Vertebrobasilar Occlusion and Verebral Artery Syndrome

Synonyms: Vertebrobasilar stroke, vertebrobasilar insufficiency

Occlusion or impairment of the vertebrobasilar blood supply affects medulla, cerebellum, pons, midbrain, thalamus and occipital cortex. Obviously the clinical features of occlusion are distinctive and quite different to those of disease affecting cerebral hemispheres. The concentration of important neurological pathways and centres of neurological control make for often dramatic and varied clinical sequelae when the blood supply is impaired or occluded. The clinical features can be complex but are readily understood from a knowledge of the blood supply and neuroanatomy. A number of clinical syndromes result from disruption of the vertebrobasilar blood supply which are usually caused primarily by atherosclerosis affecting the vertebrobasilar system. The state of other parts of the circulation to the brain will affect the clinical manifestation of vertebrobasilar disease.

The vertebral arteries branch off the subclavian arteries, passing cephalad through the costotransverse foramina of the sixth to second cervical vertebrae. They enter the skull through the foramen magnum merging at the pontomedullary junction to form the basilar artery which divides into two posterior cerebral arteries at the upper pons. At the base of the brain the carotid and basilar systems join to form the circle of Willis. This arrangement of collateral circulation may allow adequate brain perfusion even with occlusion of a main vessel. Important points to consider when assessing clinically are:

• Superior cerebellar arteries from the basilar artery supply lateral aspect of pons and midbrain together with superior surface of cerebellum
• Cerebellum supplied by branches from the basilar artery (long circumferential, posterior cerebral, anterior inferior cerebellar and superior cerebellar arteries)
• The medulla is supplied by the posterior inferior cerebellar artery and by direct smaller branches from the vertebral arteries
• The pons is supplies by small and large branches from the basilar artery
• The midbrain and thalamus are supplied by penetrating arteries from the posterior cerebral arteries
• The occipital cortex is perfused by the posterior cerebral artery.

• The commonest vascular disease affecting the vertebrobasilar system is atherosclerosis:²
  • This affects large vessels causing narrowing and occlusion.
  • It needs to produce stenosis at the origins of both vertebral arteries to cause vertebrobasilar ischaemia.
  • Even with vertebral artery occlusion collaterals (circle of Willis) may prevent ischaemia.
  • Ischaemia of the hind brain is likely to develop with the association of carotid artery disease (often at the bifurcation of the carotid artery), vertebral artery stenosis and intracerebral disease.
  • Note that the circle of Willis is only intact in 50% of patients.
• Lipohyalinosis affects small vessels eventually causing occlusion. This frequently occurs in association with hypertension. Lipohyalinosis also weakens vessel walls and rupture of the vessels causing focal haemorrhage. Almost all intracerebral haemorrhages come from such rupture of small penetrating vessels.
• Embolic occlusion of the vertebrobasilar system is uncommon and emboli are typically from the aortic arch, subclavian artery and vertebral arteries. Emboli usually occlude the basilar artery.

A relatively uncommon form of stroke. However:

• Stroke is the third biggest cause of death in the United Kingdom³
• Stroke of all types is common and more common in men than women
• Incidence rises with age
• Incidence is higher in some racial groups
• Most strokes are ischaemic (80-85%)
• 20% of lesions causing stroke occur in the vertebrobasilar circulation
• 15 to 20% of strokes are caused by haemorrhage
• The cerebellum around the dentate nucleus is involved in 7% of strokes
• 6% of haemorrhagic strokes involve the pons

• Age
• Alcohol abuse
• Coronary and other heart disease
• Diabetes mellitus
• Drug abuse^4,5
• Family history of stroke
• Giant cell arteritis⁶
• Hypertension
• Obesity and physical inactivity⁷
• Previous stroke
• Race
• Smoking^5,8

Death or major disability is the result of occlusion of large vessels in the vertebrobasilar system. However many lesions arise in smaller vessels with a wide variety of focal neurological deficits. Stroke scoring systems to evaluate patients have been developed but are of limited use for vertebrobasilar stroke.⁹

History

Onset and duration of symptoms may vary with aetiology.

