Continuing Education Activity

Posterior cerebral artery (PCA) strokes can be challenging due to the variability and nonspecific initial presentation of this condition. This activity provides a concise overview of the vertebrobasilar and posterior cerebral artery (PCA) circulation, emphasizing the vascular supply to the thalamus, midbrain, cerebellum, and occipital and temporal cortices, including the anatomic variability of the vertebral arteries and PCA origins, segmentation of the PCA (P1–P4), and the functional territories supplied by deep and superficial branches. The course also reviews the epidemiology, mechanisms, and risk factors of PCA strokes, highlighting common etiologies such as atherosclerosis, embolism, and small vessel disease, as well as less frequent causes including migraine, mitochondrial disorders, and fibromuscular dysplasia.

Additionally, this activity reviews PCA stroke presentations, which are often subtle, fluctuating, and underestimated by standard scales. Participants will also gain an understanding of clinical syndromes associated with PCA infarction, appropriate diagnostic imaging and laboratory evaluation, and current acute and secondary prevention strategies. This activity for healthcare professionals is designed to enhance the learner's competence in identifying PCA stroke, performing the recommended evaluation, and implementing an appropriate interprofessional approach when managing this condition.

Objectives:

• Determine the etiology of a posterior cerebral artery stroke by integrating diagnostic evaluation findings.
• Differentiate the presentations of posterior cerebral artery stroke from those of other neurologic conditions.
• Apply evidence-based acute management strategies tailored to posterior cerebral artery stroke.
• Collaborate management strategies with interprofessional team members to improve care coordination and outcomes for patients affected by posterior cerebral artery strokes.

Introduction

Vertebrobasilar and Posterior Cerebral Artery Anatomy

Vascular supply to the thalamus and infratentorial structures begins with the proximal vertebral arteries and continues distally through the posterior inferior cerebellar arteries (PICA), anterior inferior cerebellar arteries (AICA), basilar artery, pontine branches of the basilar artery, superior cerebellar arteries (SCA), posterior cerebral artery (PCA), and posterior communicating arteries (PComm). The vertebral arteries commonly arise from the subclavian arteries and merge to form the basilar artery at the pontomedullary junction near the level of the fourth ventricle, with substantial anatomic variability. Please see StatPearls' companion resource, "Neuroanatomy, Vertebrobasilar System," for further information. In approximately half of the population, the left vertebral artery demonstrates a larger diameter than the right. At the basilar artery apex, the terminal large vessels, the PCAs, emerge near the pituitary stalk at the pontomesencephalic junction.

Posterior cerebral arteries originate from the basilar artery in approximately 70% of cases, from the PComms in 20%, and from a mixed origin in 10%.[1] PCA branches supply the midbrain, subthalamic nucleus, basal nucleus, thalamus, and the temporal, occipital, and occipitoparietal cortices (see Image. Stroke, Posterior Cerebral Artery).

Posterior cerebral artery segments

The PCA divides into 4 segments, designated P1 through P4, which can also be classified as deep or superficial, corresponding to proximal and distal segments. P1 and P2 represent the deep segments. The P1 segment extends from the termination of the basilar artery to the PComm. Thalamic-subthalamic arteries arising from P1 supply the paramedian upper midbrain and thalamus. Tuberothalamic arteries typically originate from the PComm and supply the anterior and anterolateral thalamus. A rare anatomic variant, the artery of Percheron, arises from the proximal P1 segment and supplies bilateral thalamic and midbrain structures.[2]

Additional P2 branches include the thalamogeniculate arteries, which supply the ventrolateral thalamus, and the posterior choroidal arteries, which supply the lateral geniculate body, pulvinar, posterior thalamus, hippocampus, and parahippocampal gyrus. P3 and P4 constitute the superficial segments. The P3 (quadrigeminal) segment gives rise to the anterior and posterior inferior temporal arteries. The P4 segment represents the cortical portion within the calcarine fissure and continues as the calcarine artery, with additional branches including the occipitotemporal and occipitoparietal arteries.

Etiology

Acute isolated PCA occlusions account for 5% to 10% of all ischemic events.[1] PCA stroke mechanisms demonstrate considerable heterogeneity and include atherothrombosis, Moyamoya disease,[3][4] embolism, arterial dissection, hemorrhage, migraine, fibromuscular dysplasia, mitochondrial disease, reversible cerebral vasoconstriction syndrome or posterior reversible encephalopathy syndrome (RCVS/PRES), cerebral amyloid angiopathy, and vasculitis. Despite this diversity, the 3 most common etiologies remain atherosclerosis, embolism, and hypertension-related small artery disease caused by lipohyalinosis, characterized by vessel wall thickening, luminal stenosis, and fibrinoid necrosis.

