Chronic basilar artery occlusion (CBAO) refers to long-term occlusion of the basilar artery. As the occlusion becomes chronic, collateral circulation develops, reducing the high mortality and morbidity associated with acute basilar artery occlusion.
The clinical presentation of CBAO includes the following three patterns.
Posterior circulation strokes account for approximately 15–20% of all ischemic strokes. Basilar artery occlusion (BAO) accounts for only 1–4% of these, but acute and complete BAO leads to high morbidity and mortality (up to 90%) if spontaneous recanalization does not occur 2). Basilar artery stenosis has been reported in approximately 1.43% of patients with acute ischemic stroke 1).
CBAO can cause impairment in both the afferent and efferent visual pathways. Rarely, a single lesion may produce symptoms in both pathways.
Acute basilar artery occlusion causes severe brainstem ischemia and locked-in syndrome due to underdeveloped collateral circulation, with extremely high mortality. In contrast, chronic occlusion allows sufficient collateral circulation development, resulting in mild symptoms or sometimes asymptomatic presentation.
In basilar artery occlusion, the latency period from initial prodromal symptoms to stroke onset can range from several days to several months. Depending on the location of the brainstem lesion, the following symptoms may occur.
In CBAO, various neuro-ophthalmological findings appear in both efferent and afferent pathways.
Efferent Pathway Findings
Internuclear ophthalmoplegia (INO): Unilateral or bilateral adduction deficit and contralateral dissociative nystagmus due to medial longitudinal fasciculus (MLF) lesion.
One-and-a-half syndrome: Combination of ipsilateral conjugate gaze palsy and INO. Horizontal eye movements are severely limited.
Eight-and-a-half syndrome: One-and-a-half syndrome plus ipsilateral facial nerve (CN VII) palsy.
Afferent findings
Homonymous hemianopia: Most common visual field defect due to posterior cerebral artery (PCA) lesion. Occipital lobe lesions may show macular sparing and congruous visual field defects.
Cortical visual impairment: Due to bilateral occipital lobe ischemia. Light reflex is preserved but visual acuity is severely reduced.
Homonymous sectoranopia: Occlusion of the anterior or posterior choroidal artery causes a wedge-shaped defect near the horizontal meridian.
Pontine ischemia impairs the horizontal gaze pathway involving the abducens nucleus (CN VI) and the medial longitudinal fasciculus. Vertebrobasilar circulatory disorders are common in ophthalmology and present with various brainstem syndromes depending on the lesion site.
When the medial longitudinal fasciculus (MLF) in the pons is damaged, adduction of the ipsilateral eye is impaired, and dissociated nystagmus (nystagmus on abduction) appears in the contralateral eye. Bilateral INO strongly suggests a brainstem lesion. For details, see the “Main Symptoms and Clinical Findings” section.
The main causes of basilar artery occlusion are as follows:
Treatable vascular risk factors include the following:
Complete prevention is difficult, but managing vascular risk factors such as treating hypertension, diabetes, and hyperlipidemia, smoking cessation, and maintaining a healthy weight can improve prognosis. For details, see the “Standard Treatment” section.
The diagnosis of basilar artery occlusion involves a combination of multiple imaging tests.
| Test | Features | Main Use |
|---|---|---|
| CT + CTA | Fast, high accuracy, can assess calcification and plaque | Initial test, stenosis evaluation |
| MRI (DWI) | Detects hyperacute ischemic changes as high signal | Visualization of acute ischemic infarction |
| MRA | Noninvasive, low contrast dose | Evaluation of vascular course and stenosis |
| DSA | Highest resolution, excellent for visualizing collateral circulation | Detailed evaluation, endovascular treatment |
Non-contrast head CT and CT angiography (CTA) are the initial tests for BAO. CTA has high sensitivity for identifying the degree of stenosis and the extent of infarction. Diffusion-weighted MRI (DWI) can detect lesions as hyperintense areas in hyperacute cerebral infarction that are difficult to detect on T2-weighted or FLAIR images.
