How are patients with vestibular syndrome treated? Acute vestibular syndrome Central vestibular syndrome in humans how to treat

Central vestibular syndromes occur when neurons and pathways of the vestibular analyzer are damaged, starting from the vestibular nuclei and ending with the cortical zones of this analyzer, as well as when similar lesions occur in brain structures adjacent to the central vestibular structures. Central vestibular syndromes are characterized by the obliteration of the vestibular symptoms proper, which lose the signs of directionality (vectoriality) characteristic of peripheral lesions; this syndrome is accompanied by many signs of disturbance of other specific functions of the central nervous system, including other sensory organs. This circumstance determines the polymorphism of the clinical picture of central vestibular syndromes, which can combine signs of proper vestibular dysfunction with alternating stem and cerebellar syndromes, with signs of damage to the pyramidal, extrapyramidal and limbic-reticular systems, etc. All central vestibular syndromes are divided into stem, or subtentorial, and suprastem, or supratentorial. Information about these syndromes is an important part of otoneurology and is essential in the differential diagnosis of peripheral and central lesions of the vestibular system.

Subtentorial vestibular syndromes. Signs of damage to the brain stem are determined by the level of its damage. The brain stem includes the legs of the brain, the bridge, the medulla oblongata. When these formations are affected, alternating syndromes occur, characterized by dysfunction of the cranial nerves on the side of the lesion and central paralysis of the limbs or conduction disorders on the opposite side. The basis of subtentorial vestibular syndromes are bulbar alternating syndromes: Avellis syndrome (damage to the nuclei of the glossopharyngeal and vagus nerves and adjacent pyramidal and sensory pathways); Babinski-Najotte syndrome (infarction or hemorrhage of the lower cerebellar peduncle; cerebellar hemiataxia, nystagmus, miosis, enophthalmos, ptosis, etc.); Wallenberg-Zakharchenko syndrome (thrombosis of the inferior posterior cerebellar artery; extensive infarctions and necrosis in the corresponding half of the medulla oblongata with damage to the vestibular nuclei and nuclei of the vagus, trigeminal and glossopharyngeal nerves; dissociated sensitivity disorders, vomiting, dizziness, spontaneous nystagmus, lateropulsion towards the lesion; Bernard-Horner syndrome (damage to C7-Th1; a triad of symptoms - ptosis, miosis, enophthalmos; occurs with syringobulbia and syringomyelia, tumors, tumors of the trunk and spinal cord; Jackson syndrome (thrombosis of the vertebral artery, circulatory disorders in the upper sections of the medulla oblongata; nucleus lesion hypoglossal nerve on the side of the lesion, central paralysis of the limbs on the opposite side), etc.

Signs of damage to the cerebellum are caused by damage to both its tissue and neighboring anatomical structures. These signs include:

• violation of coordination of movements of the limbs (one-sided violation of the proportionality and rhythm of movements, for example, adiadochokinesis of the upper limbs;
• cerebellar paresis (decrease in the strength of muscle contraction on the side of the lesion);
• hyperkinesis (ataxic tremor, aggravated by voluntary targeted movements of the upper limbs, and myoclonus, characterized by rapid twitches of individual muscle groups or muscles that occur in the limbs, neck and swallowing muscles;
• cerebellar ataxia (violation of statics and gait);
• cerebellar disorders of muscle tone (spontaneous overshooting of the upper limb with closed eyes on the side of the lesion);
• asynergy (violation of the symmetry of movements with both limbs);
• speech disorders (bradilalia and scanned speech).

Supratentorial vestibular syndromes. These syndromes are characterized by significant polymorphism, manifesting both specific "direct" signs and associative symptoms mediated through the thalamic system.

Optico-striatal vestibular syndromes. Many authors admit that the nuclei of the optic-striate system are the second vestibular center, since signs of vestibular dysfunction also appear in some pathological conditions of this system. For example, in Parkinson's disease, chorea and other processes developing in the extrapyramidal system, many authors describe spontaneous pathological vestibular symptoms, indicating involvement in the pathological process of the vestibular system. However, these symptoms are indistinct and not systematic. Most often, vestibular dysfunction is manifested by non-systemic dizziness, experimental vestibular tests are normal, however, with a caloric test, along with the usual nystagmus with closed eyes, an involuntary deviation of the head towards the MK of nystagmus occurs, lasting exactly as long as the climax phase of nystagmus continues.

Cortical vestibular syndrome. It is generally accepted that the cortical projections of the vestibular apparatus are located in the temporal lobes of the brain, however, the central pathological vestibular reactions cause damage not only to the temporal lobes, but also to all others. This is explained by the fact that, probably, the vestibular apparatus has its own projections in all parts of the cerebral cortex. Other explanations are based on the existence of interlobar connections and the influence of the cortical pathological focus on the nuclei of the optic-striate system.

With tumors of the temporal lobe and often with lesions of other lobes, spontaneous nystagmus is observed, less often horizontal, more often circular and positional. In the Romberg position, patients usually deviate to the healthy side with tumors of the temporal lobe and to the diseased side with tumors of the parietal lobe. As a rule, provocative vestibular tests are normal or indicate some hyperreactivity of the vestibular analyzer. Spontaneous nystagmus is usually absent. The vertigo, if it occurs, is of an indeterminate nature, and rather resembles the peculiar aura sometimes observed before an epileptic seizure.

