Posterior Cerebral Artery (PCA) Stroke: A High-Yield Clinical Guide
A 68-year-old who "forgot how to read" his own book — the ER case that opens this clinical guide to posterior cerebral artery (PCA) stroke syndromes.
What every clinician should recognize about back-of-the-brain strokes.
- →PCA strokes account for roughly 5–10% of all ischemic strokes and rarely cause classic limb weakness — they present with vision, memory, or behavioral changes instead.
- →Three functional zones to remember: the cortex ("brain cinema"), the thalamus ("grand central station"), and the midbrain ("cable trunk").
- →Alexia without agraphia — writing intact, reading lost — is a near-pathognomonic sign of a left PCA stroke involving the splenium.
- →The NIHSS underestimates posterior strokes. A devastating PCA infarct can score as low as 1–3. Suspicion matters more than the score.
- →Treat new, unexplained vision loss, "out-of-proportion" sleepiness, or sudden memory failure as a stroke until proven otherwise.
It is 2:00 a.m. in the ER. A 68-year-old man is wheeled in by his wife. He has no facial droop. His speech is perfectly fluent. His grip strength is 5/5 on both sides. The triage nurse has put him down for an "ocular problem" or maybe an atypical migraine, because his only complaint is bizarre: he suddenly "forgot how to read" his book.
I walk into the room and hand him a clipboard and a pen. "Can you write a sentence for me?"
Without hesitating, he writes, in clean cursive: I am at the hospital because my vision is weird.
I take the clipboard, wait a minute, and hand it back. "Read what you just wrote." He stares at his own handwriting. He turns the paper sideways. He turns it back. Nothing. He cannot read a single word he just produced. Next, I sweep my fingers through his visual fields and watch his eyes. He misses every motion on the right side — a clean right homonymous hemianopia.
How did I get there? By recognizing that the perfectly normal motor exam was a red herring. The fact that he can write but cannot read is a disconnection syndrome called alexia without agraphia. Combined with the right-sided field cut, this points to exactly one culprit: a stroke in the left posterior cerebral artery (PCA) territory, involving the dominant occipital lobe and the splenium of the corpus callosum.1
Welcome to TheVascularBrain.com. This is your high-yield walkthrough of one of the most under-recognized strokes in clinical medicine.
What is a PCA stroke?
The posterior cerebral artery supplies the back third of the brain. It feeds the occipital cortex, the inferior surface of the temporal lobe (including the hippocampus), large portions of the thalamus, and parts of the midbrain. PCA strokes make up roughly 5–10% of all ischemic strokes.2 Most are embolic, frequently from the heart or the vertebrobasilar circulation. A smaller fraction are caused by in-situ atherosclerosis of the PCA itself or by extension of a basilar artery occlusion.
Because the PCA's territory is so functionally diverse, a single artery occlusion can present in radically different ways. The trick to localizing PCA strokes is to remember three distinct zones — each with its own signature syndrome.
Zone 1 — "The Brain Cinema" (Cortex)
When the distal PCA is occluded, the damage hits the visual and cognitive pathways of the occipital and temporal lobes. This is where most of the classic, board-question PCA syndromes live.
Contralateral homonymous hemianopia
This is the single most characteristic finding of a PCA stroke. Both eyes lose the same half of their visual field — opposite to the side of the stroke. A patient with a left PCA stroke loses the right half of vision in both eyes. The central (macular) field is often spared because the occipital pole receives collateral supply from the middle cerebral artery.2
Patients rarely walk in saying, "I'm blind on the right." They walk in saying, "I keep bumping into things," or "people keep startling me from the side." Confrontation visual fields take 20 seconds and will catch this every time.
Alexia without agraphia
This is the syndrome our ER patient had. A left PCA stroke damages two structures: the left occipital cortex (so he cannot see the right side of the page) and the splenium of the corpus callosum (so the visual information his right occipital lobe is still receiving cannot cross over to the left-sided language network).
