The most basic diagnoses for dizziness. Dizziness: causes and treatment

Dizziness is a common problem among people today and one of the most common reasons for visiting a medical facility. According to statistical information obtained from various authoritative sources, over 5% of the world's population have experienced dizziness at least once. This phenomenon is located at the second level among the complaints described by neurological patients. In neurology, dizziness is more common only when patients indicate cephalgia - headache.

Despite this global distribution, dizziness remains one of the most difficult problems in medical practice. This is explained by the fact that such a phenomenon can occur for a variety of reasons, coexist with completely different symptoms and be a sign of a wide range of somatic diseases, neurological defects, and mental disorders. In fact, any malfunction in the functioning of the nervous, cardiovascular, endocrine systems, any pathology of the ENT organs and visual sensory system can make itself felt by dizziness.

Another difficulty in choosing a treatment strategy for dizziness is that this symptom itself is a rather abstract phenomenon. Complaints about dizziness reflect the patient’s subjective experiences, since it is quite difficult to objectively describe and select specific words that accurately reflect the essence of this phenomenon. The term “dizziness” means different sensations to different people. Also complicating medical work is the current lack of precise unambiguous criteria for confirming this diagnosis.

Dizziness: general information

The overwhelming majority of contemporaries use the term “dizziness” to mean doubts about the placement of their body in relation to other objects in the environment. The subject may imagine that his own torso is rotating in space. Or he may sense instability and various movements of surrounding objects. By dizziness, a person may refer to the inability to maintain a stable position. He may say that he cannot keep his body still even for several seconds. The patient may describe that the ground is disappearing from under his feet.

Dizziness may be accompanied by discomfort in the epigastric region. Vomiting may occur, the appearance of which cannot be explained by food intake. This anomaly may be accompanied by increased sweating, sudden jumps in blood pressure, and changes in heart rate. Involuntary oscillatory movements of the eyeballs may occur - a phenomenon called nystagmus in neurology. The duration of dizziness attacks also varies: for some people, the crisis lasts a matter of minutes, while others feel discomfort for several hours.

The mechanism of development and causes of dizziness have been well studied. This symptom occurs if the flow into the central structures of the brain is disrupted or the information transmitted by the visual, auditory, vestibular, sensory systems and proprioceptor organs is distorted. Dizziness can develop if there is a failure in the central processing of incoming information or the process of the motor act is disrupted in its efferent part (in the organization of the response). Such anomalies are often observed with damage to the frontal lobe, whose function is motor behavior. This symptom can occur when the basal ganglia are damaged. The cause of dizziness is pathology of the cerebellum, which is responsible for coordinating movements and regulating balance.

Clinical studies have shown that in the vast majority of patients, the causes of dizziness were one of the following factors or a combination of them:

  • peripheral vestibular syndrome - pathological conditions that developed as a result of damage to the peripheral vestibular neuron;
  • sensory deprivation (insufficiency), which occurs when the functions of the main sense organs are disrupted;
  • psychogenics - abnormal mental states, psychotic reactions to stimuli;
  • disturbances of blood circulation in the medulla oblongata, pons, midbrain;
  • diseases of the central nervous system of other origins;
  • heart pathologies, defects in the structure of blood vessels.

Dizziness: types

Experts divide the anomaly into two large groups:

  • systemic vertigo, otherwise called vestibular or true;
  • non-systemic, otherwise called physiological.

In turn, non-systemic dizziness is differentiated into three clinical types:

  • presyncope, or cardiogenic appearance;
  • psychogenic dizziness;
  • imbalance.

Systemic dizziness

This type is a phenomenon characteristic of people who have lesions of various origins in the structure of the vestibular sensory system - a group of sensory organs that act to analyze the position of the body in space and assess its movement relative to other surrounding objects. The vestibular system is a structural and functional construct designed for the perception and analysis of spatial information, which plays a leading role in a person’s orientation in space: both during active and passive movements.

With systemic vertigo, the patient may feel that his torso is making rotational movements, falling, bending or swaying. Illusions of nearby objects oscillating, spinning, or swaying may also occur. Very often this type of dizziness is accompanied by other unpleasant symptoms, including:

  • nausea and vomiting;
  • sudden hearing loss or deafness;
  • sensations of fullness, noise in the ears;
  • excessive sweating all over the body or in specific areas;
  • imbalance;
  • nystagmus;
  • sudden onset of deafness;
  • the illusion of rapid oscillatory movements from surrounding objects.

Scientists have established the main reasons for the development of this symptom. These include:

  • infectious diseases of the middle ear;
  • traumatic brain injuries;
  • otological surgical procedures;
  • impaired blood supply to parts of the brain;
  • labyrinthine infarction.

The most common is benign paroxysmal positional vertigo, the symptoms of which occur periodically when changing posture. Attacks of dizziness are short-lived, lasting no more than one minute.

This condition is characterized by its onset between the ages of 60 and 70 years. It is worth noting that women suffer from this type of dizziness twice as often as representatives of the stronger sex.

A clinical variant of systemic vertigo is also Meniere's disease, which is characterized by a feeling of fullness in one ear.

Systemic dizziness, which has an abrupt onset, associated with a history of acute respiratory viral infection, may indicate vestibular neuronitis. Attacks of this disease occur without hearing impairment.

In some patients, systemic dizziness is a sign of neurological diseases, for example: epilepsy. In this variant, during an attack, a person may experience discomfort in the abdominal cavity, nausea, illusions and hallucinations.

Treatment of systemic dizziness depends on the reasons that provoked this symptom. Vestibulolytics are used as symptomatic therapy: antihistamines, benzodiazepines. Complex treatment may include vasoactive agents and nootropics. The use of histaminomimetics shows a good effect.

It should be remembered that self-medication of systemic dizziness is fraught with disastrous consequences that pose a threat to the life and health of a person.

Presyncope: provoking factors and treatment

One of the types of dizziness is a pathological condition that patients describe as fainting. In cardiogenic vertigo, the subject reports a sudden onset of an attack in which he feels an empty, light feeling in the cranium. He anticipates the approach of loss of consciousness.

Very often, a presyncope is manifested by other vegetative symptoms, including:

  • painful pallor of the skin;
  • pathological myasthenia – weakness that appears in muscle tissue;
  • feeling of lack of air when breathing;
  • increased heart rate, irregular heartbeats, or slow pulse;
  • intense unreasonable fear;
  • sudden darkening of the eyes;
  • nausea;
  • increased sweating.

Presyncope can occur for various reasons, the most common of which are the following conditions. The main culprit of weakness and dizziness is a sharp decrease in blood pressure (systolic and diastolic). The phenomenon of orthostatic hypotension occurs in a subject when moving from a horizontal position to a vertical position. A sharp drop in blood pressure occurs due to insufficient blood flow to the brain. Presyncope most often occurs in people with weakened blood vessel tone. This type of dizziness can be caused by delayed reactions or insufficient intensity of the heart’s response to changes in body position.

A common reason for the development of pre-fainting conditions is dehydration (dehydration) of the body. Dizziness can be caused by hypovolemia - a decrease in circulating blood volume due to massive blood loss or as a result of taking certain medications, for example: diuretics. Often, a pre-fainting state is recorded in people suffering from anemia - a decrease in the concentration of hemoglobin in the blood with a simultaneous decrease in the number of red blood cells, a change in their qualitative composition. The causes of pre-fainting include hypoglycemia - a decrease in blood glucose levels.

Feelings of impending fainting arise not only due to physiological disruptions in the body, but also for a number of mental reasons. This condition is often experienced by people suffering from vegetative-vascular dystonia and anxiety-phobic disorders. A crippling attack of panic anxiety in most cases at the beginning of its development is manifested by dizziness and a feeling of impending loss of consciousness. Often, a fainting state is the result of a person’s exposure to strong stress factors. Rapidly developing stress “rewards” a person with neurocircular dystonia with a mass of unpleasant vegetative symptoms associated with changes in heart rate, surges in blood pressure, and increased breathing.

