Systemic dizziness treatment. Non-systemic dizziness causes

Robert B. Daroff

Dizziness is a fairly common and often distressing symptom. Patients use this term to describe a variety of sensations (eg, lightheadedness, weakness, dizziness, lightheadedness), although some do not fit this definition at all, such as blurred vision, blindness, headache, tingling, “walking on wobbly legs,” etc. Moreover, some patients with gait disturbances will describe their difficulties by also calling them dizziness. It is necessary to carefully collect anamnesis to accurately determine which of the patients talking to the doctor that he is dizzy is actually experiencing this condition.

After excluding sensations such as blurred vision, dizziness may turn out to be either a feeling of weakness (similar to the sensations preceding a fainting state) or systemic dizziness (an illusory sensation of movement of surrounding objects or the body). In other cases, none of these definitions provides an accurate description of the patient's symptoms, and only when spasticity, parkinsonism, or another cause of gait disturbance is identified during a neurological examination do the main sources of complaints become clear. For clinical purposes, dizziness is divided into four categories: syncope; systemic dizziness; various mixed sensations from the head and gait disturbances.

Fainting state. Fainting (syncope) is a loss of consciousness due to ischemia of the brain stem (see Chapter 12). Before the development of true syncope, prodromal signs (a feeling of weakness) are often noted, reflecting ischemia to a degree insufficient to cause loss of consciousness. The sequence of symptoms is quite similar and includes an increasing feeling of lightness in the head, partial or complete loss of vision and heaviness in the legs, increasing to postural instability. Symptoms increase until loss of consciousness occurs or ischemia is eliminated, for example, the patient is placed in a horizontal position. True systemic dizziness almost never develops during presyncope.

The causes of fainting are described in Chapter. 12 and include decreased cardiac output of various etiologies, postural (orthostatic) hypotension, as well as conditions resembling fainting such as vertebrobasilar insufficiency and epileptic seizures.

Systemic dizziness. Systemic vertigo is the apparent movement of surrounding objects or own body. Most often it manifests itself as a sensation of rapid rotation around its axis, usually due to damage to the vestibular analyzer. The peripheral section of the vestibular analyzer, located in the bony labyrinth of the inner ear, consists on each side of three semicircular canals and the otolithic apparatus (elliptical and spherical sacs). The semicircular canals convert angular acceleration, while the otolithic apparatus converts linear acceleration and static gravitational forces, which provide a sense of the position of the head in space. From peripheral part information is transmitted via VIII pair cranial nerves into the vestibular nuclei of the brain stem. The main projections from the vestibular nuclei go to the nuclei of the III, IV and VI cranial nerves, spinal cord, cerebral cortex and cerebellum. The vestibulo-ocular reflex serves to maintain constancy of vision during head movements and depends on direct projections from the vestibular nuclei to the nucleus of the VI cranial nerve (abducens) in the pons and through the medial longitudinal fasciculus to the nuclei of the III (oculomotor) and IV (trochlear) cranial nerves in the midbrain . These projections are responsible for nystagmus (repetitive movements eyeballs), which is an almost obligatory component of vestibular function disorder. The vestibulospinal tracts help maintain a stable body position in space. Connections with the cerebral cortex through the thalamus provide awareness of body position and head movements. The vestibular nerves and nuclei are connected to the cerebellar formations (mainly the flocculus and nodule), which modulate the vestibulo-ocular reflex.

The vestibular analyzer is one of three sensory systems responsible for spatial orientation and body position; the other two include the visual analyzer (from the retina to the occipital cortex) and the somatosensory system, which transmits information from the periphery from skin, joint and muscle receptors. These three stabilizing systems overlap each other sufficiently to compensate for the deficiency (partial or complete) of any of them. Dizziness can be a consequence of either physiological arousal or pathological disruption of the activity of any of these three systems.

Physiological dizziness. It develops in cases where there is a discrepancy between the three above-mentioned systems or the vestibular apparatus is subjected to unusual loads to which it was never adapted, for example, with seasickness. The discrepancy between the sensory systems explains the appearance of sensations of motion sickness when driving in a car, dizziness at altitude, and visual dizziness, which most often occurs while watching films with chase scenes; in the latter case, the visual sensation of movement of surrounding objects is not accompanied by corresponding vestibular and somatosensory motor signals. Another example of physiological dizziness is space sickness, caused by active head movement in conditions of weightlessness.

Pathological dizziness. It occurs as a result of damage to the visual, somatosensory or vestibular analyzers. Dizziness due to visual impairment occurs when wearing new or incorrectly selected glasses or with double vision due to suddenly developed paresis of the muscles of the eyeball, in any case as a result of compensatory activity of the central nervous system quickly the dizziness stops. Somatosensory dizziness, more often found in combination with other types of dizziness, usually occurs in the case of peripheral neuropathy with a decrease in the amount of sensitive information necessary to activate central compensatory mechanisms in cases where there is a disturbance in the activity of the vestibular or visual analyzers.

