Vertebrobasilar insufficiency: causes and treatment

Vertebrobasilar insufficiency is a condition in which blood flow is impaired in the vertebral and basilar arteries, which supply the brainstem, cerebellum, and occipital lobes. Today, it is more accurate to use the terms "vertebrobasilar ischemia" and "stroke or transient ischemic attack in the vertebrobasilar system," as vascular events determine the prognosis and treatment. It is important to understand that isolated vertigo is extremely rarely explained solely by "chronic vertebrobasilar insufficiency" without objective vascular causes. [1]

Strokes in the vertebrobasilar system account for approximately 20% of all ischemic strokes. These strokes often masquerade as benign vestibular disorders, leading to delays in diagnosis and treatment. Moreover, basilar artery occlusion is among the most severe forms of stroke, with a high risk of adverse outcome without timely reperfusion. [2]

The term "vertebrobasilar insufficiency" has historically been applied to transient disturbances of blood flow in the posterior cerebral circulation. Current guidelines recommend assessing such episodes as transient ischemic attacks or strokes using neuroimaging and vascular studies, rather than simply labeling them as "insufficiency." This allows for more precise prevention and reduces the risk of recurrent stroke. [3]

The key to proper management is early recognition of posterior circulation "red flags," prompt neuroimaging with a focus on vascular techniques, and subsequent management of risk factors. In the acute phase, timely thrombolytic therapy and mechanical thrombectomy for large vessel involvement are crucial. [4]

Code according to ICD-10 and ICD-11

In ICD-10, "vertebrobasilar artery syndrome" is classified under the category of transient cerebral ischemia, code G45.0. In the presence of stenosis or occlusion without infarction, codes I65.0 "vertebral artery occlusion and stenosis" and I65.1 "basilar artery occlusion and stenosis" are used. If ischemia leads to infarction, codes from the I63 range are used. [5]

In ICD-11, transient ischemic attack is classified under the section "Cerebral ischemia" and is coded 8B10 with specifications, while ischemic stroke itself is classified in other categories of the section on cerebrovascular diseases. The transition from ICD-10 to ICD-11 is ongoing in a number of countries, and local correspondence tables may differ. [6]

Table 1. Basic codes

Classification	Code	Name
ICD-10	G45.0	Vertebrobasilar artery syndrome
ICD-10	I65.0	Occlusion and stenosis of the vertebral artery
ICD-10	I65.1	Occlusion and stenosis of the basilar artery
ICD-11	8B10	Transient ischemic attack
ICD-11	8B25.0 and others.	Consequences of ischemic stroke and other positions in the stroke section

Epidemiology

Ischemic strokes in the vertebrobasilar system account for approximately 20% of all ischemic strokes. Among transient circulatory disorders, the proportion of posterior circulation is also significant, but varies across studies and populations. These data highlight the clinical significance of posterior circulation and the need for specific diagnostics. [7]

The presence of hemodynamically significant vertebral or basilar artery stenosis after a posterior circulation stroke increases the risk of early recurrence. Recurrent stroke has been shown to occur significantly more frequently in patients with stenosis within the first 90 days compared to those without stenosis. This requires aggressive risk factor management and optimal antithrombotic prophylaxis. [8]

Basilar artery occlusion is a rare but extremely serious condition with high mortality and disability. Randomized trials in recent years have confirmed the benefit of mechanical thrombectomy in certain clinical and radiological criteria, improving outcomes in this subgroup of patients. [9]

The rate of false-negative results on diffusion-weighted magnetic resonance imaging in the first 24 hours is higher for posterior circulation strokes than for anterior circulation strokes, which impacts the assessment of true incidence and requires clinical vigilance. This explains some of the underreporting of vertebrobasilar circulation strokes in the early stages. [10]

Table 2. Epidemiological landmarks

Indicator	Grade
The proportion of posterior circulation strokes among all ischemic strokes	about 20%
Risk of early recurrence in vertebral or basilar artery stenosis	increased in the first 90 days
False-negative rate of diffusion MRI in the first 24 hours of posterior circulation stroke	higher than with anterior circulation

