree occurs when looking towards the slow phase of the N. Spontaneous vestibular N. usually intensifies when looking towards the fast phase, and the appearance of spontaneous N. with a direct look and towards the slow phase indicates stronger irritation of the vestibular apparatus.

Usually both eyes are involved in nystagmus (binocular N.). Often, with brainstem lesions of the vestibular apparatus, the eyeballs participate in N. not equally: one eye moves with a greater amplitude, and the other with a smaller one. In rare cases, only one eye takes part in N., while the other remains motionless (monocular N.). Monocular N. may be the result of damage to the posterior longitudinal fasciculus or the nuclei of the oculomotor and abducens nerves.

Often spontaneous N. prevails in some direction. The prevalence of N. can be based on its degree, when N. appears at a smaller angle of eye abduction or even with direct gaze, as well as in amplitude and tonicity. More often, horizontal N. is prevalent, less often vertical. The prevalence of horizontal N. in any direction indicates uneven, asymmetrical damage to the labyrinths and roots of the VIII pair cranial nerves. In case of acute loss of function of one of the labyrinths (purulent labyrinthitis, thrombosis of the labyrinthine artery, fissures of the pyramid temporal bone) spontaneous N. appears, directed towards the healthy labyrinth, and disappears after 2-3 weeks.

Changing spontaneous N. is called positional or positional nystagmus, since it often changes or appears only in certain positions. Thus, when changing position, N. can change amplitude, degree, frequency (most often), direction, or occurs only in certain positions of the patient, or sharply changes its character without changing position (with tumors of the cerebellum and fourth ventricle).

Spontaneous vestibular K. consists of rhythmically alternating fast and slow phases. During the slow phase, the eyeballs slowly retract; when they reach a certain abduction amplitude, a fast N. phase occurs, during which the eyeballs return to their original position. Normal ratio Between the fast and slow phases, the duration is usually 1:3, 1:5. Depending on the nature of the alternation of phases, N. is divided into the following types. Pendulum-shaped, trembling, or undulating, N., in which the slow and fast phases are the same and eye movements resemble the movements of a pendulum, as a rule, is not associated with damage to the vestibular system, but is caused by low vision, which arose in early childhood, and impaired gaze fixation. In rare cases of severe primary brainstem lesions (pontine tumors, strokes, encephalitis), pendulum-shaped trembling N. of vestibular origin appears.

Clonic jerky N. occurs in the compensated form of the central vestibular syndrome that occurs when the peripheral part vestibular analyzer.

Tonic N. is observed during strokes in the acute period, with moderate and severe degrees of traumatic brain injury, in acute stage stem encephalitis, during the period of decompensation of hypertensive syndrome due to brain tumors (see Hypertensive syndrome).

A sharply expressed unevenness of N. in amplitude, rhythm, and duration of alternation of phases is characteristic of severe stem lesions (strokes, stem tumors, and encephalitis). The loss of the fast phase of N., when the eyeballs “float” towards the slow phase during the caloric test and remain motionless, is a formidable symptom characteristic of patients in a comatose state. In an even deeper comatose state, the slow phase N also occurs.

Depending on the location, peripheral and central spontaneous vestibular II are distinguished. Peripheral spontaneous N. occurs when the labyrinth or root of the VIII pair of cranial nerves is damaged. In direction, this type of spontaneous N. is horizontal-rotatory, less often rotatory. Vertical, diagonal and converging N. do not occur with peripheral lesions. When one of the labyrinths dies, spontaneous N. is directed in the healthy direction, and when one of the labyrinths is irritated, it is directed towards the irritated labyrinth. N.'s character is rhythmic, with regular alternation of phases, binocular. It is often accompanied by an increase in vestibulo-vegetative and vestibulosensory reactions, as well as other vestibulosomatic reactions (spontaneous deviation of the arms and torso), while the deviation coincides in direction with the slow phase of spontaneous N. Peripheral N. disappears after 2-3 weeks. due to compensatory restructuring in the central sections of the vestibular analyzer.

Central spontaneous N., in contrast to peripheral one, is caused by damage to the vestibular nuclei and vestibuloculomotor connections in the system of the posterior longitudinal fasciculus. In direction, along with horizontal and rotatory, there are vertical, diagonal and converging N.; often N. becomes dysrhythmic, tonic, and monocular. The reaction of deviation of the arms and body does not always correspond to the slow phase of spontaneous N. (vestibular disharmony). With severe central N., patients often do not experience dizziness and do not experience vestibulo-vegetative reactions. Central N. can remain for a very long time, sometimes for life.