Most often, pathological dizziness develops as a result of a disorder of vestibular functions. Dizziness is often accompanied by nausea, clonic nystagmus, postural instability, and ataxia when walking.

Labyrinth defeats. Lesions of the labyrinth lead to the development of dizziness, which creates the impression of rotation or linear movement of surrounding objects or one’s own body, directed in the direction opposite to the lesion. The fast phase of nystagmus is also directed in the direction opposite to the lesion, but there is a tendency to fall towards the lesion.

In the case of a direct, stationary position of the head, the peripheral parts of the vestibular analyzer generate tonic resting potentials with a frequency that is the same on both sides. With any rotational acceleration, due to the semicircular canals, an increase in potentials occurs on one side and a compensatory weakening on the other. These changes in the activity of potentials are transmitted to the cerebral cortex, where they are summed up with information from the visual and somatosensory analyzers, and a corresponding conscious sensation of rotational movement is developed. After the cessation of prolonged rotation, the peripheral parts continue to respond to inhibition for some time. A decrease in potentials below the resting level on the side with an initial increase in activity and a corresponding increase on the other side are noted. There is a sensation of rotation in the opposite direction. Since there was no true movement of the head, this apparent sensation should be considered dizziness. Dizziness is caused by any lesion in the peripheral part of the vestibular analyzer that changes the frequency of potentials, leading to unequal transmission of signals to the brain stem and ultimately to the cerebral cortex. The symptom can be explained both in the form of inadequate interpretation by the cerebral cortex of pathological signals from the brain stem, and in the form of information about the movement of the head in space. Transient deficiency leads to short-term symptoms. With persistent unilateral damage, central compensatory mechanisms ultimately reduce the symptoms of dizziness. Since compensation depends on the plasticity of connections between the vestibular nuclei and the cerebellum, in patients with damage to the brainstem and cerebellum, the compensatory ability is reduced and symptoms may remain unchanged for an unlimited time. In cases of severe, persistent bilateral lesions, recovery will always be incomplete, despite the fact that cerebellar connections are preserved; Patients with such lesions will feel dizzy constantly.

Acute unilateral damage to the labyrinth occurs when infectious diseases, injuries, ischemia and poisoning with drugs or alcohol. Often it is not possible to establish the etiology of the pathological process and the term acute labyrinth or, preferably, acute peripheral vestibulopathy is used to describe it. It is impossible to make a forecast about the further condition of a patient with first-time attacks of dizziness.

Schwannomas affecting the vestibular nerve (acoustic neuroma) progress slowly and lead to such a gradual decline in labyrinthine function that central compensatory mechanisms usually prevent or minimize vertigo. The most common manifestations are hearing loss and tinnitus. Since dizziness can occur suddenly with damage to the brain stem or cerebellum, accompanying objective and subjective signs will help differentiate them from lesions of the labyrinth (Table 14.1). Sometimes, with acute damage to the vestibulocerebellar tract, dizziness may occur as the only symptom, which makes it difficult to distinguish it from labyrinthopathy.

Repeated unilateral dysfunctions of the labyrinth in combination with objective and subjective signs of cochlear damage (progressive hearing loss and tinnitus) usually occur with Meniere's disease. If there are no hearing symptoms, the term vestibular neuronitis is used to indicate repeated dizziness, which is the only symptom. Transient ischemic attacks in the posterior cerebral basin (vertebrobasilar insufficiency) almost never produce repeated attacks of dizziness without accompanying motor and sensory disorders, dysfunction of the cerebellum, or signs of damage to the cranial nerves.

Table 14.1. Differential diagnosis of peripheral and central vertigo

* In Meniere's disease, the direction of the fast phase changes.

Positional vertigo is aggravated by lying on your side. Benign paroxysmal positional vertigo (BPPV) is especially common. Although these disorders may result from traumatic brain injury, in most cases no precipitating factor is identified. Typically, dizziness goes away on its own within a few weeks or months. Dizziness and accompanying nystagmus have a characteristic latency period, recurrence and termination, which distinguishes them from the less common central positional vertigo (CPV) (Table 14.2), which occurs with lesions of the fourth ventricle.

Positional vertigo should be distinguished from the installation. The latter is caused by movement of the head in space rather than by its position, and is an integral feature of all vestibulopathies, central and peripheral. Since dizziness intensifies with sudden movements, patients try to keep their head still.

Vestibular epilepsy, dizziness associated with the presence of epileptic activity in the temporal lobe, is rare and is almost always closely associated with other manifestations of epilepsy.

Psychogenic dizziness, usually in combination with agoraphobia (fear of large open spaces, crowds of people), is characteristic of patients who are so “out of commission” after an attack of dizziness that they cannot leave their home for a long time. Despite the inconvenience, most patients with dizziness of organic origin strive for active activity. Vertigo should be accompanied by nystagmus. In the absence of nystagmus during an attack, dizziness is most likely of a psychogenic nature.

