Makindo Medical Notes

Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Causes of Stroke

Introduction

Basilar artery thrombosis (BAT) is a rare but life-threatening condition that accounts for approximately 1% of all strokes. It involves the occlusion of the basilar artery, leading to ischaemia in areas supplied by the posterior circulation. The prognosis is generally poor; however, advancements in imaging techniques such as magnetic resonance angiography (MRA) and computed tomography angiography (CTA) have improved the identification of patients with partial or progressive occlusions who may have limited ischaemia and a better prognosis. Early intervention with mechanical thrombectomy or intra-arterial thrombolysis can significantly improve outcomes.

Anatomy

The basilar artery is a critical vessel in the posterior circulation of the brain. It is formed by the fusion of the right and left vertebral arteries at the level of the lower pons. The artery ascends in the basilar sulcus on the ventral surface of the pons and divides at the upper pons/midbrain junction into the right and left posterior cerebral arteries (PCAs).

Branches of the Basilar Artery

• Anterior Inferior Cerebellar Artery (AICA): Supplies parts of the cerebellum and pons.
• Labyrinthine Artery: Usually a branch of the AICA; supplies the inner ear.
• Pontine Arteries: Numerous small branches supplying the pons; occlusion can cause unilateral or bilateral pontine infarcts.
• Superior Cerebellar Artery (SCA): Supplies the superior aspect of the cerebellum and portions of the midbrain.
• Posterior Cerebral Arteries (PCAs): Terminal branches of the basilar artery; supply the occipital lobes, medial temporal lobes, thalamus, and parts of the midbrain.

Anatomical Illustrations

Below are illustrations of the basilar artery and its branches:

Etiology and Pathophysiology

Basilar artery occlusion can result from various mechanisms:

• Cardioembolism: Emboli originating from the heart, especially in atrial fibrillation.
• Artery-to-Artery Embolism: Emboli from atherosclerotic plaques in the vertebral or basilar arteries.
• Thrombus in Situ: Localized thrombosis due to atherosclerosis or vessel injury.
• Arterial Dissection: Vertebral artery dissection extending into the basilar artery.
• Inflammatory Conditions: Arteritis or vasculitis affecting the vertebrobasilar system.

The occlusion may develop progressively, with a slow accumulation of thrombus leading to gradual worsening of symptoms, or it may occur suddenly, causing catastrophic neurological deficits.

Risk Factors

• Atherosclerosis
• Atrial fibrillation and other cardiac arrhythmias
• Hypertension
• Diabetes mellitus
• Smoking
• Hyperlipidemia
• Cervical artery dissection
• Substance abuse (e.g., cocaine)
• Inflammatory vasculopathies (e.g., arteritis, meningitis)
• Genetic arteriopathies

Clinical Presentation

The presentation of basilar artery thrombosis can be variable and may include:

• Sudden collapse and loss of consciousness
• Coma or decreased level of consciousness
• Quadriparesis or quadriplegia: Weakness or paralysis of all four limbs
• Diplopia: Double vision due to cranial nerve involvement
• Dysarthria and Dysphagia: Difficulty speaking and swallowing
• Cerebellar Ataxia: Uncoordinated movements
• Pinpoint Pupils: Indicative of pontine involvement
• Lateralizing sensory or motor deficits
• Locked-In Syndrome: Patient is conscious but unable to move except for vertical eye movements

Early symptoms can be subtle, making diagnosis challenging without high clinical suspicion and focal neurological examination.

Investigations

• Laboratory Tests: FBC, U&E, LFTs, glucose, lipid profile, CRP, coagulation studies.
• Non-Contrast CT Scan: May show a hyperdense basilar artery (HDBA) in 70-80% of cases, but early ischemic changes may not be visible.
• CT Angiography (CTA): Essential for visualizing vessel occlusion and planning endovascular treatment. It can also assess collateral circulation via posterior communicating arteries (PCOMs).
• MRI with Diffusion-Weighted Imaging (DWI): Detects acute ischemic changes and extent of infarction.
• ECG: To identify cardiac arrhythmias like atrial fibrillation.
• Echocardiography: Evaluates cardiac sources of emboli.

