Vertebro-basilar insufficiency( VBI) - Causes, symptoms and treatment. MF.

Vertebral-basilar insufficiency ( synonyms Vertebro-basilar insufficiency and VBN ) is a reversible impairment of brain functions caused by decreased blood supply to the area fed by vertebral and main arteries.

Synonym "Vertebrobasilar arterial system syndrome" is the official name of vertebro-basilar insufficiency.

Due to the variability of vertebral-basilar insufficiency, the abundance of subjective symptoms, the complexity of instrumental-laboratory diagnosis of vertebrobasilar insufficiency and the fact that the clinical picture resembles a number of other pathological conditions - in clinical practice, the diagnosis of VBI often occurs when a diagnosis is established without validfor that reason.

Reasons for VBI

Currently, the causes of vertebrobasilar insufficiency or VBI are considered:

1. Stenosing defeat of the main vessels, primarily:

• extracranial vertebral department
• subclavian arteries
• nameless arteries

In most cases,arteries is caused by an atherosclerotic lesion, with the most vulnerable being:

• the first segment - from the beginning of the artery to its entry into the bone channel of the transverse outgrowthCAS and C6 vertebrae
• the fourth segment - the fragment of the artery from the place of the perforation of the dura to the confluence with another vertebral artery at the interface between the bridge and the medulla oblongata, in the region of the formation of the main artery

. Frequent damage to these zones is caused by local features of the geometry of the vessels predisposing tothe appearance of areas of turbulent blood flow, damage to the endothelium.

2. Congenital features of the structure of the vascular bed:

• abnormal separation of vertebral arteries
• hypoplasia / aplasia of one of the vertebral arteries
• pathological tortuosity of the vertebral or main arteries
• inadequate development of anastomoses on the basis of the brain, primarily the arteries of the Willis circle,collateral blood supply in conditions of affection of the main artery

3. Microangiopathy against arterial hypertension, diabetes mellitus may occur whenanother occurrence of VBN( the defeat of small cerebral arteries).

4. Depression of vertebral arteries with pathologically altered cervical vertebrae: in spondylosis, spondylolisthesis, osteophytes of considerable size( recent years, the role of compression effects on vertebral arteries has been reconsidered as an important cause of VBI, although in some cases there is quite pronounced compression of the artery during head turns, which in additionreduction of blood flow along the vessel may be accompanied by arterio-arterial embolism)

5. Extravasal compression of the subclavian artery hypertrophic lstitch muscle, hyperplastic transverse processes of the cervical vertebrae.

6. Acute trauma of the cervical spine:

• Transport( whiplash injury)
• iatrogenic with inadequate manipulations of manual therapy
• abnormal performance of gymnastic exercises

7. Inflammatory lesions of the vascular wall: Takayasu's disease and other arteritis. The most vulnerable in this case are women of childbearing age. Against the background of the already defective wall of the vessel with the thinning of the media and a thickened, compacted intima, it is possible to separate it even in conditions of minor traumatization.

8. Antiphospholipid syndrome: may be the cause of a combination of impaired patency of extra- and intracranial arteries and increased thrombosis in young people.

Additional factors contributing to cerebral ishmia in vertebro-basilar insufficiency( VBI):

• changes in the rheological properties of blood and microcirculation disorders with increased thrombus formation
• cardiogenic embolism( whose frequency reaches 25% according to T. Glass et al., 2002)
• small arterio-arterial embolisms of which the source is a friable parietal thrombus
• complete occlusion of the lumen of the vessel as a consequence of atherosclerotic stenosis of the vertebral artery with the formation of the pristenochthrombus

Increased thrombosis of the vertebral and / or main artery at a certain stage of its development can manifest itself as a clinical picture of transient ischemic attacks in the vertebral-basilar system. The likelihood of thrombosis increases in areas of traumatizatsii arteries, for example, when passing in the bone channel of the transverse processes of СVI-СII.Probably, the provoking moment of development of thrombosis of the vertebral artery in a number of cases can be a long stay in an uncomfortable position with a forced position of the head.

The data of the sectional and neuroimaging methods of investigation( primarily MRI) reveal the following changes in brain tissue( brain stem, bridge, cerebellum, occipital cortex) in patients with VBI:

•
lacunar infarctions of different ages • signs of neuronal death and proliferation of glialelements
• Atrophic changes in the cerebral cortex of the

These data, confirming the existence of an organic substrate of the disease in patients with VBI, indicate the need for a thorough searchcause of disease in each particular case.