Thrombosis secondary to atherosclerosis represents the dominant pathology in PCA disease. Infarctions involving 1 or more PCA cortical territories demonstrate proximal arterial disease in approximately a third of affected patients.[5] Small vessel lacunar infarctions constitute the most frequent stroke subtype, accounting for over a third of cases in the Sagrat Cor Hospital of Barcelona Stroke Registry.[6] PCA stroke patients with a fetal-type posterior cerebral artery (FTP), a common anatomic variant present in 3% to 36% of the general population, more frequently demonstrate small vessel occlusion and ventrolateral thalamic involvement, likely related to altered hemodynamic conditions associated with FTP.[7][8]

Cardioembolic events to the PCAs pose a particularly high risk, especially in isolated PCA infarction. Sources include valvular disease, atrial fibrillation as the most common etiology, left atrial or ventricular thrombus, dilated cardiomyopathy, patent foramen ovale (PFO), and congestive heart failure.[9] Migraine-associated PCA strokes remain reported, although thrombotic arterial occlusions and PFO complicate causal attribution. Even so, strokes affecting the superficial PCA territory occur in approximately 3.5% of patients with a migraine history.[10]

Intracranial involvement associated with fibromuscular dysplasia occurs infrequently. Reported cases include fibromuscular dysplasia of the basilar artery presenting with multiple cerebral infarctions involving the PCA territory.[11] Patients with Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes (MELAS) commonly carry a mitochondrial DNA mutation at base pair 3243 (A3243G). Within the “young stroke” population aged 18 to 45 years, occipital infarctions appear in approximately 12.5% of cases.[12] Vertebrobasilar dolichoectasia, defined by elongation and dilation of the vertebral artery system, represents another less common cause of PCA stroke.[13] Most patients exhibit multiple modifiable and nonmodifiable stroke risk factors, although mean age at onset and atrial fibrillation prevalence remain lower than in anterior circulation strokes.[14]

Epidemiology

PCA strokes account for an estimated 5% to 12% of all ischemic strokes and affect males slightly more often.[1][15] Carotid-fetal-posterior (CFP) syndrome, defined as a PCA territory ischemic stroke or transient ischemic attack resulting from symptomatic carotid stenosis or occlusion of 50% or more via a fetal posterior communicating artery, demonstrates a prevalence of 2.9% among patients with symptomatic carotid stenosis or occlusion of 50% or more and an incidence of 4.23 per 1,000,000 person-years.[16]

Pathophysiology

Signs and symptoms in PCA syndrome vary according to the location and severity of vascular occlusion, involving the occipital lobe, inferomedial temporal lobe, large portions of the thalamus, and the upper brainstem and midbrain. Deep or proximal occlusion may produce ischemia affecting the thalamus, midbrain, and cortex. Well-developed PComm collateral flow may limit infarction despite proximal occlusion. Superficial or distal PCA occlusion typically restricts ischemia to cortical structures.

In chronic intracranial atherosclerosis with robust collateralization, thrombotic occlusion may spare portions of the vascular territory, whereas acute cardioembolic events often cause larger infarcts due to limited collateral flow.[17] Atherothrombosis may result in artery-to-artery embolism, complete branch occlusion, in situ thrombosis, or hemodynamic instability. Small artery disease encompasses lipohyalinosis and hyaline arteriolosclerosis, most commonly associated with chronic hypertension, uncontrolled diabetes, and aging.

Underlying Pathophysiology of Clinical Manifestations

Clinical manifestations, eg, diplopia, visual field deficits, dysphagia, vertigo, altered consciousness, memory impairment, and alexia, assist in localizing PCA territory involvement.[18] Cortical lesions account for 42% of cases, isolated thalamic lesions for 21%, and combined involvement for 37%. The greatest overlap of PCA ischemia occurs within the ventral and medial occipitotemporal cortex and adjacent white matter association tracts. Dorsal and peripheral occipitotemporoparietal regions remain less frequently affected, contributing to visual field defects as the most common presentation, followed by sensorimotor deficits, dizziness, cognitive and oculomotor dysfunction, and ataxia.[19]

Visual Field Defects

PCA branches and deep branches of the middle cerebral artery (MCA) supply the optic radiations. The inferior optic radiations receive PCA blood flow, whereas the superior optic radiations receive MCA perfusion. Unilateral occipital lobe infarction commonly produces contralateral homonymous hemianopia with macular sparing. Limited defects may result in quadrantanopia. Temporal lobe infarction involving the Meyer loop or infracalcarine region may cause superior quadrantanopia.

Inferior quadrantanopia, reported in 22% of patients with visual field impairment, follows infarction of the inferior parietal optic radiations or supracalcarine region.[10] Occlusion of the posterior choroidal artery may produce visual field defects, hemisensory loss, and neuropsychological dysfunction, including transcortical aphasia and memory disturbances. Bilateral occipital lobe infarctions may lead to cortical blindness with visual anosognosia, during which patients deny visual loss and may confabulate.[20]

Visual Dysfunction

Visual dysfunction includes several distinct syndromes. Visual agnosia presents in apperceptive and associative forms. Apperceptive agnosia reflects impaired perception and comprehension, whereas associative agnosia reflects impaired object recognition and use. Large left PCA infarctions may produce visual agnosia through disruption of the visual-language network connectivity.[21] Prosopagnosia manifests as impaired recognition of familiar faces and results from lesions involving the inferior occipital regions, fusiform gyrus, and anterior temporal cortex, typically within the right PCA territory.[22]

Alexia denotes impaired reading ability. Alexia without agraphia, or pure alexia, follows lesions of the dominant occipital lobe and splenium of the corpus callosum and commonly accompanies right homonymous hemianopia. Achromatopsia involves impaired color perception due to infarction of the ventral occipital cortex or infracalcarine region. Unilateral lesions may produce hemi-achromatopsia.[23] Diagnostic evaluation includes Ishihara color plates and the Farnsworth-Munsell 100-hue test. PCA territory strokes may also cause spatial neglect, with both PCA and MCA infarctions disrupting the same perisylvian attentional network.[24]

Cognitive and Behavioral Dysfunction

Cognitive and behavioral dysfunction frequently accompanies PCA strokes. Aphasia may develop following infarctions extending into the left parietal or temporal lobes. Transcortical sensory aphasia arises from left parietal-occipital involvement. Amnestic aphasia, characterized by impaired naming with preserved repetition and comprehension, follows infarction of the left temporal lobe within the PCA territory. Memory impairment results from hippocampal and thalamic infarctions, with no consistent correlation with lesion laterality.

