What are the symptoms of posterior cerebral artery syndrome?

The core symptom is sudden loss of the same half of the visual field in both eyes (a contralateral homonymous hemianopia), often with central vision spared and limb strength normal. Depending on the branch involved, patients may also be unable to read (left PCA), fail to recognize faces (right PCA), have trouble forming new memories, develop one-sided numbness and later burning pain (thalamus), or have a droopy eyelid and double vision with weakness of the opposite limbs (midbrain). Because strength is often normal, PCA strokes are easy to miss.

Why is the macula spared in a PCA stroke?

The classic exam answer is dual blood supply: the occipital pole, where central (macular) vision is mapped, receives collateral flow from the middle cerebral artery as well as the PCA, so it often survives a PCA occlusion. Other explanations are the macula's disproportionately large cortical representation, anastomoses with the opposite side at the occipital pole, and bilateral representation of the macula. Macular sparing points to the occipital cortex, but it is not specific, and its absence does not exclude a PCA stroke.

Can a posterior cerebral artery stroke cause weakness?

Yes, although many PCA strokes leave strength intact. A proximal PCA occlusion can infarct the cerebral peduncle in the midbrain, causing contralateral hemiparesis, often with an ipsilateral third nerve palsy (Weber syndrome). Thalamic infarction causes contralateral sensory loss that can mimic a middle cerebral artery stroke. A homonymous hemianopia, a third nerve palsy, drowsiness or a vertical gaze palsy, without aphasia or neglect, points back to the PCA.

What is alexia without agraphia, and which artery is involved?

Alexia without agraphia, or pure alexia, is loss of reading with preserved writing, speech and comprehension: patients can write a sentence but cannot read it back. It classically follows a left posterior cerebral artery stroke that infarcts the left occipital cortex and the splenium of the corpus callosum, usually with a right homonymous hemianopia. In the classic explanation, the intact right visual cortex sees the words but cannot send them across the damaged splenium to the left-hemisphere language areas; imaging studies also implicate the left fusiform visual word form area.

What is the difference between Anton syndrome and Balint syndrome?

Anton syndrome is cortical blindness from bilateral occipital infarction, often an embolus at the basilar tip blocking both posterior cerebral arteries, in which the patient denies being blind and confabulates; pupillary light reflexes and fundi are normal. Balint syndrome is the triad of simultanagnosia, optic ataxia and oculomotor apraxia from bilateral parieto-occipital damage. In stroke it usually reflects bilateral border-zone (watershed) infarcts between the middle and posterior cerebral artery territories rather than a PCA occlusion.

How is an acute PCA stroke treated?

Under the 2026 AHA/ASA acute ischemic stroke guideline, a patient with a disabling deficit within 4.5 hours of onset should receive IV thrombolysis as fast as possible, with tenecteplase 0.25 mg/kg (maximum 25 mg) as a single bolus or alteplase 0.9 mg/kg. Basilar artery occlusion within 24 hours with an NIHSS of 10 or more and only limited early infarction calls for thrombectomy, but thrombectomy is not routinely recommended for an isolated PCA occlusion. Afterward, look for the source; atrial fibrillation calls for anticoagulation.

Posterior Cerebral Artery Syndrome: Signs & USMLE Case

Posterior cerebral artery (PCA) syndrome is an ischemic stroke in PCA territory: the occipital lobe, the inferomedial temporal lobe including the hippocampus, the splenium of the corpus callosum, the thalamus and the upper midbrain. Its signature is a contralateral homonymous hemianopia, often with macular sparing, frequently with full strength and normal speech. The branch involved adds the classic exam clues: alexia without agraphia (left PCA plus splenium), prosopagnosia (right or bilateral occipitotemporal cortex), hemisensory loss followed by Dejerine–Roussy thalamic pain (thalamic branches) or Weber syndrome, an ipsilateral CN III palsy with contralateral hemiparesis (midbrain perforators). In an isolated PCA infarct, hunt for an embolic source, classically atrial fibrillation.