Examination of patients with pathological vestibular vertigo. The nature of the examination is determined by the possible etiology of the disease. If there is suspicion about the central origin of dizziness (see Table 14.1), a computed tomography scan of the head is indicated. Special attention in this case, attention should be paid to the formations of the posterior cranial fossa. Such an examination is rarely informative in the case of repeated isolated dizziness with no neurological symptoms at the time of examination. BPPV does not require further testing once the diagnosis has been made (see Table 14.2).

Table 14.2. Benign paroxysmal positional vertigo (BPPV) and central positional vertigo (CPV)

a - time between establishing the position of the head and the appearance of symptoms; b - disappearance of symptoms when maintaining the accepted position; c - reduction of symptoms during repeated studies; d - the probability of reproducing symptoms during the examination.

Vestibular tests are used for the purpose of differential diagnosis of dizziness of organic and psychogenic etiology; establishing the localization of the lesion; conducting differential diagnosis of dizziness of peripheral and central origin. The standard test is electronystagmography (ENG) with irritation of the eardrums with warm and cold water(or air) and comparing the frequency of the slow phases of the resulting nystagmus on the right and left. Decreased speed on either side indicates hypofunction (“channel paresis”). A condition in which nystagmus cannot be caused by the action of ice water is defined as “death of the labyrinth.” In some clinics, doctors are able to quantify various elements of the vestibulo-ocular reflex using computerized swivel chairs and accurately record eye movements.

In case of acute dizziness, bed rest should be prescribed, as well as drugs that suppress vestibular activity, such as antihistamines [Meclizine, dimenhydrinate, diprazine], centrally acting anticholinergic drugs (scopolamine), tranquilizers with a GABAergic effect (diazepam). In cases where dizziness continues for more than a few days, most authors recommend walking in order to induce a beneficial effect of central compensatory mechanisms, despite the fact that this may cause some temporary inconvenience for the patient. Chronic dizziness of labyrinthine origin can be treated with a course of systematic exercises that help stimulate compensatory mechanisms.

Preventive measures taken to prevent recurrent attacks of dizziness have varying degrees efficiency. In these cases, antihistamines are usually used. For Meniere's disease, a salt-restricted diet in combination with diuretics is recommended. In rare cases of persistent (4 to 6 weeks) BPPV, a clear improvement, usually within 7-10 days, is noted after performing a special set of exercises.

There are many surgical methods Treatment of all forms of persistent chronic and recurrent dizziness, but they are rarely necessary.

Mixed sensations from the head. This definition is used to describe non-systemic dizziness that is not syncope or true dizziness. In cases where cerebral ischemia or vestibular disorders are of minor severity, a slight decrease in blood pressure or mild vestibular instability, sensations other than overt lightheadedness or dizziness may occur, which could be properly characterized by provocative testing. Other causes of this type of dizziness may include hyperventilation syndrome, hypoglycemia, and somatic manifestations of clinical depression. At neurological examination Similar changes in patients are not detected.

Gait disturbances. In some cases, people with gait disturbances complain of dizziness, despite the absence of systemic dizziness or other pathological sensations from the head. The causes of such complaints may be peripheral neuropathy, myelopathy, spasticity, parkinsonian rigidity, cerebellar ataxia. In these cases, the term dizziness is used to describe the loss of mobility. There may be a feeling of lightness in the head, especially if sensitivity in the lower limbs, and weakened vision; This condition is defined as dizziness due to multiple sensory disorders, and it occurs in elderly people who complain of dizziness only when walking. Motor and sensory disturbances due to neuropathy or myelopathy or weakened vision due to cataracts or retinal degeneration create an increased load on the vestibular analyzer. A less precise but more comforting term is benign instability of aging.

Examination of patients with complaints of dizziness. The most important diagnostic tool is a carefully collected history, aimed at establishing the true meaning of the term “dizziness” in each specific case. Is this condition called fainting? Is it accompanied by a feeling of spinning? If this is confirmed, and no pathological abnormalities are detected during a neurological examination, then appropriate examinations should be undertaken to identify possible reasons cerebral ischemia or damage to the vestibular analyzer.

To identify the source of dizziness, provocative tests are used. Such procedures reproduce the signs of cerebral ischemia or vestibular insufficiency. These reasons are confirmed if dizziness occurs with orthostatic hypotension. Then a Valsalva test is performed, which reduces cerebral blood flow and provokes symptoms of cerebral ischemia.

The simplest provocative test is a quick rotation on a special swivel seat, followed by sudden stop movements. This procedure always causes dizziness, which the patient can compare with his feelings. Intense provoked systemic vertigo may not look like spontaneous symptoms, but soon after the test, when the vertigo subsides, it is followed by a feeling of lightness in the head, which can be identified by the patient as the kind of vertigo that he feels. In such cases, a patient with an initial diagnosis of mixed head sensations is diagnosed with vestibulopathy.

Another way to provoke dizziness is caloric tests. Eardrum irritate with cold water until dizziness occurs; this sensation is then compared with the patient’s complaints. Since visual fixation suppresses the caloric reaction, before conducting a provocative caloric test (as opposed to a diagnostic quantitative thermal test with ENG), you should ask the patient to close his eyes or put on special glasses that interfere with fixing the gaze (Frenzel lenses). Patients with signs of positional dizziness should perform appropriate tests (see Table 14.2). Like provocative caloric tests, positional tests are more sensitive if gaze fixation is eliminated.