It is necessary to treat attacks of presyncope not negligently, but responsibly, since this symptom can be one of the signs of various disorders, which only an experienced doctor can diagnose. The treatment program is determined after identifying the true culprit of the anomaly and a complete examination of the patient. Treatment of presyncope involves more than just pharmacological therapy. To save the patient from this phenomenon, it is necessary to eliminate all factors that provoke attacks. To solve this problem, you will need the help of a psychotherapist who will tell the patient about the original source of his problem and help him master constructive ways of responding to stress.

Psychogenic dizziness: causes and treatment

The psychogenic form of dizziness is taken to mean unpleasant sensations that are quite difficult to specifically describe in words. Most often, patients complain of a feeling of fog or heaviness in the head. The patient describes his symptoms as being similar to alcohol intoxication. Others describe feeling lightheaded and unwell. Many people suffering from psychogenic dizziness complain that during an attack they experience intense fear: they are afraid of falling and getting hurt, they are afraid of losing consciousness, they are worried that they will suddenly die.

A distinctive sign of psychogenic dizziness from others is the causes of the painful phenomenon. Psychogenic dizziness occurs solely for psychological reasons. The development of this symptom is in no way associated with any somatic disease or neurological pathology.

Psychogenic dizziness is almost always not a separate independent symptom: this phenomenon is observed with other signs that accompany neurotic diseases and psychopathological conditions. Examinations of patients with suspected psychogenic dizziness most often determine that they have anxiety-phobic disorders, in particular agoraphobia. Psychogenic dizziness is often observed in panic disorder. This type often accompanies depressive states of varying severity.

Dizziness can be interpreted by people as spontaneously arising and quickly disappearing sensations of illusory instability of the body. Such experiences most often occur when a person overcomes certain areas, for example: walking along a bridge, climbing stairs, crossing a desert area. With agoraphobia, psychogenic dizziness occurs in a person when he moves away from his own home, especially if he travels in vehicles that move at high speed.

The causes of psychogenic dizziness are factors that a person perceives as dangerous. An unpleasant symptom can develop when the subject is in busy places: supermarkets, at meetings, in the subway. The onset of the disease can immediately follow an episode of stress or develop under the influence of long-term traumatic factors.

The clinical picture of diseases manifested by psychogenic dizziness almost always includes other psychotic symptoms. Among them:

  • intense uncontrollable anxiety;
  • causeless uncontrollable fear;
  • high level of anxiety of the subject;
  • tendency to worry about little things;
  • feeling of tension and stiffness;
  • irritability, nervousness;
  • fussiness, impatience;
  • inability to relax;
  • frequent illogical mood swings.

A person who regularly experiences episodes of psychogenic dizziness complains of difficulty concentrating and notices memory impairment. Such a subject cannot withstand prolonged mental and physical stress and gets tired very quickly.

An episode of psychogenic dizziness is very often accompanied by a variety of somatic and autonomic symptoms, including:

  • increased heart rate;
  • hot flashes followed by chills;
  • increased sweating;
  • sensation of a “lump” in the throat;
  • difficulty taking a deep breath, feeling of lack of air;
  • irresistible thirst, dry mouth;
  • nausea, vomiting, dyspeptic disorders;
  • tremor of the limbs.

The medical task in the treatment of psychogenic dizziness includes two areas of work. The first goal of treatment is to reduce the intensity of painful symptoms, minimize the number of episodes of psychogenic dizziness, and eliminate complications of the underlying disorder. The second goal of treatment is to ensure the patient’s complete recovery by identifying and eliminating the cause that gave rise to psychotic disorders and neuroses.

The use of tricyclic antidepressants or drugs from the serotonin reuptake class shows high effectiveness in the treatment of psychogenic dizziness. Antidepressants help break the vicious circle that occurs during prolonged periods of anxiety, depression, and spiritual exhaustion.

An important step in the treatment of psychogenic disorders is the use of psychotherapy. Psychotherapeutic techniques help to detect the harmful factor that triggered the cascade of psychotic reactions, and subsequently eliminate its negative impact on the human psyche. As a result of psychotherapy sessions, the patient’s reactions to the current stimulus change, thereby his psyche ceases to suffer from “attacks” of harmful agents.

Psychotherapeutic treatment also involves conducting explanatory and educational work. This is extremely important in the treatment of psychogenic dizziness, since the patient’s conviction that his condition is mortally dangerous is a serious psychologically traumatic factor that contributes to even greater suffering for the person.

In the treatment of psychogenic dizziness, a special role is assigned to the performance of vestibular gymnastics, which helps reduce the excitability of the vestibular apparatus. A good effect is shown by performing specially designed breathing exercises.

Benzadiazepine anxiolytics are also used in treatment. Some patients are helped to overcome dizziness by taking low doses of antipsychotics. H1-histamine receptor blockers can be used, which can eliminate not only dizziness, but also lightheadedness.

Balance imbalance

Some patients describe dizziness as a partial loss of balance. They describe a feeling of lack of stability while standing. There is often unsteadiness when walking, which resembles the gait of a drunk person. In this case, imbalance is determined exclusively when standing or performing movements. If a person sits or lies, unpleasant sensations do not arise.

Another feature of this dizziness is an increase in imbalance in the dark, when a person does not have the ability to compensate for the existing defect with the help of the organs of vision. A person can feel an illusory movement (swing) of the external environment before the eyes. This phenomenon is called oscillopsia.

The causes of imbalance are varied. Most often, this type of dizziness occurs as a result of:

  • lesions of the floculonodular lobe of the cerebellum;
  • cervical proprioception disorders;
  • numerous subcortical infarctions;
  • Hakim-Adams syndrome (normotensive hydrocephalus);
  • idiopathic parkinsonism syndrome;
  • progressive supranuclear palsy or Shy-Drager syndrome;
  • chronic SDH (hemorrhage).

This pathological condition is observed in pathology of the cervical spine. Its cause is a decrease in blood flow through the vertebral artery due to osteochondrosis of the cervical spine. This phenomenon can occur due to congenital defects in the structure of the vertebral arteries.

Balance disorders can develop with a variety of benign and malignant neoplasms in the structures of the cranium, especially if the tumors are localized in the frontal lobes of the hemispheres.

A common cause of imbalance is the use of certain pharmacological agents., such as: anticonvulsants, benzodiazepine tranquilizers, antipsychotics, some mood stabilizers. Anamnesis data and clinical assessment of the condition of patients with complaints of balance disorders show that the anomaly often develops against the background of sensory function disorders.

Treatment of imbalance is focused on eliminating the underlying somatic pathology. The therapeutic program is drawn up for each individual patient, depending on the causes of this symptom. Histaminergic drugs demonstrate a good response in the treatment of imbalance, as well as other types of dizziness.

25.09.2011 12295

Dizziness is one of the most common symptoms in medical practice. About 80 diseases have been described that may cause dizziness.

DIZZINESS - one of the most common symptoms in medical practice. About 80 diseases have been described that may cause dizziness.

When examining a patient with complaints of dizziness, you first need to find out what he calls dizziness.

Under vestibular (systemic) dizziness understand the illusion of movement of the person himself or objects in the environment. All other sensations that differ from systemic dizziness (equilibrium disorders - instability, staggering; feeling of intoxication and lightheadedness; syncope and fainting states; “veil” before the eyes, “emptiness and lightness” in the head and other sensations of discomfort in the head) are called non-vestibular (non-systemic) dizziness and are not associated with pathology of the vestibular analyzer. Vestibular (systemic) dizziness indicates a pathology of the vestibular analyzer, both its peripheral and central parts. Depending on the level of damage to the vestibular analyzer, peripheral (PVS) and central (CVS) vestibular syndromes are distinguished.