PCA syndrome at a glance

Feature	What to know
Territory	Occipital lobe, inferomedial temporal lobe and hippocampus, splenium, thalamus, upper midbrain
How common	About 5–12% of ischemic strokes
Signature sign	Contralateral homonymous hemianopia, often with macular sparing; strength often normal
Left PCA extras	Alexia without agraphia when the splenium is involved; sometimes color anomia
Right PCA extras	Prosopagnosia (face blindness)
Both PCAs	Cortical blindness with normal pupillary reflexes; Anton syndrome if the patient denies it
Thalamic branches	Contralateral hemisensory loss, later burning central pain (Dejerine–Roussy)
Midbrain branches	Weber syndrome, vertical gaze palsy
Main causes	Cardioembolism (atrial fibrillation), vertebrobasilar atherosclerosis, small-vessel disease, dissection; a fetal PCA lets carotid disease cause it
Imaging	Noncontrast CT first to exclude hemorrhage (often normal early), CT angiography, diffusion-weighted MRI to confirm
Acute treatment (2026 AHA/ASA)	IV tenecteplase or alteplase within 4.5 hours for a disabling deficit; thrombectomy for basilar occlusion, not routinely for an isolated PCA occlusion

PCA anatomy: segments and territories

In about 70% of people the PCAs arise from the basilar bifurcation as the terminal branches of the posterior circulation. In a fetal PCA, a large posterior communicating artery (PComm) fills the PCA from the internal carotid, so carotid stenosis or a carotid embolus can infarct the occipital lobe.

Segment	Course	Key branches	Supplies
P1	Basilar tip to the PComm junction	Thalamoperforating (thalamic–subthalamic) and paramedian midbrain perforators; artery of Percheron (variant)	Paramedian thalamus, subthalamic region, rostral midbrain
P2	Curves around the midbrain from the PComm	Thalamogeniculate arteries, posterior choroidal arteries, peduncular perforators	Ventrolateral thalamus (sensory relay nuclei), lateral geniculate body, pulvinar, hippocampus and parahippocampal gyrus, lateral midbrain
P3	Quadrigeminal cistern	Anterior and posterior inferior temporal arteries	Inferior temporal lobe
P4	Calcarine fissure	Calcarine and parieto-occipital arteries	Primary visual cortex, medial occipital lobe

Two details show up in questions: the splenium is the only part of the corpus callosum fed by the vertebrobasilar system (terminal and choroidal PCA branches), and the anterior thalamus is fed by the tuberothalamic artery from the PComm, not by the PCA.

Signs of PCA syndrome: lesion-to-deficit map

Visual field loss is the most common presentation, followed by sensorimotor deficits, dizziness, cognitive and eye-movement problems, and ataxia.

Territory (branch)	Deficit	Vignette clue
Calcarine cortex, one side (P4)	Contralateral congruous homonymous hemianopia, often with macular sparing	Bumps into things on one side; strength normal
Cuneus (above the calcarine fissure) vs lingual gyrus (below)	Contralateral inferior vs superior quadrantanopia	Quadrant field cut, nothing else
Left occipital cortex + splenium	Alexia without agraphia with a right hemianopia	Writes a note, cannot read it back
Right or bilateral fusiform (occipitotemporal) cortex	Prosopagnosia	Knows his wife by her voice, not her face
Ventral occipital cortex below the calcarine fissure	Achromatopsia (hemiachromatopsia if one-sided)	Colors drain to gray
Occipitotemporal association cortex	Visual agnosia: apperceptive (form not perceived) or associative (meaning not attached)	Cannot name a key by sight, names it by touch
Hippocampus (P2 branches) or thalamus	Anterograde memory loss	Keeps asking the same question
Both occipital lobes	Cortical blindness; Anton syndrome if denied	Blind with brisk pupils, insists she can see
Ventrolateral thalamus (thalamogeniculate, P2)	Contralateral hemisensory loss, later Dejerine–Roussy pain	Burning pain weeks after a "numb" stroke
Subthalamic nucleus	Contralateral hemiballismus	Sudden flinging of one arm
Ventromedial midbrain (perforators)	Weber syndrome: ipsilateral CN III palsy + contralateral hemiparesis	Ptosis, down-and-out eye, weak opposite limbs
Artery of Percheron (one P1 perforator to both sides)	Bilateral paramedian thalamic ± midbrain infarcts: altered consciousness, memory loss, vertical gaze palsy	Will not stay awake, cannot look up

Why the macula is spared

A one-sided occipital infarct often leaves an island of central vision inside the hemianopia. StatPearls lists four explanations:

Dual blood supply (the classic exam answer). The occipital pole, where the macula is mapped, receives collateral flow from the middle cerebral artery (MCA) as well as the PCA, so it can survive a PCA occlusion.
A huge cortical map. The macula's cortical representation is disproportionately large, so a partial infarct rarely removes all of it.
Anastomoses at the occipital pole with branches from the opposite side.
Bilateral representation of the macula in both occipital lobes.