Vestibular disorders in intracranial hypertensive syndrome. Intracranial hypertensive syndrome occurs when the circulation of cerebrospinal fluid is disturbed as a result of obstruction of the CSF pathways. It is manifested by the following characteristic features: headache; nausea and vomiting, more often in the morning and with a change in head position; congestive optic discs are detected, sometimes with visual impairment. Vestibular symptoms appear more frequently with tumors in the posterior cranial fossa than with bulky supratentorial processes, with systemic dizziness, horizontal or multiple spontaneous nystagmus, and positional nystagmus occurring. Patients endure provocative tests with difficulty because of the occurrence of a Meniere-like syndrome during their conduct. If it is possible to conduct a caloric test, then a pronounced interlabyrinth asymmetry is revealed in the direction with a predominance of nystagmus in the healthy direction.

Central auditory syndromes. These syndromes occur when the conduction pathways and auditory nuclei are damaged in any of their areas. The resulting hearing impairments progress along with the main pathological process and are distinguished by the fact that the higher this process is localized, the less “tonal” and more “speech” hearing suffers, while the noise immunity of the sound analyzer sharply decreases. Tonal threshold audiograms in central auditory syndromes G.Greiner et al. (1952) classifies into three types:

1. primary hearing loss at low frequencies occurs with lesions of the bottom of the IV ventricle;
2. a decrease in the tonal curve to both low and high frequencies, with an even sharper decrease in the curve in the region of the so-called speech frequencies, is characteristic of bulbar lesions of the brain stem;
3. atypical mixed tone audiograms may indicate both an extramedullary pathological process and an intramedullary disease, such as syringobulbia or multiple sclerosis.

Central auditory syndromes are characterized by bilateral impairment of auditory function, loss of musical hearing, and the absence of FUNG. With cortical lesions of the auditory zones, auditory hallucinations and speech perception disorders often occur.

The expression “I have a weak vestibular apparatus” has probably been heard by every reader of this article. Usually people who get motion sickness in transport say this. However, few people know that the concept of "vestibular system" is somewhat broader, and that such ailments are often directly related to pathologies in the inner ear or brain,

Our sense of balance and coordination in space depend on the state of the vestibular system, the functions of which are to fix the image perceived by the eyes on the retina, as well as transmit information about the position of the head for further analysis to the brain.

An important organ of this system, responsible for the balance of the body, is the labyrinth of the inner ear. Some diseases can give complications in the form of a disorder of the vestibular analyzer, which leads to vestibular syndrome.

Most common symptoms of vestibular syndrome:

• dizziness
• a feeling of unsteadiness ("sickness"), both in sitting and standing positions
• nausea
• vomit
• before the eyes everything "floats" and "circles"
• tachycardia or bradycardia
• problems with blood pressure
• weakness
• confusion
• disorientation
• fatigue
• difficulty concentrating
• involuntary nystagmus
• anxiety, restlessness

The above symptoms of the disease, as a rule, are not permanent. Most often they appear paroxysmal, and then disappear. The periods between attacks can be different.

On the Causes of Vestibular Disorders from a Tibetan Perspective

Eastern doctors believe that in diseases associated with brain dysfunctions, the "culprit" defiant imbalance of basic constitutions"wind"-"bile"-mucus" is "wind"(nervous system)."Indignation" of this Yin (cold) constitution, most often, occurs due to unjustified frequent anxieties and fears, experienced grief, prolonged grief, mental or physical exhaustion, abuse of diets, dry food or foods with cold properties. In addition, age is a risk factor. In older people, the activity of the "wind" increases, and its balance is quite easy to disturb.

vestibular syndromeusually accompanies:

• traumatic brain injury, some of which cause positional vertigo (for example, loss of balance during a sharp turn of the head up or to the side)
• consequences of surgery
• labyrinthitis - the penetration of a viral or bacterial infection into the membranous labyrinth, provoking the development of an inflammatory process in the inner ear. May be a complication of otitis media that has passed in an acute form
• labyrinth infarction, most often occurs in old age, but it can also appear in a young person, together with atherosclerosis of blood vessels and increased blood clotting. The patient has an intense syndrome of dizziness, unsteadiness and uncertainty of gait, other neurological symptoms
• Meniere's disease, manifested by hearing loss, noise and pressure in the ears. The head is spinning paroxysmal, nausea and vomiting occur in parallel, this condition can last for several hours, then it passes
• basilar migraine, in moments of acute headache of which a sense of stability is lost, a painful reaction to loud sounds and photophobia appears, in some cases hearing loss is also possible. Dizziness in most cases precedes an attack of pain
• multiple sclerosis is often accompanied by impaired vestibular function
• vestibular neuritis (dizziness, nausea and vomiting with too sudden a change in the position of the head characterizes inflammation of the vestibulocochlear nerve, possibly associated with the herpes virus)
• some diseases of the central nervous system and the musculoskeletal system (vertebrobasilar insufficiency, vegetative-vascular dystonia, cervical osteochondrosis, etc.)
• hypertonic disease
• a brain tumor
• psychogenic disorders

Besides, vestibular cider may be the result of a banal motion sickness in a vehicle or an "unloading" disease (when the traffic has already been stopped, and the symptoms persist for some time). The state of drug intoxication also causes weakness in the legs and lack of a sense of balance.

