Dizziness

Dizziness is a feeling of imaginary movement of one's own body or surrounding objects.

In practice, the term "dizziness" is interpreted much broader and includes sensations and conditions caused by disturbances in the arrival of sensory information (vestibular, visual, proprioceptive, etc.), its processing and manifested by difficulties in orientation in space.

Dizziness is one of the most frequent reasons for seeking medical help. In an outpatient setting, 2-5% of patients present dizziness complaints. The frequency of dizziness complaints increases with age and reaches 30% or more in persons over 65 years of age. According to Lopez-Gentili et al. (2003), of 1,300 patients who sought medical help for vestibular disorders, systemic dizziness occurred in 896 (68.9%); in others, vertigo was non-systemic, associated with psychogenic disorders, and less often with syncopal conditions. More than half of patients with systemic dizziness had a positional character, and in a third of cases it tended to repeat.

[1], [2], [3], [4], [5], [6], [7]

Causes of dizziness

The mechanism of ensuring the maintenance of equilibrium is one of the oldest, acquired by man in the process of evolution. Ensuring the balance is achieved by integrating the activity of the vestibular, visual, proprioceptive and tactile sensory systems, close connections with other structures of the brain, in particular, subcortical formations and the bark of the cerebral hemispheres.

The vestibular analyzer has a very complicated neurochemical organization. The leading role in the transmission of information from the receptors of the semicircular canals is played by histamine, which acts on histamine H ₁ and H ₃ receptors (but not H ₂ receptors, mainly located in the gastrointestinal mucosa). Modulating effect on histaminergic neurotransmission is provided by cholinergic transmission. Acetylcholine provides the transfer of information from the receptors to the lateral vestibular nuclei, as well as to the central parts of the analyzer. Existing experimental data suggest that due to the interaction of choline and histaminergic systems, vestibulo-vegetative reflexes are realized. Vestibular afferentation to the medial vestibular nucleus is provided by both histamine and glutamatergic routes. In addition, GABA, dopamine, serotonin, and some neuropeptides play an important role in the modulation of ascending impulses.

Mechanisms of vertigo development are extremely diverse, which is due to the possibility of damage to various parts of the nervous system in general and the vestibular analyzer in particular. The main cause of systemic vertigo is the damage to the peripheral part of the vestibular analyzer (semicircular tubules, vestibular nerve, vestibular ganglia) due to degenerative, toxic, traumatic processes. Relatively rarely, the leading mechanism of vertigo development is acute ischemia of these formations. The defeat of higher structures (brain stem, subcortical structures, white matter and cortex of the large hemispheres) is usually associated with vascular pathology (arterial hypertension, atherosclerosis), traumatic, degenerative diseases (Parkinsonism, multisystem degeneration, etc.).

Causes of dizziness are manifold: Ménière's disease, vestibular neuronitis, benign postural vertigo, vertebrobasilar ischemia, the influence of ototoxic drugs, labyrinthitis, destructive lesions of the middle ear (cholesteatoma), neuroma of the auditory nerve, herpetic infection, obstruction of the Eustachian tube, syphilis.

[8],

Benign positional vertex

It is provoked by the movement of the head (often this happens when the patient turns his head in bed) and lasts for a few seconds. This condition is often observed after a head injury, which may be due to damage to the elliptical sac ("darts") in the vestibular apparatus. Provocation test: put the patient on the couch, ask him to turn his head to the side towards the doctor. If you keep this position of the head, quickly put the patient on his back, while the head is held 30 ° below the level of the couch and remains in this position for 30 seconds. Nystagmus with a benign positional vertex has a circular character, and its movements "beat" in the direction of the ear on which the patient's head lies. Nystagmus begins after a latent period lasting for a few seconds, and stops after 5-20 seconds; Nystagmus becomes weaker when the test is repeated, but is accompanied by a vertigo. If any of the signs are missing, look for the central cause of dizziness. This is a self-limiting disease.

[9], [10], [11], [12]

Vestibular neuronitis

The disease occurs after a febrile condition in adults, usually in the winter, and is probably associated with a viral infection. In such cases, sudden vertigo, vomiting and prostration are caused by the movement of the head. Treatment is symptomatic (eg, cyclizine 50 mg every 8 hours). Recovery comes in 2-3 weeks. The disease is difficult to differentiate from the viral labyrinthitis.