Symptoms of vertebrobasilar insufficiency VBN

The diagnosis of circulatory insufficiency in the air force is based on a characteristic symptom complex, combining several groups of clinical symptoms:

• visual disorders
• oculomotor disorders( and symptoms of violation of the function of other cranial nerves)
• static and motion coordination
•vestibular( cochleovestibular) disorders
• pharyngeal and laryngeal symptoms of
• headache
• asthenic syndrome
• vegvascular dystonia
• conductive symptoms( pyramidal, sensitive)

This symptomatic complex is found in the majority of patients with circulatory failure in the vertebrobasilar basin. In this case, the presumptive diagnosis is determined by the presence of at least two of these symptoms. They are usually short-lived and often go by themselves, although they are a sign of trouble in this system and require a clinical and instrumental examination. Especially, a thorough anamnesis is needed to clarify the circumstances of the occurrence of certain symptoms.

The clinical manifestations of VBI are based on the combination of:

• characteristic complaints of the patient
• objectively detectable neurological symptoms, indicative of the involvement of structures circulating from the vertebral-basilar system.

The core of the clinical picture of vertebral-basilar insufficiency is the development of neurologic symptoms, reflecting transient acute cerebral ischemia in the zones of vascularization of peripheral branches of vertebral and main arteries. However, some pathological changes can be detected in patients after the end of ischemic attack. One and the same patient with VBI usually has several clinical symptoms and syndromes, among which it is not always easy to identify a presenter.

All the symptoms of VBI can be conventionally divided into:

• paroxysmal( symptoms and syndromes that are observed during an ischemic attack)
• permanent( marked for a long time and can be detected in a patient during the interictal period).

In the basin of the arteries of the vertebral-basilar system it is possible to develop:

• transient ischemic attacks of
• ischemic strokes of various severity, including lacunar ones.

Uneven arterial lesion leads to the fact that ischemia of the brain stem is characterized by mosaic, "spotting".

The combination of symptoms and the degree of their severity are determined by:

• localization of the lesion
• the size of the lesion
• the possibilities of collateral circulation

The neurological syndromes described in the classical literature are relatively rare in the pure form due to the variability of the blood supply system of the cerebral trunk and cerebellum. It was noted that during the attacks, the side of primary motor disorders( paresis, ataxia), as well as sensitive disorders, can change.

1. Movement disorders in patients with VBN are characterized by a combination of:

• central paresis of
• coordination disorders due to cerebellar involvement and its associations

As a rule, there is a combination of dynamic ataxia in the limbs and intentional tremor, gait disorders, unilateral reduction of muscle tone.
It should be noted that clinically, it is not always possible to identify the involvement of the blood supply zones of carotid or vertebral arteries in the pathological process, which makes application of methods of neuroimaging desirable.

2. Sensory disorders are manifested:

• symptoms of prolapse with the appearance of hypo- or anesthesia in one limb, half of the trunk.
• Paresthesias may appear, usually the skin of the limbs and face are involved.
• Surface and deep sensitivity disorders( occur in a quarter of patients with VBI and are usually caused by a ventrolateral thalamus lesion in the areas of the blood supply of a. Thalamogeniculata or posterior external villous artery)

3. Visual disorders can be expressed as:

• loss of visual fields(scotoma, homonymous hemianopsia, cortical blindness, less often - visual agnosia)
• appearance of
photopsy • blurred vision, obscurity of vision of
objects • appearance of visual images - "mushto "," lights "," stars ", etc.

4. Disorders of cranial nerve functions

• oculomotor disorders( diplopia, convergent or diverging strabismus, vertical eyeball separation),
• peripheral paresis of the facial nerve
• bulbar syndrome( less often pseudobulbar syndrome)

These symptoms appear in different combinations, muchless common is their isolated occurrence due to reversible ischemia in the vertebral-basilar system. It should be taken into account the possibility of combined damage to brain structures, blood supply from the systems of carotid and vertebral arteries.

5. Pharynx and guttural symptoms:

• Sore throat, pain in the throat, difficulty in swallowing food, spasms of the pharynx and esophagus
• hoarseness, aphonia, foreign body sensation in the larynx, coughing

6. Dizziness attacksduration from several minutes to hours), which may be due to the morphofunctional features of the blood supply of the vestibular apparatus, its high sensitivity to ischemia.

Dizziness:

• as a rule, is systemic in nature( in some cases dizziness is non-systemic and the patient experiences a feeling of falling, rocking, unsteadiness of the surrounding space)
• is manifested by the feeling of rotation or rectilinear motion of surrounding objects or own body.
• characterized by associated vegetative disorders: nausea, vomiting, profuse hyperhidrosis, changes in heart rate and blood pressure.

Over time, the intensity of the sensation of dizziness may be weakened, while the focal symptoms( nystagmus, ataxia) become more pronounced and become permanent.
It must, however, be taken into account that the feeling of dizziness is one of the most common symptoms, the frequency of which increases with age.