What is the treatment of vestibular syndrome in the clinic of Tibetan medicine?

Doctors of modern medicine often cannot decide which specialist should treat this disease: a neurologist or an otolaryngologist, which makes it difficult for a patient to contact a specialist and make a diagnosis.

The Naran clinic believes that the approach to each disease should be comprehensive, the main attention is directed not to the elimination of visible external symptoms, but to the fight against the cause that causes the disease. Therefore, at a preliminary consultation in Tibetan medicine clinics, an additional diagnosis is necessarily carried out, consisting of:

• survey
• inspection
• traditional oriental pulse diagnostics

On the basis of conversations with the patient and the results of his examination, the personal doctor decides which procedures will be included in the treatment. Among them:

• advice on nutrition, lifestyle

Karataev Pavel Sergeevich, veterinarian, neurologist, VK "Zoolyuks", Kiev.
Abbreviations: PVA- Peripheral vestibular syndrome. CVS- Central vestibular syndrome.

Anatomy of the vestibular system

vestibular system is a component of the nervous system that is responsible for maintaining the balance and position of the body and head.

Functionally, the vestibular system consists of two parts(Fig. 1) - peripheral (outside the brain stem) and central (located in the brain stem and cerebellum). Determination of localization (peripheral or central vestibular syndrome) is a very important step in the diagnosis of patients with vestibular disorders.

The peripheral part of the vestibular apparatus (Fig. 2, 3) is located in the petrous part of the temporal bone (osseous labyrinth). The bony labyrinth consists of semicircular tubules, vestibule and cochlea (which takes part in the formation of hearing). Inside the bony labyrinth contains a membranous (webbed) labyrinth. The space between the walls of the bone and membranous labyrinth is filled with a fluid - perilymph, similar in properties to cerebrospinal fluid. Inside the membranous labyrinth contains another type of fluid - endolymph.
The three semicircular canaliculi are located at right angles to each other. Each semicircular canal at one end has an extension - an ampulla, in which receptor cells are located (ciliated cells extending their villi into a jelly-like structure - a cupula). When the endolymph in the semicircular tubules moves, the cupula also moves and displaces the villi, stimulation of the dendritic endings of sensory neurons of the 8th cranial nerve (CN) occurs.
The utriculus and sacculus also contain a receptor organ, the macula, which is covered with ciliated cells. The cilia extend into a jelly-like structure (otolithic membrane) and are embedded in crystals (otoliths). As the otolithic membrane moves with respect to gravity, the villi are displaced and an action potential is generated.
Nerve fibers extending from the nerve cells of the semicircular tubules and sacs are collected in nerve bundles and exit through the internal auditory canal along with the facial nerve into the cranial cavity (in the rostral part of the medulla oblongata). The combination of vestibular and auditory axons at this level form the 8th pair of cranial nerves. Next, the axons enter the brainstem at the level of the trapezoid body and the caudal cerebellar peduncles.

After entering the brainstem, the axons travel in different directions. Most of the axons form synapses with the vestibular nuclei (Fig. 4). A small number of axons bypass the vestibular nuclei and reach the cerebellum via the caudal cerebellar peduncles. Some axons synapse in the fastigial nucleus of the cerebellum, others ascend to the cerebellar cortex, in the flocculonodular lobe.
There are 4 vestibular nuclei on each side of the brainstem. They are located on the ventral wall of the 4th cerebral ventricle. Axons from these nuclei go to the spinal cord (lateral vestibulospinal tract) and rostral to the brainstem (medial longitudinal bundle).
The fibers of the vestibulospinal tract affect the tone of the extensors of the extremities.
The medial longitudinal fasciculus (medial longitudinal fasciculus) passes rostrally (axons terminate in the nuclei of cranial nerves III, IV, VI and affect the position of the eyes) and caudally into the spinal cord (forms the medial vestibulospinal tract).
Information from the vestibular system is also projected to other areas of the brain stem (vomit center in the reticular formation) and the brain (including synapses in the thalamus).

Study of the vestibular system

The main function of the vestibular system is to maintain balance, the position of the body in space. The vestibular system also affects the extraocular muscles.
The influence of the vestibular system on maintaining balance is achieved by acting on the muscles of the extensors. Each side of the vestibular apparatus enhances the function of the extensors ipsilaterally. In the normal state, the right and left sides act in the same way, and therefore balance is maintained. If there is a problem on one side of the vestibular apparatus, the function of the extensors of the opposite side is enhanced, which leads to the main symptoms that can be observed with vestibular syndrome.
With vestibular syndrome, ataxia is observed (possibly with a fall on the side), while there will be no paresis or paralysis.

The vestibular system also influences the formation of the oculovestibular reflex, so the assessment of pathological eye movements is of great importance in the localization of pathology. The brain always focuses vision on some object. When moving the head from side to side, for example to the left, the extraocular muscles on the right will “pull” the eye back (to the right) to ensure focus on the object. When the limit of muscle contraction is reached, the eye quickly moves in the direction of head movement (to the left) to focus on a new object. This reflex activity is called the oculocephalic reflex (physiological nystagmus), and the slow phase will be observed in the opposite direction of head movement.

Pathological nystagmus occurs on its own, without head movements. Nystagmus can be without fast and slow phases (pendular - pendular nystagmus) or have a fast and slow phase (jerk - clonic nystagmus).
Pendulum nystagmus is not a symptom of vestibular disorders, it is observed in some breeds (Siamese, Himalayan, etc.) as a congenital pathology of the visual pathways.