Reasons

The main cause is atherosclerosis of the extracranial portions of the vertebral arteries and basilar artery, resulting in stenosis and thrombosis. Cardioembolic sources also contribute significantly, especially in atrial fibrillation, necessitating a search for cardiac causes. [11]

Vertebral artery dissection occurs in middle-aged patients and can be triggered by minor neck trauma. Current guidelines allow for both antiplatelet and anticoagulant therapy for up to 6 months, as no differences in stroke prevention have been identified between the approaches. [12]

Hemodynamic mechanisms include a "critical" drop in perfusion due to a combination of stenosis and systemic hypotension, or in subclavian artery steal syndrome, when blood "leaks" into the working arm via retrograde flow through the vertebral artery. This leads to transient or persistent cerebral symptoms. [13]

Rare causes include large-vessel vasculitis, fibromuscular dysplasia, congenital vertebral artery hypoplasia, and dynamic compression during head rotation, known as "bow hunter" syndrome. These mechanisms require targeted testing and tailored treatment strategies. [14]

Risk factors

Modifiable risk factors include hypertension, diabetes mellitus, dyslipidemia, smoking, obesity, physical inactivity, and poor dietary habits. Controlling these factors can prevent a significant proportion of recurrent vascular events after stroke or transient ischemic attack. [15]

Non-modifiable factors include age, male gender, and hereditary predisposition. Certain anatomical variants, such as vertebral artery hypoplasia, may be associated with a higher risk of posterior circulation ischemia. These features are taken into account when interpreting imaging and choosing prophylaxis. [16]

Subclavian artery steal syndrome is more often associated with atherosclerosis in individuals with significant risk factors and is characterized by differences in blood pressure between the arms and symptoms during exercise of the affected arm. Identifying and correcting these factors reduces the incidence of ischemic episodes. [17]

The combination of several risk factors has a cumulative effect and requires a multicomponent secondary prevention strategy guided by evidence-based guidelines. This strategy includes lifestyle modification and drug therapy. [18]

Table 3. Risk factors

Group	Factors
Modifiable	Arterial hypertension, diabetes mellitus, dyslipidemia, smoking, obesity, physical inactivity, excessive salt intake
Non-modifiable	Age, heredity, male gender
Anatomical and hemodynamic	Vertebral artery hypoplasia, subclavian artery steal syndrome
Behavioral	Unsustainable diet, low adherence to therapy

Pathogenesis

Posterior circulation ischemia develops through embolic, thrombotic, or hemodynamic mechanisms. Emboli originate from atherosclerotic plaques in the vertebral artery, basilar artery, or the heart, especially in atrial fibrillation. Thrombotic occlusion develops against the background of critical stenosis. [19]

Hemodynamic events occur when systemic pressure decreases or when there is competitive blood flow, as in subclavian artery steal syndrome. In these situations, even moderate stenosis with impaired autoregulation can provoke transient neurological symptoms. [20]

The contribution of microcirculatory disorders and arteriolopathies is less studied but is important in lacunar infarctions of the brainstem and cerebellum. These cases often have less pronounced vascular stenosis and require careful clinical and radiological correlation. [21]

Understanding the dominant mechanism in a particular patient determines the choice of therapy: anticoagulation is indicated for cardioembolic genesis, antiplatelet agents and statins for the atherosclerotic process, and endovascular treatment for occlusion of a large artery with clinical and radiological indications. [22]

Symptoms

Typical symptoms include sudden vertigo, unsteadiness, double vision, dysarthria, dysphagia, visual field loss, unilateral weakness or numbness, and severe occipital headache. Symptoms often appear suddenly and may occur in combination.[23]

Isolated vertigo without neurological deficit is more often associated with peripheral vestibular disorders, but when combined with gait disturbance, diplopia, dysarthria, or dysphagia, posterior circulation ischemia should be considered as a probable cause. [24]

Basilar artery occlusion can lead to severe complications, including coma and locked-in syndrome. Rapid recognition and transfer to a stroke center are critical to the chances of recovery. [25]

In some patients, transient episodes precede stroke, serving as "warning blows." Ignoring them increases the risk of a serious event in the coming weeks. [26]

