A solid understanding of the pathophysiology of a posterior cerebral artery (PCA) stroke as well as the syndrome relating to it, requires adequate knowledge of the structures and vascular anatomy of the brain. Anterior and posterior circulations provide the primary blood circulation of the brain. Both circulations are connected by the posterior communicating arteries (PCOM), which make up the circle of Willis. When there is an occlusion in the cerebral vasculature, the circle of Willis, as well as collateral circulations, provide blood to the occluded areas. Posterior circulation is supplied by the vertebral arteries (VA), posterior inferior cerebellar arteries (PICA), basilar artery (BA), anterior inferior cerebellar arteries (AICA), pontine branches of the basilar artery, superior cerebellar arteries (SCA), PCA, and PCOM. The VAs arise from the subclavian arteries and fuse into the BA within the cranium. The BA typically divides into PCAs near the pituitary stalk at the pontomesencephalic junction. PCAs can originate from BA 70 percent of the time, 20 percent of the time from PCOMs, and 10 percent of the time from a mix of the two.  The PCAs then give off branches to the midbrain, subthalamic nucleus, basal nucleus, thalamus, temporal, occipital and occipitoparietal cortices (See Figure).
PCA is divided into four segments, P1 to P4. The segments can be further categorized into deep and superficial segments or proximal and distal, respectively.
The mechanism of PCA strokes are variable and include large artery disease, small artery disease, atherothrombosis of PCA, BAand VA, embolism (cardiac, aortic, coagulopathy), dissection, hemorrhagic, migraine, Moyamoya disease, fibromuscular dysplasia (FMD), mitochondrial disease, reversible cerebral vasoconstriction syndrome, vertebrobasilar dolichoectasia (VBD), and vasculitis as well as central nervous system (CNS) infections. The most common causes are still atherosclerosis, embolism, and small artery disease.
Stroke, a leading cause of adult disability,  is the fifth leading cause of death in the United States. Each year, nearly 800,000 people experience a new or recurrent stroke as well as nearly 140,000 deaths each year. There are approximately 7 million stroke survivors. A stroke is reported every 40 seconds, and every 4 minutes someone dies from a stroke. The risk of experiencing a first stroke is nearly twice as high for African Americans as Caucasians, and African Americans also have the highest rate of death due to stroke. 
The incidence of PCA strokes can be estimated between 5% to 10%.  Some studies include only pure PCA. One study shows that pure PCA strokes account for 232 (6.1%) cases of stroke (n = 3808). Other factors, such as being male and the mean age, are also shown in the same study 128/232 (55.2%) and 73.9 (11.9 SD), respectively.
Patients may present with different signs or symptoms when PCA restricts the blood supply of multiple brain regions (the occipital lobe, the inferomedial temporal lobe, a large portion of the thalamus, and the upper brainstem and midbrain). Signs and symptoms may change in a patient with PCA syndrome based upon the location and severity of the occlusion,
It is essential to understand the mechanism of stroke. Acute and chronic management, preventive measures can be instituted.
Symptoms associated with PCA strokes like diplopia, visual field defects, dysphagia, vertigo, alteration in consciousness, memory impairment, or difficulty reading may help us to understand the localization of stroke.
Visual Field Defects
Cognitive and Behavioral Dysfunction
Stroke is an emergency, and the timing of the onset of symptoms is the most important information in acute settings. Time of onset can be challenging in posterior circulation strokes because patients may be unaware of their symptoms. If a patient is unaware of having symptoms, at practitioner should ascertain when the patient last appeared and behaved in the manner that they were known or accustomed. Once this question is answered, a brief history of presentation and complete physical exam should be obtained. When taking a history, there should be an emphasis on determining the risk factors for stroke in the patient's past medical history. The Two main categories or risk factors are non-modifiable and modifiable.
Patients may present in a comatose state via ambulance or may walk to an emergency department without assistance. Patients with a PCA stroke may present with only a headache and mild visual changes such as 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 problems such as grayness, spots, voids, and difficulties focusing.  Patient history may include unilateral weakness, sensory deficits, language dysfunction, dizziness, nausea, vomiting, cognitive, and behavioral disturbances.
A physical exam is performed as soon as a physician sees the patient. The National Institutes of Health Stroke Scale (NIHSS) is a systematic assessment tool that provides a quantitative measure of stroke-related neurologic deficits. NIHSS gives us a brief evaluation of acuity, determination of appropriate treatment, and can predict patient outcomes. It should be completed in less than 10 minutes and ranges from 0 (no deficit) to 42 (maximum). Posterior circulation strokes, including PCA strokes, may be underestimated by NIHSS when compared to anterior circulation strokes.  For example, a patient with complete homonymous hemianopsia has only two NIHSS points, but the patient might have a significant infarct in the occipital cortex, and their daily life will be affected drastically.
