Left PCA stroke
Executive summary
A left posterior cerebral artery (PCA) stroke is an ischemic event in the vascular territory supplying the left occipital lobe, medial temporal lobe and parts of the thalamus and midbrain that most commonly produces visual and visual‑cognitive deficits — notably contralateral homonymous hemianopia and, when the splenium is involved, alexia without agraphia — and can present subtly, delaying care [1] [2] [3]. Diagnosis and acute management hinge on rapid recognition of often‑mild visual symptoms, timely imaging, and consideration of thrombolysis or endovascular therapy despite limited trial evidence specific to PCA territory strokes [4] [1] [3].
1. What “left PCA stroke” means anatomically and clinically
A left PCA stroke denotes infarction of brain tissue perfused by the left posterior cerebral artery, which supplies the occipital cortex (visual processing), inferomedial temporal structures (memory and visual recognition), and thalamic and midbrain territories; clinical manifestations therefore cluster around visual field loss (contralateral homonymous hemianopia or quadrantanopia), visual agnosia including prosopagnosia, memory disturbance, sensory thalamic syndromes and occasional brainstem signs depending on branch involvement [1] [5] [6].
2. Typical presentation and why it’s often missed
Patients with PCA strokes may present with isolated headache, vague visual changes, difficulty reading, color perception problems, diplopia, or inability to see half of the field, and because these symptoms can be mild the NIH Stroke Scale can under‑score their severity — for example, complete homonymous hemianopia scores only two points — which contributes to diagnostic delays and higher misdiagnosis rates in posterior circulation events [3] [7] [8].
3. Causes, risk factors and stroke mechanism
Cardioembolism — most often from atrial fibrillation and left atrial thrombus — is the leading identifiable cause of PCA ischemia, although large‑artery atherosclerotic stenosis and small‑vessel disease can also produce PCA territory infarcts; anatomical variants (fetal PCA) can alter source attribution because a carotid lesion may then produce an occipital infarct [3] [7] [8].
4. How it’s diagnosed and the limits of current imaging/scores
Prompt neuroimaging (CT and diffusion MRI) is essential to confirm occipital/temporal or thalamic infarction and to exclude hemorrhage; however, small vessel size, variable onset timing and subtle clinical scores mean ischemia can be missed on noncontrast CT early on and that NIHSS underestimates posterior deficits, so clinicians must combine history, visual field testing and advanced imaging when suspicion exists [4] [3] [7].
5. Acute treatment options and controversies
Time‑sensitive thrombolysis (IV or intra‑arterial) remains the standard when patients meet criteria and present within treatment windows, and case series suggest some patients with isolated PCA occlusions benefit from intra‑arterial therapy or mechanical thrombectomy, but major randomized thrombectomy trials largely excluded PCA strokes so evidence for routine endovascular therapy is limited and practice varies by center and occlusion location [3] [1] [9].
6. Prognosis, complications and rehabilitation needs
Outcomes depend on infarct size and location: small thalamic infarcts can have relatively good recovery while cortical occipital or bilateral PCA infarcts cause persistent disabling visual impairment and cognitive/reading deficits that affect quality of life and require multidisciplinary rehab (visual field training, occupational therapy, neuropsychology); risk of recurrence is managed by addressing embolic sources (e.g., anticoagulation for AF) and vascular risk factors [10] [5] [7].
7. Diagnostic pitfalls, alternative explanations and research gaps
Migraine with brainstem aura, ophthalmologic disease and atypical headaches can mimic PCA stroke and posterior circulation ischemias are misdiagnosed about twice as often as anterior circulation strokes; importantly, the literature shows a shortage of high‑quality randomized data on thrombectomy for PCA occlusions and variable inclusion of PCA territory in trials — an implicit clinical‑trial gap that shapes conservative treatment paradigms in many centers [7] [8] [1].