Approximately 30% of memory-related lesions localize outside the hippocampus, involving the ventral occipitotemporal cortex and long occipital white matter tracts.[25] PCA strokes may also provoke aggressive behavior. In a cohort of 41 PCA stroke patients, 3 patients, representing 7.3%, demonstrated behaviors, eg, shouting obscenities and physical aggression.[26] Environmental stimulation may exacerbate anxiety, aggression, and frustration. Hallucinations occur infrequently but may develop following PCA infarction on either side. Palinopsia, characterized by persistent visual images after stimulus removal, is associated with infarction of the lingual and fusiform gyri.

Other Dysfunctions

Additional neurologic syndromes reflect involvement of subcortical and brainstem structures. Midbrain infarctions present variably depending on lesion location, with anterolateral infarctions producing ataxic hemiparesis and paramedian rostral infarctions causing oculomotor or pupillary abnormalities. Pure sensory stroke may result from lesions of the ventral posterolateral nucleus, supplied by thalamogeniculate (inferolateral) arteries.

Occlusion of the artery of Percheron may cause bilateral paramedian thalamic infarction with or without midbrain involvement, presenting with confusion, hypersomnolence, dysarthria, amnesia, and ocular movement disorders. Balint syndrome arises from bilateral occipitoparietal border infarctions and includes optic ataxia, oculomotor apraxia, and simultanagnosia.[27][28] Anton syndrome follows acute bilateral occipital infarction, leading to cortical blindness with denial of visual loss.[29] Alien hand syndrome, although rare, may also occur following PCA territory involvement.[30]

History and Physical

Clinical History

Time of onset can be challenging in posterior circulation strokes because patients may be unaware of their symptoms. If a patient is unaware of symptoms, a practitioner should ascertain when the patient last appeared and behaved in the manner they were known or accustomed to. Once this question is answered, a brief history of presentation and a complete physical exam should be obtained. When taking a history, clinicians should emphasize identifying the risk factors for stroke in the patient's past medical history. The following categories of risk factors are the primary categories: 

• Nonmodifiable: These risk factors include age, gender (male > female), race (higher in African Americans), history of transient ischemic attack (TIA), cerebrovascular disease (CVA), and hypercoagulable states, as well as a family history of hypercoagulable state or CVAs. 
• Modifiable: These risk factors include hypertension, diabetes mellitus, hyperlipidemia, smoking, heart disease (atrial fibrillation, endocarditis), oral contraceptives, substance abuse (cocaine), poor diet, obesity, immobility, and sleep apnea. 

Patients with a PCA stroke may present with only a headache and mild visual changes, eg, vision loss, diplopia, inability to see half of the view, or difficulty reading, perceiving colors, or recognizing familiar faces. Mild symptoms in the setting of a PCA stroke may delay a patient from getting medical treatment. Many times, they are also unaware of their visual problems. Patients may report visual issues, eg, grayness, spots, voids, and difficulties focusing.[31] Patient history may include unilateral weakness, sensory deficits, language dysfunction, dizziness, nausea, vomiting, cognitive, and behavioral disturbances. More severely, patients may present in a comatose state.

However, posterior circulation strokes, including PCA strokes, may be underestimated by the National Institutes of Health Stroke Scale (NIHSS) when compared to anterior circulation strokes.[32] For example, a patient with complete homonymous hemianopsia has only 2 NIHSS points, yet daily life will be severely affected.[33]

Physical Examination

A complete neurological exam remains essential, along with a cardiovascular exam for abnormal rhythm or valvular murmurs, and listening for vertebral artery bruits at the posterior cervicocranial junction. The physical exam may demonstrate the following findings:

• Homonymous Hemianopia with macular sparing
• Superior or inferior quadrantanopia 
• Hemisensory loss/paresthesia
• Cortical blindness or visual anosognosia
• Visual Agnosia
• Prosopagnosia 
• Alexia without agraphia (pure alexia)
• Achromatopsia
• Transcortical sensory aphasia
• Amnestic aphasia
• Memory impairment
• Aggression and hyperactive delirium
• Visual hallucinations
• Palinopsia
• Hemiparesis with/without ataxia
• Oculomotor or pupillary deficits
• Hypersomnolence/lethargy
• Optic ataxia, oculomotor apraxia, and simultanagnosia

Evaluation

PCAs and other posterior circulation strokes are more difficult to diagnose because of nonspecific and fluctuating symptoms at presentation. In the acute setting, management should begin after obtaining the following:

• Vitals
• Finger-stick blood glucose
• Initial non-contrast head computerized tomography (CT)

The Alberta Stroke Program Early CT Score (ASPECTS) system is a simple and reliable 10-point scale for evaluating early ischemic changes in acute middle cerebral artery stroke. ASPECTS is modified to pc-ASPECTS for the posterior circulation strokes.[34] Points are lost for each area affected, eg, the thalamus (1 point each), occipital lobes (1 point each), midbrain (2 points), pons (2 points), and cerebellar hemispheres (1 point each).