A full neurologcial exam is still essential for a better understanding. A cardiovascular exam also should be performed to check for carotid bruits and abnormal rhythm or heart sounds as well as signs of a DVT. The physical exam may show:
PCA and other posterior circulation strokes are more difficult to diagnose because of nonspecific and fluctuating symptoms at presentation. Time of onset it essential for further evaluation with tests. In the acute setting, management should begin after obtaining the following:
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. Points are lost for each area affected such as thalamus (1 point each), occipital lobes (1 point each), midbrain (2 points), pons (2 points), and cerebellar hemispheres (1 each point).
Tests 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 such as 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.
In many cases, noninvasive imaging may be enough for diagnosis and management. Stroke imaging includes CT, magnetic resonance imaging (MRI), CT angio (CTA), MRA, doppler ultrasound, PET, and SPECT. A four-vessel angiogram can be ordered when unclear findings or more information is needed.
In most cases, cardiac pathology should be ruled out with the following test: electrocardiogram, chest X-ray, transthoracic echocardiogram, transesophageal echocardiogram, Holter monitoring, and extensive cardiac monitoring.
2018 AHA/ASA guidelines address prehospital care, urgent and emergency evaluation, and treatment with intravenous (IV) and intra-arterial therapies for acute ischemic stroke (AIS).  Patients with AIS should be checked for airway, breathing, and adequate oxygenation. Intravenous tissue plasminogen activator (tPA) can be administered up to 4.5 hours after AIS. Eligibility recommendations in the 2018 guidelines should be checked before administering IV tPA. The guidelines suggest that the patient must have a blood pressure less than 180/110, finger-stick glucose more than 50 mg/dL, and absence of hemorrhage on initial noncontrast head CT. The dose of tPA is 0.9 mg/kg; the maximum dose is 90 mg over 60 min with an initial 10% of the dose given as a bolus over 1 min.
A patient with AIS may present after a 4.5-hour window and might still be a candidate for endovascular treatment (EVT), 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 AIS. The DAWN and DEFUSE 3 trials selected patients presenting after 6 hours for treatment using imaging-based criteria.  Unfortunately, the results of this study apply to patient MCA or internal carotid artery (ICA) occlusions. A randomized study on posterior circulation AIS treated with intra-arterial therapy was terminated prematurely because of poor recruitment.  The Basilar Artery International Cooperation Study (BASICS) group completed an observational registry study on 619 patients with BA occlusion to see any superiority of intra-arterial therapy to intravenous thrombolysis.  The study did have all the limitations of a non-randomized study. Intra-arterial therapy was more accessible every other day. Following this study, a randomized trial for BA occlusion began in 2011 and is still active. The results of the trial may support other possible studies in the future such as a trial of PCA strokes. Despite the lack of information, there are still good outcomes with some case series in literature after intra-arterial therapy for PCA stokes. Intra-arterial thrombolysis is superior to intravenous thrombolysis in 18 patients with isolated PCA.  There is a case study with isolated PCA that also underwent an endovascular clot aspiration with significant improvement on the patient's symptoms.  Briefly, challenging factors in the acute treatment of PCA stroke include an unclear time of symptom onset, the small size of the vessel, low NIH stroke scale, and the lack of specific guidelines.
The rest of the treatment should be a focus on preventing further cerebrovascular accidents. Antiplatelet or anticoagulation should be started based on the etiology of the stroke. Other secondary risk factors should be addressed with better-controlled hypertension, cholesterol, and diabetes.
Stroke is a leading cause of disability and the fifth leading cause of death in the United States. The disability and mortality are less likely from pure PCA stroke compared to other strokes. 
Stroke care is a multidisciplinary approach. All rehabilitation services should be involved including physical, occupational, and speech/cognitive therapies. Poststroke complications should be followed closely for prevention and management.
"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.
To help prevent strokes, one should:
Patients with a stroke are usually managed by a multidisciplinary team that includes the emergency department physician, neurologist. ICU nurses, radiologist, physical therapist, occupational and speech therapist and other specialists depending on the functional deficit. The key is to restore the patient to pre-stroke functioning levels, if possible. For patients with a minor stroke recovery is good but those who have gross neurological deficits at the time of admission usually require prolonged rehabilitation and there is often no guarantee of full recovery.
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