Peripheral vestibular syndrome occurs when the receptor formations of the inner ear, vestibular ganglion and root of the VIII pair of cranial nerves are damaged. The most common nosological forms accompanied by PVS are Meniere's disease, benign paroxysmal positional vertigo (BPPV), acute and chronic labyrinthitis, acute circulatory disorders in the internal auditory artery.

Characteristic features of dizziness with PVS are:

· paroxysmal course - dizziness has a sudden beginning and end;

· limited duration of the attack (the attack rarely exceeds 24 hours);

combination of dizziness with severe autonomic disorders;

good health of the patient between attacks;

· rapid onset of compensation due to the inclusion of central compensatory mechanisms - the duration of residual vestibular dysfunction rarely exceeds a month.

Dizziness with damage to the peripheral part of the vestibular analyzer is necessarily accompanied by unilateral horizontal or horizontal-rotatory spontaneous nystagmus, the direction of which is determined by the stage of irritation or inhibition of the labyrinth. As a rule, at the beginning of an attack, patients feel the movement of objects in the direction of the diseased ear, and nystagmus is also directed in the same direction (stage of irritation of the labyrinth). Subsequently, as the labyrinth is depressed, dizziness and nystagmus can change their direction to the opposite (towards the healthy ear). Mandatory for peripheral vertigo is the presence of spontaneous deviation of the arms and torso in the direction opposite to the direction of spontaneous nystagmus. PVS is characterized by auditory disorders (hearing loss, tinnitus).

Central vestibular syndrome develops with damage to the vestibular nuclei and pathways in the posterior cranial fossa, as well as vestibular formations in the cortical-subcortical regions of the brain. CVT is usually observed in pathologies of the central nervous system of various origins.

Dizziness with CVS is characterized by:

· chronic course, lack of clear time boundaries;

· moderate intensity;

· combination with symptoms of damage to the central nervous system;

· long-term (months, years) presence of residual vestibular dysfunction due to limited compensatory capabilities with central damage;

· absence of hearing impairment.

Spontaneous nystagmus during CVS is either absent or observed in several directions. Vertical, diagonal, or converging spontaneous nystagmus may be present. There is no spontaneous deviation of the arms and torso, or its direction coincides with the direction of spontaneous nystagmus.

If a process in the central nervous system acutely affects the vestibular formations, then dizziness in nature and intensity is largely similar to that observed with pathology of the peripheral part of the vestibular analyzer.

EXAMINATION OF PATIENTS WITH Dizziness

1. Collection of complaints and medical history. Determination of the type of dizziness and the type of vestibular syndrome, determination of the nature of dizziness (paroxysmal, chronic), determination of factors provoking dizziness, etc.

2. Nystagmus. Determination of direction, connection with head movements, changes in expression when fixing gaze.

3. Romberg test. With a unilateral lesion of the labyrinth, the patient deviates in the direction of the lesion. To increase sensitivity, you can perform the Romberg test on one leg or place your legs on the same line.

4. Stato-kinetic tests (finger-nose, finger-toe, heel-knee tests). Damage to the cerebellum is characterized by hypermetria (excessive range of movements) and intention tremor (i.e., increasing when performing fine and precise movements) tremor

5. Gait study. Damage to the cerebellum is characterized by a gait with widely spaced legs.

6. Test for adidochokinesis. The patient is asked to quickly alternately turn the hand with the palm up and down. If the cerebellum is damaged, rapid changes in movements are impossible, resulting in awkward, incorrect movements.

VERTEBRO-BASILLAR INSUFFICIENCY (VBI) - this is reversible ischemia of brain structures supplied with blood from the vessels of the vertebral and basilar arteries.

The following symptoms are characteristic of lesions of the vertebrobasilar region:

1. Movement disorders in patients with VBI are characterized by a combination of:

central paresis

· coordination disorders due to damage to the cerebellum and its connections

2. Sensory disorders manifest themselves:

· symptoms of prolapse with the appearance of hypo- or anesthesia in one limb, half of the body.

· Paresthesia may occur, usually involving the skin of the limbs and face.

disorders of superficial and deep sensitivity (occur in a quarter of patients with VBI and, as a rule, are caused by damage to the ventrolateral thalamus in the areas of blood supply to the a. thalamogeniculata or posterior external villous artery)

3. Visual impairment can be expressed as:

Loss of visual fields (scotomas, homonymous hemianopsia, cortical blindness, less often - visual agnosia)

· appearance of photopsia (visual images - “flies”, “lights”, “stars”, etc.)

blurred vision, blurred vision of objects

4. Cranial nerve dysfunction

oculomotor disorders (diplopia, convergent or divergent strabismus, vertical separation of the eyeballs),

peripheral paresis of the facial nerve

Bulbar syndrome (less commonly pseudobulbar syndrome)

à feeling of a lump in the throat, pain, sore throat, difficulty swallowing food, spasms of the pharynx and esophagus

5. Systemic dizziness similar to central vestibular syndrome.

Clinically, this condition can develop acutely and is manifested by repeated episodes of transient ischemic attacks (TIA) or small strokes in the vertebrobasilar system with reversible neurological deficit. In this case, it is reasonable to assume Acute circulatory disturbance in the vertebral-basilar circulation. According to the literature (T.S. Barykova, E.V. Fastakovskaya, 2010), only 7.7% of patients hospitalized for acutely developed vestibular disorders were diagnosed with cerebral infarction in the dorsolateral parts of the medulla oblongata (Wallenberg-Zakharchenko syndrome), infarctions in the anterior and inferior posterior cerebellar arteries.

If this condition develops gradually, then we can judge chronic cerebrovascular accident (synonyms: cerebrovascular disease, dyscirculatory encephalopathy, chronic cerebral ischemia).

Distinctive feature VERTEBROGENIC VERTIGO is an acute onset associated with a certain position of the head (bending forward, throwing it back, sharply turning to the side, etc.), often in the morning, after sleep. Dizziness, which occurs as a result of a change in the position of the head, can be caused by both irritation of the inner ear and the central vestibular structures of the brain (trunk, cerebellum). Compression of the arteries develops with osteophytes and lateral disc herniations in the uncovertebral areas, anterior exostoses of the articular processes, as well as with subluxation. Dizziness is systemic. Both peripheral vestibular syndrome and central vestibular syndrome may occur.

BENIGN PAROXYSMAL POSITIONAL VERTIGO (BPPV)- a disease of the labyrinth, which is manifested by attacks of vestibular vertigo that occur when the position of the head changes.

BPPV occurs when the head position changes, for example when it tilts back. Dizziness is usually preceded by a short (several seconds) latent period. The dizziness itself lasts, as a rule, 10-15 s, but no more than 1 minute and is accompanied by a specific positional (horizontal or horizontal-rotatory) nystagmus, the direction of which depends on which of the semicircular canals is affected. When BPPV attacks follow one another at short intervals, nausea and vomiting may occur. This is observed if, instead of avoiding unnecessary movements, the patient moves restlessly, constantly changes the position of the head and thereby involuntarily provokes new attacks. In such cases, patients may complain of continuous (several hours or even days) dizziness, which complicates diagnosis.

MENIERE'S DISEASE - This is a non-inflammatory disease of the inner ear, which is associated with a violation of the hydrodynamics of the membranous ear labyrinth. For this pathology, a natural combination of cochlear (hearing impairment) and vestibular (dizziness, imbalance) disorders is required. The diagnosis of Meniere's disease is established in the presence of the following mandatory signs:

· sudden onset of systemic dizziness with vegetative symptoms;

· one-sided (at the initial stage of development of the disease) hearing loss;

progressive hearing loss

fluctuating noise in the ear

· feeling of fullness or pressure in the ear.

· recurrence of attacks of dizziness while the patient feels well and remains functional during the interictal period of the disease.