Laboratory Studies

Laboratory studies should include a complete blood count (CBC), prothrombin time (PT), activated partial thromboplastin time (aPTT), international normalized ratio (INR), electrolytes, comprehensive metabolic panel (CMP), troponin, lipid panel, and A1c. Additional tests can be ordered, eg, ANA with titers, ESR, CRP, ANCA for vasculitis, hypercoagulable panel for coagulopathy, and genetics tests for an unknown cause of stroke after the first workup.

Imaging Studies

In many cases, noninvasive imaging may be enough for diagnosis and management. Stroke imaging includes CT, magnetic resonance imaging (MRI), CT angiogram (CTA), MRA, Doppler ultrasound, and CT perfusion. A 4-vessel angiogram can be ordered when findings are unclear or additional information is required, such as when evaluating for vasculitis, moyamoya, or fibromuscular dysplasia.

Cardiovascular Testing

In most cases, cardiac pathology should be ruled out with the following test:

• Electrocardiogram
• Chest x-ray
• Transthoracic echocardiogram
• Transesophageal echocardiogram
• Holter monitoring
• Extensive cardiac monitoring/loop recorders to maximize the yield for detecting atrial fibrillation

Treatment / Management

The 2018 American Heart Association (AHA)/American Stroke Association (ASA) guidelines address prehospital care, urgent and emergency evaluation, and treatment with intravenous (IV) and intra-arterial therapies for acute ischemic stroke.[35] Intravenous tissue plasminogen activator (tPA) or tenecteplase can be administered up to 4.5 hours after an acute ischemic stroke. Challenging factors in the acute treatment of PCA stroke include an unclear time of symptom onset, the medium size of the vessel, low NIH stroke scale, and the lack of specific guidelines. 

A patient with acute ischemic stroke may present after a 4.5-hour window and might still be a candidate for endovascular treatment, which may include angioplasty, stenting, mechanical embolectomy, or intra-arterial thrombolysis. Randomized trials have shown the safety and efficacy of intra-arterial thrombolysis given within 6 hours of symptom onset of acute ischemic stroke. The DAWN and DEFUSE 3 trials selected patients presenting more than 6 hours after symptom onset for treatment using imaging-based criteria.[36][37] The variable patient presentation makes the potential benefit of mechanical thrombectomy controversial.[38] Unlike ICA/M1 LVO, isolated PCA occlusions were underrepresented in pivotal thrombectomy RCTs, so decision-making remains individualized.

Observational data suggest endovascular thrombectomy (EVT) is feasible (including distal P2/P3 occlusions), with higher reperfusion and early neurologic improvement in some cohorts, but meta-analyses generally show no consistent improvement in 90-day functional independence (mRS) compared with best medical management, and safety signals (sICH/hemorrhage) vary by study and selection. In practice, many comprehensive stroke centers consider EVT most strongly when the following are present:

• proximal PCA (P1) or dominant-territory occlusion
• clearly disabling deficits (eg, dense hemianopia, alexia, profound neglect)
• favorable imaging (small core/limited established infarct with evidence of salvageable tissue)

This balances anticipated benefit against procedural risk and the reality that some PCA deficits may not translate into differences in mRS despite having a high morbidity.[39][40][41] 

Parenthetically, patients with isolated PCA occlusion undergoing endovascular thrombectomy have a better outcome when treated under general anesthesia, with a higher reperfusion rate, although functional outcomes remain unchanged.[42] Antiplatelet or anticoagulation should be started based on the etiology of the stroke. Other secondary risk factors should be addressed by better controlling hypertension, cholesterol, and diabetes.

Differential Diagnosis

The differential diagnoses that should also be considered when evaluating a patient with a suspected PCA stroke include:

• Hypoglycemia
• Hypotension/hypertension
• Mass in the occipital, temporal, or parietal area
• Migraine
• Seizure with a postictal state
• Subarachnoid hemorrhage
• Vasculitis

Prognosis

The majority of patients with PCA stroke function with mild-to-moderate visual field deficit. In those treated with endovascular thrombectomy for higher NIHSS compared with medical management alone, no disabling deficit at 90 days can be observed, but no functional independence and higher odds of spontaneous intracerebral hemorrhage are noted.[40] Poor outcome is observed in over half of patients, depending on age, NIHSS score, infarct volume, and lack of fibrinolytic use.[43]

Complications

A small deficit, eg, a quadrantanopsia, may not be noticed by the patient and may be incidentally detected on a confrontational peripheral field exam by an optometrist or an astute clinician. Thalamic lesions have the potential to cause long-lasting central dysesthesia and central pain syndrome, eg, Dejerine-Roussy syndrome (see StatPearls, 2025).[44] When the stroke is large and under pressure, hemorrhagic transformation does occur. Postfibrinolysis or postmechanical thrombectomy also poses a greater risk of intracerebral hemorrhage, but generally the hemorrhage does not alter long-term survival or recovery, although it prolongs the length of hospital stay.

Postoperative and Rehabilitation Care

Stroke care requires an interprofessional approach involving coordination among all rehabilitation services, including physical, occupational, and speech/cognitive therapies. Close monitoring and management of poststroke complications remain essential for optimizing recovery and preventing secondary morbidity.