Vertigo in patients with VBI, as well as in patients with other forms of cerebral vascular disease, may be due to the suffering of the vestibular analyzer at various levels, and its nature is determined not so much by the characteristics of the underlying pathological process( atherosclerosis, microangiopathy, hypertension);but localization of the ischemic focus:

• lesions of the peripheral part of the vestibular apparatus
• defeat of the central department of the vestibular apparatus
• psychiatric

abnormalities Suddenly developing systemic dizziness, especially when combined with acute unilateral deafness and a sense of ear noise, may be a characteristic manifestation of a labyrinth infarction( although isolated dizziness is rarely the only manifestation of VBI).

Differential diagnosis of vertebrobasilar insufficiency

A similar clinical picture other than vertebrobasilar insufficiency can have:

• benign paroxysmal positional dizziness( due to lesion of the vestibular apparatus and not associated with blood supply disorders, a reliable test for its diagnosis are Hallpike samples)
• vestibular neuronite
• acute labyrinthitis
• Ménière disease, labyrinth hydrosis( due to chronic otitis)
•perilymphatic fistula( caused by a previous trauma, operation)
• neural sinus nerve
• demyelinating diseases
• normotensive hydrocephalus( combination of persistent dizziness, imbalance, unstable walking, cognitive impairment)
• emotional and mental disorders( anxious, depressive disorders)
• pathology of the degenerative and traumatic nature of the cervical spine( cervical dizziness), as well as the craniocerephalic transition syndrome

Hearing impairment( reduction of its acuity, sensation of noise in the ears) are also frequent manifestations of VBI.It should be borne in mind, however, that about a third of the older population systematically notes the sense of noise, with more than half of them assessing their feelings as intense, causing them considerable inconvenience. In this regard, one should not regard all audiological disorders as manifestations of cerebrovascular pathology, given the high incidence of degenerative processes developing in the middle ear.

At the same time, there is evidence that short-term episodes( up to several minutes) of unilateral reversible hearing loss in combination with ear noise and system dizziness are prodromes of the anterior lower cerebellar artery thrombosis, which requires close attention to such patients. As a rule, the source of hearing loss in this situation is directly the snail, which is extremely sensitive to ischemia, the retrochlear segment of the auditory nerve, which has a rich collateral vascularization, is relatively less affected.

Diagnosis of vertebrobasilar insufficiency

In the diagnosis of VBN, ultrasonic methods for studying the cerebral vascular system of the brain have become the most accessible and safe:
• Ultrasonic dopplerography allows obtaining data on the permeability of vertebral arteries, the linear velocity and the direction of blood flow in them. Compression-functional tests provide an opportunity to assess the status and resources of collateral circulation, blood flow in the carotid, temporal, supra-block and other arteries.
• Duplex scanning demonstrates the condition of the artery wall, the nature and structure of stenotic lesions.
• Transcranial Doppler( TCD) with pharmacological samples is important for determining the cerebral hemodynamic reserve.
• Ultrasonic dopplerography( UZDG), - detection of signals in the arteries gives an idea of ​​the intensity of microembolic flow in them, cardiogenic or vascular embologenic potential.
• Data on the condition of the main arteries of the head, obtained with MRI in the angiography mode, are extremely valuable.
• When deciding whether to perform thrombolytic therapy or surgery on the vertebral arteries, contrast X-ray pangography becomes important.
• Indirect data on vertebrogenic effects on vertebral arteries can also be obtained with routine radiography performed with functional samples.

The best method of neuroimaging of stem structures is MRI, which allows you to see even small foci.

A special place is taken by otoneurological examination, especially if it is supported by computer-assisted electro-histogram and electrophysiological data on auditory evoked potentials characterizing the state of the brain stem structures.

Research on the coagulating properties of blood and its biochemical composition( glucose, lipids) is of particular importance.

The sequence of application of the listed instrumental methods of investigation is determined by the peculiarity of determining the clinical diagnosis.

Treatment of vertebrobasilar insufficiency

The majority of patients with VBI receive conservative treatment on an outpatient basis. It should be borne in mind that patients with acute focal neurological deficit should be hospitalized in a neurological hospital, since the possibility of increasing thrombosis of a large arterial trunk with the development of a stroke with a persistent neurologic deficit should be taken into account.

1. Modern understanding of the mechanisms of the development of VBI, in particular the recognition of the leading role of stenosing lesions of the extracranial departments of the main arteries, and the introduction of new medical technologies into clinical practice, allows the angioplasty and stenting of the corresponding vessels, endarterectomy, superintracranial superpositionAnastomosis, in some cases, the possibility of thrombolysis can be considered.