• Basilar artery thrombosis may have a gradual onset with half of patients experiencing transient ischaemic attacks for days or weeks prior to occlusion.
• Embolic events cause sudden and dramatic symptoms without prodrome.
• It may (rarely) be brought on by turning the head (temporarily occluding one vertebral artery, with insufficient collaterals due to advancing atherosclerosis).

Symptoms reported with vertebrobasilar strokes include:

• Vertigo - common - and this may be the only symptom.
• Nausea and vomiting
• Disturbance of consciousness
• Headache
• Visual disturbance (oculomotor signs such as nystagmus, diplopia and pupillary changes)
• Visual field defects
• Speech disturbance (for example dysarthria and dysphonia)
• Sensory changes face and scalp
• Ataxia
• Contralateral motor weakness (may cause a "drop attack")
• Sensory disturbance affecting pain and temperature
• Incontinence

There may be a history of associated risk factors.

Examination

Diagnosis can be made from careful clinical examination, but the complexity of signs requires careful and detailed neurological examination. Common findings:

• 70% of patients will exhibit:
  • Abnormal level of consciousness
  • Hemiparesis or quadriparesis (usually asymmetric)
• 40% of patients have bulbar manifestations (facial weakness, dysphagia, dysarthria, dysphonia)
• Also common are pupillary and oculomotor abnormalities

The physical findings can be very varied and complex according to the site of the brain affected:

• Abducens nucleus, horizontal gaze centre (located in the pontine paramedian reticular formation) and medial longitudinal fasciculus lesions cause oculomotor signs. These can result in:
  • ipsilateral lateral gaze palsy
  • Conjugate gaze palsy
  • Ocular bobbing
• Midbrain syndromes:
  • Vertical gaze palsy
  • Third cranial nerve palsy
• Pontine syndromes:
  • Tremor, ataxia and mild hemiparesis
  • Horizontal gaze palsy
  • Cranial nerve 6 and 7 palsy
• Medullary syndromes:
  • Loss of facial pain and temperature sensation (ipsilateral)
  • Horner syndrome
  • Ataxia (ipsilateral)
  • Tongue, soft palate, vocal cord, sternocleidomastoid paralysis (ipsilateral)
  • Contralateral loss of pain and temperature sensation elsewhere
• Posterior cerebral artery syndromes:
  • Contralateral hemianopia
  • With macular sparing

Clinical syndromes and scenarios¹

A variety of different combinations of signs and symptoms have been described. See table.

A wide variety of conditions may need to be considered particularly tumours and demyelination:

• Secondary brain tumours
• Primary brain tumours specifically cerebellopontine angle tumours
• Lesions in the supratentorial hemispheric region causing brainstem compression and herniation
• Subarachnoid haemorrhage
• Meningitis
• Basilar migraine
• Multiple sclerosis
• Guillain-Barre syndrome.¹⁰

Giant cell arteritis has been identified as a cause of vertebrobasilar infarcts.⁶

• Basic bloods including FBC, ESR, blood chemistry, clotting and lipid profile
• Screen for hypercoaguable states if under 45 for example:
  • Lupus anticoagulant and anticardiolipin antibodies
  • Antithrombin III deficiency
• Imaging studies:
  • CT scanning is usually the first imaging study done but may miss early ischaemia
  • MRI scanning is better than CT scanning particularly for ischaemia, demyelination, tumours and diseases of blood vessels
  • New MRI techniques allow even better definition of pathology.²
• ECG:
  • Mandatory for all stroke patients
  • 20% of stroke patients have an arrhythmia and about 2% have had myocardial infarctions.
• Echocardiography:
  • Identifies valvular defects, vegetations and other sources of emboli particularly in young patients with basilar artery occlusion.
• Cerebral angiography:
  • Used less because of noninvasive imaging
  • Useful when thrombolysis or recanalisation contemplated