The last provocative test requiring the use of Frenzel lenses is vigorous shaking of the head in a supine position for 10 s. If nystagmus develops after shaking has stopped, then even in the absence of dizziness, this indicates a violation of vestibular functions. The test can then be repeated in a vertical position. If, using provocative tests, it has been established that the dizziness is vestibular in nature, carry out the above assessment of vestibular dizziness.

In many patients with anxiety, the cause of dizziness is hyperventilation; however, they may not feel tingling in their hands and face. Patients with dizziness of unknown etiology and absence of neurological. For symptoms, two minutes of forced hyperventilation is indicated. Symptoms of depression (which the patient states are secondary to dizziness) indicate to the physician that depression is more often a cause than a consequence of dizziness.

Damage to the central nervous system can cause all types of dizzy sensations. Therefore, a neurological examination is always necessary, even if the history and provocative tests suggest a cardiac, peripheral vestibular or psychogenic origin of symptoms. Any changes detected during neurological examination should prompt physicians to conduct appropriate diagnostic studies.

Bibliography

Baloh R.W. Dizziness, Hearing Loss and Tinnitus: The Essentials of Neurology. -

Philadelphia: Davis, 1984. Brandt T., Daroff R. B. The multisensory physiological and pathological vertigo

syndromes. - Ann. Neurol., 1980, 7, 195. Hinchcliffe F.R. Hearing and Balance in the Elderly. - New York: Churchill

Livingstone, 1983, sect. II, 227-488. Leigh R. /., Zee D. S. The neurology of Eye Movements. - Philadelphia: Davis,

1984, Chaps 2 and 9. Oosterveld W.I. Vertigo - Current concepts in management. - Drugs, 1985,

The most common complaint a neurologist hears is a feeling of dizziness. But few people know that there are many varieties of it. One of them - non-systemic dizziness. How it differs from other types, the main causes, methods of diagnosing and treating this condition - all this is discussed further in the article.

What is dizziness

First, it’s worth understanding what doctors mean by dizziness. This is the illusion of feeling the environment spin around you or yourself around space. Everyone has experienced this feeling after a long ride on a carousel. But some people mean by this symptom unsteadiness when walking, lightheadedness, heaviness inside the head, a feeling of lightheadedness, swaying.

There is confusion with terms in Russian literature. In some sources you can find the concept of “vertigo”, borrowed from in English. It is used to indicate the illusion of rotation. And “dizziness” is used as a collective concept for all other complaints. This is probably more logical. This article will also use the collective concept of "dizziness" and the term "vertigo".

Types of symptom

There are several types of dizziness. Each of them has different reasons. And the choice of diagnostic and treatment method directly depends on the reasons. The following types of this symptom are distinguished:

1. Non-systemic - typical for diseases not associated with damage to the nervous system (pathologies of the heart and blood vessels, hormonal imbalance, blood diseases).
2. Systemic – develops as a result of dysfunction of the vestibular system, including brain structures.
3. Psychogenic – typical for people with mental neurotic disorders.
4. Mixed - they take part in the development of the symptom various factors, the reason is difficult to find out.

Relevance of the problem

About 5% of people coming to the clinic complain of dizziness. Moreover, at the age of over 65 years, the number increases to 30%. By their complaint, patients most often mean dizziness of a non-systemic nature. A wide variety of sensations can be hidden under this term. Below are just a few of them:

• feeling of instability;
• staggering when walking;
• fainting state;
• feeling of intoxication;
• blurred vision;
• a state as if there would be a loss of consciousness;
• general lightheadedness, weakness.

Unsystematic dizziness is usually one of the first signs of illness internal organs. Moreover, the range of pathologies is extremely wide. Therefore, the relevance of studying non-systemic dizziness is difficult to overestimate.

The main reasons for the development of symptoms

Non-systemic dizziness is a very non-specific symptom. It can be a manifestation of almost any pathology in the body. This article will discuss the most common diseases, which include:

• Hypertension is a persistent increase in blood pressure.
• Chronic debilitating diseases of the body - oncology, heart failure, impaired liver or kidney function.
• Anemia is a decrease in the level of hemoglobin and oxygen in the blood.
• Acute or chronic bleeding.
• Hypoproteinemia is a decrease in protein levels in the blood due to liver or kidney disease.
• Dehydration is dehydration of the body due to intestinal infections and blood loss.
• Vegetovascular dystonia (VSD) is a dysfunction of the autonomic nervous system.

An attack can be caused by any sudden change in blood pressure. Often people experience this symptom when it decreases. There is a syndrome called orthostatic hypotension. The main manifestation is a sharp decrease in pressure after transition from horizontal position to vertical. Many have experienced it more than once after quickly getting out of bed. For a few seconds, it seems as if you are about to lose consciousness. This is an attack of non-systemic dizziness.