To judge the topic of spontaneous N., it is necessary to analyze the signs of spontaneous vestibular disorders, data from studies of experimental vestibular tests and hearing, and also take into account the wedge and picture of the disease. Vestibular symptoms, including vestibular N., are especially clearly manifested in the acute development of patol, the process, for example, in acute labyrinthitis (see), acute swelling of the labyrinth during an attack of Meniere's disease (see Meniere's disease), in the acute period traumatic brain injury (see), stroke (see), subarachnoid hemorrhages, with rapidly increasing hypertension due to malignant brain tumors. Most often, spontaneous N. occurs when the labyrinth and stem sections of the brain in the posterior cranial fossa (pons) are damaged. With tumors of the posterior cranial fossa, spontaneous N. occurs in 92% of cases, varies greatly in direction, degree, amplitude, and the nature of the alternation of phases depending on the location, size, direction of growth, the nature of the tumor and the age of the patients. The closer the tumor is located to the primary arc of the vestibular reflex (vestibular nuclei, vestibulo-oculomotor connections in the posterior longitudinal fasciculus at the bottom of the fourth ventricle), the more pronounced spontaneous H.

So, for example, with tumors of the pons, spontaneous N. occurs in 100% of cases, of the cerebellopontine angle - in 95%, of the fourth ventricle - in 92.7%, of the cerebellum - in 84.2% of cases. With tumors of the cerebral hemispheres, spontaneous N. occurs only in 11-12% and is much less pronounced than with tumors of the posterior cranial fossa.

Spontaneous N. often occurs with cracks in the pyramid of the temporal bone, in the acute period of any traumatic brain injury, with vascular disorders in the vertebrobasilar system, with brainstem encephalitis, arachnoiditis and arachnoencephalitis, localized mainly in the posterior cranial fossa, with multiple sclerosis.

Usually spontaneous N. is examined visually (nystagmoscopy) or recorded (nystagmography). The method of electronystagmography (see), which allows accurate recording of nystagmus, has become widespread.

N.'s study is carried out in the following sequence: with direct gaze; with extreme aversions of gaze; tilting the head to the sides and back; lying on your back and side. Often spontaneous N. changes especially sharply when the head is tilted to the sides and when the patient lies on his side (positional nystagmus).

To clarify the diagnosis, they use functions, loads on the vestibular apparatus, using calorization, rotation and galvanic current.

Artificially induced vestibular nystagmus is caloric, rotational, post-rotational and pressor; Galvanic N is studied much less frequently.

Caloric N. refers to the movements of the eyeballs that occur during artificial cooling or warming of the labyrinth. Heat or cold causes movement of the eidolymph in the semicircular canals (cold particles go down, hot particles go up), which is an adequate stimulus to the vestibular analyzer. There are several options for performing a caloric test; The most rational option is to inject 100 ml of water at t°25° into the external auditory canal for 10 seconds. If there is no reaction, pour in water at a temperature of 19°. If there is a clear asymmetry of the vestibular reflexes obtained from both labyrinths, pour in 100 ml of hot water (over 37°). Normally, caloric N. according to this method appears after 25-30 seconds. and lasts 50-70 seconds. Sometimes, normally, caloric N. is absent, but the reactive deviation of the hands towards the slow phase of N. with eyes closed after calorization always remains clear. The caloric test allows you to explore each maze separately. For irritation of the horizontal semicircular canal it is given a vertical position, for which the patient’s head is tilted 60° back. When the horizontal semicircular canal is irritated with cold water, a horizontal caloric N. appears, which is directed in the direction opposite to the ear being examined, and when hot water is infused (over 37°), a N. appears, directed towards the ear being examined. The change in caloric N. can be in duration (normal, increased, decreased, no reaction) and in qualitative characteristics, which have the same meaning as with spontaneous vestibular N.

In case of peripheral and nuclear damage to the vestibular analyzer during calorization with hot and cool water, the severity of N. depends on the labyrinth being studied: regardless of the direction of the caloric N., reactions from the labyrinth will be normal, increased or decreased. With subcortical lesions during hot and cold calorization, N. will be expressed more in one direction, often towards the lesion, regardless of which labyrinth is irritated. Distinct vestibular asymmetries of caloric N. of the peripheral-nuclear or subcortical type are usually found in the decompensated phase of diseases of c. n. With. and with damage to the peripheral part of the vestibular analyzer.

