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Nasretdinova M. T., Karabaev H. E., Samarkand Medical Institute, Department of Otorhinolaryngology, the city of Samarkand Uzbekistan. Tashkent Pediatric Medical Institute Department of children's Otorhinolaryngology, dentistry course Tashkent Uzbekistan E-mail: [email protected]
VESTIBULAR NEURONITIS - THE PROBLEM OF SYSTEMIC DIZZINESS
Abstract. The Vestibular Neuritis is often mistakenly diagnosed pathology manifested by a sudden acute systemic dizziness, nausea, vomiting, unsteadiness when walking and peripheral nystagmus. The vestibular Neuritis is a quite rare pathology, which may cause diagnostic difficulties for physicians of different specialties. As the diagnosis of "vestibular neuritis" is primarily a "diagnosis of exclusion", it is necessary to know peculiarities of clinical picture, course and differential diagnosis with other similar netalogue. The diagnosis of the disease requires the joint and coordinated work of medical specialists: neurologists, ENT, specialists of functional and laboratory diagnostics and laboratory services. Due to the low awareness of this disease doctors of different specialties often make mistakes in diagnosis and treatment.
Keywords: vertigo, vestibular neuritis, ischemic stroke in the vertebral-basilar pool.
Vestibular neuronitis (VN) or sharp peripheral ves-tibulopatia is this disease of vestibular vehicle, that does not threaten to life of man. First clinical presentation of VN was described by Eric Ruttin in 1909, and a term is inculcated in 1949 by Dix and Hallpike. The met of VN is 3.5 case on 100000 persons [1]. Vestibular neuronitis (VN) or acute peripheral vestibulopathy is a disease of the vestibular apparatus that does not threaten human life. The age of onset of the disease is different, but more often it debuts within 30 to 60 years [2; 3]. The etiology is not entirely clear. The cause of the disease is associated with selective inflammation (viral or infectious-allergic Genesis) of the vestibular nerve, as indicated by the results of pathomorphological studies[1; 4]. Studies have shown serological signs of recent upper respiratory infections caused by hepatitis a virus, influenza virus, adenovirus, as well as infections caused by herpes simplex, cytomegalovirus, Ep-stein-Barr virus, rubella and parainfluenza [3]. Herpes simplex virus type 1 was isolated in 2/3 of cases in vestibular ganglion autopsy by PCR [3; 4]. The histological pattern of the vestibular nerve in LN is similar to that of the nerve in herpes zoster [4]. Much less common is the defeat of the lower branch of the vestibular nerve. The pathological picture is characterized by a decrease and degeneration of the vestibular nerve fibers, and sometimes changes in the scarp node [3].
The main complaints of a patient with VN are:
1. Incessant rotational vertigo.
2. Imbalance at rest and when walking with a tendency to fall towards defeat.
3. Nausea and vomiting.
For vestibular neuronitis characterized by monophasic course, when clinical symptoms develop acutely or subacutely and most pronounced from a few days to several weeks.
The patient should be specifically interviewed about the presence of neurological symptoms such as impaired speech, vision, severe headache, numbness or severe weakness in the limbs. These symptoms are typical for lesions of the brain stem and cerebellum and indicate a Central vestibular pathology, primarily a stroke.
In a clinical examination of a patient with VN pathognomonic for this disease are the following symptoms:
1. Sp N. Most often there is a horizontal nystagmus in the direction of a healthy ear with a rotator component, in which the upper pole of the pupil is twisted also in the direction of a healthy ear. This type of SpN is observed in the combined lesion of the upper and lower vestibular nerves, which explains the absence of a vertical component in SpN by the defeat of the receptors of both vertical channels [2].
2. The slope of the subjective visual vertical in the direction of the patient's ear. This occurs as a result of asymmetry of the tone of the vestibular nuclei with a unilateral violation of afferent impulses from the vertical channels, or from the otolith receptor, or from both of them with a joint lesion.
3. Positive head turn test (Halmagi test). During the fixation of the patient's gaze on the target with a sharp low-amplitude turn of the patient's head in the horizontal plane in the
Section 2. Medical science
affected direction, a corrective saccade is fixed, which returns the patient's eyes to the target after the turn.
4. Deviation in stato-coordination and stato-kinetic tests. In a simple pose Romberg, sensitized pose Romberg, walking in a straight line there is a deviation in the direction of the affected maze. In the finger-nose, finger-index and the BarreFisher sample, a harmonious deviation of the hands towards the affected labyrinth can be detected.
5. In oculomotor tests, such as the saccade test and smooth tracking, disturbances can be detected, especially when the target moves in a horizontal plane in the direction opposite to the affected ear.
6. There is no change in hearing. In the case of a combination of the described symptoms and unilateral acute hearing loss, the detected pathology is called labyrinthitis.