Imaging Findings

Hyperdense Basilar Artery (HDBA)

The HDBA sign on a non-contrast CT scan indicates thrombosis within the basilar artery.

Posterior Circulation Infarctions

Infarctions may be evident in the brainstem, cerebellum, occipital lobes, and thalamus.

Prognostic Indicators

Poor Prognostic Indicators

• Advanced age
• Current smoking
• Hyperlipidemia
• Delayed time to treatment
• Need for intubation at presentation or within 24-48 hours
• History of minor strokes
• High baseline NIH Stroke Scale (NIHSS) score
• NIHSS ≥ 28 at 24-48 hours
• BATMAN score < 7 on CTA

Favorable Prognostic Indicators

• Successful recanalization of the occluded artery
• Presence of bilateral PCOMs on pre-treatment CTA
• NIHSS ≤ 4 at 24-48 hours

BATMAN Score on CTA

The Basilar Artery on Computed Tomography Angiography (BATMAN) score assesses collateral circulation in basilar artery occlusion:

• Flow in both vertebral arteries: +1 (considered as one segment)
• Flow in proximal basilar artery: +1
• Flow in middle basilar artery: +1
• Flow in distal basilar artery: +1
• Flow in P1 segments of the PCAs: +1
• Filling of each PCOM:
  • Normal PCOM: +2 (each)
  • Hypoplastic PCOM: +1

A maximum score of 10 indicates normal posterior circulation filling, while a score of 0 suggests no filling. A BATMAN score less than 7 is independently associated with poor outcomes (modified Rankin Scale ≥ 4).

Management

Management of basilar artery thrombosis is time-sensitive and requires a multidisciplinary approach:

• Initial Stabilization:
  • Ensure airway patency; may require intubation due to bulbar weakness.
  • Support breathing and circulation; monitor vital signs closely.
  • Admit to an intensive care unit (ICU) for continuous monitoring.
• Imaging and Diagnosis: Immediate CTA to confirm occlusion and assess for thrombectomy eligibility.
• Reperfusion Therapy:
  • Intravenous Thrombolysis: Consider within 4.5 hours of symptom onset; may extend to 6 hours on a case-by-case basis.
  • Mechanical Thrombectomy: Emergent endovascular treatment is the preferred therapy, effective up to 12 hours or more from symptom onset, especially if there is a small infarct core with a high NIHSS score.
  • Intra-Arterial Thrombolysis: May be considered in some cases, often in conjunction with mechanical thrombectomy.
• Supportive Care: Manage blood pressure, glucose levels, and prevent complications such as deep vein thrombosis.
• Secondary Prevention: Address modifiable risk factors, initiate antithrombotic therapy as appropriate, and consider long-term rehabilitation needs.
• Palliative Care: In cases with a very poor prognosis, focus on comfort measures and end-of-life care may be appropriate.

Prognosis

The prognosis of basilar artery thrombosis is often grave, with high rates of mortality and morbidity. Early diagnosis and successful recanalization are critical for improving outcomes. Patients may survive with significant disabilities, including locked-in syndrome, which necessitates comprehensive rehabilitation and support.

Suggested Management Algorithm

An algorithm for the management of basilar artery occlusion includes rapid assessment, imaging, and consideration of reperfusion therapies. Always follow local guidelines and protocols.

References

• Schwartz NE, Vertinsky AT, Hirsch KG, Albers GW. Basilar Occlusion Syndromes: An Update. The Neurohospitalist. 2015;5(3):142-150.
• Lindsberg PJ, Mattle HP. Basilar artery occlusion. Lancet Neurol. 2011;10(11):1002-1014.
• Rangaraju S, Streib C, Aghaebrahim A, et al. Neurologic Examination at 24 to 48 Hours Predicts Functional Outcomes in Basilar Artery Occlusion Stroke. Stroke. 2016;47(10):2534-2540.
• Kang DH, Jung C, Yoon W, et al. Posterior circulation CT angiography collaterals predict outcome of endovascular acute ischaemic stroke therapy for basilar artery occlusion. J Neurointerv Surg. 2016;8(8):783-786.