Macular sparing points to the occipital cortex but is not specific: it also occurs with optic radiation and optic tract lesions, and a hemianopia that splits the macula does not exclude a PCA stroke. Congruous defects (nearly identical in the two eyes) point posteriorly; an incongruous hemianopia with a relative afferent pupillary defect points to the optic tract. Occipital lesions cause about 45% of homonymous hemianopias. After stroke, 20–60% of patients improve within a month, most recovery comes by 3 months, and gains after 6 months are rare.

Named syndromes that get confused

Alexia without agraphia (pure alexia)

Lesion: a left PCA infarct of the left occipital cortex and the splenium, usually with a right homonymous hemianopia; some patients also cannot name colors.
What is lost: reading. Speech, comprehension, repetition and writing are spared, so the patient writes a sentence and then cannot read it. Many read slowly, letter by letter.
Classic mechanism: pure alexia is a classic disconnection syndrome and one of the first described. With the left visual cortex infarcted, written words reach only the right visual cortex, and the damaged splenium cannot relay them to the left-hemisphere language areas. Imaging studies also implicate the left fusiform visual word form area; either way, the lesion sits in left PCA territory.
Contrast: alexia with agraphia follows damage to the left angular gyrus and impairs both reading and writing, usually with aphasia.

Cortical blindness, Anton syndrome and Balint syndrome

Feature	Cortical blindness	Anton syndrome	Balint syndrome
Lesion	Both occipital lobes	Both occipital lobes	Both parieto-occipital regions (dorsal stream)
Usual stroke cause	Both PCAs, e.g., an embolus to the basilar tip	Same	Bilateral border-zone (watershed) infarcts where MCA and PCA territories meet
Key findings	No vision; pupillary light reflexes and fundi normal	Cortical blindness plus denial and confabulation	Simultanagnosia, optic ataxia, oculomotor apraxia

Why Balint is usually not a PCA stroke: its triad needs damage to both dorsal parieto-occipital regions, the border zone between the MCA and PCA territories. A PCA occlusion mainly hits medial occipital and inferior temporal cortex, so its signature is field loss or blindness.

Thalamic syndromes

Thalamogeniculate (P2) infarct: contralateral sensory loss in the face, arm and leg from the ventral posterior nuclei.
Dejerine–Roussy syndrome (central post-stroke pain): constant, burning, poorly localized pain on the numb side, with allodynia in over two-thirds. Most cases start within a month, but some appear years later. Amitriptyline is the best-studied drug and lamotrigine the best-supported anticonvulsant.
Pure sensory stroke without a field cut is usually a small-vessel lacune in the ventral posterior thalamus, not a cortical PCA syndrome: compare the lacunar syndromes and the thalamic nuclei.
Paramedian infarcts (P1 thalamoperforators or an artery of Percheron) cause drowsiness or confusion, memory loss and vertical gaze palsy. The artery of Percheron itself is small and hard to see on vascular imaging, so the clue is the bilateral paramedian thalamic pattern on MRI.

Midbrain: Weber syndrome and the top of the basilar

Weber syndrome (ventromedial midbrain: CN III fascicles and cerebral peduncle): ipsilateral CN III palsy (ptosis, eye down and out, sometimes a dilated pupil) with contralateral hemiparesis. It most often results from occlusion of a PCA branch.
Benedikt syndrome (midbrain tegmentum) pairs the CN III palsy with contralateral involuntary movements such as tremor; Claude syndrome pairs it with contralateral ataxia. Drill them with the brainstem syndromes mnemonic.
Top of the basilar: a basilar-tip embolus can infarct both PCA territories, both thalami and the midbrain: bilateral visual loss or cortical blindness, vertical gaze palsy, impaired awareness, sometimes peduncular hallucinosis.

Causes of PCA stroke

Cardioembolism: especially important in isolated PCA infarction; atrial fibrillation is the most common source.
Large-artery atherosclerosis: vertebral, basilar or proximal PCA disease is found in about a third of patients with cortical PCA infarcts.
Small-vessel disease: hypertension-related disease of the P1 and P2 perforators causes thalamic and midbrain lacunes, the most frequent subtype (over a third) in one large registry.
Vertebral artery dissection: one of the most common causes of stroke before age 45; expect one-sided neck pain or occipital headache, often after minor neck trauma or manipulation.
Fetal PCA: a carotid stenosis or carotid embolus causes the PCA-territory infarct.
Others: migraine, MELAS in young patients with occipital infarcts, and PCA compression during transtentorial herniation.