The condition quickly returns to normal after the pressure stabilizes.

How various diseases lead to dizziness

Feeling of lightheadedness, unsteadiness when walking and other symptoms of non-systemic dizziness are a consequence of ischemia of the central nervous system. The greatest impact is caused by a lack of oxygenation of the brain. What is it? Ischemia is an insufficient amount of oxygen in an organ. It develops due to a weak inflow of arterial blood or a decrease in the outflow of venous blood.

Ischemia of the brain stem leads to irritation of the vestibular nuclei - clusters of nerve cells that pick up information from the inner ear. Other structures associated with the vestibular system also suffer - the cerebral cortex, cerebellum, subcortical nuclei. Impaired functioning of one or more formations leads to the development of the corresponding symptom.

Symptoms accompanying non-systemic dizziness

An attack of unsystematic dizziness is accompanied by increasing fatigue and general weakness. The patient may have dark vision, ringing or noise in the ears. Sometimes hearing decreases or, conversely, sensitivity to sounds increases. In the medical literature, this condition can be found under the name “hyperacusis”.

Symptoms of concomitant activation of the autonomic nervous system are characteristic. During an intense or prolonged attack, a person feels nauseous. Possible vomiting. The skin turns pale and there is profuse sweating. There is a feeling of unreasonable fear of death, anxiety.

There is a separate type of non-systemic dizziness - disturbance of balance and gait. This group of diseases includes paresis (weakness of the limbs) due to stroke, shuffling gait due to Parkinson's disease, and side deviations and instability due to diseases of the cerebellum. Patients can describe all these conditions in one word – dizziness.

Basic diagnostic methods

Diagnosis of diseases manifested by non-systemic dizziness must be comprehensive. Other symptoms of the disease should be assessed. For example, hypoproteinemia is characterized by swelling on the face and upper torso. Attacks of high blood pressure are accompanied by headaches and flickering spots before the eyes.

Since there are many diagnoses hidden under non-systemic dizziness, consultation with different specialists may be required: neurologist, cardiologist, hematologist, endocrinologist, infectious disease specialist. After a thorough conversation and examination of the patient, additional methods examinations. The following diagnostic methods will help determine the cause:

• Measuring blood pressure - to look for a connection between its changes and the appearance of a symptom.
• General analysis blood - to exclude the presence inflammatory processes in organism.
• A general urine test excludes infection of the genitourinary system.
• Magnetic resonance or CT scan brain - allows you to exclude organic lesion central nervous system.
• Electrocardiogram, echocardiogram (ultrasound of the heart) – detection of cardiac pathology.

Symptom treatment algorithm

To effectively treat non-systemic dizziness, it is necessary to accurately understand the cause of its development. Therapy includes the following aspects:

• Symptomatic treatment is elimination of the attack.
• Etiotropic treatment is an effect on the cause.
• Pathogenetic treatment – ​​influence on the mechanisms of symptom occurrence.

To reduce the severity unpleasant symptom use "Betaserc", psychogenic dizziness "Clonazepam". For the same purposes, drugs are used that improve metabolism in the cells of the nervous system: Cavinton, Piracetam. Patients often experience decreased tone venous wall. Troxevasin and Detralex are effective for increasing it.

Attacks of mild non-systemic dizziness can be stopped with medications traditional medicine. Infusions of motherwort and rosehip herbs are effective. Take one cup of decoction three times a day.

Sometimes, to get rid of an unpleasant symptom, it is enough to breathe fresh air. To reduce the frequency of attacks, aerobic exercise will help: jogging, race walking, morning work-out.

The most important thing in dealing with a symptom is eliminating the cause. The choice of drug directly depends on the underlying disease. In the presence of hypertension, medications that lower blood pressure are prescribed: Enalapril, Nifedipine, Propranolol. If dizziness is caused by heart pathology, antiplatelet agents (Acetylsalicylic acid), Nitroglycerin, and antiarrhythmic drugs (Cordarone) are used.

Drug treatment dizziness is permissible only after consulting a doctor.

Conclusion

Unsystematic dizziness is a multifaceted symptom. It hides radically different diseases. It is extremely difficult to get rid of it on your own. Therefore, if you experience frequent or prolonged dizziness, a consultation is required. family doctor, who, if necessary, will refer you to a more specialized specialist.

G dizziness is one of the symptoms most often encountered in medical practice. Among the reasons for visiting doctors of all specialties, it accounts for 2-5%.

The cause of dizziness is an imbalance of sensory information coming from the main afferent systems that provide spatial orientation - vestibular, visual and proprioceptive. Disturbances in central information processing and the efferent part of the motor act are also of great importance. In addition, pathology of the musculoskeletal system plays a certain role.

In most cases Dizziness is based on one of the following conditions : peripheral vestibular disorders, multiple sensory deficits, psychogenic causes, circulatory disorders in the brain stem, other diseases of the central nervous system, cardiovascular diseases. There may be a combination of several reasons.