With unilateral damage to the vestibular apparatus, an imbalance of nervous activity occurs, because. the vestibular apparatus on the healthy side continues to constantly send impulses. This imbalance is interpreted by the brainstem as body movement, and nystagmus will occur with a rapid phase away from the lesion.

Nystagmus can be spontaneous and positional, the latter occurs at certain positions of the body (when lifting the head up, position on the back).

Depending on the direction of movement, nystagmus is horizontal, vertical and rotational.
Another symptom that is often observed in vestibular syndrome is strabismus (abnormal position of the eyes, often ventral or lateral ipsilateral displacement). Strabismus can be spontaneous (always present) and positional (observed only in certain positions, for example, when raising the head up) (Fig. 5).
Nausea and vomiting are rarely seen in dogs and cats with vestibular syndrome. The vomiting center is located in the reticular formation in the medulla oblongata and has a direct connection with the vestibular nuclei.

Determination of localization (peripheral or central vestibular syndrome) is a very important part in the diagnosis of vestibular disorders. A thorough history, physical and neurological examination are of great help in this. The main task in determining the localization is to identify signs that are characteristic only of the central vestibular syndrome.

Head tilt is observed in both peripheral and central vestibular syndrome. With PVS, the head tilt always occurs in the direction of the lesion, with CVS, the head tilt can be in the direction of the lesion or the opposite (see below - paradoxical vestibular syndrome).

Head tilt can be combined with walking in a circle.

Nystagmus - horizontal and rotational - is possible at any localization (PVA or CVA). Vertical nystagmus indicates CVD. With PVS, the fast phase of nystagmus is directed in the opposite direction from the lesion, with CVS, the fast phase can be directed in any direction. Since animals with PVS are able to quickly compensate for lesions, nystagmus may be observed for only a few days. In PCV, nystagmus is often positional and may change direction (eg, rotational/vertical) with changes in head position. The number of eye movements per minute can also help a little in differentiation - with PVS, the frequency is usually greater than 66 movements per minute. With bilateral vestibular syndrome, there will be no nystagmus and head tilt.
Strabismus in PVS is ventral or ventrolateral, while it is observed on the side of the lesion. Strabismus is often positional. With PCV, strabismus can be in any direction.
The facial nerve (VII) passes through the internal auditory canal of the petrous bone and dorsal to the middle ear cavity. Due to the proximity to the peripheral part of the vestibular apparatus, some diseases can cause dysfunction of the facial nerve (paresis / paralysis).
The sympathetic innervation of the eye also passes near the middle and inner ear, so Horner's syndrome can also be observed in peripheral vestibular syndrome (Fig. 6).

The presence of a deficit of cranial nerves (except VII and VIII) indicates a central vestibular syndrome. Changes in consciousness can also be seen with PCV.
Another sign of PCV is a deficit of proprioceptive responses. Since the proprioceptive pathways have no connection with the peripheral vestibular system, decreased postural responses are indicative of PCV.
Also, with PCV, there may sometimes be signs of damage to the cerebellum.
Symptoms of a forebrain lesion (convulsions, loss of vision, behavioral disturbances, etc.) in combination with a vestibular syndrome indicate multifocal lesions.
Paradoxical vestibular syndrome occurs when the central vestibular system is affected. In this case, the tilt of the head will be observed in the opposite direction from the lesion. Normally, the cerebellum sends inhibitory impulses to the vestibular nuclei. With the loss of inhibition, the vestibular nuclei on the same side will send more impulses to the extensors ipsilaterally, as a result of which the body will strive in the opposite direction from the lesion. In such cases, the localization of the lesion can be determined by proprioceptive deficit - a decrease in postural reactions will occur ipsilaterally. Paradoxical vestibular syndrome occurs when the flocculo-nodular lobe of the cerebellum, the caudal cerebellar peduncles, and the rostral and medial vestibular nuclei in the brainstem are affected.

Diseases leading to peripheral vestibular syndrome (PVS)

Degenerative diseases/abnormalities
Congenital malformations are more common in young animals and may be associated with deafness. With a bilateral problem, the patient may not have nystagmus and no head tilt. There will often be symmetrical ataxia, wide stance, and side-to-side movement of the head.
Symptoms begin to appear when the animals begin to walk. Many of the animals can compensate for vestibular disorders (up to the ability to walk). At the same time, deafness (if any) remains. Congenital anomalies of the vestibular system are more common in breeds such as the German Shepherd, English Cocker Spaniel, Doberman Pinscher, Siamese and Burmese cats.

Metabolic Causes
Hypothyroidism is a common metabolic cause of vestibular syndrome in older animals. Involvement of the peripheral vestibular system may be the first sign of hypothyroidism. Usually, hypothyroidism has an acute onset, a non-progressive course. Almost all animals show head tilt and positional strabismus, and many patients also show other signs of facial nerve involvement, including decreased threat response and palpebral reflex. Such patients may also have systemic signs of hypothyroidism, such as hypercholesterolemia.
Hypothyroidism can cause both peripheral and central vestibular syndrome; central may be associated with ischemic infarction.
Treatment consists of replacement therapy, most patients with early treatment return to normal.
Neoplasms can cause PVS by compression or invasion of the vestibulocochlear nerve. Peripheral nerve neoplasms may initially present as PVS, but over time the tumor may invade the brainstem.
Ear neoplasms (eg, adenocarcinoma of the ceruminal glands) may invade the middle and inner ear and cause PVS.