Imaging and workup

First minutes: fingerstick glucose and noncontrast head CT to exclude hemorrhage. CT is often normal in the first hours, and small infarcts may show only on MRI.
Vessels: CT angiography of the head and neck shows a basilar occlusion, a PCA cutoff, a dissection or a fetal PCA.
Diffusion-weighted MRI is highly sensitive for early ischemia and confirms occipital, thalamic or midbrain infarcts.
pc-ASPECTS scores early posterior-circulation ischemia out of 10, subtracting 1 point each for the left and right thalamus, cerebellum and PCA territory and 2 points each for the midbrain and pons; the 2026 guideline's basilar thrombectomy recommendation, like the trials behind it, requires a score of ≥6.
Find the source: ECG and prolonged cardiac monitoring for atrial fibrillation, and echocardiography (transthoracic, transesophageal when needed).

Acute management under the 2026 AHA/ASA guideline

The AHA/ASA 2026 Guideline for the Early Management of Patients With Acute Ischemic Stroke (published online 26 January 2026) replaces the 2018 guideline and its 2019 update. Applied to a PCA stroke:

IV thrombolysis within 4.5 hours for a disabling deficit, as fast as possible, regardless of NIHSS score and without waiting for advanced imaging: tenecteplase 0.25 mg/kg (maximum 25 mg) as a single bolus or alteplase 0.9 mg/kg (maximum 90 mg; 10% as a bolus, the rest over 60 minutes).
Non-disabling deficits: thrombolysis showed no benefit; dual antiplatelet therapy is preferred. PCA strokes often score low on the NIHSS, so judge whether the deficit is disabling, not the number.
Extended window: for wake-up strokes or 4.5–9 hours from onset, thrombolysis may be considered when MRI shows a DWI–FLAIR mismatch (an infarct probably less than about 4.5 hours old) or perfusion imaging shows salvageable penumbra.
FDA status: tenecteplase (TNKase) has been FDA-approved for acute ischemic stroke in adults since February 2025. Its label gives a weight-tiered single 5-second bolus (maximum 25 mg) started within 3 hours of onset, the same window as alteplase's US label, so treatment from 3 to 4.5 hours rests on the guideline rather than the labels.
Thrombectomy: strongly recommended for basilar artery occlusion within 24 hours in patients with NIHSS ≥10, limited early infarction (pc-ASPECTS ≥6) and no significant disability before the stroke (mRS 0–1); its benefit with NIHSS 6–9 is not well established. For an isolated PCA occlusion, a medium or distal vessel, it is not routinely recommended outside a clinical trial: in the 2025 DISTAL trial, which included P1–P3 occlusions, thrombectomy did not reduce disability or death compared with best medical treatment.
Blood pressure: below 185/110 mm Hg before thrombolysis and below 180/105 mm Hg for at least 24 hours afterward; the 2026 guideline advises against intensive lowering of systolic pressure to below 140 mm Hg after thrombolysis or thrombectomy.
Secondary prevention: anticoagulation for atrial fibrillation; antiplatelet therapy, a statin and blood pressure control for atherosclerotic and small-vessel causes.

Practice these decisions with tPA and thrombectomy questions and the anticoagulation side with atrial fibrillation.

PCA vs MCA vs ACA vs basilar stroke

Feature	PCA	MCA	ACA	Basilar
Territory	Occipital lobe, inferomedial temporal lobe, thalamus, midbrain	Lateral frontal, parietal and temporal lobes; basal ganglia and internal capsule	Medial frontal and parietal lobes (leg cortex)	Pons, midbrain, cerebellum; both PCAs and thalami at the tip
Weakness	Often none; contralateral hemiparesis if the midbrain is hit	Contralateral, face and arm worse than leg	Contralateral, leg worse than arm	Hemiparesis or quadriparesis, crossed signs
Vision	Contralateral homonymous hemianopia, often macular sparing	Contralateral field cut from the optic radiations	Usually spared	Bilateral visual loss or cortical blindness (tip)
Higher function	Left: alexia without agraphia; right: prosopagnosia; memory loss	Left: aphasia; right: neglect and apraxia	Apathy, confusion, mutism, grasp reflex	Impaired consciousness, coma
Other clues	Thalamic sensory loss and pain, CN III palsy, hemiballismus	Contralateral sensory loss, dysarthria	Urinary incontinence, gait apraxia	Cranial nerve deficits, ataxia, dizziness, labile blood pressure

For every territory side by side, see stroke localization by artery; the cortical counterparts are middle cerebral artery syndrome and anterior cerebral artery syndrome.