Patients receiving tPA or tenecteplase (TNK) may experience acute angioedema. Life-threatening angioedema or laryngospasm requires immediate discontinuation of thrombolytic therapy. Neurological deterioration often peaks between 72 and 96 hours following stroke in cases of hemorrhagic transformation or malignant cerebral edema. Posterior circulation strokes carry a higher risk of hydrocephalus compared with anterior circulation strokes, and surgical interventions such as craniotomy or placement of an external ventricular drain should be considered when indicated.

Venous thromboembolism, including pulmonary embolism and deep venous thrombosis (DVT), presents an elevated risk during the initial months after stroke due to reduced mobility. Hospitalized patients should receive chemical DVT prophylaxis unless contraindicated, eg, within 24 hours of tPA administration or in the setting of hemorrhagic transformation. Dysphagia requires evaluation by speech therapists, and patients who fail swallowing tests should receive percutaneous endoscopic gastrostomy tube placement before discharge.

Poststroke patients exhibit increased susceptibility to infections, including pneumonia and urinary tract infections, although prophylactic antibiotics are not recommended. Similarly, seizure risk rises after stroke without an indication for prophylactic antiepileptic therapy. Spasticity may respond to muscle relaxants, with resistant cases treated with onabotulinumtoxinA injections in addition to oral medications. Bedbound patients remain at risk for decubitus ulcers, and repositioning every 2 hours offers a preventative benefit. Early mobilization, facilitated by family and rehabilitation teams in hospital, home, or nursing home settings, supports the prevention of DVT and physical deconditioning.

Deterrence and Patient Education

"BEFAST" is a good and handy acronym to recognize common signs of a stroke, regardless of the etiology. Stroke is an emergency. Time is brain. BEFAST stands for the following clinical considerations:

• Balance: Is there a sudden onset of loss of balance or coordination?
• Eye: Is there a sudden onset of blurred or double vision, or any sudden onset or persistent vision problems?
• Face: When the person smiles, does 1 or both sides of the face hang limply?
• Arms: Ask the person to raise both arms. Does 1 side slope downward? Is there a sudden onset of weakness/numbness on 1 side?
• Speech: Does the person have slurred or garbled speech? Can the patient repeat simple phrases?
• Time: Call 911 for immediate medical attention upon noticing 1 or more of these signs. Also, clinicians should take note of when the symptoms began.

To help prevent strokes, the following recommended strategies should be advised:

• Monitor blood pressure.
• Control cholesterol and blood sugar.
• Increase activity to help maintain a healthy weight.
• Eat healthily.
• Stop smoking cigarettes.
• Control obstructive sleep apnea.
• Establish primary care to provide routine and urgent medical attention.

Pearls and Other Issues

Although most distal PCA territory strokes display low morbidity, proximal PCA strokes could be devastating and involve key structures, eg, the thalamus, hippocampus, and the upper midbrain, leading to stupor and chronic neurologic disability. Poor outcomes occur in more than half of medically treated PCA-related strokes. Facilitating the use of thrombolytics may improve functional outcome. Therapeutic approaches aimed at enhancing recanalization and reducing hemorrhagic transformation warrant further investigation.[45]

Enhancing Healthcare Team Outcomes

Stroke represents a leading cause of long-term disability and requires a comprehensive, interprofessional approach to care. Effective management spans from acute intervention to poststroke rehabilitation, with goals of minimizing neurologic injury, preventing complications, and optimizing functional recovery. Patients may present with a wide range of deficits, including visual, cognitive, motor, and speech impairments, which influence the intensity and duration of rehabilitation. Early recognition, accurate localization of the stroke, and timely interventions such as thrombolysis or thrombectomy are critical to improve outcomes and reduce secondary complications such as hemorrhagic transformation, hydrocephalus, venous thromboembolism, infections, and spasticity.[46]

Optimizing patient-centered care demands coordinated skills and responsibilities across the healthcare team. Physicians and advanced practitioners evaluate stroke severity, determine etiology, and implement acute and secondary prevention strategies, while radiologists provide critical imaging interpretation. Nurses and therapists monitor neurologic status, mobilize patients safely, manage dysphagia, and provide rehabilitative therapies. Pharmacists ensure appropriate medication selection, dosing, and monitoring for thrombolytics, anticoagulants, and spasticity agents. Interprofessional communication and care coordination facilitate timely intervention, reduce complications, enhance patient safety, and support functional recovery. Collaborative planning with family members ensures continuity of care across hospital, home, or skilled nursing environments, ultimately improving outcomes and team performance.

Review Questions

• Access free multiple choice questions on this topic.
• Click here for a simplified version.
• Comment on this article.

References

1.

Cereda C, Carrera E. Posterior cerebral artery territory infarctions. Front Neurol Neurosci. 2012;30:128-31. [PubMed: 22377879]

2.

Kichloo A, Jamal SM, Zain EA, Wani F, Vipparala N. Artery of Percheron Infarction: A Short Review. J Investig Med High Impact Case Rep. 2019 Jan-Dec;7:2324709619867355. [PMC free article: PMC6689919] [PubMed: 31394937]

3.

Mazzotta S, Baltsavias G, Hebeisen M, Khan N. Posterior Cerebral Artery Involvement in Paediatric Moyamoya: Angiographic Patterns and Stroke Burden. Cerebrovasc Dis. 2025;54(6):937-944. [PMC free article: PMC12060807] [PubMed: 40112781]

4.