The most common toxic causes leading to PVA are aminoglycosides, various ear cleaners. The onset of development of the vestibular syndrome is usually acute. Treatment is to stop using the drugs.

Injuries rarely lead to PVS. In this case, the vestibular syndrome will often be combined with signs of injury to other parts of the brain.

Diseases leading to central vestibular syndrome
In principle, any brain disease can also involve the central part of the vestibular system. There are no diseases involving only the central part of the vestibular system.

Neoplasms can be primary or secondary. It may be chronic or acute onset. Neoplasms cause compression, ischemia, or infiltration. The prognosis depends on the location, size, type of neoplasm. Treatment is conservative (eg, corticosteroids to relieve peritumoral edema), chemotherapy, surgical removal, and radiation therapy.
Inflammatory diseases can be infectious (canine distemper, infectious peritonitis of cats, toxoplasmosis, bacterial meningoencephalitis, etc.) and non-infectious origin (considered to be autoimmune diseases). Treatment depends on the cause (for non-infectious meningoencephalitis, treatment consists of various immunosuppressive drugs). Forecasts are always very cautious.
Metronidazole intoxication- one of the possible causes of damage to the central vestibular system. The onset of the disease is acute, usually observed after prolonged use of high doses of metronidazole. Symptoms of intoxication - generalized ataxia, nystagmus, vomiting; in more severe cases - depression, convulsions, opisthotonus. Treatment is the abolition of metronidazole, after which patients return to normal, usually within 1-2 weeks. The use of diazepam usually speeds up recovery.
Thiamine deficiency can cause damage to the vestibular system. It can occur due to a lack of thiamine in the feed, the destruction of the vitamin during cooking, the content in food of a large amount of thiaminase (a substance that destroys thiamine; it is found in fish in abundance). Thiamine deficiency causes bilateral foci of necrosis, hemorrhages in the brain stem. In cats, the vestibular nuclei are primarily affected, and there may also be evidence of cerebellar involvement. Treatment is thiamine administration, with early detection and treatment, the prognosis is usually favorable.

Vascular disorders

The cerebellum is one of the most common areas for the development of vascular disorders. The causes of a heart attack can be arterial hypertension, heart disease, bleeding disorders, neoplasms, etc.; in many cases, the cause may not be identified. The onset is acute or hyperacute (development of the central vestibular syndrome, as well as symptoms of cerebellar damage), during the first day there may be progression. The prognosis is usually good.

Literature:

1. Michael D. Lorenz. Handbook of veterinary neurology.
2. Evans H. E., A. de Lahunta. Miller's anatomy of the dog.
3. Curtis W. Dewey. Practical guide to canine and feline neurology.
4. Platt S., Garosi L. Small animal neurological emergencies.

Vestibular syndrome is a pathological condition caused by dysfunction of the vestibular system, which is responsible for balance and coordination of movements. The vestibular system is a statokinetic analyzer that, with the help of tonogenic mechanisms and various vegetative reactions, maintains a stable position of the body in space. The main functional component of the system is the vestibular nerve. It consists of sensory and motor fibers that start from the nuclei of the medulla oblongata and end with a large node in the auditory analyzer. Its peripheral processes have receptor cells localized in the semicircular canals. They react to any change in the position of the body in space and transmit the information received to the central nervous system. When the structures of the vestibular system are affected, it ceases to perform its main functions, and neurological, somatic and autonomic disorders develop in the body.

The labyrinth is an important organ of the vestibular system. It consists of three semicircular canals located in mutually perpendicular planes and filled with endolymph. With their help, signals are sent to the brain when a person makes head movements: nods or turns it to the sides. The structures of the vestibular system, the organ of vision and the musculoskeletal system control and maintain the position of the body at rest and during movement. The visual system prevents blurred vision and the formation of a blurry picture of the image when moving the head. Sensory receptors located in the joints, ligaments and muscle fibers perceive external irritation, convert its energy into nerve impulses transmitted to the central nervous system. Such processes allow you to maintain balance and prevent a fall. In the labyrinth, mechanical forces are registered, including gravity, which has a direct effect on the structures of the vestibular system. The brain receives information, after processing which it becomes easy and simple to control your body.

The syndrome is a manifestation of various diseases and pathological conditions caused by taking certain medications. Diseases of the inner ear disrupt the functioning of the vestibular apparatus, the brain begins to receive false information, which is clinically manifested by characteristic signs. These diseases include: inflammation of the labyrinth, otitis media, tumors and injuries, intoxication, hypertension, angioedema.

The disease develops as the body ages. Elderly people often complain of dizziness and imbalance. Vestibulopathy can also appear at an early age with failure of the otolith apparatus. In children, the causes of the syndrome are mental exhaustion and physical overstrain, nervousness and stressful conditions. In them, the disease is manifested by motion sickness on a swing, in an elevator and public transport.

Patients with vestibular syndrome often feel dizzy, their consciousness is clouded, it seems that they are spinning and are about to fall. These signs are usually accompanied by nausea, vomiting, impaired stool, anxiety and restlessness, pressure fluctuations, tachycardia, and unstable body position. According to ICD-10, vestibulopathy has the code H81 and refers to diseases of the inner ear.