Ménière's disease

At the heart of the disease is the expansion of the endolymphatic spaces of the membranous labyrinth, which leads to paroxysms of vertigo lasting up to 12 hours with prostration, nausea and vomiting. Attacks of the disease tend to happen as if by "bundles" with complete remission between them. There is a noise in the ears and progressive sensory-neural deafness. Acute attack of the vertigo in such cases, stop symptomatically (cyclizin 50 mg every 8 hours). Betagistin 8-16 mg every 8 hours inside gives less predictable results, but it should also be tried to appoint a patient. The operative decompression of the endolymphatic sac can rid the vertigo, prevent the progression of the disease and preserve the ability to hear. Labyrinthectomy relieves vertigo, but causes complete bilateral deafness.

What causes dizziness?

Classification of dizziness

Isolate systemic (vestibular) and non-systemic dizziness; to the latter include disorders of balance, pre-stupor states, as well as psychogenic dizziness. In some cases, the term "physiological dizziness" is justified.

Systemic dizziness is pathogenetically associated with direct damage to the vestibular analyzer. Depending on the level of its damage or irritation, peripheral and central systemic dizziness is isolated. In the first case, the disease is caused by the damage directly to the semicircular canals, vestibular ganglia or nerves, in the second - to the vestibular nuclei of the cerebral trunk, the cerebellum or their connections with other structures of the central nervous system. Within the system it is possible to isolate proprioceptive dizziness (sensation of passive movement of one's own body in space), tactile, or tactile (sensation of movement of the support under the feet or hands, rocking on the waves, failing or lifting the body, swinging forward-backward, right-left, down, fluctuation of the soil - "walking like a bump") and visual (sensation of translational movement of objects of visible environment).

Inconsistent dizziness:

• Balancing disorders are characterized by a sense of instability, difficulty walking or maintaining a certain posture, possibly increasing unpleasant sensations when performing actions that require a clear coordination of movements. At the heart of the imbalance is the mismatch of the activity of the vestibular, visual and proprioceptive sensory systems that occurs at different levels of the nervous system.
• The pre-mental state is distinguished by a feeling of faintness, the proximity of loss of consciousness, and the true sense of rotation of the sick or surrounding world is absent.
• Psychogenic dizziness is seen in anxious and depressive disorders.

Physiological dizziness occurs with excessive irritation of the vestibular apparatus. It is observed in the case of a sudden change in the speed of motion (motion sickness), with prolonged rotation, observation of moving objects, being in a state of weightlessness, etc. It enters the motion sickness syndrome (seasickness, kinetosis).

In a number of patients, a combination of manifestations of both systemic and non-systemic dizziness with different manifestations of concomitant emotional and vegetative disorders is observed.

With non-systemic vertigo, in contrast to the systemic, there is no sensation of movement of the body or objects. Systemic dizziness (vertigo) can be peripheral (vestibular) or central origin (VIII pair of cranial nerves or brain stem, its vestibular nuclei, medial oblong fasciculus, cerebellum, pre-spinal cord). Vertigo of vestibular origin, often very harsh. It can be accompanied by nausea and vomiting, loss of hearing or noise in the ears, and nystagmus (usually horizontal). With vertigo of central origin, which usually does not manifest itself so sharply, hearing loss and noise in the ears are noted less often. Nystagmus can be horizontal or vertical.

Symptoms of dizziness

[13], [14], [15], [16], [17],

Inspection of the patient for dizziness

Carefully examine the head, neck and check the condition of the cranial nerves. It is necessary to perform tests for the safety of the cerebellar function, check the tendon reflexes, perform a Romberg test (positive if the balance deteriorates with closed eyes, which may indicate a pathological positional feeling in the joints of the joints or associated with vestibular disorders). It is necessary to check whether there is nystagmus.

Diagnosis of dizziness

Tests

These are audiometry, electrostemagmography, stem auditory evoked reactions (potentials), calorimetric assay, CT studies, electroencephalography and lumbar puncture.