Patients can describe a wide variety of sensations as “dizziness,” so the primary diagnostic task is to clarify the nature of the patient’s complaints. Typically, they can be classified into one of four clinical types of vertigo.

Systemic or vestibular vertigo - a feeling of spinning, falling, tilting or swaying of your own body or surrounding objects. Often accompanied by nausea, vomiting, hyperhidrosis, impaired hearing and balance, as well as oscillopsia (the illusion of rapid small-amplitude vibrations of surrounding objects). Systemic vertigo is characteristic of damage to the vestibular system - both its peripheral and central parts.

Pre-fainting state . Patients note a feeling of lightheadedness, impending loss of consciousness, and “lightness” in the head. Often combined with pallor of the skin, palpitations, a feeling of fear, darkening of the eyes, nausea, and increased sweating. The most common causes are heart disease and orthostatic hypotension.

In some cases, by “dizziness” patients mean imbalance . There is instability, unsteadiness when walking, and a “drunk” gait. It is characterized by a combination with paresis, sensitivity disorders, incoordination and oscillopsia. Symptoms caused by imbalance occur when standing and walking and are absent when sitting or lying down.

For psychogenic dizziness observed, in particular, within the framework of anxiety, conversion disorders or depression, characterized by difficult-to-describe sensations that do not correspond to the previous types of dizziness. Patients may complain of “fog,” “heaviness” in the head, a feeling of intoxication, and lightheadedness. It should be noted that similar vague symptoms can occur in the early stages or during the atypical course of organic diseases.

Along with the clinical type of dizziness, its course, the presence of provoking factors and accompanying symptoms. A single episode of systemic vertigo is most often caused by a brainstem or cerebellar stroke. Repeated attacks of dizziness can develop either for no apparent reason or due to certain provoking factors. Spontaneous attacks of dizziness, not provoked by sudden movements of the head, usually serve as a manifestation of arrhythmias, transient ischemic attacks (TIA) in the vertebrobasilar region, Meniere's disease or epileptic seizures. Recurrent attacks of dizziness, in which provoking factors are identified (changes in body position, turning the head), are most often caused by benign paroxysmal positional vertigo (BPPV) or fainting, in particular orthostatic.

Systemic dizziness

Most common cause systemic vertigo is BPPV. The disease usually develops after middle ear infections, traumatic brain injury, or otological surgery. Characteristic are short-term (no more than 1 minute) attacks of systemic dizziness that occur when changing body position. In the pathogenesis of BPPV, the leading role is played by cupulolithiasis - the formation of a clot of calcium carbonate crystals in the cavity of the semicircular tubule, which leads to an increase in the sensitivity of the receptors of the semicircular tubules. To identify positional vertigo, a test is performed Nilena-Barani . From a sitting position, the patient quickly lies on his back, with his head tilted back 45° and turned to the side 45°. The position is maintained for 30-40 seconds. The test is repeated with the head positioned along the midline and when turned in the opposite direction. The development of positional vertigo and nystagmus confirms the diagnosis. Isolated positional nystagmus also speaks in favor of BPPV - when the eyeballs are fixed in the middle position, the nystagmus is vertical-rotatory, with a fast phase directed upward and towards the underlying ear. When looking towards the underlying ear, the fast phase of nystagmus is directed in the same direction, horizontal-rotatory nystagmus, when looking in the opposite direction - vertical, beating upward. There is a characteristic latent period (30-40 seconds) between the start of the test and the onset of nystagmus. The nystagmus fades when the test is repeated. Positional nystagmus is observed inconsistently, more often during an exacerbation. BPPV must be differentiated from central positional vertigo and nystagmus, the most common causes of which include spinocerebellar degenerations, brainstem tumors, Arnold-Chiari malformation, and multiple sclerosis. Central positional nystagmus has no latent period, its duration exceeds 1 minute, the direction of nystagmus can vary, often vertical nystagmus does not fade with repeated examination. To treat BPPV, exercises are used to move calcium carbonate crystals from the semicircular tubule into the cavity of the elliptical sac. Repeated provocation of dizziness is also effective, which leads to its gradual regression due to central compensation.

The combination of systemic dizziness with focal neurological symptoms is characteristic of circulatory disorders in the vertebrobasilar system, as well as tumors of the cerebellopontine angle and posterior cranial fossa. With vertebrobasilar insufficiency, dizziness usually develops suddenly and persists for several minutes, often accompanied by nausea and vomiting. As a rule, it is combined with other symptoms of ischemia in the vertebrobasilar region. Early stages of vertebrobasilar insufficiency may present with episodes of isolated systemic vertigo. Longer episodes of isolated systemic vertigo suggest other diseases, particularly peripheral vestibular disorders. Along with systemic vertigo, TIAs and strokes in the vertebrobasilar region may also present with balance disorders.