A harbinger of an attack of dizziness in Meniere's disease is often a change in the tone and strength of ear noise; gain “feelings of pressure/fullness” in the area of ​​the sore ear. The classic course of Meniere's disease is characterized by increased noise in the affected ear, followed by an increase in vestibular disorders. An attack of dizziness lasts up to several hours, is accompanied by nausea and vomiting, and occurs at any time of the day. The disease has a chronic course. Over time, hearing loss increases, and attacks become less frequent and may stop altogether.

VESTIBULAR NEURONITIS - the third most common cause of acute vestibular vertigo after BPPV and Meniere's disease. The disease occurs mainly at the age of 30-60 years, men and women get sick equally often.

The development of vestibular neuronitis is associated with selective inflammation of the vestibular nerve. It is believed that the cause of inflammation is herpes simplex virus type I. Vestibular neuronitis manifests itself as a sudden and prolonged attack of systemic dizziness, accompanied by nausea, vomiting and imbalance. The disease may be preceded by a respiratory viral infection. Sometimes brief episodes of dizziness or unsteadiness occur several hours or days before the onset of an acute vestibular attack. Symptoms of vestibular neuronitis intensify with head movements or changes in body position, but unlike BPPV, they do not go away with rest. Dizziness may improve with fixed gaze. Hearing does not decrease. Neurological examination shows no symptoms of damage to the brainstem or other parts of the brain. The duration of dizziness ranges from several hours to several days. After the dizziness stops, patients continue to experience instability for several days or weeks.

ACUTE CIRCULATION IN THE LABYRINTH ARTERY OR HEMORRHAGE IN THE EAR LABYRINTH manifests itself as severe, sudden dizziness, nausea, vomiting, loss of balance and coordination of movements. At the same time, noise appears in one ear and a sharp decrease in hearing, up to complete deafness. This condition is called labyrinthine apoplexy. Apoplexy of the labyrinth should be differentiated from an attack of Meniere's disease and stroke. Unlike Meniere's disease, which occurs with repeated attacks of dizziness, with apoplexy of the labyrinth, a single vestibular crisis is observed, resulting in persistent deafness in one ear, which is not typical for Meniere's disease. Labyrinthine apoplexy is distinguished from stroke by the absence of focal neurological symptoms.

Esin G.V.

Literature

1. P.R.Kamchatnov, A.V.Chugunov, V.A.Li, B.B.Radysh. Vertebrobasilar insufficiency: treatment options. CONSILIUM MEDICUM VOLUME 10; No. 7; pp. 81-84.

2. N.V. Boyko. Dizziness in the practice of a general practitioner. Attending Physician, April 2010, No. 4.

3. O. V. Veselago. Dizziness in neurological practice. Attending Physician, May 2010, No. 5

4. N. S. Alekseeva. Dizziness caused by pathology of the cervical spine. Attending Physician, August 2009, No. 7.

5. Lilenko S.V. Auditory and vestibular disorders in the early stages of Meniere's disease: diagnosis and treatment. Treatment of diseases of the nervous system No. 2(2), 2009

6. T.S. Barykova, E.V. Fastakovskaya. Vestibular dizziness in emergency neurology and cervical osteochondrosis. Neurology, neuropsychiatry, psychosomatics, 2010, No.2, pp. 55-58.

7. Zamergrad M.V. Vestibular vertigo. Neurology, neuropsychiatry, psychosomatics, No. 1, pp. 14-18, 2009.

Dizziness (or scientifically vertigo) is a symptom that manifests itself as a sensation of rotation of surrounding objects around the patient, or, on the contrary, as the rotation of the person himself around his own axis. This symptom is almost never isolated; it is usually accompanied by other manifestations of trouble in the body. There are a number of pathological conditions that cause dizziness, and often they can only be identified after a serious examination.

Balance regulation system

Several organs take part in the regulation of balance:

  • visual analyzer;
  • vestibular apparatus;
  • proprioceptive apparatus;
  • brain structures.

Visual analyzer

A person sees surrounding objects and, based on the information received, can realize his position in space. It is no coincidence that in pitch darkness sometimes instability occurs in a vertical position.

Located in the skull in the cavity of the inner ear. Anatomically combined with the auditory analyzer. It consists of three hollow tubes (semicircular canals) located at an angle to each other, lined from the inside with a special shell with a mass of receptors and filled with liquid. When you change the position of the body (or rather, the head) in space, the liquid shifts, irritating the receptors. The transmission of information from them is carried out through the vestibular nerve, which sends impulses to intracerebral structures

Proprioceptive (somatosensory) system

All organs, muscles, ligaments and bones of the body are penetrated by millions of nerve endings. Some of them are equipped with sensitive receptors, from which the brain receives information about changes in body position. Evidence of this is the inability to maintain balance when the nerves of the limbs are damaged.

Intracerebral structures

The main center of balance is located in the cerebellum. However, there are several more structures (reticular formation, vestibular nuclei of the brain stem and cerebellum, extrapyramidal system) that perceive and process information coming from the receptor systems of the visual analyzer, vestibular apparatus and nerve endings of the body.

Disruption of the functions of any part of this incredibly complex mechanism leads to a distortion of the patient’s perception of his position in space, which is also manifested by dizziness.

There are two main types of dizziness:

  1. systemic associated with dysfunction of the vestibular apparatus at different levels; in turn is divided into:
    • central – with damage to brain structures;
    • peripheral – with damage to nerve ganglia, nerves, semicircular canals;
  2. non-systemic, which includes:
    • imbalances associated with the uncoordinated action of all three systems for maintaining balance - the visual analyzer, the vestibular apparatus and the proprioceptive mechanism;
    • presyncope, in which dizziness is caused by a sharp deterioration in nutrition of any of the elements described above;
    • psychogenic dizziness that occurs during anxiety or depression.

There is a separate form of vertigo - physiological dizziness. This type of symptom is not associated with any pathology and is caused by excessive irritation of the vestibular apparatus. Seasickness is a classic example of this type of vertigo.

Features of dizziness depending on the cause

The cause of dizziness is the main factor influencing its characteristics. The nuances of vertigo are determined by the level of damage to the balance system and the accompanying neurological symptoms that appear in the underlying disease.

30-50% of all patients complaining of vertigo suffer from its systemic form. It is caused by a number of diseases:

At Meniere's disease Along with repeated attacks of dizziness, tinnitus, periodic hearing loss, and severe autonomic disorders are noted. Vertigo lasts from several minutes to a day, the frequency of attacks is very diverse - from once a year to several times a day. Often before an attack there are sensations of stuffiness in the ears, a feeling of heaviness, noise in the head, and impaired coordination of movements.

Vestibular neuronitis– inflammation of the vestibular nerve, in which the most striking symptom is intense dizziness for several hours. This pathology occurs acutely and is caused by infectious causes or intoxication. Vestibular neuronitis is characterized by the complete absence of focal neurological and meningeal symptoms and complete preservation of hearing.

BPPV– a syndrome that occurs when calcium crystals form in the semicircular canals. Changing the position of the head causes their displacement and severe irritation of the receptors of the vestibular apparatus. At the same time, an attack of sweating occurs and the pulse rate decreases. There are no auditory phenomena (noise, hearing loss) or neurological symptoms.

Tumors cerebellum, brainstem and paracerebellar region often present with dizziness. This symptom may be the only sign of a space-occupying process in the brain for a long time.

Dizziness occurring immediately after TBI, usually indicates labyrinthine trauma. There are no meningeal, focal symptoms, but there is severe headache, often nausea and vomiting. Sometimes vertigo appears only a few days after the injury, and then one can suspect the development of inflammation of the labyrinth - serous labyrinthitis.

Use of aminoglycoside antibiotics often provokes toxic damage to the auditory and vestibular apparatus. Thus, gentamicin primarily damages the structures of the labyrinth. Such damage is almost always irreversible.

Vertebro-basilar insufficiency is a disease in which there is a deterioration in the blood supply to both the labyrinth and intracerebral structures. Along with dizziness, other neurological symptoms are also detected: motor and sensory disorders associated with damage to the nuclei of the cranial nerves, visual disturbances, and coordination disorders. The cause of this condition can be osteochondrosis, atherosclerosis, anomalies in the development of the main and vertebral arteries, that is, any conditions leading to a decrease in the lumen of these vessels.

