Basilar artery occlusion
The incidence of BAO is approximately 1 patient per 100 000 per year. The most common cause of BAO is atherosclerotic occlusion with local thrombosis due to severe stenosis as well as embolic occlusions from cardiac or larger artery sources. BAO can also result from extension of vertebral artery dissection, an important consideration in younger patients without the usual cerebrovascular risk factors.
Unlike middle cerebral and anterior cerebral circulation occlusions, in which acute onset of focal symptoms is common, BAO can mimic nonstroke conditions such as gastroparesis and vertigo, and symptoms are commonly nonspecific with nausea, headache, and neck pain. Latency between initial prodromal symptoms and actual stroke is also prolonged compared with anterior and middle cerebral circulation strokes; it can be days to months, with symptoms increasing in frequency leading up to the stroke.
Basilar artery occlusion commonly results in ischemia to the pons, usually involving the middle of the pons, which impacts descending long-motor tracts and crossing cerebellar fibers as well as oculomotor fibers. As a result, the predominant consequences of pontine ischemia are motor and oculomotor.
Level of consciousness can also be affected, and patients with BAO may present with coma in the setting of bilateral ischemia. Large pontine infarctions due to BAO are the most common cause of locked-in syndrome.
Due to the presence of descending long-motor tracts and crossing cerebellar fibers, patients with BAO and pontine ischemia present with lateralized paresis as well as some motor or reflex abnormality on the non-hemiparetic side, although these can be subtle (slight weakness, hyperreflexia, abnormal spontaneous movements, shivering, jerking, etc).
Bulbar involvement results in facial weakness, dysarthria, dysphagia, and in some cases dysphonia. Somatosensory symptoms are generally uncommon with BAO but can occur.
Related topic: Drug-induced stroke
I65.1 – Occlusion and stenosis of basilar artery
195180004 – Basilar artery occlusion
- Acute peripheral vestibulopathy – Rapid onset of vertigo, nausea / vomiting, and gait unsteadiness with head motion intolerance and nystagmus. Can last for days to weeks, usually self-limited viral etiology.
- Subarachnoid hemorrhage
- Nonconvulsive status epilepticus or post-ictal state
- Hypoxic ischemic encephalopathy
- Central nervous system infection (meningitis or encephalitis)
- Bilateral hemispheric strokes
- Guillain-Barré syndrome
- Miller Fisher syndrome
- Myasthenic crisis
- Benign positional vertigo
- Basilar-type migraine