Classification, forms and stages

Classification by mechanism includes embolic, thrombotic, and hemodynamic forms. The embolic form is most often associated with cardiac sources or atherosclerotic plaques, the thrombotic form is associated with local progression of stenosis, and the hemodynamic form is associated with a decrease in perfusion. [27]

Anatomical classification is based on involvement of the vertebral arteries, basilar artery, posterior cerebral arteries, and cerebellar arteries. Clinical syndromes correspond to the affected area; for example, lateral medullary syndrome is characterized by dizziness, nystagmus, dysarthria, and sensory disturbances. [28]

Based on the course of the disease, transient ischemic attacks (TIAs) and strokes are distinguished. Transient ischemic attacks (TIAs) require the same urgent evaluation and secondary prevention as strokes, due to the high early risk of recurrence. [29]

Standard thresholds similar to those used for carotid pathology are used to assess the degree of stenosis; however, decisions are made individually, taking into account hemodynamics and collaterals. This is particularly important for the vertebral artery of the ostial region. [30]

Table 4. Classification

Axis	Options
Mechanism	Embolic, thrombotic, hemodynamic
Anatomy	Vertebral artery, basilar artery, posterior cerebral artery, cerebellar arteries
Flow	Transient ischemic attack, stroke
Comorbidity	Cardioembolic sources, multifocal atherosclerosis

Complications and consequences

The main complications are recurrent ischemic events, including disabling stroke. The risk is particularly high in the presence of hemodynamically significant vertebral or basilar artery stenosis within 90 days. This necessitates early intensification of prophylaxis. [31]

Basilar artery occlusion is associated with high mortality and permanent neurological deficits, but endovascular reperfusion, with proper patient selection, reduces these risks and increases the proportion of functional independence. [32]

Patients may experience chronic gait disturbances, dysphagia with risk of aspiration, visual impairment, and cognitive impairment. Early multidisciplinary rehabilitation helps improve outcomes and quality of life. [33]

Psychological and social consequences include decreased ability to work and the need for long-term care. Comprehensive secondary prevention and rehabilitation programs can reduce the burden of disease. [34]

When to see a doctor

Seek emergency medical attention immediately if you experience sudden weakness or numbness, slurred speech, double vision, severe headache, loss of balance, sudden blindness in one eye, or other focal neurological symptoms. Even if symptoms resolve quickly, prompt evaluation is necessary. [35]

Dizziness accompanied by an inability to walk straight, severe unsteadiness, dysarthria, or dysphagia are particularly concerning. These combinations increase the likelihood of posterior circulation damage and require urgent neuroimaging. [36]

Neck pain following minor trauma with the development of neurological symptoms may indicate vertebral artery dissection and requires prompt evaluation and antithrombotic therapy.[37]

When loading one arm, the occurrence of dizziness, weakness, blurred vision with a simultaneous greater difference in pressure between the arms requires testing for subclavian artery steal syndrome. [38]

Table 5. "Red Flags"

Situation	Action
Sudden focal symptoms	Call emergency help immediately
Vertigo with dysfunction of the cerebellum or brainstem	Urgent neuroimaging
Neck pain after injury with neurology	Exclude vertebral artery dissection
Symptoms during arm loading and pressure differences	Rule out steal syndrome

Diagnostics

The initial neurological examination is supplemented by targeted vestibular testing in acute vertigo. Signs of central nystagmus and vertical ocular misalignment during the eye cover test combined with the head impulse test are important. These clinical findings direct prompt visualization of the posterior circulation. [39]

Magnetic resonance imaging of the brain with diffusion-weighted sequences is the method of choice, but some posterior circulation strokes may not be detected in the first 24 hours. If suspicion persists, the study is repeated and supplemented with a perfusion assessment. [40]

Vascular imaging of the neck and head is essential early on. Computed tomography angiography and magnetic resonance angiography quickly reveal stenoses and occlusions of the vertebral and basilar arteries and allow planning of reperfusion treatment. [41]

Cardiac evaluation includes electrocardiography, echocardiography, and long-term rhythm monitoring if cardioembolism is suspected. Basic tests are performed in parallel to rule out metabolic mimics and assess risk factors. [42]