The result is striking: the patient can write a perfect sentence — because the language and motor systems are intact — but cannot read what he just wrote. Letters look like meaningless shapes. It is one of the few times in neurology that having the patient do something he already did, two minutes later, makes the diagnosis for you.1
Prosopagnosia and visual agnosia
Right (non-dominant) PCA strokes can produce "face blindness" (prosopagnosia) — patients no longer recognize family members by face, though they recognize them instantly by voice. A broader inability to recognize familiar objects, despite intact basic vision, is called visual agnosia. The eye works. The seeing-and-knowing pipeline is broken.
Cortical blindness and Anton syndrome
Bilateral occipital infarcts — often from a "top of the basilar" embolic event involving both PCAs — cause complete cortical blindness.3 What makes this fascinating, and dangerous, is that a subset of these patients have Anton syndrome: they deny being blind. They confabulate vivid, confident descriptions of a room they cannot see. Families often interpret this as confusion or delirium. The bedside clue is asking them to describe something specific in the room — and watching the descriptions fall apart.
Zone 2 — "Grand Central Station" (Thalamus)
The proximal PCA gives off deep penetrating branches that supply most of the thalamus. The thalamus is the brain's relay hub — every sensory pathway except smell, every arousal signal, and large parts of memory and behavior pass through it. Strokes here cause syndromes that look less like "stroke" and more like a psychiatric or metabolic problem.4
Dejerine-Roussy (thalamic pain syndrome)
A stroke in the thalamogeniculate artery territory often presents first with simple contralateral numbness. Weeks to months later, that numb side begins to burn. Patients describe a deep, relentless pain that is triggered by touch — clothes against the skin, a bedsheet, a breeze — a phenomenon called allodynia. It is one of the most difficult-to-treat pain syndromes in neurology, and it can develop long after the acute stroke has been forgotten.
Artery of Percheron infarction
In roughly 4–11% of people, both paramedian thalamic territories — plus the rostral midbrain — are supplied by a single arterial trunk arising from the proximal PCA. This anatomical variant is called the artery of Percheron.5 When it occludes, a single small lesion produces a devastating bilateral thalamic stroke.
The classic presentation is a triad: fluctuating consciousness or profound hypersomnolence, severe memory impairment, and vertical gaze palsy. Patients are frequently misdiagnosed as encephalopathic, intoxicated, or post-ictal. The clue is the vertical gaze — once you check it and see they cannot look up, the differential collapses.
Any patient who arrives with sudden, unexplained sleepiness or memory loss out of proportion to other findings deserves an MRI before they get labeled "altered mental status." Bilateral paramedian thalamic infarcts often look unremarkable on early CT and will get missed by every screening tool except diffusion-weighted MRI.
Zone 3 — "The Cable Trunk" (Midbrain)
When the PCA's penetrating branches into the midbrain are involved, the result is a small lesion in a very high-density piece of wiring — cranial nerve nuclei, descending motor tracts, and gaze pathways are all crammed into a few cubic centimeters. The classic eponymous brainstem syndromes live here.
Parinaud syndrome (dorsal midbrain syndrome)
A stroke in the dorsal (posterior) midbrain, near the pretectal area, produces a distinctive constellation:
- Upward gaze palsy — patients cannot look up.
- Convergence-retraction nystagmus — on attempted upgaze, the eyes jerk inward and the globes retract.
- Light-near dissociation ("pseudo-Argyll Robertson pupils") — pupils respond poorly to light but constrict normally with accommodation.
- Collier's sign — bilateral upper eyelid retraction, giving a "wide-eyed" look.
Classically described with pineal tumors, Parinaud syndrome can also be the presenting picture of a small dorsal midbrain stroke.
Weber, Benedikt, and Claude syndromes
These are the classic "crossed" midbrain syndromes. The shared rule: a "down and out" eye on the side of the stroke (an ipsilateral third nerve palsy) paired with contralateral findings that depend on exactly which tract the lesion clips:
- Weber syndrome — CN III palsy + contralateral hemiparesis (cerebral peduncle).
- Benedikt syndrome — CN III palsy + contralateral ataxia and tremor (red nucleus involvement).
- Claude syndrome — CN III palsy + contralateral ataxia (red nucleus and superior cerebellar peduncle, without strong motor signs).