The classification is divided into:

• Central vestibular syndrome develops with damage to the trunk and cerebral hemispheres. Symptoms of pathology are: loss of balance, minor auditory symptoms, unilateral deafness, neurological disorders.
• Peripheral vestibular syndrome- a manifestation of labyrinthitis, inflammation of the roots of the spinal cord, damage to receptor cells and the vestibular nerve. It is manifested by horizontal nystagmus, tinnitus and hearing loss.

Etiology

Factors provoking the development of the syndrome:

1. Anxiety and restlessness
2. Prolonged sorrow and grief
3. Stress and nervousness
4. Psycho-emotional exhaustion and physical overstrain,
5. Improper nutrition, starvation, debilitating diets,
6. Elderly age.

Diseases manifested by vestibular disorders include pathologies of the labyrinth, brain, spine, nervous system, traumatic head injuries, neoplasms, acute infections, as well as age-related features.

• TBI with loss of balance with a sharp movement of the head.
• Labyrinthitis is an inflammation of the inner ear of an infectious etiology, manifested by dizziness and cochlear disorders.
• Labyrinth infarction in the elderly and in young people against the background of atherosclerosis or increased blood clotting, manifested by uncertainty in determining one's position in space, ataxia, neurological signs, and discoordination of movements.

• Meniere's disease with paroxysmal dizziness, stuffy ears, dyspeptic symptoms, sensorineural hearing loss.
• Basilar migraine - dizziness, acute headache, loss of stability, hypersensitivity to loud sounds and bright lights.
• Multiple sclerosis is manifested by staggering while walking, ataxia, tremor, horizontal nystagmus, debilitating headache, deafness, paresthesia, emotional lability.
• Vestibular neuritis caused by the herpes virus aggravates in autumn or spring and is manifested by dizziness, dyspeptic symptoms. Symptoms of the disease last for several days and gradually regress.

Rarer causes of the syndrome include:

• acute inflammation of the middle ear,
• vertebrobasilar arterial system syndrome,
• cardiopsychoneurosis,
• degenerative-dystrophic lesions of the intervertebral discs in the cervical spine,
• arterial hypertension,
• neoplasms and cysts in the brain,
• psychogenic disorders
• acute conditions after ear surgery.

Weakness in the legs and loss of balance can also be caused by ordinary motion sickness or drug poisoning. Idiopathic vestibular syndrome has no known cause. Its origin is not related to other conditions or diseases of the patient.

Signs of vestibular disorders can occur with damage to the central part of the vestibular apparatus - the brain, as well as peripheral parts - the labyrinth, nerves, receptors. A normally functioning vestibular system ensures a stable position of the human body and its correct orientation in space.

Symptoms

Dizziness and a sense of rotation are the main clinical manifestations of the disease, which most often patients with the syndrome complain about at the doctor's office. With systemic dizziness, patients complain about the rotation of environmental objects in front of them, with non-systemic dizziness, they complain of unsteadiness of gait, rocking of the body from side to side. Such sensations arise suddenly and have a strong influence on the psyche of patients. They begin to grab onto a bed or a chair to keep from falling.

Dizziness, depending on the damage to the structures of the vestibular system, is of three types:

1. proprioceptive dizziness is perceived by patients as a change in the position of their own body,
2. tactile - the feeling that "the earth is leaving under your feet",
3. visual - rotation of surrounding objects around the patient.

Symptoms of vestibular syndrome also include the following clinical signs:

• unstable body position
• the feeling that "everything around moves and rotates",
• nausea and vomiting, diarrhea,
• flies and dark circles before the eyes, decreased visual acuity,
• inability to fix one's gaze on a particular object,
• hazy look,
• heart rate change,
• fluctuations in blood pressure
• violation of the rhythm of breathing and pulse,
• decrease in body temperature,
• change in the size of the pupils,
• general weakness, malaise, depression,
• clouding of consciousness,
• disorientation in time and space,
• fast fatiguability,
• headache of varying intensity,
• impaired concentration,
• nystagmus,
• unsteady gait,
• tremor and myoclonus,
• muscle hypotonia,
• speech disorder,
• anxiety, anxiety, panic fear,
• ringing or noise in the ears, hearing loss,
• pale skin on the face and neck,
• profuse sweating,
• blurred vision.

Clinical symptoms of pathology do not occur simultaneously and are not constantly present. Usually the syndrome is manifested by short-term attacks that occur at various intervals. The onset of an attack can be triggered by sharp sounds or smells, a change in the weather. In the intervals between attacks, patients do not complain about anything and feel satisfactory.

Forms of vestibulopathy:

1. Vertebrogenic vestibulopathy develops as a result of pathological processes in the cervical spine - osteochondrosis, protrusion, hernia. Patients develop characteristic clinical signs: prolonged dizziness, headache, inability to fix their eyes.
2. Vestibular neuronitis is an acute infectious inflammation of the nerve fibers of the inner ear and vestibular ganglion, manifested by imbalance, eye nystagmus, paroxysmal dizziness, fear, nausea, vomiting, congestion and tinnitus, autonomic disorders. Patients note that the appearance of these symptoms was preceded by SARS. A complication of the disease is encephalopathy.
3. Post-traumatic vestibulopathy is the result of traumatic damage to the labyrinth, perforation of the tympanic membrane and hemorrhage into the middle ear cavity. The causes of such processes are: concussion, contusion, compression of the brain, barotrauma, fractures of the base and cranial vault, epidural and intracerebral hematomas. Dizziness in patients is persistent with nausea, vomiting, nystagmus, ataxia, and hearing impairment.