Tigchelaar SS, Wang AR, Vaca SD, Li Y, Steinberg GK. Incidence and Outcomes of Posterior Circulation Involvement in Moyamoya Disease. Stroke. 2024 May;55(5):1254-1260. [PubMed: 38567531]

5.

Yamamoto Y, Georgiadis AL, Chang HM, Caplan LR. Posterior cerebral artery territory infarcts in the New England Medical Center Posterior Circulation Registry. Arch Neurol. 1999 Jul;56(7):824-32. [PubMed: 10404984]

6.

Arboix A, Arbe G, García-Eroles L, Oliveres M, Parra O, Massons J. Infarctions in the vascular territory of the posterior cerebral artery: clinical features in 232 patients. BMC Res Notes. 2011 Sep 07;4:329. [PMC free article: PMC3180463] [PubMed: 21899750]

7.

Frid P, Wasselius J, Drake M, Wu O, Petersson J, Rost NS, Lindgren A., MRI-GENIE study, the ISGC. Fetal posterior cerebral artery configurations in an ischemic stroke versus an unselected hospital population. Acta Neurol Scand. 2022 Mar;145(3):297-304. [PubMed: 34811730]

8.

Ryu JC, Kim JS. Mechanisms of Stroke in Patients with Fetal Posterior Cerebral Artery. J Stroke Cerebrovasc Dis. 2022 Aug;31(8):106518. [PubMed: 35605387]

9.

Ntaios G, Spengos K, Vemmou AM, Savvari P, Koroboki E, Stranjalis G, Vemmos K. Long-term outcome in posterior cerebral artery stroke. Eur J Neurol. 2011 Aug;18(8):1074-80. [PubMed: 21435108]

10.

Cals N, Devuyst G, Afsar N, Karapanayiotides T, Bogousslavsky J. Pure superficial posterior cerebral artery territory infarction in The Lausanne Stroke Registry. J Neurol. 2002 Jul;249(7):855-61. [PubMed: 12140669]

11.

Tashiro K, Shigeto H, Tanaka M, Kawajiri M, Taniwaki T, Kira J. [Fibromuscular dysplasia of the basilar artery presenting as cerebral infarction in a young female]. Rinsho Shinkeigaku. 2006 Jan;46(1):35-9. [PubMed: 16541792]

12.

Majamaa K, Turkka J, Kärppä M, Winqvist S, Hassinen IE. The common MELAS mutation A3243G in mitochondrial DNA among young patients with an occipital brain infarct. Neurology. 1997 Nov;49(5):1331-4. [PubMed: 9371917]

13.

Passero S, Filosomi G. Posterior circulation infarcts in patients with vertebrobasilar dolichoectasia. Stroke. 1998 Mar;29(3):653-9. [PubMed: 9506608]

14.

Liu EA, Murali S, Rivera-de Choudens R, Trobe JD. Demographics, Risk Factors, and Etiology of Posterior Cerebral Artery Stroke Causing Homonymous Hemianopia. J Neuroophthalmol. 2023 Sep 01;43(3):387-392. [PubMed: 37436886]

15.

Nichols L, Bridgewater JC, Wagner NB, Karivelil M, Koelmeyer H, Goings D, Hope TD. Where in the Brain do Strokes Occur? A Pilot Study and Call for Data. Clin Med Res. 2021 Sep;19(3):110-115. [PMC free article: PMC8445664] [PubMed: 33985981]

16.

Cruz-Rojas A, Gu T, Kellomäki E, Nordanstig A, Fox AJ, Johansson E. Prevalence and Incidence of Carotid-Fetal-Posterior Syndrome. Cerebrovasc Dis. 2023;52(6):643-650. [PMC free article: PMC10733935] [PubMed: 36921590]

17.

Wong KS, Caplan LR, Kim JS. Stroke Mechanisms. Front Neurol Neurosci. 2016;40:58-71. [PubMed: 27960181]

18.

Javed K, Reddy V, Das JM. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 1, 2023. Neuroanatomy, Posterior Cerebral Arteries. [PubMed: 30860709]

19.

Benke T, Dazinger F, Pechlaner R, Willeit K, Clausen J, Knoflach M. Lesion topography of posterior cerebral artery infarcts. J Neurol Sci. 2021 Sep 15;428:117585. [PubMed: 34371243]

20.

Kondziella D, Frahm-Falkenberg S. Anton's syndrome and eugenics. J Clin Neurol. 2011 Jun;7(2):96-8. [PMC free article: PMC3131545] [PubMed: 21779298]

21.

Larrabee GJ, Levin HS, Huff FJ, Kay MC, Guinto FC. Visual agnosia contrasted with visual-verbal disconnection. Neuropsychologia. 1985;23(1):1-12. [PubMed: 3974844]

22.

Gainotti G, Marra C. Differential contribution of right and left temporo-occipital and anterior temporal lesions to face recognition disorders. Front Hum Neurosci. 2011;5:55. [PMC free article: PMC3108284] [PubMed: 21687793]

23.

Damasio A, Yamada T, Damasio H, Corbett J, McKee J. Central achromatopsia: behavioral, anatomic, and physiologic aspects. Neurology. 1980 Oct;30(10):1064-71. [PubMed: 6968419]

24.