Table 6. Step-by-step diagnostic algorithm

Step	Method	Task	Note
1	Neurological examination and vestibular tests	Identify the central features	In case of central signs - urgent visualization
2	Diffusion magnetic resonance imaging	Confirm acute myocardial infarction	False negative results are possible in the first 24 hours.
3	Computed or magnetic resonance angiography	Identify stenosis and occlusions	Basis for the decision on reperfusion
4	Ultrasound of the vertebral arteries, including transcranial examination	Screening of hemodynamics and dynamic phenomena	Useful when subclavian artery steal is suspected
5	Cardiological examination	Search for the source of embolism	Echocardiography and rhythm monitoring

Differential diagnosis

Posterior circulation ischemia must be distinguished from peripheral vestibular disorders, such as benign paroxysmal positional vertigo and acute vestibulocochlear neuritis. Central signs of nystagmus, gait disturbance, and neurological deficits increase the likelihood of stroke. [43]

Migraine with aura, including brainstem symptoms, can mimic posterior cranial ischemia. The history of migraine, reversibility of symptoms, and the absence of vascular changes on imaging during recurrent episodes are important. [44]

Metabolic and toxic disturbances, such as hypoglycemia and drug intoxication, can cause similar symptoms. Screening blood tests and correlation with imaging help exclude these causes. [45]

Demyelinating diseases and inflammatory lesions of the brainstem are also included in the differential, but the clinical context and the nature of the lesion on magnetic resonance imaging allow for the distinction to be made. [46]

Table 7. How does a posterior circulation stroke differ from its “doubles”?

State	Key Features	What helps to distinguish
Posterior circulation ischemia	Suddenness, central nystagmus, cerebellar ataxia, focal symptoms	Visualization of blood vessels and brain, central tests
Peripheral vestibular disorders	Positional provocation, horizontal nystagmus, no focal deficit	Peripheral tests, normal vessels
Migraine with aura	History of migraine, gradual development of aura	Negative visualization between attacks
Metabolic mimics	Hypoglycemia, electrolyte shifts	Blood tests, correction of condition

Treatment

In acute posterior circulation stroke, in the absence of contraindications, intravenous thrombolysis is considered within the therapeutic window. Early reperfusion is associated with better outcomes and should be performed in a specialized stroke center, followed by secondary prevention. [47]

In basilar artery occlusion, mechanical thrombectomy has shown superior functional outcomes in randomized trials with selection based on clinical and radiological criteria. This applies to both the early window and the extended window in the presence of tissue viability criteria. [48]

Antiplatelet therapy is the mainstay of secondary prevention for non-cardioembolic strokes. In the first weeks after a minor stroke or transient ischemic attack, a short course of dual antiplatelet therapy can reduce the early risk of recurrence, after which monotherapy is used. Drug selection and duration are determined by current guidelines. [49]

Anticoagulant therapy is indicated for cardioembolic mechanisms, such as atrial fibrillation. The choice of drug and timing of initiation after stroke is individualized, balancing the risk of bleeding and recurrent ischemia. [50]

In vertebral artery dissection, scientific evidence shows comparable efficacy of antiplatelet and anticoagulant therapy in preventing stroke, so either approach is acceptable for up to 6 months with subsequent reassessment. The decision is made based on the bleeding risk, patient dynamics, and patient preference. [51]

Intensive risk factor management is essential for all patients: target blood pressure, high-intensity statin therapy for atherosclerosis, tobacco cessation, weight control, a low-salt diet, and adequate physical activity. These measures account for the greatest share of preventable recurrent events. [52]

Stenting of the vertebral artery ostium for symptomatic stenosis remains a controversial strategy. A pooled analysis of randomized trials showed no significant reduction in stroke risk compared with optimal medical therapy and an increased periprocedural risk in intracranial stenoses. Therefore, medical management is preferred, and interventions are considered in exceptional cases. [53]

In subclavian artery steal syndrome, subclavian artery intervention is considered in symptomatic patients, particularly those with posterior circulation ischemia or arm ischemia during stress, to restore antegrade blood flow. The choice between endovascular and surgical techniques depends on anatomy and local expertise. [54]