Systemic dizziness, nausea and vomiting are the earliest symptoms of ischemia in the anterior inferior cerebellar artery. , leading to the development of infarction of the caudal parts of the tegmentum of the pons (lateral inferior pontine syndrome, Gasperini syndrome). Similar symptoms are observed with cerebellar infarction. Such symptoms require a differential diagnosis with peripheral vestibular disorders. With damage to the cerebellum, in contrast to damage to the labyrinth, the fast component of nystagmus is directed towards the lesion. Its direction changes depending on the direction of gaze, but nystagmus is most pronounced when looking in the direction of the lesion. Fixing the gaze on any object does not affect nystagmus and dizziness. In addition, there is discoordination in the limbs, which is absent when the labyrinth is affected.

Acute systemic dizziness, both isolated and in combination with suddenly developed deafness, is characteristic of infarction of the labyrinth . Deafness caused by labyrinthine infarction is usually irreversible, while the severity of vestibular disorders gradually decreases. A combination of labyrinthine and brainstem infarction is possible.

Systemic dizziness is a cardinal symptom of peripheral vestibular disorders . The most important sign that makes it possible to differentiate peripheral vestibular disorders from central ones is nystagmus - most often horizontal, directed in the direction opposite to the lesion and intensifying when looking in the same direction. Unlike a central lesion, gaze fixation reduces nystagmus and vertigo.

Acute development of systemic dizziness in combination with nausea and vomiting is typical for viral neurolabyrinthitis (vestibular neuronitis, vestibular neuritis). Symptoms usually regress within a few days, in severe cases - after 1-2 weeks. Typically, symptoms develop 1-2 weeks after respiratory infection.

Meniere's disease manifests itself as repeated episodes of severe systemic dizziness, accompanied by decreased hearing, a feeling of fullness and noise in the ear, nausea and vomiting. Within a few minutes, the dizziness reaches its maximum and gradually, over the course of several hours, goes away. Hearing impairment in the early stages of the disease regresses completely and then becomes irreversible. Balance problems may occur for several days after an attack of Meniere's disease. The first attacks of the disease may manifest as isolated systemic dizziness. To confirm the diagnosis, audiometry is performed. A hearing loss of more than 10 dB at two different frequencies is typical. The cause of Meniere's disease is recurrent swelling of the labyrinth, which develops as a result of rupture of the membrane separating the endolymph from the perilymph.

Treatment

Treatment of systemic dizziness is largely determined by its cause; in addition, symptomatic therapy plays an important role. Specific treatment for systemic vertigo is known only for a limited range of diseases. Dizziness as part of vertebrobasilar insufficiency requires prescription antiplatelet agents (acetylsalicylic acid 75-330 mg/day, ticlopidine 500 mg/day), and if symptoms increase - anticoagulants. For viral neurolabyrinthitis, symptomatic therapy is carried out. Efficiency antiviral drugs and glucocorticoids has not been proven.

Treatment of attacks of Meniere's disease is symptomatic. Most effective betahistine . For prevention, a low-salt diet and diuretics are prescribed.

For symptomatic treatment For systemic dizziness, vestibulolytic agents are used that act on vestibular receptors or on central vestibular structures, mainly the vestibular nuclei. The first include antihistamines : meclozine is prescribed 12.5-25 mg orally 4 times a day, promethazine - 25-50 mg orally, intramuscularly or rectally 4-6 times a day. Have a central vestibulolytic effect benzodiazepines : oxazepam - 10-15 mg orally 4 times a day, diazepam - 5-10 mg orally, IM or IV 4-6 times a day. A stimulant is also used histamine receptors betahistine - 8-16 mg orally 2-3 times a day, calcium antagonists (cinnarizine 25-50 mg orally or intramuscularly 4 times a day, flunarizine 10 mg per day in the afternoon).

An effective remedy for the treatment of dizziness is combination drug Fezam , containing 400 mg of piracetam and 25 mg of cinnarizine. The effect of the drug is complex, including vasoactive and metabolic effects. The combination of two components in the drug leads to their enhancement therapeutic effect without increasing toxicity. In addition, Phezam was noted to be more effective and tolerable compared to separate administration of its components.

A number of double-blind, placebo-controlled studies have shown high efficiency Phezam for systemic vertigo caused by both central and peripheral vestibular disorders. The drug also reduced the severity of dizziness during the presyncope state. Fezam is effective in patients with chronic cerebrovascular insufficiency, who showed significant improvement in cognitive functions during treatment. The drug is prescribed 2 capsules 3 times a day for 3-6 weeks.

For relief of nausea and vomiting Prescribe prochlorperazine 5-10 mg orally or intramuscularly 4 times a day, 25 mg rectally once a day or metoclopramide - 5-50 mg orally, intramuscularly or intravenously 4-6 times a day. Thiethylperazine has a central vestibulolytic and antiemetic effect. Prescribe 6.5 mg orally, rectally, subcutaneously, intramuscularly or intravenously 1-3 times a day. A combination of antihistamines and benzodiazepines is effective. To reduce the sedative effect of vestibulolytic drugs, it is recommended to prescribe methylphenidate hydrochloride 5 mg orally 2 times a day (in the first half of the day). Vestibulolytic agents should be prescribed only for acute systemic dizziness. Their use should be as short as possible, since long-term use slows down the process of central compensation of the defect.

