posterior cerebral artery

**Anatomy** - Origin: The basilar artery bifurcates at the pontomesencephalic junction into the two PCAs. In ~15-20% of people there is a fetal-type PCA, in which the PCA arises from the internal carotid artery via a large posterior communicating artery (PCom). - Segments: P1 (precommunicating, from the basilar bifurcation to the PCom), P2 (ambient, runs around the midbrain), P3 (quadrigeminal), P4 (calcarine and parieto-occipital branches). - Circle of Willis: The PCom connects the PCA to the ICA, linking the anterior and posterior circulations. The PCA is also the posterior border of the circle. - Relationship to the oculomotor nerve (CN III): CN III passes between the PCA and the superior cerebellar artery (SCA). Aneurysms of the PCA or PCom can compress CN III, causing a "down and out" eye, ptosis, and a dilated pupil.

**Territory supplied** - Cortical branches: Occipital lobe (primary visual cortex/calcarine cortex), inferior and medial temporal lobe, and the splenium of the corpus callosum. - Penetrating (central) branches from P1/P2: Thalamoperforators (thalamogeniculate and paramedian thalamic arteries) supply the thalamus, subthalamic nucleus, and midbrain (the artery of Percheron is a single trunk from P1 supplying both paramedian thalami). - Macular sparing: The occipital pole (macular representation) has dual blood supply from the PCA and MCA, so central vision is spared.

**Clinical syndromes of PCA occlusion (usually embolic, e.g., from the vertebrobasilar system or heart)** - Contralateral homonymous hemianopia with macular sparing (calcarine cortex infarct). - Visual agnosia, prosopagnosia, and alexia without agraphia (dominant PCA infarct involving the left occipital lobe plus the splenium of the corpus callosum; disconnects the intact right visual cortex from the left angular gyrus/language areas). - Cortical blindness (bilateral PCA infarcts) and Anton syndrome (denial of blindness). Balint syndrome with bilateral parieto-occipital lesions (simultanagnosia, optic ataxia, oculomotor apraxia). - Memory impairment (medial temporal/hippocampus involvement). - Thalamic involvement: Dejerine-Roussy (thalamic pain) syndrome, with contralateral hemisensory loss followed by severe central pain (thalamogeniculate branches/VPL/VPM nuclei). - P1 or midbrain involvement: CN III palsy with contralateral hemiplegia (Weber syndrome, involving the cerebral peduncle), contralateral ataxia/tremor (Benedikt syndrome, red nucleus), vertical gaze palsy (rostral interstitial nucleus of the MLF/Parinaud), "top of the basilar" syndrome. - Artery of Percheron infarct: Bilateral paramedian thalamic infarcts with altered consciousness, vertical gaze palsy, and memory deficits.

**Distinguishing from MCA/ACA stroke** - MCA: contralateral face and arm weakness and sensory loss, aphasia (dominant) or hemineglect (nondominant). Hemianopia may occur but is usually accompanied by motor/sensory deficits. - PCA: isolated visual field defect, often without motor weakness (a key point for boards).

**Diagnosis and management** - Noncontrast head CT first to exclude hemorrhage; then CT angiography/MRI with diffusion-weighted imaging (DWI). Posterior circulation strokes can be missed on CT, so MRI is more sensitive. - IV alteplase/tenecteplase if within the window (up to 4.5 hours) and no contraindications. Endovascular thrombectomy may be considered for select basilar/PCA occlusions. Secondary prevention with antiplatelets, statins, BP control, and anticoagulation if atrial fibrillation.

**High-yield pearls** - PCA stroke = contralateral homonymous hemianopia with macular sparing. - Left PCA + splenium = alexia without agraphia. - Thalamic branch = Dejerine-Roussy syndrome. - CN III runs between the PCA and SCA; PCom aneurysm = painful CN III palsy with pupil involvement. - Bilateral PCA = cortical blindness (pupillary light reflex intact because the lesion is post-geniculate). - Uncal (transtentorial) herniation can compress the PCA and cause an occipital infarct.