Vestibular ataxia is a violation of the coordination of movements and the ability to maintain a pose associated with damage to the vestibular apparatus at any level. Vestibular ataxia is manifested by shakiness in standing and sitting positions, as well as when walking. It is accompanied by systemic dizziness and nystagmus; nausea and vomiting, vegetative disorders and symptoms characteristic of the pathological process that caused the development of vestibular ataxia can be observed. Diagnosis of the latter is the main purpose of examination of patients with vestibular ataxia. Treatment is symptomatic. The main therapy should be aimed at the causal disease.
R27.0 Unspecified ataxia
The orientation of the body in space in the human body is provided by the vestibular analyzer. It is responsible for determining the position and nature of the movement of the body and its individual parts, provides the perception of gravity. Any change in the position of the body in space is perceived by vestibular receptors — the so-called hair cells located in the labyrinth of the inner ear. From the receptors, nerve impulses go along the vestibular nerve, which, together with the auditory nerve, enters the VIII pair of cranial nerves. Further, the impulses enter the vestibular nuclei of the medulla oblongata, where information synthesis takes place and motor reactions are controlled. From the vestibular nuclei, regulating nerve impulses diverge into various parts of the central nervous system: the cerebellum, spinal cord, reticular formation, autonomic nerve nodes, oculomotor nuclei and the cerebral cortex. They provide redistribution of muscle tone and reflex reactions to maintain balance.
Vestibular ataxia is associated with damage to any structure of the vestibular analyzer. Most often it is caused by damage to hair cells as a result of an inflammatory process in the inner ear — labyrinthitis. In turn, labyrinthitis can occur as a result of ear injury or during the transition of infection from the middle ear cavity with acute otitis media, chronic purulent otitis media, complicated aerotitis. The death of hair cells, leading to the development of this disease, may occur as a result of invasive growth of an ear tumor or toxic effects of secretions of ear cholesteatoma. Paroxysmal vestibular ataxia accompanies Meniere’s disease.
Less often, vestibular ataxia is caused by a lesion of the vestibular nerve, which can be infectious, tumor (with neurinoma of the auditory nerve) or toxic (when taking ototoxic drugs). Vestibular neuritis is often associated with a viral infection: ARI, herpes virus, influenza, etc.
Vestibular ataxia can occur when the vestibular nuclei located in the medulla oblongata are affected. Thus, vestibular ataxia occurs as a result of compression of the medulla oblongata in individuals with craniovertebral anomalies (Chiari anomaly, Atlas assimilation, platybasia), with brain stem tumors, encephalitis and arachnoiditis of the posterior cranial fossa, demyelinating diseases (multiple sclerosis, acute encephalomyelitis). Vestibular ataxia is a clinical manifestation of chronic brain stem ischemia caused by a violation of vertebral-basilar circulation in connection with vertebral artery syndrome, atherosclerosis, hypertension, cerebral vascular aneurysm. In acute circulatory disorders of this area (TIA, ischemic or hemorrhagic stroke), vestibular ataxia is also observed.
Vestibular ataxia is often observed after a traumatic brain injury. At the same time, it can be caused both by the direct impact of a traumatic factor on the nuclei and roots of the vestibular nerve, and with concomitant circulatory disorders (post-traumatic vascular spasm).
Vestibular ataxia manifests itself both in movement (dynamic ataxia) and in a standing position (static ataxia). Vestibular ataxia differs from other types of ataxia by the dependence of its severity on the turns of the head and trunk. Increased ataxia when turning the head, eyes and torso make patients avoid such movements or perform them smoothly and slowly. Visual control of movements partially compensates for violations of the function of the vestibular analyzer, therefore, with closed eyes, the patient feels more insecure and the manifestations of vestibular ataxia increase.
Lesions of the vestibular analyzer are most often unilateral in nature. In such cases, vestibular ataxia is manifested by shakiness when walking with a deviation of the body constantly in the same direction — in the direction where the lesion is localized. In the standing or sitting position, the patient also deviates to the affected side. This symptom is easily detected in the Romberg pose and when the patient tries to walk several steps smoothly with his eyes closed.
A characteristic feature is the presence of systemic dizziness, in which the patient experiences a feeling of rotation of his own body or movement of surrounding objects around him. Dizziness can be noted even in the supine position with closed eyes. In such cases, it is usually accompanied by a sleep disorder with difficulty falling asleep. The activation of vestibular-visceral nerve connections leads to the fact that dizziness in vestibular ataxia is often accompanied by nausea and vomiting. Vestibulo-vegetative interactions cause the appearance of vegetative reactions: pallor or redness of the face, feelings of fear, tachycardia, pulse lability, hyperhidrosis.
In most cases, vestibular ataxia is accompanied by horizontal nystagmus, the direction of which is opposite to the side of the lesion. Bilateral nystagmus is possible. When the vestibular nuclei are affected, vertical nystagmus with a rotatory component may be noted. If there is a violation at the level of the peripheral vestibular analyzer, the nystagmus increases with head turns, but with repeated turns, the nystagmus may decrease. In the presence of craniovertebral anomaly, vestibular ataxia is accompanied by nystagmus, which increases with head tilts.
Pathology can be detected by the characteristic complaints of the patient and during his neurological examination. To differentiate vestibular ataxia from other types of ataxia (cerebellar, sensory, cortical), as well as to establish the level and nature of damage to the vestibular analyzer, the neurologist needs the results of instrumental examination methods: REG, Echo-EG, EEG, CT and MRI of the brain, X-ray examinations. Since vestibular ataxia as a syndrome occurs in many diseases of the central nervous system, the most important point in clinical neurology is to identify the cause of its development.
REG allows you to obtain indirect data on the state of blood circulation of the brain. If necessary, it can be supplemented with angiography or MRI angiography of cerebral vessels. With the help of Echo-EG, the state of the cerebrospinal fluid system is assessed. The displacement of the Echo indicates the presence of a volume formation (tumor, hematoma or abscess of the brain), the presence of which may be associated with disease. EEG is used to analyze the bioelectric activity of the brain. CT and MRI can diagnose bulky formations and demyelinating processes, which can also be the cause of vestibular ataxia. If a craniovertebral anomaly is suspected, an X-ray of the spine in the cervical region and an X-ray of the skull are performed.
The study of the vestibular analyzer in patients with vestibular ataxia is carried out by a vestibulologist, and in his absence, a neurologist or an otolaryngologist. The examination includes vestibulometry, stabilography, videoculography or electronystagmography, as well as a caloric sample. Since vestibular ataxia is often combined with hearing impairment (hearing loss), a hearing study is carried out: threshold audiometry, tuning fork examination, electrocochleography, promontory test, etc.
Therapy of vestibular ataxia is primarily aimed at curing the disease that caused it. In the presence of an infectious lesion of the ear, antibiotic therapy, washing of the middle ear, sanitizing surgery, labyrinthotomy, etc. are carried out. measures aimed at eliminating the purulent focus. If vestibular ataxia is caused by vascular disorders, then drugs that improve blood supply to the brain are used. In severe cases of craniovertebral anomalies, their surgical correction is performed. Appropriate therapy is necessary in the presence of bulky formations, encephalitis, arachnoiditis.
Disease itself is subject to symptomatic treatment, usually consisting in taking drugs that improve the metabolism and functioning of nerve cells: piracetam, gamma-aminobutyric acid, ginkgo biloba, vitamins of group B. In addition, patients are recommended a special complex of exercise therapy aimed at training coordination of movements and strengthening muscles.