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.
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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.
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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.
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?