The basilar artery (BA) is formed over the surface of pons by two vertebral arteries to supply the critical areas of the brain and brainstem. Anatomically, it can subdivide into three arbitrary segments: proximal form vertebral artery (VA) to anterior inferior cerebellar arteries (AICA), middle from AICA to the origin of superior cerebellar arteries (SCA) and finally distal segment from SCA to the terminal posterior cerebral arteries (PCA). Basilar artery infarct or occlusion (BAO) results from the obliteration of blood supply to the posterior circulation or vertebrobasilar system of arteries to the brain. BAO was first described in 1828 by Scottish physician John Abercrombie.
The most common causes are atherosclerosis and thromboembolism from large vessel occlusion (LVO) or heart. The clinical presentation can be very mild as nausea, dizziness, headache, confusion, vertigo to the severe symptoms like aphasia, dysarthria, dysphagia, hemiparesis/quadriparesis, loss of consciousness, coma, cranial nerve abnormalities, vision loss and even cardiac or respiratory compromise which is usually lethal unless immediately identified to achieve revascularization. Reduced consciousness is the hallmark of basilar artery occlusion. A patient presenting with these brainstem symptoms and signs qualifies for a rapid evaluation, consult to the stroke and endovascular teams and an urgent imaging confirmation with computed tomography (CT) scan of head, CT angiography of head and neck and/or magnetic resonance imaging (MRI) with or without perfusion imaging are usually done. The whole process should not delay the administration of intraarterial thrombolytics like alteplase (tPA) or tenecteplase and transfer to angiography suite for mechanical thrombectomy (MT) in the eligible patients to achieve potentially good clinical outcomes.
The common causes of ischemic stroke can also cause infarct in the basal artery territory. Interruption to the blood supply due to atherosclerosis or from an embolus anywhere form the heart to the basilar artery can cause the obliteration of flow through the basilar artery leading to an infarct of the brainstem (mainly pons) or brain region supplied by the basilar artery and its branches. The most commonly involved segments are proximal and middle segments of the basilar artery. Atherosclerosis of the phenomena by which cholesterol and repeat injury to the vessels leading to injury to the intimal side of blood vessels, exposing collagen and releasing factors leading to platelet adhesion to the surface forming a thrombus or plaque. When the plaque rupture, it can either close the vessel, ultimately leading to the high-grade vessel stenosis, and the organizing thrombus can further breakdown and throw the emboli in the cerebral circulation.
Alternatively, a small part of the thrombus can detach and cause occlusion of small vessels distally. Both mechanical symptoms eventually can cause the occlusion of several vessels leading to an infarct in the corresponding cerebral territories. Another mechanism is cardioembolism from the heart, where a clot in the heart mainly composed of fibrinogen, usually forms due to dysrhythmias like atrial fibrillation, metallic valve, severe mitral stenosis, large MI, acute heart failure and wall motion abnormalities, etc. Rarely, external compression of the vertebral artery (bow hunter syndrome or vertebrobasilar insufficiency) can cause posterior circulation stroke, which needs either endovascular deconstruction or reconstruction, external surgical decompression, surgical bypass techniques.
Although the exact incidence of basilar artery occlusion remains unknown, it is estimated to account for 1% of all ischemic strokes. Data from the center, including 129 patients with an LVO, showed that the estimated incidence was four persons per 100000/year. As per the BASICS registry, among 592 patients with basilar artery occlusion, the average age of the aorta is 63 years, females being 37%, and admission NIHSS of 22 (11 to 30). In this era of advanced imaging in diagnosing techniques, we need further prospective randomized studies to determine the current incidence and prevalence of this disease, mainly because we have more treatment options for this patient population.
Almost 30 to 35% of the strokes in posterior circulation are due to an embolus originated from an LVO in VA, BA, and PCA. An occlusion of BA is often due to an LVO by an embolism from heart, aorta or VA (36%), atherosclerosis of BA (35%), dissection (5%) of BA and occasionally dolichoectasia or vasculopathy or undetermined (24%) causes. Emboli usually arise from the heart or large arteries to cause occlusion of BA. In contrast, thrombus may arise directly from the basilar artery due to atherosclerosis to produce BAO or may propagate from a thrombus from a VA due to atherosclerosis or dissection. Often, both proximal and middle segments get occluded due to thrombi arising from bilateral vertebral arteries, and an embolus from VA can lodge into the distal section directly.
The perfusion pressure drops due to the presence of an embolus in the proximal portion of BA, causing a reversal of blood flow from bilateral PCAs, and this reflux can prevent an embolus from reaching the distal segment of the BA. Basilar syndrome is mostly caused by distal basilar artery occlusion and involves behavioral disturbance, confusion, oculomotor, and visual abnormalities but often spares motor findings. The extent of thromboembolism can be a single segment occlusion of BA or may involve all three segments of BA, and we can visualize this on the vessel imaging, preferably CT angiography of the head and neck. With time, as the occlusion ages, the embolus becomes harder to get extracted by thrombectomy. Hence time is of utmost importance.