Combining neck CT or MRI with CTA or MRA can identify not only the occlusion site but also more proximal causative lesions (e.g., vertebral artery dissection). Digital subtraction angiography (DSA) may be required for detailed evaluation of collateral circulation or pre-treatment assessment.
Cortical or brainstem lesions causing efferent or afferent symptoms are considered in the differential diagnosis.
Consensus on the optimal acute management of BAO has not been established, but it is generally treated similarly to other large vessel occlusive diseases.
Rapid stroke evaluation is critical, and aggressive intervention should be considered if within the therapeutic time window.
Some patients with chronic BAO have sufficient collateral circulation to vital structures, and the following secondary prevention is the mainstay of treatment.
Intravenous thrombolysis (t-PA) is indicated within 4.5 hours of onset. Mechanical thrombectomy may be effective within 6 to 24 hours. In any case, prompt consultation and diagnosis greatly influence prognosis.
The basilar artery begins at the medullopontine junction and ends at the pons-midbrain junction. Anatomically, it is divided into three segments: proximal, middle, and distal, and bifurcates into the left and right posterior cerebral arteries (PCA) as terminal branches.
The posterior cerebral artery is a branch of the basilar artery and supplies the following structures.
Blood flow to the visual cortex is mostly supplied by the calcarine artery, a terminal branch of the posterior cerebral artery, but also by the posterior temporal artery and the parieto-occipital artery. Occlusion of the main trunk of the posterior cerebral artery causes homonymous hemianopia and thalamic syndrome with contralateral sensory disturbance, while occlusion of only the calcarine artery results in homonymous hemianopia alone.
Occlusive lesions can occur at any site in the basilar artery. Ischemia most often occurs in the paramedian region of the pontine base, but sometimes extends to the paramedian region of the pontine tegmentum. Atherosclerotic lesions are common in the proximal and middle portions of the basilar artery.
Top of the basilar syndrome and thrombus extension are life-threatening. In locked-in syndrome, consciousness is clear, but all voluntary movement is lost, and only vertical eye movements may be preserved.
Collateralization is a compensatory mechanism against ischemia. In CBAO, sufficient development of collateral circulation to the PCA is crucial for symptom reduction. Unlike acute occlusion, chronic occlusion may result in mild symptoms due to the development of collateral blood flow.
Even in complete homonymous hemianopia due to occipital lobe lesions, a visual field of approximately 5 to 10 degrees around the center may remain (macular sparing). Causes include dual blood supply to the occipital pole (the calcarine artery, a branch of the posterior cerebral artery, and branches of the middle cerebral artery) and the large cortical area corresponding to the macular visual field.
The benefit of endovascular treatment for large vessel occlusion in the anterior circulation is established, but challenges remain for the posterior circulation. Mechanical thrombectomy has shown promising results in BAO patients within 6 to 24 hours of symptom onset, and expansion of the treatment time window is being considered.
Akram et al. (2025) reported a case of a 76-year-old diabetic patient with basilar artery stenosis, noting that 50% basilar artery stenosis carries a 46% risk of recurrence within 90 days. The SAMMPRIS trial showed that stenting of the basilar artery had a higher perioperative risk compared to medical therapy (20.8% vs 6.7%), indicating that the indication for intracranial stenting should be carefully considered 1).
Wong et al. (2022) reported a case in which giant cell arteritis (GCA) caused bilateral vertebral artery thrombosis and posterior circulation stroke. The patient presented with cortical blindness due to bilateral occipital lobe infarction, and diagnosis was confirmed by temporal artery biopsy. Giant cell arteritis should be considered as a rare cause of posterior circulation stroke in the differential diagnosis 3).
Costa et al. (2022) reported a case of bilateral vertebral artery occlusion treated with V4 segment stenting, resulting in good recovery. This suggests the efficacy of endovascular treatment for vertebrobasilar artery occlusion refractory to medical therapy 4).