Why the NIHSS misses PCA strokes
The NIH Stroke Scale was built around anterior circulation strokes, and it shows. A full hemianopia scores only 2 points. Memory loss, executive dysfunction, vertical gaze palsy, and behavioral change score zero. A patient with a devastating bilateral thalamic stroke from an artery of Percheron occlusion can score 1–3 on the NIHSS — well below the cutoff most centers use to trigger advanced imaging.6
A low NIHSS in a patient who suddenly cannot read, recognize his wife, or stay awake is not a reassuring score. It is a missed posterior circulation stroke.
The bottom line
PCA strokes are camouflaged. They look like ocular problems, migraine, dementia, delirium, or psychiatric episodes. The unifying clue is that something specific in vision, memory, attention, or eye movement has changed suddenly — and the motor exam is reassuringly, misleadingly normal.
The single highest-yield bedside maneuver is a careful confrontation visual field exam. The second is a quick test of reading versus writing. The third is checking vertical gaze. None of them take more than a minute. All of them have caught strokes the NIHSS would have missed.
If the back of your brain is in trouble, the front of your brain often does not know — but a careful clinician at the bedside will.
Frequently asked questions.
What is a posterior cerebral artery (PCA) stroke?
A PCA stroke is an ischemic stroke in the territory supplied by the posterior cerebral artery, which feeds the occipital and inferior temporal cortex, the thalamus, and parts of the midbrain. It accounts for 5–10% of ischemic strokes and classically presents with visual, memory, or behavioral changes rather than weakness.
What is the most common symptom of a PCA stroke?
The single most characteristic symptom is contralateral homonymous hemianopia — both eyes lose the same half of the visual field. Patients rarely describe it as blindness; they describe bumping into things or being startled by people on one side.
What is alexia without agraphia?
Alexia without agraphia is a disconnection syndrome in which a patient writes fluently but cannot read what they just wrote. It is caused by a left PCA stroke that damages both the left occipital cortex and the splenium of the corpus callosum, disconnecting visual input from the language network.
What is Anton syndrome?
Anton syndrome is cortical blindness with denial of blindness. Patients are completely unable to see but confidently confabulate visual descriptions, often delaying the recognition of a stroke. It is most commonly caused by bilateral occipital infarcts from a top-of-the-basilar embolic event.
What is artery of Percheron infarction?
The artery of Percheron is an anatomical variant in which a single trunk off the proximal PCA supplies both paramedian thalami and part of the rostral midbrain. Occlusion produces a classic triad of fluctuating consciousness or hypersomnolence, severe memory loss, and vertical gaze palsy — a presentation easily mistaken for encephalopathy.
Why does the NIHSS miss PCA strokes?
The NIHSS was built around anterior circulation strokes. Hemianopia scores only 2 points, and memory loss, executive dysfunction, behavioral change, and vertical gaze palsy score zero. A devastating PCA stroke can score 1–3 on the NIHSS, below most centers' thresholds for advanced imaging. Clinical suspicion beats the score.
How are PCA strokes diagnosed?
Diffusion-weighted MRI is the most sensitive test for PCA territory infarcts. Non-contrast CT often appears normal early. CT or MR angiography evaluates for PCA, basilar, or vertebral artery occlusion. Any patient with a new visual field defect, alexia, sudden hypersomnolence, or unexplained memory loss should be considered for urgent neuroimaging.
References.
- Geschwind N. Disconnexion syndromes in animals and man. Brain. 1965;88(2):237-294. PubMed
- Brandt T, Steinke W, Thie A, Pessin MS, Caplan LR. Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome. Cerebrovasc Dis. 2000;10(3):170-182. PubMed
- Caplan LR. "Top of the basilar" syndrome. Neurology. 1980;30(1):72-79. PubMed
- Schmahmann JD. Vascular syndromes of the thalamus. Stroke. 2003;34(9):2264-2278. PubMed
- Lazzaro NA, Wright B, Castillo M, et al. Artery of percheron infarction: imaging patterns and clinical spectrum. AJNR Am J Neuroradiol. 2010;31(7):1283-1289. PubMed
- Martin-Schild S, Albright KC, Tanksley J, et al. Zero on the NIHSS does not equal the absence of stroke. Ann Emerg Med. 2011;57(1):42-45. PubMed
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