Any disease, including vestibular syndrome, should be treated in the early stages, when it has not yet developed to the maximum and has not caused irreversible changes. If the syndrome is started and left to chance, the body's resources will not survive. The body itself can not cope with the disease. All patients with signs of pathology should consult a specialist and undergo a thorough examination to make an accurate diagnosis and receive recommendations for a quick recovery. For therapy to be effective, it is necessary to determine the cause of the disease. It is necessary to treat not the symptoms, but to eliminate all the etiopathogenetic factors that provoked the disease.

Diagnostics

Since vestibular syndrome has many causes, its diagnosis is quite difficult. Patients are examined by a neurologist and an ENT doctor. They listen to complaints, take anamnesis, examine patients and study symptoms in detail. Then the specialists conduct a direct standard examination of the organ of hearing and determine the neurological status of patients. With the help of cold and warm water, diagnostic tests are carried out, the essence of which is to act on the middle ear and determine the difference in nystagmus.

Special medical procedures include:

• Audiometry allows you to accurately determine the violations in the perception of sounds,
• Electronystagmography - graphic registration of changes in the biopotentials of the eyeball,
• Ophthalmoscopic examination - examination of the fundus with the help of special instruments,
• Magnetic resonance and computed tomography,
• Vestibulometry is performed to determine the causes of dizziness and assess the severity of disorders.

Treatment

Complex treatment of the syndrome of vestibular disorders is aimed at eliminating the causes and clinical manifestations of the disease. The scheme of therapeutic measures is determined by the pathogenesis of vestibular dysfunctions.

In Meniere's disease, patients are shown to reduce the consumption of salty foods, limit alcohol, and stop smoking. Antibacterial drugs or steroid hormones are injected into the tympanic cavity. In severe cases, surgery is indicated. For the treatment of otitis media, anti-inflammatory and antimicrobial drugs are prescribed.

For all types of pathology, regardless of the cause, symptomatic therapy is carried out. Patients are prescribed:

1. anticholinergic drugs - "Platifillin", "Atrovent",
2. antihistamines - Dimedrol, Suprastin, Tavegil,
3. benzodiazepines - Relanium, Lorazepam,
4. antiemetic drugs - Meterazin, Cerucal, Motilium,
5. vascular agents - Cavinton, Piracetam,
6. drugs with vasodilating, antiplatelet and neurometabolic effects - Betaserk, Betaver, Tagista.

During an attack, it is necessary to apply cold to the head and a heating pad to the legs, take Bellaspon, Cinnarizine or No-shpu. In the interictal period, patients are shown proper nutrition and an active lifestyle, treatment with medicinal herbs and herbal teas, head massage, acupuncture, exercise therapy, acupuncture, hirudotherapy, magnetotherapy.

These general therapeutic measures restore the work of the statokinetic analyzer and eliminate dizziness. In patients, a confident gait becomes, the work of the nervous system improves, anxiety, anxiety, and panic fear disappear. The structures of the vestibular apparatus begin to work much better, the immune defense and general resistance of the body increase, pain and discomfort disappear, the severity of dizziness and dyspeptic symptoms decreases, the heart rhythm and blood pressure are restored, the movements of patients become coordinated, and the body position is stable. The condition of the body improves markedly, efficiency is restored, the quality of life increases.

Vestibular rehabilitation is a set of measures that are carried out in order to normalize the functions of the vestibular apparatus as soon as possible. It includes gymnastics and gait training. At first, patients experience discomfort during exercise, and then get used to it. Vestibular gymnastics together with pharmaceuticals has a positive therapeutic effect. Surgical intervention is indicated for injuries and hemorrhages that pose a danger to the life of patients.

an example of a universal complex of vestibular gymnastics

Comprehensive treatment improves innervation and blood supply to the elements of the inner ear, has a positive effect on the entire body.

Prevention

The prognosis of vestibular syndrome with timely and proper treatment is favorable. Proper nutrition, playing sports, alternating work and rest, good sleep, giving up bad habits and competent treatment of pathologies manifested by vestibular disorders are the main measures to prevent dizziness and loss of balance.

To avoid injury to persons prone to falls, the following rules must be observed: use of low beds with restraints, comfortable and safe furniture, appropriate assistive devices for movement, special handrails in bathrooms, safety barriers and fences.

Video: about disruption of the vestibular apparatus

Disturbances in coordination of movements and the ability to maintain a posture associated with damage to the vestibular apparatus at any level. Vestibular ataxia is manifested by unsteadiness in standing and sitting positions, as well as when walking. It is accompanied by systemic dizziness and nystagmus; nausea and vomiting, autonomic disorders and symptoms characteristic of the pathological process that caused the development of vestibular ataxia may be observed. Diagnosis of the latter is the main goal of examining patients with vestibular ataxia. Treatment of vestibular ataxia is symptomatic. The main therapy should be directed to the causative disease.

