basilar artery

**Anatomy** - Formed by the fusion of the right and left vertebral arteries at the pontomedullary junction. It runs in the basilar sulcus of the pons and ends at the interpeduncular cistern (upper pons/midbrain) by bifurcating into the two posterior cerebral arteries (PCAs). - Part of the posterior (vertebrobasilar) circulation. It connects to the anterior circulation via the posterior communicating arteries, which complete the circle of Willis.

**Branches (caudal to rostral)** 1. Anterior inferior cerebellar artery (AICA): lateral pons (facial nucleus, vestibulocochlear nuclei, spinal trigeminal nucleus and tract), the inferior cerebellum, and the internal auditory (labyrinthine) artery to the inner ear. 2. Pontine perforating (paramedian) arteries: medial pons. 3. Superior cerebellar artery (SCA): the superior cerebellum and dorsolateral rostral pons. 4. Terminal branches, the PCAs: occipital lobe, inferior temporal lobe, and thalamus/midbrain via perforators. (The posterior inferior cerebellar artery, PICA, arises from the vertebral artery, not the basilar.)

**Clinical significance** - **Basilar artery occlusion/thrombosis**: Often preceded by a stuttering prodrome (vertigo, headache, neck pain, transient weakness). Causes include atherosclerosis (typically the proximal or mid portion), embolism (typically the distal portion), and vertebral dissection. Features include bilateral motor and sensory deficits, cranial nerve palsies, diplopia, dysarthria, dysphagia, coma, and high mortality. - **Locked-in syndrome**: Ventral pontine infarct, usually from basilar occlusion. Corticospinal and corticobulbar tracts are interrupted, so there is quadriplegia and facial/bulbar paralysis with preserved consciousness (the reticular formation is spared), cognition, and vertical eye movements and blinking (supranuclear control above the pons). Horizontal gaze is lost because the CN VI nuclei/PPRF are affected. - **Top of the basilar syndrome**: Embolic occlusion of the distal basilar artery. Causes midbrain, thalamic, and occipital infarcts with vertical gaze palsy, pupillary abnormalities, somnolence or coma, visual field defects or cortical blindness, and memory deficits. - **Medial pontine syndrome**: Paramedian pontine branches. Contralateral hemiparesis, ipsilateral CN VI palsy (diplopia/ipsilateral lateral gaze palsy), and a possible CN VII lesion. - **Lateral pontine syndrome**: AICA. Ipsilateral facial paralysis, deafness/tinnitus, vertigo, nystagmus, loss of facial pain/temperature sensation, and cerebellar ataxia. Contralateral loss of body pain/temperature. - **Basilar artery aneurysm**: Usually at the tip (bifurcation). It can cause subarachnoid hemorrhage or compress CN III. - **Vertebrobasilar insufficiency**: Transient episodes of the "5 Ds" (dizziness, diplopia, dysarthria, dysphagia, drop attacks) and ataxia. It is seen with subclavian steal syndrome and vertebral artery stenosis. - **Imaging/diagnosis**: Non-contrast CT may show a hyperdense basilar artery sign. CTA/MRA confirm occlusion. MRI DWI is more sensitive than CT for posterior fossa infarcts. - **Treatment**: IV thrombolysis within the standard window. Endovascular thrombectomy is beneficial for basilar occlusion (ATTENTION and BAOCHE trials). Secondary prevention includes antiplatelets, statins, and risk factor control.

**High-yield pearls** - Basilar = "base of the brain stem circulation": pons, cerebellum, and PCA territory. - Locked-in syndrome: "Can only blink and move eyes vertically." - Pontine hemorrhage causes pinpoint pupils, coma, and quadriplegia.