Attack dizziness due to migraine is not a symptom of a disease, but one of the types of aura - a condition that precedes the onset of headaches.

In temporal lobe epilepsy, vertigo is combined with powerful autonomic symptoms:

  • pain in the stomach;
  • nausea;
  • sweating;
  • increased salivation;
  • decrease in heart rate.

This form of epilepsy is not accompanied by seizures, but other sensory disturbances, such as visual hallucinations, may occur.

Encephalitis– most often a viral inflammation of the brain, beginning acutely or subacutely, followed by stabilization or gradual regression (subsidence) of symptoms. Dizziness is accompanied by other, very diverse neurological symptoms.

Vertigo often occurs with multiple sclerosis. The characteristic course of the pathology, the multifocal nature of the lesion and the results of instrumental and laboratory studies make it possible to clearly determine the presence of the underlying disease. Difficulties can arise only then. When other symptoms are mild or dizziness is the very first sign of multiple sclerosis.

At developmental anomalies of the cervical vertebrae and the base of the skull, dizziness is caused by a mechanism similar to vertebrobasilar insufficiency. Usually there are other symptoms of the underlying disease, on the basis of which the final diagnosis is made.

Unsystematic dizziness

This includes types of dizziness that are not directly related to the work of the vestibular analyzer.

Balance disorders that occur when the three systems that regulate body position are not working in a coordinated manner can result from:

  • dysfunction of the vestibular system without damage to the semicircular canals; in this case, the patient, having closed his eyes, loses the ability to maintain balance;
  • cerebellar lesions, in which visual control does not affect the severity of symptoms;
  • lesions of the subcortical nerve centers;
  • disturbances in the transmission of impulses from the visual analyzer, proprioceptors;
  • taking certain medications that affect nerve conduction.

In presyncope, dizziness is often accompanied by a feeling of lightheadedness, noise or ringing in the ears, unsteadiness, loss of balance, and “darkening in the eyes.” Emotional disorders are also noted - fear, anxiety, powerlessness, depression. Often, after the appearance of these symptoms, fainting occurs, but it happens that they gradually disappear without the patient losing consciousness.

Psychogenic dizziness most often occurs with hysteria, as well as with some phobias (fear of open spaces). This type of vertigo is characterized by great persistence and pronounced emotional perception.

Treatment

Treatment of dizziness is carried out according to the rules adopted for the treatment of the underlying disease:

  • when used, vasodilators, antiplatelet drugs;
  • in case of Meniere's disease, salt intake is limited, diuretics are used, and, if necessary, surgical intervention is performed;
  • vestibular neuronitis is treated with;
  • Benign paroxysmal positional vertigo is treated mainly non-pharmacologically; there are a number of techniques that allow you to move calcium crystals to the vestibule of the labyrinth, where they will not irritate the receptors;
  • for epilepsy, special agents are used to suppress the excessive electrical activity of the pathological focus in the brain.

Symptomatic agents are also used to interrupt the flow of impulses from the vestibular receptors (betagistine).

For some forms of dizziness, the use of meclozine, promethazine, and cinnarizine is indicated. Sedatives are widely used, which do not eliminate dizziness, but make it easier to tolerate.

Treatment of psychogenic dizziness is carried out by prescribing psychotropic drugs - antidepressants, tranquilizers, and sometimes anticonvulsants that have a sedative effect. Psychotherapy is also very effective, since vertigo in this case is not organic in nature, but rather is a feature of the perception of the surrounding reality.

Dizziness is just one of many neurological symptoms. Its appearance clearly indicates trouble in the body. That is why, with repeated attacks of vertigo, it is necessary to consult a doctor as soon as possible for examination and quality treatment.

Dizziness (GK) - this is a violation of the orientation of one’s body in the surrounding space, accompanied by instability, apparent oscillation or rotation of objects surrounding a person (clockwise, or vice versa).
Most people, practically healthy, under certain circumstances, have at some time experienced similar symptoms.
The types of dizziness depend on the causes of its origin.
In the absence of illness, dizziness may appear due to irritation of the vestibular apparatus. It can be provoked by motion sickness in transport, watching a train pass by,looking down when at height. This kind of dizziness is called physiological.

Pathological dizziness


Pathological dizziness is observed in the absence of provoking factors. Its cause is dysfunction of the vestibular complex, auditory nerve, brain stem, cerebellum, cortical brain disorders, and pathology of afferentation. More often, the cause is multiple and complex.
Depending on the clinical manifestations, the types of dizziness differ. It can be systemic (rotation of objects in front of the eyes) and non-systemic (their oscillation), constant or not, paroxysmal and have a gradual development, positional (related to the position of the body) and attitudinal (occurring when turning the head).
Depending on the location of the lesion, dizziness is divided into three large groups.
When the vestibular apparatus is damaged (semicircular canaliculi, ampullae of the vestibule, vestibular part of the auditory nerve), peripheral dizziness - the most common.
When the brain vestibular structures are damaged (in the brainstem, cerebellum, in the cortical regions), it occurs central vertigo
Dizziness due to impaired afferentation occurs with impaired vision, hearing, proprioceptive sensitivity, with tonic dysfunction of the sternocleidomastoid muscle.
In reality, especially as you age, the cause of dizziness is complex.
Dizziness combined with autonomic dysfunctions - pallor of the skin, palpitations or bradycardia, instability of blood pressure, hyperhidrosis.

Peripheral dizziness


It occurs more often than others. Accompanied by nystagmus. When the gaze is fixed, both the nystagmus and the dizziness itself decrease or disappear completely.
Peripheral dizziness, depending on the cause, has several types. It develops in many conditions - Shane , , emotional disorders, , autonomic dysfunction and other problems.
Benign positional GK has a paroxysmal character. Appears when the position of the body in space changes, or when the head turns. The most provocative is turning the head in the sagittal plane.
The reason is degenerative processes in the otolithic apparatus (usually the semicircular, posterior canal).
Neuronitis vestibular (acute vestibulopathy). Its cause is unknown. Occurs at different ages, often after a viral respiratory infection. Dizziness is paroxysmal, intense, systemic. Sometimes it is accompanied by vomiting and nausea. The attack is accompanied by imbalance, fear, and spontaneous nystagmus. Lasts for hours, even days. Hearing does not decrease. Recurs rarely.
In the post-attack period, a feeling of uncertainty when walking persists.


For Meniere's disease Characterized by recurring sudden, paroxysmal, systemic dizziness. Attacks occur against a background of good health. More often, at the age of 25 - 45 years. The cause of dizziness is an increase in endolymph in the inner ear. At the slightest movement of the head, dizziness intensifies, vomiting and nausea occur. Nystagmus appears.

The attack is combined with autonomic symptoms, noise in one ear, and ear congestion. When the attack is repeated, the noise intensifies, persists in the inter-attack period, and is combined with hearing loss.
Meniere-like syndrome occurs more often than the true disease. Occurs with cerebrovascular dysfunction in the vertebrobasilar region (main and vertebral arteries). The cause of dizziness is a violation of blood flow against the background of cervical osteochondrosis.
Hunt's syndrome. In addition to decreased hearing, herpetic eruptions appear in the external auditory canal and paresis of the facial muscles on the same side.
Acoustic nerve neuropathy. Hearing decreases and noise in the ear appears. The disease is progressive, accompanied by complaints of periodic, not intense dizziness.
Acoustic neuroma accompanied by non-systemic, intermittent dizziness.
In addition to progressive hearing loss and tinnitus, there is a suppression of the corneal reflex until it disappears. There may be weakness of the facial muscles on the affected side.
The diagnosis is confirmed by MRI examination ( ).