Data on the use of transluminal angioplasty of the main arteries, including the proximal segment in patients with VBI, have been accumulated.

2. Therapeutic tactics in patients with VBI is determined by the nature of the main pathological process, while it is appropriate to correct the major modifiable risk factors for cerebral vascular disease.

The presence of arterial hypertension requires a survey to exclude its secondary nature( vasorenal hypertension, thyrotoxicosis, hyperfunction of the adrenal glands, etc.).Systematic control of blood pressure level and rational dietary therapy are necessary: ​​

• restriction in the diet of table salt
• exclusion of alcohol consumption and smoking
• physical activity dosage

In the absence of a positive effect, medication should be started in accordance with generally accepted principles. Achieving the target level of pressure is necessary first of all in patients with the existing lesion of target organs( kidney, retina, etc.), suffering from diabetes mellitus. Treatment can be started with the administration of ACE inhibitors and angiotensin receptor blockers. It is important that these antihypertensive drugs provide not only reliable control of blood pressure level, but also possess nephro- and cardioprotective properties. A valuable consequence of their use is the remodeling of the vascular bed, the possibility of which is expected in relation to the cerebral vascular system. If there is insufficient effect, it is possible to use antihypertensive drugs from other groups( calcium channel blockers, b-blockers, diuretics).

In elderly people in the presence of stenosing lesions of the main arteries of the head, an accurate decrease in blood pressure is necessary, since there is evidence of an inverted cerebral vascular lesion with an excessively low arterial pressure.

3. In the presence of stenosing lesions of the main arteries of the head, high probability of thrombosis or arterio-arterial embolisms, an effective way of preventing episodes of acute cerebral ischemia is to restore the rheological properties of the blood and prevent the formation of cellular aggregates. To this end, antiaggregants are widely used. The most accessible drug, combining sufficient efficacy and satisfactory pharmacoeconomic characteristics, is acetylsalicylic acid. The optimal therapeutic dose is 0.5-1.0 mg per 1 kg of body weight per day( the patient should receive 50-100 mg of acetylsalicylic acid daily).When prescribing it, you should consider the risk of developing gastrointestinal complications, allergic reactions. The risk of damage to the mucous membrane of the stomach and duodenum decreases with the use of enteric-soluble forms of acetylsalicylic acid, as well as with the simultaneous administration of gastroprotective agents( eg, omeprazole).In addition, 15-20% of the population has a low sensitivity to the drug. The inability to continue monotherapy with acetylsalicylic acid, as well as the low effect of its use, requires the connection of another antiaggregant or a complete replacement for another drug. To this end, dipyridamole, an inhibitor of the GPI-1b / 111b complex clopidogrel, ticlopidine can be used.

4. Along with antihypertensive agents and antiplatelet agents, drugs from the group of vasodilators are used to treat patients with VBI.The main effect of this group of drugs is an increase in cerebral perfusion due to a decrease in vascular resistance. At the same time, recent studies suggest that some of the effects of these drugs may be due not only to vasodilator activity, but also to direct effects on brain metabolism, which must be considered when they are prescribed. The expediency of their vasoactive drugs, the doses used and the duration of treatment are determined by the patient's condition, adherence to treatment, the nature of the neurological deficit, the level of blood pressure, the rate of achievement of a positive result. It is advisable to time the course of treatment to coincide with the unfavorable in the meteorological period( autumn or spring season), a period of increased emotional and physical exertion. Treatment should begin with minimal dosages, gradually bringing the dose to therapeutic. In the absence of the effect of monotherapy with a vasoactive drug, it is desirable to use another drug of similar pharmacological action. The use of a combination of two drugs of similar effect makes sense only in individual patients.

5. For the treatment of patients with various forms of cerebrovascular pathology, drugs that have a positive effect on brain metabolism, which have neurotrophic and neuroprotective effects, are widely used. Piracetam, cerebrolysin, actovegin, semax, glycine, a large number of other drugs are used. There are data on the normalization of cognitive functions against the background of their use in patients with chronic disorders of cerebral circulation.

6. Symptomatic drugs should be used in the complex treatment of patients with NIB:

• drugs that reduce the severity of dizziness
• mood-conditioning medications( antidepressants, anxiolytics, hypnotics)
• analgesics( if indicated)

7.It is rational to connect non-pharmacological methods of treatment - physiotherapy, reflexotherapy, therapeutic gymnastics.

It should be emphasized the need for individualization of the tactics of managing the patient with VBI.It is the registration of the main mechanisms of the development of the disease, an adequately selected set of medicinal and non-medicinal methods of treatment that can improve the quality of life of patients and prevent the development of a stroke.