Of the diagnostic tests used: The caloric test.
1.With HF, Hypo - or areflexia is observed from the affected labyrinth. However, it should be taken into account that the caloric test assesses the functional state of only the vestibular-ocular reflex from the ampullary receptor of the horizontal semicircular channel at low frequencies (0.003 Hz) and does not reveal pathology in an isolated lesion of the lower vestibular nerve (with lower HF).
2. vHIT. A characteristic feature of HV is the asymmetry of gain more than 8% due to its reduction from the affected side and the presence of explicit and hidden corrective saccades [1; 2]. With the help ofvHIT, the functional state of not only horizontal semicircular channels, but also vertical ones is investigated, which allows to assess whether both branches of the vestibular nerve are affected or isolated upper (upper) or lower (lower) VN.
3. Vestibular myogenic evoked potentials (VMVP). VMVP assesses the function of otolith sacculus and utriculus receptors. VN is divided into 3 stages: symptomatic, pathogenetic therapy and vestibular rehabilitation
4. In oculomotor tests, such as the saccade test and smooth tracking, abnormalities can be detected, especially when the target is moving in a horizontal plane in the direction opposite to the affected ear.
5. Hearing doesn't change. In the case of a combination of the described symptoms and unilateral acute hearing loss, the revealed pathology is called labyrinthitis.
Diagnostic tests used:
Calorie test. In HF, Hypo-or areflexia from the affected labyrinth is observed. However, it should be taken into account that the calorie test evaluates the functional state of the vestibular-ocular reflex only from the ampullary receptor of the horizontal semicircular channel at low frequencies (0.003
Hz) and does not reveal pathology in isolated lesions of the Lower vestibular nerve (with lower HF).
2. vHIT. A characteristic feature of VH is the asymmetry of the gain of more than 8%, due to its decrease on the affected side and the presence of explicit and hidden corrective saccades [l; 2]. The functional state of not only horizontal semicircular channels, but also vertical channels is investigated with the help of vhit, which allows to assess whether both branches of the vestibular nerve are affected or the upper (upper) or lower (lower) VN are isolated.
3. Vestibular myogenic evoked potentials (VMVP). VMVP evaluates the function of otolith sacculus and utriculus receptors. VN is divided into 3 stages: symptomatic, pathogenetic therapy and vestibular rehabilitation.
Symptomatic therapy, primarily, is the use of vestibular suppressants to reduce vegetative symptoms, which include antihistamines, antiemetic agents and benzodiazepines.
Pathogenetic therapy is the appointment of high doses of corticosteroids with a gradual decrease in dose. The effectiveness of corticosteroids in NR was confirmed in several randomination kontroliruemykh studies [3].
Vestibular rehabilitation is an individual course of special physical exercises, compiled by a doctor and regularly performed by the patient under his control. First and foremost, uses exercises for adaptation based on the stimulation and consolidation of the responsiveness of the vestibular system to rotation of the head with the defeat of one of the mazes and, consequently, the vestibular-ocular reflex on the affected side through biofeedback in the form of slippage of the visual image from the retina by rotating the head. Another form of vestibular gymnastics are exercises on substitution, under which the patient is using duplicate Vestibulo-ocular reflex of the oculomotor system, such as smooth pursuit and saccades [3; 6]. Subsequently, the complex is expanded through the use of exercises that duplicate the most commonly used movements in the daily life of the patient, which helps him to quickly return to normal life.
Conclusion
VN is an acute disease of the peripheral vestibular system, manifested by rotational dizziness, nausea, vomiting, coordination disorders. The clinical picture is caused by acute unilateral lesion of the vestibular nerve and vestibular receptors. The main diagnostic criteria are the absence of hearing loss and neurological symptoms, the presence of peripheral nystagmus, a positive test of head rotation. Treatment consists in the appointment of vestibular suppressants and corticosteroids in the acute period and an individual course ofvestibular rehabilitation.
References:
1. Brandt T., Dieterich M., Strupp M. Vertigo and dizziness - common complaints. indedition. - London: Springer, 2013.
2. Gioacchini F. M., Alicandri-Ciufelli M., Kaleci S. et al. Prevalence and diagnosis ofvestibular disorders in children: a review. Int J Pediatr Otorhinolaryngol 2014; 78: 718-24.
3. Arbusow V, Derfus T., Held K. et al. Latency of herpes simplex virus type-1 in human geni-culate and vestibular ganglia is associated with infiltration of CD8+ T cells. J Med Virol 2010; 82(n): 1917; 20.
4. Esaki S., Goshima F., Kimura H. et al. Auditory and vestibular defects induced by experi-mental labyrinthitis following herpes simplex virus in mice.Acta Otolaryngol 2011; 131 (7): 684-91.