Central vertigo


It occurs against the background of damage to the cerebellum, brain stem and cerebral cortex. Nystagmus can be vertical or horizontal, with a rotational component. Unlike peripheral vertigo, nystagmus is not suppressed by gaze fixation.
With demyelinating processes (multiple sclerosis, encephalomyelitis), cerebrovascular diseases (vertebrobasilar dysfunction), syringobulbia, the brain stem is affected, which provokes Meniere-like attacks.
With a tumor of the 4th ventricle, intense dizziness is accompanied by nausea, vomiting, severe headache, slowing of the pulse, falling and convulsions. Seizures are triggered by turning the head.
GK can be the most important symptom of circulatory disorders in the cerebellar artery and damage to the cerebellum.

When the interparietal sulcus of the cerebral cortex of various origins is damaged, interparietal syndrome is observed. Accompanied by dizziness, a feeling of swaying, instability. Combined with a disorder of spatial perception of the shape, size of surrounding objects and one’s own body.
GC in epilepsy occurs when the focus is located temporally. The attacks last for seconds, the dizziness is not systemic, and is accompanied by a feeling of unreasonable fear, short-term derealization or depersonalization, and vegetative symptoms.
Afferentation disorder . Occurs when visual afferentation decreases due to damage to the extraocular muscles. Accompanied by diplopia (a feeling of double objects).
Dizziness can also be a concern if there is a violation of muscle tone in the sternocleidomastoid muscle. It is a source of orientation impulses for the head.
It is not systemic in nature, it is provoked by head movements, looking up or down, or changing a person’s posture. Lasts from several minutes to hours.
Accompanied by complaints of pain in the neck, radiating to the ear, behind the ear, and forehead area. When palpating the gudino-clavicular-mastoid muscle, its soreness and tension (defense) are detected.
In older people, dizziness has a complex origin. Its etiology is influenced by disruption of afferent signals entering the brain (decreased vision, hearing, proprioceptive sensitivity), damage to the vestibular nerve, stem and cerebellar structures.
Dizziness in the background , anxiety-depressive, depressive, anxious, phobic disorders are not accompanied by nystagmus.

To clarify the diagnosis, an otoneurological study (caloric, rotational tests), duplex scanning of the brachiocephalic arteries, magnetic resonance imaging of the brain, etc. are performed.
comprehensive, a system of therapeutic measures must be included. It is necessary to contact a neurologist, otolaryngologist, or local physician at its initial manifestations.


For quotation: Kamchatnov P.R. Dizziness in the practice of a neurologist // RMJ. 2005. No. 12. P. 824

Dizziness is an extremely common complaint that prompts you to consult a doctor. About 2–5% of outpatients complain of dizziness, while its frequency increases with age and reaches 30 percent or more in the population of people over 65 years of age. According to the modern definition, the concept of vertigo implies a sensation of imaginary rotation or translational movement of the patient in various planes or an illusory displacement of a stationary environment in any plane.