Sperber C, Clausen J, Benke T, Karnath HO. The anatomy of spatial neglect after posterior cerebral artery stroke. Brain Commun. 2020;2(2):fcaa163. [PMC free article: PMC7846084] [PubMed: 33543137]

25.

Benke T, Bodner T, Wiesen D, Karnath HO. The amnestic syndrome of posterior cerebral artery infarction. Eur J Neurol. 2022 Oct;29(10):2987-2995. [PMC free article: PMC9541518] [PubMed: 35708171]

26.

Botez SA, Carrera E, Maeder P, Bogousslavsky J. Aggressive behavior and posterior cerebral artery stroke. Arch Neurol. 2007 Jul;64(7):1029-33. [PubMed: 17620495]

27.

HECAEN H, DE AJURIAGUERRA J. Balint's syndrome (psychic paralysis of visual fixation) and its minor forms. Brain. 1954;77(3):373-400. [PubMed: 13208876]

28.

Parvathaneni A, Das JM. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jun 26, 2023. Balint Syndrome. [PubMed: 31335067]

29.

Das JM, Naqvi IA. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Apr 3, 2023. Anton Syndrome. [PubMed: 30844182]

30.

Nowak DA, Engel A, Leutbecher M, Zeller C. Alien limb phenomenon following posterior cerebral artery stroke: a distinct clinical entity. J Neurol. 2020 Jan;267(1):95-99. [PubMed: 31562560]

31.

Fisher CM. The posterior cerebral artery syndrome. Can J Neurol Sci. 1986 Aug;13(3):232-9. [PubMed: 3742339]

32.

Sato S, Toyoda K, Uehara T, Toratani N, Yokota C, Moriwaki H, Naritomi H, Minematsu K. Baseline NIH Stroke Scale Score predicting outcome in anterior and posterior circulation strokes. Neurology. 2008 Jun 10;70(24 Pt 2):2371-7. [PubMed: 18434640]

33.

Matsunaga S, Mikami T. Motor Vehicle Collision Due to Left Hemineglect Associated with a Stroke. N Engl J Med. 2025 Dec 18;393(24):e41. [PubMed: 41406447]

34.

Puetz V, Sylaja PN, Coutts SB, Hill MD, Dzialowski I, Mueller P, Becker U, Urban G, O'Reilly C, Barber PA, Sharma P, Goyal M, Gahn G, von Kummer R, Demchuk AM. Extent of hypoattenuation on CT angiography source images predicts functional outcome in patients with basilar artery occlusion. Stroke. 2008 Sep;39(9):2485-90. [PubMed: 18617663]

35.

Powers WJ, Rabinstein AA, Ackerson T, Adeoye OM, Bambakidis NC, Becker K, Biller J, Brown M, Demaerschalk BM, Hoh B, Jauch EC, Kidwell CS, Leslie-Mazwi TM, Ovbiagele B, Scott PA, Sheth KN, Southerland AM, Summers DV, Tirschwell DL. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2019 Dec;50(12):e344-e418. [PubMed: 31662037]

36.

Albers GW, Marks MP, Kemp S, Christensen S, Tsai JP, Ortega-Gutierrez S, McTaggart RA, Torbey MT, Kim-Tenser M, Leslie-Mazwi T, Sarraj A, Kasner SE, Ansari SA, Yeatts SD, Hamilton S, Mlynash M, Heit JJ, Zaharchuk G, Kim S, Carrozzella J, Palesch YY, Demchuk AM, Bammer R, Lavori PW, Broderick JP, Lansberg MG., DEFUSE 3 Investigators. Thrombectomy for Stroke at 6 to 16 Hours with Selection by Perfusion Imaging. N Engl J Med. 2018 Feb 22;378(8):708-718. [PMC free article: PMC6590673] [PubMed: 29364767]

37.

Nogueira RG, Jadhav AP, Haussen DC, Bonafe A, Budzik RF, Bhuva P, Yavagal DR, Ribo M, Cognard C, Hanel RA, Sila CA, Hassan AE, Millan M, Levy EI, Mitchell P, Chen M, English JD, Shah QA, Silver FL, Pereira VM, Mehta BP, Baxter BW, Abraham MG, Cardona P, Veznedaroglu E, Hellinger FR, Feng L, Kirmani JF, Lopes DK, Jankowitz BT, Frankel MR, Costalat V, Vora NA, Yoo AJ, Malik AM, Furlan AJ, Rubiera M, Aghaebrahim A, Olivot JM, Tekle WG, Shields R, Graves T, Lewis RJ, Smith WS, Liebeskind DS, Saver JL, Jovin TG., DAWN Trial Investigators. Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct. N Engl J Med. 2018 Jan 04;378(1):11-21. [PubMed: 29129157]

38.

Baig AA, Monteiro A, Waqas M, Cappuzzo JM, Siddiqi M, Doane J, Dossani RH, Almayman F, Khawar WI, Davies JM, Snyder KV, Levy EI, Siddiqui AH. Acute isolated posterior cerebral artery stroke treated with mechanical thrombectomy: A single-center experience and review of the literature. Interv Neuroradiol. 2023 Feb;29(1):10-19. [PMC free article: PMC9893240] [PubMed: 35001703]

39.