Rehabilitation begins early and includes neurorehabilitation methods, speech therapy for dysphagia and dysarthria, and complication prevention. An individualized rehabilitation plan significantly impacts functional recovery and quality of life. [55]

Table 8. Main treatment strategies

Direction	Content	Comment
Reperfusion	Intravenous thrombolysis when indicated	Improves outcomes with early therapy
Reperfusion	Mechanical thrombectomy for basilar artery occlusion	Shown in the selection by criteria
Antithrombotic prophylaxis	Antiplatelet agents for non-cardioembolic mechanism	A short combination mode is possible at the beginning
Antithrombotic prophylaxis	Anticoagulants for cardioembolism and dissection	The terms and conditions are individual.
Risk factor control	Pressure, lipids, behavior	The greatest contribution to the prevention of relapse

Prevention

Lifestyle modifications include quitting smoking, limiting salt intake, following a Mediterranean-style diet, engaging in regular aerobic activity, and losing weight if obese. These measures are recommended for all patients after a stroke or transient ischemic attack. [56]

Drug prophylaxis is selected individually and includes antiplatelet agents or anticoagulants as indicated, high-intensity statins for atherosclerosis, glycemic control, and treatment of arterial hypertension. Combined management, taking into account adherence, increases effectiveness. [57]

Monitoring and correction of risk factors should be ongoing: control of blood pressure, lipids, glucose, heart rate, and body weight. Informed patient participation and training in recognizing relapse symptoms improve safety. [58]

Influenza and pneumococcal vaccination in high-risk patients may reduce the incidence of exacerbations and decompensations, which indirectly affects vascular risk, although direct data for the vertebrobasilar system are limited. The decision is based on general cardio-neurological guidelines. [59]

Table 9. Preventive measures and goals

Measure	Target
Quitting smoking	Reducing the risk of stroke and cardiovascular events
Diet and activity	Control of body weight, blood pressure, lipids
Antithrombotics	Stroke prevention by mechanism
Statins	Plaque stabilization and risk reduction
Blood pressure control	Individual target values

Forecast

Prognosis depends on the mechanism, location, and timing of therapy. In basilar artery occlusion, timely reperfusion improves the chances of functional independence compared to the best medical management without reperfusion. [60]

The presence of significant vertebral or basilar artery stenosis is associated with an increased risk of early recurrence, but strict control of risk factors and adherence to therapy reduces this risk. Secondary prevention and rehabilitation programs improve long-term outcomes. [61]

Cases with false-negative early diffusion magnetic resonance imaging (DMI) require clinical suspicion and repeat imaging. Proper sequencing of examinations prevents missed stroke and worsened outcome. [62]

In general, a comprehensive strategy including early reperfusion when indicated, optimal antithrombotic prophylaxis and correction of risk factors ensures the maximum reduction in mortality and disability. [63]

Table 10. Factors influencing the prognosis

Factor	Influence
Time to reperfusion	The sooner, the better the outcome.
Presence of significant stenosis	Increased risk of relapse
Risk factor control	Reduces relapse and mortality
Stroke volume and location	Determines the degree of disability

Frequently asked questions

Is it true that "vertebrobasilar insufficiency" is often diagnosed "by eye" in cases of dizziness?
Historically, yes, but the modern approach requires confirmation with vascular and neuroimaging methods. Isolated dizziness is more often peripheral in nature without a vascular substrate. [64]

If an MRI shows no signs of infarction, does it mean there was no stroke?
Not always. In the first 24 hours of a posterior circulation stroke, diffusion MRI can be falsely negative. Repeat studies and vascular evaluation are needed. [65]

When is vertebral artery stenting justified for stenosis?
Randomized trials have shown no clinical benefit over optimal medical therapy, particularly in intracranial stenosis, where periprocedural risk is higher. The decision is individualized and is rarely used. [66]

What really reduces the risk of recurrent stroke?
Strict control of blood pressure, lipids, smoking cessation, physical activity, a Mediterranean-type diet, and appropriate antithrombotic agents and statins. This is documented in modern guidelines. [67]