The main principle of rehabilitation for peripheral vestibular disorders is stimulation of central compensation by repeated stimulation of vestibular receptors. It is necessary to start rehabilitation as early as possible. When the central vestibular structures are damaged, rehabilitation is much less effective.

Balance imbalance

One of the causes of imbalance is chronic vestibular dysfunction. Characteristically, symptoms intensify in the dark, when it is impossible to compensate for the defect with the help of vision. Oscillopsia is often observed, possibly combined with hearing impairment. The most common cause of chronic bilateral labyrinthine lesions is the use of ototoxic drugs. medicines. Worsening imbalance in the dark is also characteristic of deep sensitivity disorders. The most pronounced imbalances develop in cerebellar disorders. Visual control does not affect the severity of symptoms. With damage to the flocculonodular parts of the cerebellum, oscillopsia is often observed, as well as nystagmus, depending on the direction of gaze. One of the mechanisms of imbalance is also disorders of cervical proprioception. The causes of imbalance caused by changes in the efferent part of the motor act include multiple subcortical infarctions, normal pressure hydrocephalus, Parkinson's disease, chronic subdural hematoma, tumors frontal lobes, as well as a number of medications - anticonvulsants (difenin, phenobarbital, finlepsin), benzodiazepines, neuroleptics (phenothiazines, haloperidol), lithium preparations. Balance imbalance - characteristic symptom tumors of the cerebellopontine angle, temporal bone and posterior cranial fossa. Systemic dizziness is observed much less frequently with this pathology. In the vast majority of cases, concomitant neurological symptoms are detected. In addition, one of the causes of imbalance, observed mainly in the elderly, is multiple sensory insufficiency - a combination of moderate disorders of several sensory functions. Disturbances in the central integration of sensory information play a certain role in its development.

Psychogenic dizziness

Psychogenic dizziness most often occurs as part of agoraphobia, depression and panic attacks, and also, usually in the form of a pre-fainting state, serves as a manifestation of hyperventilation syndrome. With dizziness of an organic nature, it is also possible to develop restrictive behavior, in particular, secondary agoraphobia or reactive depression. In some cases, there is a combination of episodes of organic and psychogenic dizziness, as well as the development of dizziness of mixed origin. Treatment is determined by the nature of the underlying disorder. Psychotherapy is of great importance. It is necessary to explain to the patient the essence of his existing disorders, since often an additional psychotraumatic factor is the belief that he has a life-threatening disease.

The list of references can be found on the website http://www.site

Piracetam + Cinnarizine -

Fezam (trade name)

(Balkanpharma)

The variety of manifestations of dizziness requires a clear classification. After all, people understand dizziness as a variety of sensations; descriptions are often extremely subjective and not always informative. At the same time, there is an extremely large number of pathologies that lead to dizziness; there are features of the perception of dizziness when various structures of the brain or vestibular analyzer are affected. According to the most common classification, dizziness is divided into two types - systemic (true, vestibular) and. This article will discuss systemic vertigo.

Definition

Systemic dizziness can be called such dizziness, which is accompanied by the rotation of the world around a person or a feeling of rotation of the person’s body along a certain axis (clockwise, along the sagittal plane, etc.). At the same time, it is true, systemic dizziness that is often manifested by a number of unpleasant sensations associated with overstimulation of vegetative structures, namely nausea, vomiting, sweating, sometimes impaired coordination of movements, feelings of anxiety and fear. Often, systemic dizziness intensifies when the position of a person’s body or head in space changes.

Reasons and features

There are many causes of systemic dizziness. Among them, the most common (characteristic is fairly short-term, no more than 1-2 minutes, recurrent positional attacks with the development and gradual extinction of nystagmus during provoking maneuvers, McClure-Pagnini), (characterized by relatively long, recurrent attacks, which are accompanied by manifestations characteristic of migraine , such as photo- and phonophobia, etc.), (caused by the herpes virus, often develops after an acute respiratory viral infection, classic peripheral phobia is characteristic, intensifying when gaze fixation is turned off), (characterized by paroxysmal recurrent dizziness, acoustic complaints during an attack are also very characteristic for noise or ringing in the ears, hearing loss, which gradually progresses and becomes persistent). Often, systemic dizziness is a sign of a hemorrhagic stroke, although in isolated form (only dizziness without accompanying symptoms) it is not observed very often. Systemic dizziness also occurs during exacerbation multiple sclerosis, including (develops gradually, also tumors leading to dizziness, more often debut with unilateral acoustic complaints of decreased hearing or, head), occurs after TBI (or), (develops more often after injury), can occur, especially if there is history of an episode of true dizziness.

It is also worth saying that systemic dizziness almost never develops with chronic vascular lesions of the brain (); its acute development against the background of chronic dyscirculatory processes can signal decompensation of the condition (transient ischemic attack or stroke).

Conclusion

In conclusion, it should be noted that isolated systemic dizziness does not always indicate a health or life-threatening condition. However, it requires a careful approach to differential diagnosis and, ideally, timely treatment.