Meyer L, Stracke CP, Jungi N, Wallocha M, Broocks G, Sporns PB, Maegerlein C, Dorn F, Zimmermann H, Naziri W, Abdullayev N, Kabbasch C, Behme D, Jamous A, Maus V, Fischer S, Möhlenbruch M, Weyland CS, Langner S, Meila D, Miszczuk M, Siebert E, Lowens S, Krause LU, Yeo LLL, Tan BY, Anil G, Gory B, Galván J, Arteaga MS, Navia P, Raz E, Shapiro M, Arnberg F, Zelenák K, Martinez-Galdamez M, Fischer U, Kastrup A, Roth C, Papanagiotou P, Kemmling A, Gralla J, Psychogios MN, Andersson T, Chapot R, Fiehler J, Kaesmacher J, Hanning U. Thrombectomy for Primary Distal Posterior Cerebral Artery Occlusion Stroke: The TOPMOST Study. JAMA Neurol. 2021 Apr 01;78(4):434-444. [PMC free article: PMC7900924] [PubMed: 33616642]

40.

Chen H, Khunte M, Colasurdo M, Malhotra A, Gandhi D. Thrombectomy vs Medical Management for Posterior Cerebral Artery Stroke: Systematic Review, Meta-Analysis, and Real-World Data. Neurology. 2024 May;102(9):e209315. [PMC free article: PMC11175628] [PubMed: 38626383]

41.

Sabben C, Charbonneau F, Delvoye F, Strambo D, Heldner MR, Ong E, Ter Schiphorst A, Henon H, Ben Hassen W, Agasse-Lafont T, Legris L, Sibon I, Wolff V, Sablot D, Elhorany M, Preterre C, Nehme N, Soize S, Weisenburger-Lile D, Triquenot-Bagan A, Mione G, Aignatoaie A, Papassin J, Poll R, Béjot Y, Carrera E, Garnier P, Michel P, Saliou G, Mordasini P, Berthezene Y, Costalat V, Bricout N, Albers GW, Mazighi M, Turc G, Seners P., ACAPULCO Collaborators. Endovascular Therapy or Medical Management Alone for Isolated Posterior Cerebral Artery Occlusion: A Multicenter Study. Stroke. 2023 Apr;54(4):928-937. [PubMed: 36729389]

42.

Berberich A, Herweh C, Qureshi MM, Strambo D, Michel P, Räty S, Abdalkader M, Virtanen P, Olive Gadea M, Ribo M, Psychogios MN, Nguyen A, Kuramatsu JB, Haupenthal D, Köhrmann M, Deuschl C, Kühne Escolà J, Demeestere J, Lemmens R, Yaghi S, Shu L, Kaiser DPO, Puetz V, Kaesmacher J, Mujanovic A, Marterstock DC, Engelhorn T, Klein P, Haussen DC, Mohammaden MH, Cunha B, Fragata I, Romoli M, Hu W, Zhang C, Matsoukas S, Fifi JT, Sheth SA, Salazar-Marioni S, Marto JP, Ramos JN, Miszczuk M, Riegler C, Poli S, Poli K, Jadhav AP, Desai SM, Maus V, Kaeder M, Siddiqui AH, Monteiro A, Peltola E, Masoud H, Suryadareva N, Mokin M, Thanki S, Alpay K, Rautio R, Siegler JE, Asdaghi N, Saini V, Linfante I, Dabus G, Nolte CH, Siebert E, Möhlenbruch MA, Fischer U, Nogueira RG, Hanning U, Meyer L, Ringleb PA, Strbian D, Nguyen TN, Nagel S. Endovascular therapy of isolated posterior cerebral artery occlusion stroke with and without general anesthesia. J Neurointerv Surg. 2024 Jun 05;17(5):508-517. [PubMed: 38839282]

43.

Wang LR, Li BH, Zhang Q, Cheng XD, Jia LJ, Zhou S, Yang S, Wang JH, Yu NW. Predictors of futile recanalization after endovascular treatment of acute ischemic stroke. BMC Neurol. 2024 Jun 17;24(1):207. [PMC free article: PMC11181662] [PubMed: 38886670]

44.

Jahngir MU, Qureshi AI. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Jul 3, 2023. Dejerine-Roussy Syndrome. [PubMed: 30085589]

45.

Sabben C, Charbonneau F, Obadia M, Strambo D, Ong E, Heldner MR, Henon H, Ter Schiphorst A, Legris L, Agasse-Lafont T, Sablot D, Nehme N, Sibon I, Triquenot-Bagan A, Wolff V, Preterre C, Rosso C, Mione G, Poll R, Papassin J, Aignatoaie A, Weisenburger Lile D, Béjot Y, Moulin S, Carrera E, Garnier P, Michel P, Mordasini P, Albers GW, Turc G, Mazighi M, Seners P., ACAPULCO collaborators. Predictors of poor outcome in acute stroke patients with posterior cerebral artery occlusion and medical management. Int J Stroke. 2025 Mar;20(3):347-356. [PubMed: 39665302]

46.

Hodgson K, Adluru G, Richards LG, Majersik JJ, Stoddard G, Adluru N, DiBella E. Predicting Motor Outcomes in Stroke Patients Using Diffusion Spectrum MRI Microstructural Measures. Front Neurol. 2019;10:72. [PMC free article: PMC6387951] [PubMed: 30833925]

Disclosure: Ramsis Benjamin declares no relevant financial relationships with ineligible companies.

Disclosure: Prasanna Tadi declares no relevant financial relationships with ineligible companies.

Disclosure: Jagkirat Singh declares no relevant financial relationships with ineligible companies.