• Where should patents be treated?The government in the United Kingdom has a National Strategy to improve services and deliver the newest treatments for stroke.³
  • Where possible patients should be treated in specialist stroke units^3,11
  • Specialist neurological intensive care may be required for:
    • When patients are candidates for thrombolysis or other interventional treatments
    • Fluctuating neurological symptoms
    • Impaired levels of consciousness
    • Unstable haemodynamic indices
    • Cardiorespiratory problems
• What treatments can be given?
  • General measures:
    • Prevention aspiration pneumonitis by for example aggressive pulmonary toilet
    • Early attention to continence programs
    • Careful monitoring of catheters to avoid infection
    • Control of body temperature
    • Control of blood glucose
  • Treatment to maintain cerebral blood flow:
    • This in practice means managing blood pressure.
    • Over enthusiastic treatment of hypertension should be avoided.
    • Treat hypertension if:
      • Evidence of hypertensive encephalopathy
      • Unstable angina
      • Acute myocardial infarction
      • Heart failure
      • Renal failure
      • Diastolic over 120 or systolic over 180 mm Hg
      • Use labetalol if below 140 mm Hg diastolic
      • Use nitroprusside if over 140 mm Hg.
    • Treat hypotension:
      • Intravenous fluids to maintain intravascular volume with isotonic fluids
      • Vasopressors such as dopamine and dobutamine may be used
    • Use pulmonary artery catheter to monitor central venous pressure and pulmonary capillary wedge pressure with congestive cardiac failure and pulmonary oedema.
  • Treatments for respiratory complications:
    • Assess respiratory drive, gag reflex, cough reflex (to expel secretions)
    • Consider endotracheal intubation (Glasgow coma scale less than 8)
    • Sedation and paralysis for ventilation should be avoided as this obscures neurological observations.
  • Thrombolysis:
    • Reports in the 1980s showed benefit with use of tissue plasminogen activator in first 3 hours for acute ischaemic stroke. Use in middle cerebral artery occlusion appears beneficial.¹²
    • Less evidence available for vertebrobasilar occlusion and no randomised controlled trials. However many are encouraged by work done so far with new techniques.¹³
  • Anticoagulation:
    • Intravenous heparin has been used in acute stroke. This shows no benefit except for some improved outcome in large vessel disease after 7 days.
  • Angioplasty:
    • The place in management is yet to be decided by research evidence. Stenting of vertebrobasilar arteries needs larger comparative trials to further evaluate the technique.^14,11
  • Surgery to form an anastamosis between vertebral artery and external carotid.¹⁵
• What forms of rehabilitation may be required?
  • Nursing factors:
    • Maintain skin, nutrition and patient safety.
    • Communication with other therapists.
    • Communication with relatives and education about stroke and its effects.
  • Physiotherapy:
    • Variable needs according to severity
    • Assessment and development of programme of care
    • Mobilisation and strengthening
    • Chest care
  • Occupational therapy to help with bathing, dressing and grooming. Education of relatives.
  • Speech therapy. This may involve speech and language skills but also safety skills, assessment of swallowing and education of carers and family.
• What referrals may be required?
  • Therapies above
  • Social services referral
  • Neuropsychology
  • Neuropsychiatry

The neurological deficit can be further complicated by:

• Pneumonia (particularly aspiration pneumonia)
• Deep vein thrombosis and pulmonary embolism
• Myocardial infarction

This will depend on the extent of disease, but:

• Acute basilar artery occlusion has a very high mortality rate (85%)
• Vertebrobasilar stroke usually leaves significant neurological deficit
• The risk of recurrent stroke is 10 to 15%

Certain syndromes may have a good prognosis in terms of long term functional outcome but still carry a risk of death in the acute phase from, for example aspiration pneumonia in the lateral medullary syndrome. One study suggested that basilar artery diameter >4.3 mm could be a marker for high risk of fatal stroke.¹⁶

This depends on the cause but prevention strategies include:

• Warfarin for atrial fibrillation. Better adherence to guidelines would prevent stroke.¹⁷
• Treatment of hypertension
• Treatment of hyperlipidaemias
• Management of risk factors for stroke