How USMLE tests it: localize the field cut first

Visual finding	Lesion	Usual vessel
Hemianopia with hemiparesis and hemisensory loss, no cortical signs	Optic tract or lateral geniculate body plus posterior limb of the internal capsule	Anterior choroidal artery
Superior quadrantanopia ("pie in the sky") with Wernicke aphasia	Meyer loop, temporal lobe	MCA
Inferior quadrantanopia ("pie on the floor") with neglect or other parietal signs	Parietal optic radiations	MCA
Quadrantanopia with nothing else	Lingual gyrus (superior) or cuneus (inferior)	PCA
Congruous hemianopia with macular sparing, normal strength	Occipital cortex	PCA
Bilateral visual loss with reactive pupils	Both occipital lobes	Both PCAs, often a basilar-tip embolus

Weakness does not exclude PCA. A proximal occlusion can infarct the cerebral peduncle or thalamus, and hemianopia plus hemisensory loss without paralysis is "virtually diagnostic" of a PCA infarct.
Alexia without agraphia is not aphasia. If writing or comprehension fails too, think left MCA.
Drowsy, blind in both fields, cannot look up: think top of the basilar, a thrombectomy emergency.

Practice question: why every answer choice matters

A 71-year-old right-handed woman is brought to the emergency department 90 minutes after she suddenly could not make sense of her morning newspaper. She has atrial fibrillation and stopped taking apixaban 2 weeks ago. She speaks fluently, names objects, repeats sentences and follows three-step commands. She writes a sentence to dictation without errors but cannot read it back, and she identifies words spelled aloud to her. Visual field testing shows a right homonymous hemianopia with central vision spared. Pupils are equal and reactive, and eye movements are full. Strength, sensation, reflexes and coordination are normal. Noncontrast CT of the head shows no hemorrhage. Occlusion of which of the following arteries best explains her findings?

A. Basilar artery
B. Left anterior cerebral artery
C. Left anterior choroidal artery
D. Left middle cerebral artery, inferior division
E. Left middle cerebral artery, superior division
F. Left posterior cerebral artery
G. Right posterior cerebral artery

Answer: F, left posterior cerebral artery. A right homonymous hemianopia with macular sparing places the lesion in the left occipital cortex. Lost reading with intact writing, speech and comprehension is alexia without agraphia, which adds the splenium. Both are left PCA territory, and atrial fibrillation off anticoagulation supplies the embolus.

A. Basilar artery: a basilar-tip embolus can infarct both PCA territories, both thalami and the midbrain: bilateral visual loss or cortical blindness, vertical gaze palsy, drowsiness or coma. She is alert, with full eye movements and a one-sided field cut. Choose A for the drowsy patient who cannot look up.
B. Left anterior cerebral artery: right leg weakness worse than arm, apathy, urinary incontinence and a grasp reflex; vision is spared.
C. Left anterior choroidal artery: the classic triad is right hemiparesis (posterior limb of the internal capsule), right hemisensory loss and a right hemianopia (optic tract or lateral geniculate body). Her strength and sensation are normal, and a field cut alone slows reading rather than abolishing it.
D. Left MCA, inferior division: Wernicke aphasia, with fluent but empty speech, poor comprehension and errors in both reading and writing, often with a right visual field cut. She comprehends, repeats and writes normally.
E. Left MCA, superior division: Broca aphasia, with nonfluent, effortful speech and impaired writing, plus right face and arm weakness. Her speech is fluent and her strength normal.
G. Right posterior cerebral artery: a left homonymous hemianopia, sometimes with prosopagnosia. Reading survives because the intact left visual cortex, which sees the right visual field, connects directly to the left-hemisphere language areas without needing the splenium.

What happens next: 90 minutes in, with a deficit that can be judged disabling and no anticoagulant effect two weeks after stopping apixaban, she is a candidate for IV tenecteplase or alteplase now unless another contraindication exists. An isolated PCA cutoff on CT angiography does not call for routine thrombectomy; cardiac monitoring and long-term anticoagulation follow.

Key takeaways

PCA syndrome = contralateral homonymous hemianopia, often with macular sparing and full strength.
Macular sparing: MCA collaterals at the occipital pole (the exam answer), plus a large macular map, anastomoses and bilateral representation.
Left PCA + splenium → alexia without agraphia; right or bilateral fusiform → prosopagnosia; both occipital lobes → cortical blindness ± Anton denial; Balint is usually bilateral watershed.
Thalamic branches → sensory loss, then Dejerine–Roussy pain; midbrain branches → Weber; artery of Percheron → somnolence, vertical gaze palsy.
Causes: cardioembolism, vertebrobasilar disease, dissection, fetal PCA.
2026 AHA/ASA: tenecteplase or alteplase within 4.5 hours for a disabling deficit; thrombectomy for basilar occlusion, not routinely for an isolated PCA occlusion.