ICD-10

R27.0 Ataxia, unspecified

General information

The orientation of the body in space in the human body is provided by the vestibular analyzer. He is responsible for determining the position and nature of the movement of the body and its individual parts, provides the perception of gravity. Any change in body position in space is perceived by vestibular receptors - the so-called hair cells located in the labyrinth of the inner ear. From the receptors, nerve impulses go along the vestibular nerve, which, together with the auditory nerve, enters the VIII pair of cranial nerves. Further, the impulses enter the vestibular nuclei of the medulla oblongata, where information is synthesized and motor reactions are controlled. From the vestibular nuclei, regulatory nerve impulses diverge to various parts of the central nervous system: the cerebellum, spinal cord, reticular formation, autonomic nerve ganglions, oculomotor nuclei and cerebral cortex. They provide a redistribution of muscle tone and reflex reactions to maintain balance.

Causes

Vestibular ataxia is associated with damage to any structure of the vestibular analyzer. Most often, it is caused by damage to the hair cells as a result of an inflammatory process in the inner ear - labyrinthitis. In turn, labyrinthitis can occur as a result of an ear injury or when an infection passes from the middle ear cavity in acute otitis media, chronic purulent otitis media, complicated by aerootitis. Hair cell death leading to the development of vestibular ataxia can occur as a result of invasive ear tumor growth or toxic exposure to ear cholesteatoma secretions. Paroxysmal vestibular ataxia accompanies Meniere's disease.

Less commonly, vestibular ataxia is caused by damage to the vestibular nerve, which can be infectious, tumor (with acoustic neuroma), or toxic (with ototoxic drugs) in nature. Often, vestibular neuronitis is associated with a viral infection: SARS, herpes virus, influenza, etc.

Vestibular ataxia can occur when the vestibular nuclei located in the medulla oblongata are affected. Thus, vestibular ataxia occurs as a result of compression of the medulla oblongata in individuals with craniovertebral anomalies (Chiari anomaly, atlas assimilation, platybasia), brain stem tumors, encephalitis and arachnoiditis of the posterior cranial fossa, demyelinating diseases (multiple sclerosis, acute encephalomyelitis). Vestibular ataxia is a clinical manifestation of chronic ischemia of the brain stem caused by a violation of the vertebrobasilar circulation due to vertebral artery syndrome, atherosclerosis, hypertension, cerebral aneurysm. In acute circulatory disorders in this area (TIA, ischemic or hemorrhagic stroke), vestibular ataxia is also observed.

Vestibular ataxia is often observed after a traumatic brain injury. At the same time, it can be caused both by the direct impact of a traumatic factor on the nuclei and roots of the vestibular nerve, and with circulatory disorders associated with trauma (post-traumatic vascular spasm).

Symptoms of vestibular ataxia

Vestibular ataxia manifests itself both in movement (dynamic ataxia) and in the standing position (static ataxia). Vestibular ataxia differs from other types of ataxia in the dependence of its severity on head and torso rotations. Increasing ataxia when turning the head, eyes, and torso causes patients to avoid such movements or perform them smoothly and slowly. Visual control of movements partially compensates for violations of the function of the vestibular analyzer, therefore, with the eyes closed, the patient feels more insecure and the manifestations of vestibular ataxia increase.

The lesions of the vestibular analyzer are most often unilateral. In such cases, vestibular ataxia is manifested by unsteadiness when walking with the deviation of the body constantly in the same direction - in the direction where the lesion is localized. In a standing or sitting position, the patient also deviates to the affected side. This symptom is easily detected in the Romberg position and when the patient tries to walk a few steps evenly with his eyes closed.

A characteristic sign of vestibular ataxia is the presence of systemic vertigo, in which the patient experiences a feeling of rotation of his own body or movement of surrounding objects around him. Dizziness may occur even when lying down with eyes closed. In such cases, it is usually accompanied by sleep disturbance with difficulty falling asleep. The triggering of the vestibulo-visceral nerve connections leads to the fact that dizziness with vestibular ataxia is often accompanied by nausea and vomiting. Vestibulo-vegetative interactions cause the appearance of autonomic reactions: pallor or redness of the face, feelings of fear, tachycardia, pulse lability, hyperhidrosis.

In most cases, vestibular ataxia is accompanied by horizontal nystagmus, the direction of which is opposite to the side of the lesion. Possible bilateral nystagmus. When the vestibular nuclei are affected, vertical nystagmus with a rotatory component may be noted. If there is a violation at the level of the peripheral part of the vestibular analyzer, nystagmus increases with head turns, however, with repeated turns, nystagmus may decrease. In the presence of a craniovertebral anomaly, vestibular ataxia is accompanied by nystagmus, which increases with head tilt.

Diagnostics

Vestibular ataxia can be detected by the patient's characteristic complaints and during his neurological examination. To differentiate vestibular ataxia from other types of ataxia (cerebellar, sensitive, cortical), as well as to establish the level and nature of damage to the vestibular analyzer, the neurologist needs the results of instrumental examination methods: REG, Echo-EG, EEG, CT and MRI of the brain, x-ray studies . Since vestibular ataxia as a syndrome occurs in many diseases of the central nervous system, the most important moment in clinical neurology is to identify the cause of its development.

REG allows you to obtain indirect data on the state of blood circulation in the brain. If necessary, it can be supplemented with angiography or MRI angiography of the cerebral vessels. With the help of Echo-EG, the state of the cerebrospinal fluid system is assessed. Echo displacement indicates the presence of a volumetric formation (tumors, hematomas or