Rotational and post-rotational N. occur during and after rotation. In this case, the right and left semicircular canals are always irritated simultaneously, however, according to Ewald’s law, the greatest irritation will be in that semicircular canal where the endolymph flow goes in the direction of the ampulla: this stronger irritation masks the irritation from the other labyrinth, where the endolymph flow comes from the ampulla .

Therefore, rotational N. is directed in the direction of rotation, and post-rotational - in the opposite direction. Rotation is a stronger and short-term irritant than calorization. The rotational test is performed either in a Barany chair or on special electronically controlled vestibular stands, which make it possible to accurately dose angular positive and negative accelerations, rotation speeds and stop stimuli over a wide range, carry out rotation according to a variety of programs and objectively record vestibular reflexes.

In healthy people, as well as with unilateral loss of vestibular function, post-rotational N. is preserved during intense vestibular irritation. Post-rotational N. falls out only with bilateral death of the labyrinths or roots of the vestibular nerves (bilateral total neuritis of the VIII pair of cranial nerves after meningitis, the use of ototoxic antibiotics), as well as in the decompensated phase of diencephalic-subcortical lesions, but in the latter case, vestibular-vegetative, sensory and motor ones sharply increase reactions. Pressor N. can be caused directly by pressing a finger on the tragus. The appearance of pressor N. indicates the presence of a destructive process (fistula) in the bone wall of the labyrinth, most often in the horizontal semicircular canal, due to hron, purulent inflammation middle ear (see Otitis).

Galvanic N. occurs under the influence of irritation of the labyrinth by direct electric current.

Optokinetic nystagmus is caused artificially by rotating a special drum under study in front of the eyes; like the vestibular one, it has a slow and fast phase, but its reflex path is different: visual stimulation from the retina goes through the visual pathways to the occipital lobe of the brain, where the optomotor path begins, which crosses into upper sections brain stem at the level of the posterior cranial fossa and ends in the vestibular nuclei, and irritation through the system of vestibulo-oculomotor connections goes to the oculomotor nuclei.

Violations of optokinetic N. are of great practical importance in the clinic. When the peripheral vestibular analyzer is damaged, optokinetic N. does not change; when lesions appear in the posterior cranial fossa, it is directed towards the lesion. Lesions in the cerebral hemispheres cause contralateral loss or weakening of horizontal optokinetic N. (when lesions are localized in the occipital and temporal regions, homonymous hemianopia appears on the side opposite to the lesion, and in the frontal region it proceeds without hemianopsia).

Other types of nystagmus. Professional N. of coal miners, miners, associated with a violation of gaze fixation in low light, working in a half-bent position, has a tremulous pendulum-like character. Due to the improvement of working conditions in mines, this pathology is rare.

Congenital (hereditary) N. often accompanies others hereditary diseases nervous system; it is caused by insufficient development of the vestibular system.

Fixation and adjustment N. occur in healthy people with extreme gaze aversion. Fixation N. is longer, installation N. quickly disappears. These types of N. are caused by fatigue of the eye muscles with extreme aversion of gaze.

Voluntary N. is caused in rare cases by Ch. arr. in persons who have the ability to contract other muscles that do not normally obey voluntary activity (for example, movement of the ears).

Bibliography: Ageeva-Maikova O.G. and Zhukovich A.V. Fundamentals of otorino-laryngoneurology, M., 1960; Blagoveshchenskaya N. S. Clinical otoneurology for brain lesions, M., 1976; Differential diagnosis otogenic and vascular vestibular disorders, Study of positional nystagmus, Guidelines, comp. G. M. Grigoriev, Chelyabinsk, 1976; Kalinovskaya I. Ya. Stem vestibular syndromes, M., 1973; X e h i n a sh v or whether S. N. Vestibular function, Tbilisi, 1968, bibliogr.; To e x and y about in A. N. Differential diagnostic problems in otoneurology, Sofia, 1962, bibliogr.; K t o n a s P. Y. a. O. Effect of electronic filters on electro-nystagmographic recordings, Arch. Otola-rvng., v. 101, p. 413, 1975; Ryu J. H. a". McCabe B. F. Central vestibular compensation, ibid., v. 102, p. 71, 1976; Spector M. Electronystagmographic findings in central nervous system disease-Ann. Otol. (St Louis), v. 84, p. 374, 1975, Tantchev K. S. Particularites diffe; rentielles et diagnostiques de position peripherique et centrale, Rev. Laryng, t. 95, p. 449.

N. S. Blagoveshchenskaya.