In the domestic literature, it is customary to distinguish two main clinical syndromes of dizziness - systemic and non-systemic. Systemic dizziness (vertigo) refers to a false sensation of rotational or linear movement of one’s own body or surrounding objects. The pathophysiological basis for the occurrence of dizziness is a mismatch in the activity of the vestibular, visual and propriceptive systems, which occurs at different levels of the nervous system. This kind of mismatch can be observed in a healthy person under the influence of appropriate high-intensity stimuli - during prolonged rotation, observing moving objects, being in a state of weightlessness, etc., which allows us to talk about physiological dizziness.
Systemic dizziness can be considered as a consequence of direct damage to the vestibular apparatus. In this case, it is possible to isolate proprioceptive dizziness, i.e. sensations of passive movement of one’s own body in space; tactile or tactile dizziness - sensations of movement of the support under the feet or hands (floor, table), rocking on the waves, a feeling of sinking or lifting the body, rocking forward and backward, left-right, up-down, unsteadiness of the soil (walking as if over bumps) and visual dizziness, perceived as forward movement of objects in the visible environment.
Non-systemic dizziness is a feeling of lightheadedness, loss of stability, loss of balance, “loss of ground under your feet,” “darkening in the eyes,” and ringing in the ears. Often, these conditions precede the development of fainting (lipothymia), although complete loss of consciousness may not occur. Characteristic of states of non-systemic dizziness are pronounced emotional disorders - a feeling of restlessness, anxiety, fear or, conversely, depression, powerlessness, a sharp loss of strength.
A number of patients experience a combination of manifestations of both systemic and non-systemic dizziness. Especially often, a similar picture occurs in elderly and senile patients, against the background of a combination of several predisposing factors.
It is noteworthy that there is concomitant pronounced autonomic dysfunction in the form of decreased blood pressure, bradycardia (less commonly, tachycardia), distal or diffuse hyperhidrosis, and increased salivation. Autonomic disorders occur in patients with various types of dizziness; they often play an important role in the formation of the clinical picture of the disease.
The causes of systemic dizziness are extremely varied; it may occur when the vestibular analyzer is damaged at various levels. It can be caused by damage to both the peripheral part of the vestibular analyzer and its central parts. In this regard, it should be noted that it is extremely difficult, based only on clinical data, to accurately establish the cause of dizziness and topically localize the pathological process. It is believed that lesions of the vestibular analyzer account for 30 to 50% of all patients who complain of a feeling of dizziness.
The most common form of attacks of systemic vertigo (up to 30%) is benign paroxysmal positional vertigo. Extremely important in its diagnosis is the occurrence of an attack depending on the position of the head, as well as positive Dix-Hallpike tests. Repeated episodes of dizziness also occur quite often in patients with Meniere's disease. In relatively rare cases, isolated systemic vertigo is a consequence of a tumor of the cerebellopontine angle, infectious diseases (syphilis, HIV infection, etc.). Cases of the development of an attack of dizziness as an aura preceding a migraine attack have been described. Diagnostic difficulties arise if the headache attack itself is absent or occurs in a reduced form.
In the practice of a neurologist, one often has to deal with dizziness caused by cerebral circulatory disorders, primarily vertebrobasilar insufficiency. There is evidence that approximately 6% of all cases of dizziness are the result of cerebrovascular pathology. As a rule, such patients also exhibit other neurological symptoms (lack of cranial innervation, conduction motor, sensory disorders, visual, coordination disorders). It should be borne in mind that extremely rarely dizziness is the only manifestation of vascular pathology of the brain. Despite the fact that isolated systemic vertigo can be observed in patients with acute occlusion of the auditory artery, anterior inferior cerebellar artery, accompanied by the formation of an infarct zone, such cases are rare and further diagnostic search is required to exclude other causes of vestibular disorders. It should be emphasized that it is inappropriate to associate most episodes of paroxysmal dizziness, provoked by a change in head position, with compression of the vertebral arteries by altered cervical vertebrae. As a rule, these patients have benign paroxysmal positional vertigo or other forms of damage to the peripheral part of the vestibular analyzer. In case of a single episode of systemic dizziness lasting a day or more, the differential diagnosis should be made with vestibular neuronitis.
The causes of non-systemic dizziness are extremely diverse. The most common condition is arterial hypotension - with orthostasis, increased vasovagal reactions, cardiac arrhythmias and conduction disturbances. Similar episodes are possible in cases of carbohydrate metabolism disorders (hypoglycemia), endogenous intoxications, pregnancy, and anemia. A large number of somatic diseases, especially those accompanied by intoxication, are accompanied by a feeling of non-systemic dizziness. It should be borne in mind that a wide range of medications can provoke or intensify existing dizziness. These drugs include some antihypertensives (b-blockers), anticonvulsants (carbamazepine), sedatives (benzodiazepines), diuretics, and drugs containing L-DOPA. The likelihood of dizziness increases when combining drugs, using them in high doses, in elderly patients, as well as against the background of concomitant somatic pathology.
A manifestation of non-systemic dizziness are imbalances caused by impaired functioning of various parts of the central nervous system, in particular, those ensuring the integration of sensory pathways of various modalities. Violations of statics, coordination, and often falls, manifest themselves as various organic, often multifocal, lesions of the brain substance (vascular, traumatic, toxic origin, neurodegeneration). It is considered possible that non-systemic dizziness may occur due to degenerative changes in the cervical spine and the formation of myofascial syndrome. In this case, proprioceptive impulses from the altered muscles of the neck and shoulder girdle can play a certain pathogenetic significance. Balance disorders not accompanied by severe dizziness are observed in patients with bilateral peripheral lesions of the vestibular apparatus. Deterioration of coordination in such patients is observed when walking on an uneven, soft surface, in a dark room.
The mechanism for ensuring balance is one of the oldest acquired by man in the process of evolution. In addition to the close integration of the vestibular, visual, proprioceptive and tactile sensory systems, it has close, extensive connections with a wide variety of brain structures. In this regard, dysfunction of the vestibular analyzer (in particular, the appearance of a feeling of dizziness) is accompanied by severe emotional disorders. It is well known that the feeling of dizziness is painful for patients, especially when combined with other neurological disorders - impaired coordination, hearing loss, a feeling of tinnitus (which is often found in circulatory disorders in the vertebrobasilar system). A significantly higher prevalence of anxiety and depressive disorders was established in patients with dyscirculatory encephalopathy and suffering from dizziness. The presence of dizziness, even if not accompanied by imbalances and coordination that are significant for everyday activities, leads not only to emotional disturbances, but also to a significant decrease in the quality of life of patients.
On the other hand, dizziness itself may be a manifestation of emotional disorders. Dizziness is one of the most common complaints made by patients with psychogenic disorders, and is observed in 79% of patients with hypochondriacal syndrome, in 80% of patients with hysterical neurosis, and in a significant number of patients with depressive conditions. A particular form of psychogenic disorders of the function of the vestibular apparatus is phobic positional vertigo, which is characterized by a feeling of instability, unsteadiness of the floor underfoot, subjective disturbances in gait and coordination of movements in the limbs in the absence of objective signs of ataxia and satisfactory performance of coordination tests. It is characteristic that this condition occurs predominantly in people with high levels of anxiety and obsessive-compulsive disorders and is not a direct analogue of phobic conditions such as agoraphobia, although in some cases differential diagnosis can be difficult. The presence of dizziness in patients with panic attacks is undoubtedly common (of the 13 symptoms characteristic of panic attacks included in the DSM-IV, dizziness is one of the most common).
It is noteworthy that patients with vestibular disorders experience progressive impairment of cognitive functions, and this concerns not only spatial thinking, but also, in particular, functions such as visual pattern recognition. The authors found that bilateral lesions of the vestibular analyzer are accompanied by a decrease in the volume of the hippocampus (according to MRI data) and a decrease in the quality of performance on spatial memory tests. It is important that the severity of cognitive impairment correlated with symptoms of depression and anxiety, but not with the severity of dizziness.
The vestibular analyzer has a very complex neurochemical organization. It has been established that histamine plays an important role in the transmission of information from the receptors of the semicircular canals, in particular histamine H1 and H3 receptors (but not H2 receptors, predominantly located in the mucous membrane of the gastrointestinal tract). Cholinergic transmission has a modulating effect on histaminergic neurotransmission. It is believed that acetylcholine is one of the main neurotransmitters that ensures the transmission of information from receptors to the lateral vestibular nuclei, as well as to the central parts of the analyzer. Experimental data suggest that it is thanks to the interaction of the choline and histaminergic systems that vestibulo-vegetative reflexes are realized. Vestibular afferentation to the medial vestibular nucleus is provided by both histamine and glutamatergic pathways. A significant role in the modulation of ascending impulses is played by g-aminobutyric acid, dopamine, serotonin, and possibly neuropeptides. GABAergic fibers have an inhibitory effect on afferent impulses, which makes it possible to consider influencing them as a therapeutic option for dizziness.
Examination of a patient with complaints of dizziness involves establishing the very fact of the presence of dizziness and clarifying its topical and nosological affiliation. It should be noted that patients can often put very different meanings into the concept of dizziness, including, for example, blurred vision, a feeling of nausea, headache, etc. In this situation, the doctor’s task is to carry out a differential diagnosis between dizziness and complaints of a different nature. During questioning, you should not push the subject to name a specific term; it is much more advisable to get from him the most detailed description of the existing complaints.
A neurological examination is of great importance, in particular, identifying and determining the nature of nystagmus (its direction, symmetry, connection with the position of the head, etc.), the state of the cranial nerves and the accuracy of the coordination tests. Many patients require examination by an otialogist (vestibulologist) or otoneurologist using instrumental methods for diagnosing the condition of the vestibular apparatus, hearing, and vision. Even a full and comprehensive examination in some cases does not allow establishing a diagnosis, which requires dynamic monitoring of the patient. Diagnosis of combined forms of dizziness is especially difficult.
Treatment of a patient with dizziness should first of all consist of eliminating the cause of its occurrence. This is especially true for patients with inflammatory, vascular and other causes of the disease that can be cured. It is extremely important to timely relieve attacks of dizziness, as well as eliminate concomitant vegetative and psycho-emotional disorders. Subsequently, it is necessary to carry out therapeutic measures aimed at compensating for the impaired functions of the vestibular apparatus. It is believed that as acute dizziness is relieved, it is necessary to carry out active rehabilitation of the patient, including therapeutic exercises, dosed physical activity, and physiotherapeutic measures. The main focus of these classes is to ensure maximum independence in everyday life and minimize the risk of falls, as a potential source of injury.
In order to reduce the intensity of dizziness, drugs are used - vestibulolytics, which inhibit the activity of vestibular receptors and ascending conduction systems. It is believed that the duration of such treatment should not be excessively long, since vestibulolytics, by inhibiting the activity of nerve formations, prevent the development of compensatory reparative reactions. Moreover, some drugs used for a long time to relieve dizziness can not only lead to the elimination of subjective symptoms, but also provoke an increase in the manifestations of ataxia, balance disorders, and general weakness.
The use of vestibulolytic drugs is largely determined by the characteristics of the neurotransmitter organization of the vestibular system. In this regard, to relieve and prevent attacks of systemic dizziness, drugs that interact with histamine H1 and H2 receptors, in particular, betahistine hydrochloride, are widely used. Drugs that limit the entry of calcium ions into the cell (cinnarizine, flunarizine) are widely used, although the exact mechanism of their action in this situation has not been fully disclosed. A rather difficult problem is the management of patients with predominantly non-systemic dizziness. The therapeutic approach is determined by the nature of the leading pathological process (psycho-emotional disorders, level of organic brain damage, disorders of propriocetal afferentation, etc.) and often the choice of therapeutic tactics is made empirically. Drugs from the pharmacological groups of antidepressants, anxiolytics, anticonvulsants, and neuroleptics are used; when choosing them, it should be borne in mind that most of these drugs themselves in a certain situation (for example, with inadequate dosage) can cause dizziness.
One of the most common approaches to the treatment of patients with dizziness is the use of combination drugs that have vestibulolytic and sedative effects, helping to eliminate vegetative manifestations. A representative of this group of drugs is Bellataminal, which contains 0.1 mg of belladonna alkaloids, 0.3 mg of ergotamine tartrate and 20 mg of phenobarbital. The main active component of belladonna alkaloids is the active levorotatory isomer hyoscyamine, which has antagonistic properties towards cholinergic receptors. Being a non-selective anticholinergic blocker, however, hyoscyamine has a greater affinity for m-cholinergic receptors, which explains most of its pharmacological effects. An important property is the ability to penetrate the blood-brain barrier, due to which the effect of the drug is realized not only at the level of postganglionic parasympathetic nerves, but also due to its effect on the autonomic formations of the central nervous system.
In relation to patients with dizziness, both the ability of hyoscyamine to reduce the intensity of the sensation of rotation and to reduce the intensity of autonomic disorders is important. Clinically significant are the reduction of nausea, hyperhidrosis, hypersalivation, bradycardia, as a result of which episodes of dizziness are tolerated much easier. Due to the peculiarities of their pharmacological properties, belladonna alkaloids can be used to relieve various forms of dizziness - systemic, non-systemic, accompanied by autonomic disorders, motion sickness and other kinetoses. It is necessary to take into account the presence of a number of undesirable effects due to anticholinergic properties, which preclude the use of belladonna preparations in patients with intracardiac conduction disorders and glaucoma.
Ergotamine tartrate, which is part of Bellataminal, has a moderate ability to block α-adrenergic receptors. At the same time, the blocking effect on adrenergic receptors of the drug is low (about 20 times lower than that of dihydrogenated ergot derivatives - dihydroergotoxin and dihydroergotamine), while ergotamine has its own adrenomimetic effect on peripheral arteries. The resulting effect, as a rule, is vasospasm (its severity depends on the dose of the drug) and a moderate increase in systemic blood pressure. In addition, like other ergot derivatives, ergotamine has a moderate antiserotonin effect. Given the ability to cause vasospasm, drugs containing ergot alkaloid should be used with caution in patients with severe stenotic lesions of the coronary arteries and retinal arteries. Finally, phenobarbital, which is part of Bellataminal, in small doses has a moderate sedative effect, which, as a rule, does not reach the degree of depression. When prescribing Bellataminal, one should also take into account its good pharmacoeconomic indicators - the relatively low cost of the drug makes it accessible to most patients.
Thus, it seems that a successful combination of pharmacological effects of the components allows the use (taking into account existing limitations) of the drug Bellataminal for the relief of dizziness of various origins.

