Vertebral Basilar Insufficiency - Symptoms

The patient complains of attacks of systemic or non-systemic dizziness, which are accompanied by a balance disorder. Complaints also include nausea and vomiting, tinnitus, and hearing loss. Attacks are often recurrent in nature, associated with fluctuations in blood pressure, head turns and tilts, and stress.

Vestibular dysfunction in vertebrobasilar circulatory insufficiency is manifested by a wide range of various clinical manifestations of peripheral cochleovestibular syndromes. Attacks of systemic rotational vertigo are characteristic, which occur in elderly patients more often against the background of arterial hypertension and combination with atherosclerosis, and in young patients - against the background of vegetative-vascular dystonia; attacks are accompanied by acute unilateral sensorineural hearing loss, occurring as an inner ear infarction. Attacks of vertigo can be isolated or combined with other otoneurological manifestations and hearing loss, and sometimes as an attack of Meniere's disease.

The onset of the disease is characterized by the development of an acute attack of dizziness of a systemic nature with nausea, vomiting, imbalance, and sometimes short-term loss of consciousness. Before the development of an attack of dizziness, some patients note the appearance of noise and hearing loss, often more pronounced on one side; in some cases, hearing impairments are expressed insignificantly and are characterized by patients as a violation of speech intelligibility. Relapses of dizziness attacks are associated with an increase or fluctuations in blood pressure, turning the head and body, and a change in body position.

An analysis of observations and literature data allowed us to conclude that there are anatomical and physiological prerequisites against which peripheral cochleovestibular syndrome is formed. These include anomalies of the vertebral arteries, such as asymmetry of diameters, hypoplasia of the vertebral artery on the right or left, and the absence of the posterior communicating arteries.

According to ultrasound methods of studying blood flow in the main arteries of the head (ultrasound Doppler, duplex scanning, transcranial Doppler and magnetic resonance angiography), structural changes in the vertebral arteries are characterized by deformations (usually unilateral), hypoplasia, and in isolated cases, stenosis and occlusion. The identified changes in the structure of these arteries cause chronic blood flow insufficiency in the vertebral-basilar system,

Deformations and stenosis of the internal carotid arteries also occur in a significant number of cases, which indicates the frequency of combination of lesions of the vertebral and internal carotid arteries in the group of patients with arterial hypertension. Vestibular dysfunction in combination with mild hearing impairment (noise and congestion in the ear) in patients with bilateral lesions of the internal carotid arteries (occlusion and critical stenosis) are the only clinical manifestation of carotid basin lesions.

Since patients with vestibular dysfunction of vascular genesis often suffer from arterial hypertension and atherosclerosis, it is important to study their blood pressure and the state of central hemodynamics.

Most often, patients with peripheral cochleovestibular syndrome have a “mild” form of arterial hypertension, relatively stable central hemodynamics; at the same time, a decrease in the stroke volume and minute volume of blood is observed, which contributes to circulatory insufficiency in the vertebrobasilar system.

Cochleovestibular disorders in vertebrobasilar vascular insufficiency.

Causes and pathogenesis. The causes of vertebrobasilar vascular insufficiency are spondyloarthrosis and osteochondrosis of the cervical spine, pathological tortuosity, loop formation, compression, atherosclerotic narrowing of the vertebral arteries, irritation of the sympathetic plexus of the vertebral arteries by osteophytes in the openings of the transverse processes of the cervical vertebrae, etc. All these factors ultimately lead to degenerative changes and thromboembolism of the vertebral arteries, as well as to a reflex spasm of the terminal vessels extending from the basilar artery, including branches of the labyrinthine artery. The above factors are the cause of ischemic phenomena in the VN and the development of a complex of cochleovestibular disorders, similar in their clinical picture to Meniere's syndrome.

Labyrinthine angiovertebral syndrome manifests itself in the following clinical forms:

1. erased forms with undefined subjective symptoms, characterized by a gradual, year after year, increase in hearing loss (unilateral or bilateral), the appearance of interlabyrinthine asymmetry first of a peripheral and then of a central type, an increase in the sensitivity of the vestibular apparatus to accelerations and optokinetic stimuli; over time, this form progresses to spontaneous vestibular crises and the neurological stage of vertebrobasilar vascular insufficiency;
2. frequent sudden Meniere-like crises that occur in the absence of any cochleovestibular disorders; gradually, with this form, unilateral or bilateral hearing loss occurs in the form of impaired sound perception and hypofunction with interlabyrinthine asymmetry of the vestibular apparatus;
3. sudden attacks of spatial discoordination with brief periods of clouding of consciousness, loss of balance and unpredictable falls;
4. persistent, prolonged vestibular crises (from several hours to several days), combined with boulevard or diencephalic disorders.