Literature
1. Golubev V.L., Vein A.M. Neurological syndromes. M., Eidos-Media, 2002.
2. Gorbacheva F.E., Matveeva L.A., Chuchin M.Yu. About cervical dizziness. RMJ, Vol. 12 No. 10, 2004.
3. Gusev E.I., Nikonov A.A., Skvortsov V.I., Avakyan G.N., Gordeeva T.N., Katunina E.A., Atayan A.V. Treatment of dizziness with the drug betaserc in patients with vascular and traumatic brain lesions Journal of Neurology and Psychiatry, 1998; 11; 43–47.
4. Dix M.R., Hood D.D. (ed.) Dizziness. M., Medicine, 1989.
5. Nikiforov A.S., Konovalov A.N., Gusev E.I. Clinical neurology M., Medicine, 2002.
6. Patyakina O.K. Therapeutic tactics for vestibulogenic dizziness. Consilium Medicum2001; 4; 15.
7. Sokolov S.Ya., Zamotaev I.P. Handbook of medicinal plants M., Medicine, 1984.
8. Tabeeva G.R., Vein A.M. Dizziness in psychovegetative syndromes Consilium–Medicum, Volume 4, N15, 2001.
9. Sheremet A.S. Dizziness as a sign of damage to the vestibular analyzer. Diagnostic stereotypes. Consilium Medicum. Otolaryngology. 2001; 04; 15.
10. Baloh R.W. Dizziness and verigo. Office practice of neurology Eds M A Samuels, S Feske – New York, 1996 – P 83–91.
11. Bird JC, Beynon GJ, Prevost AT, Baguley DM. An analysis of referral patterns for dizziness in the primary care setting. Br J Gen Pract 1998, 48:1828–1832.
12. Brandt T; Kapfhammer HP; Dieterich M Phobic postural vertigo.” A further differentiation of psychogenic vertigo conditions seems necessary. Nervenarzt. 1997; 68(10):848–849.
13. Brandt T. Vertigo. Its Multisensory Syndromes. 2nd ed. Springer, London, 2000. p.441–451
14. Baloh RW. Dizziness, hearing loss, and tinnitus. New York: Oxford University Press, 1998:107–25.
15. Cesarani A., Alpini D., Monti B, Raponi G. The treatment of acute vertigo. Neurological Sciences 2004; 25; s1; 26–30.
16. Colledge NR, Wilson JA, Macintyre CC, MacLennan WJ. The prevalence and characteristics of dizziness in an elderly community. Age Aging 1994, 23: 117–120.
17. Sloan PD. Dizziness in primary care. Results from the National Ambulatory Care Survey. Fam Pract 1989, 29: 33–38.
18. Dieterich M Zurich Vertigo Meeting – phobic postural vertigo. Schweiz Rundsch Med Prax, 1997; 86(40):1554–1557.
19. Drachman DA, Hart CW. An approach to the dizzy patient. Neurology 1972, 22: 323–34.
20. Gil–Loyzaga PE. Neurotransmitters of the olivocochlear lateral efferent system: with an emphasis on dopamine. Acta Otolaryngol. 1995 Mar;115(2):222–6.
21. Halmagyi GM. Diagnosis and management of vertigo. Clin Med. 2005;5(2):159–65.
22. Herdman SJ, Schubert MC, Tusa RJ. Strategies for balance rehabilitation: fall risk and treatment. Ann N Y Acad Sci. 2001 Oct;942:394–412.
23. Horii A, Takeda N, Mochizuki T, Okakura–Mochizuki K, Yamamoto Y, Yamatodani A, Kubo T. Vestibular modulation of the septo-hippocampal cholinergic system of rats. Acta Otolaryngol Suppl. 1995;520 Pt 2:395–8.
24. Housley GD, Norris CH, Guth PS. Histamine and related substances influence neurotransmission in the semicircular canal. Hear Res. 1988 Sep 1;35(1):87–97.
25. Kroenke K, Hoffman RM, Einstadter D. How Common are various causes of dizziness. Southern Medical Journal 2000, 93: 160–167.
26. Kwong K. C., Pimlott J. G. Assessment of dizziness among older patients at a family practice clinic: a chart audit study BMC Family Practice 2005, 6:2 doi:10.1186/1471–2296–6–2
27. Lawson J, Johnson I, Bamiou DE, Newton JL. Benign paroxysmal positional vertigo: clinical characteristics of dizzy patients referred to a Falls and Syncope Unit. Q.J.M. 2005 May;98(5):357–64.
28. Matsuoka I, Ito J, Takahashi H, Sasa M, Takaori S. Experimental vestibular pharmacology: a minireview with special reference to neuroactive substances and antivertigo drugs. Acta Otolaryngol Suppl. 1984;419:62–70.
29. Murray JB. Psychophysiological aspects of motion sickness. Percept Mot Skills. 1997 Dec;85(3 Pt 2):1163–7.
30. Rascol O, Hain TC, Brefel C, Benazet M, Clanet M, Montastruc JL. Antivertigo medications and drug–induced vertigo. Alogical pharmacological review. Drugs. 1995 Nov;50(5):777–91.
31. Serafin M, Khateb A, Vibert N, Vidal PP, Muhlethaler M. Medial vestibular nucleus in the guinea pig: histaminergic receptors. I. An in vitro study. Exp Brain Res. 1993;93(2):242–8.
32. Setness PA, Van Beusekom M. Patient Notes: motion sickness. Postgrad Med. 2004 Oct;116(4):64.
33. Swartz R, Longwell P. Treatment of vertigo. Am Fam Physician. 2005 Mar 15;71(6):1115–22.
34. Smith PF, Darlington CL. Pharmacology of the vestibular system. Bailliers Clin Neurol. 1994 Nov;3(3):467–84
35. Smith P. F., Zheng Y., Horii A., Darlington C. L. Does vestibular damage cause cognitive dysfunction in humans? Journal of Vestibular Research 2005; 15; 1:1–9.
36. Tusa RJ. Dizziness. Med Clin North Am. 2003 May;87(3):609–641.
37. Yardley L, Owen N, Nazareth I, Luxon L. Prevalence and presentation of dizziness in a general practice community sample of working age people. Br J Gen Pract 1998, 8:1131–1135.