Symptoms of labyrinthine angiovertebral syndrome are determined by its form. In latent forms, by the end of the working day there is tinnitus, mild directed (systemic) dizziness, unstable balance when walking down the stairs or when turning the head sharply. In the early stages of the disease, when angiodystonic processes affect only the structures of the inner ear, and the blood supply to the brainstem is compensated, compensatory-adaptive processes prevail in the patient's condition, allowing him to recover within two or three days of rest. When vascular disorders spread to the brainstem, which contains the auditory and vestibular centers, the processes of cochlear and vestibular decompensation begin to prevail, and the disease passes into the stage of persistent labyrinthine dysfunctions and transient neurological symptoms. At this stage, in addition to the interlabyrinthine asymmetry revealed by provocative vestibular tests, unilateral hypoacusis of the peripheral type and then of the central type arises and progresses, and then with the involvement of the other ear.

The occurrence of persistent and prolonged vestibular attacks is caused not only by angiodystonic crises in the vertebral-basilar vascular system, but also by gradually occurring organic changes in the ear labyrinth, similar to those that occur in stages II and III of Meniere's disease (fibrosis of the membranous labyrinth, narrowing of the endolymphatic spaces, up to their complete desolation, degeneration of the vascular strip, etc.), which lead to chronic irreversible hydrops of the labyrinth and degeneration of its hair (receptor) cells. Two well-known syndromes are associated with damage to the cervical spine - Barre - Lieou.

Barre-Lieou syndrome is defined as a neurovascular symptom complex that occurs with cervical osteochondrosis and deforming spondylosis of the cervical spine: headache, usually in the occipital region, dizziness, loss of balance when standing and walking, noise and pain in the ears, visual and accommodation disorders, neuralgic pain in the eye area, arterial hypothesis in the retinal vessels, facial pain.

Bertschy-Roshen syndrome is defined as a neurovegetative symptom complex in patients with diseases of the upper cervical vertebrae: unilateral paroxysmal headache and paresthesia in the facial area, tinnitus and photopsies, scotomas, difficulty in head movements. The spinous processes of the upper cervical vertebrae are sensitive to palpation. When tilting the head to one side, the pain in the neck on the other side increases. X-ray picture of osteochondrosis, traumatic injury or other type of lesion (for example, tuberculous spondylitis) of the upper cervical vertebrae.

The diagnosis of labyrinthine angiovertebral syndrome is based on the results of X-ray examination of the cervical spine, REG, Doppler sonography of the cerebral vessels, and, if necessary, brachiocephalic angiography. Of great importance are the patient's survey data and complaints. The overwhelming majority of patients suffering from labyrinthine angiovertebral syndrome note that when turning their heads they experience or intensify dizziness, feel nauseated, weak, and unsteady when standing or walking. Such patients experience discomfort when watching movies, television programs, or riding in public transport. They do not tolerate sea and air pitching, drinking alcohol, or smoking. Vestibular symptoms are of primary importance in the diagnosis of labyrinthine angiovertebral syndrome.

Dizziness is the most common symptom, observed in 80-90% of cases.

Cervical positional nystagmus usually occurs when the head is thrown back and turned to the side opposite to the vertebral artery in which more pronounced pathological changes are observed.

Impaired coordination of movements is one of the typical signs of vertebrobasilar vascular insufficiency and depends not only on the dysfunction of one of the vestibular apparatus, but also on vestibulocerebellar-spinal discoordination caused by ischemia of the brainstem, cerebellar and spinal motor centers.

Differential diagnosis of labyrinthine angiovertebrogenic syndrome is very complex, since, unlike Meniere's disease, which is typically characterized by the absence of visible causes, vertebrogenic labyrinthine pathology may be based, in addition to the above causes, on many neck diseases, such as injuries to the cervical spine and spinal cord and their consequences, cervical osteochondrosis and deforming spondyloarthrosis, cervical ribs, giant cervical processes, tuberculous spondylitis, rheumatic lesions of the joints of the spine, cervical sympathetic ganglionitis, various developmental anomalies of the skull, brain and spinal cord, such as Arnold-Chiari syndrome (a hereditary syndrome caused by brain anomalies: downward displacement of the cerebellum and medulla oblongata with disorders of the dynamics of the cerebrospinal fluid and hydrocephalus - and manifested by occlusive hydrocephalus, cerebellar disorders with ataxia and nystagmus, signs of compression of the brainstem and spinal cord (cranial nerve palsies, diplopia, hemianopsia, attacks of tetanoid or epileptiform seizures, often anomalies of the skull and cervical vertebrae), etc. Such pathological processes as labyrinthine angiovertebral syndrome and space-occupying processes in the posterior cranial fossa, lateral cistern of the brain, and pyramid of the temporal bone should not be excluded from differential diagnosis. The presence of chronic purulent otitis media should also be considered as a possible cause of chronic limited labyrinthitis or labyrinthosis, possibly also cystic arachnoiditis MMU with compression syndrome. It is also necessary to consider the possibility of the presence of such diseases as syringobulbia, multiple sclerosis, various cerebral vasculitis, which often occur with atypical forms of "labyrinthopathy".

Treatment of patients suffering from labyrinthine angiovertebral syndrome is complex, pathogenetic - aimed at restoring normal blood supply to the inner ear, symptomatic - at blocking pathological reflexes emanating from the nerve structures exposed to pathological influence. It is carried out in neurological hospitals under the supervision of an otoneurologist and audiologist.