Microscopic examination of the brain tissue in the autopsies shows ischemic changes due to a thrombus or an embolus. The histopathology examination of thrombus shows an increased amount of aggregated platelets consistent with the atherosclerotic disease. In contrast, there is an increased amount of fibrinogen in the emboli extracted from basilar arteries consistent with the cardioembolic etiology.
To guide history and physical examination, the following is a summary of specific signs or symptoms based on the infarct location :
On arrival to ED, the first test should be a CT head without contrast to rule out hemorrhagic stroke. In the meantime, quickly gather information including blood pressure, blood glucose level, the time of last known normal (LKN) or onset of stroke signs/symptoms (s/s), National Institute of Health Stroke Scale (NIHSS), use of anticoagulants/antiplatelets, past medical and surgical history, renal function, and if indicated run the alteplase (tPA) checklist. If CT head is negative for bleed and there is a concern for basilar artery occlusion (BAO), subsequent intravenous access and CT angiogram of head and neck is advised to rule out an LVO. If CT angiogram is unobtainable, an MR angiogram can be used to evaluate cerebral vessels provided no contraindication. MRI brain without contrast can be done later to characterize the stroke further, but it should not delay the revascularization treatment with intraarterial thrombolysis (IAT) and mechanical thrombectomy (MT). In the diffusion-weighted imaging (DWI) sequence of the MRI scan, the nerve density of the tracts in the pons may appear "SMOGGY" or "hazy," due to the diffusion restriction in the axonal tracts. This "smog sign" is a predictor of a good predictor of neurologic outcomes after mechanical thrombectomy.
After the initial management, stroke workup should be done to evaluate the cause to guide the goal-directed treatment. After the evaluation of vertebral and basilar circulations other workup includes a transcranial doppler (TCD to find out stability of plaque), transthoracic echocardiogram (TTE or TEE to rule out the clot, valvular abnormalities, wall motion abnormalities, and PFO), electrocardiogram, telemetry, event monitor or loop recorder (to rule out arrhythmias), and blood workup (HbA1c, lipid panel, homocysteine, and other workup based on etiology: antiphospholipid antibody syndrome, verify-now for platelet function, malignancy workup etc.).
If the patient has arrived within the tPA window (less than 3 to 4.5 hours since LKN) and has no contraindication to tPA, he/she should immediately receive alteplase/tPA or tenecteplase for the intraarterial thrombolysis. If eligible, the patient should be transferred to the angiography suite for mechanical thrombectomy (MT) within 24 hours of LKN. Everyone should be considered for tPA if the patient has arrived in the ED within the window and has no contraindication is present. The patient should first receive tPA if eligible, and after tPA administration, the patient should transfer to an angiography suite for MT. Admit patients to the neuroscience ICU for the post-tPA and post-MT care, including neuromonitoring, hemicraniectomy watch, airway watch, respiratory support, blood pressure management, and symptomatic care. Further management should take place at the stroke unit with a multidisciplinary team approach rather than an admission to the general ward.
Patients who are not tPA candidates, and who have a plaque burden in the posterior circulation are manageable through acute anticoagulation or antiplatelet regimen. Recent data is supporting the use of single or dual antiplatelets, over anticoagulation for large artery atherosclerotic disease, particularly if there is a large infarct burden. For intracranial atherosclerosis, it is recommended to use dual antiplatelets for 90 days after stroke and followed by aspirin only. Further details regarding the management of basilar artery occlusion and ischemic stroke of currently available and ongoing data can be found in the "pertinent studies and ongoing trial" section of this review. However, be advised that most of the currently available data came from anterior circulation strokes rather than posterior circulation strokes. Secondary prevention, including the use of aspirin, atorvastatin, and anticoagulants if indicated. At the time of discharge, vascular risk factor modification with LDL goal below 70, a blood pressure goal less than 130/80, and reasonable glycemic control with A1c goal under 6.5, as well as the goal-directed treatment, should be considered based on the etiology of stroke. Also, lifestyle modification, including the Mediterranean diet, smoking cessation, limit alcohol, and no illicit drugs, have proven benefits in preventing stroke recurrence.
Heparin after an acute ischemic stroke
TPA (tissue Plasminogen activator or alteplase) after an acute ischemic stroke
Thrombectomy in LVO
Carotid Endarterectomy (CEA) for atherosclerotic LVO
Aspirin+Plavix (dual antiplatelets) appeared to superior to aspirin alone in preventing strokes after TIA/small ischemic strokes
Intracranial Arterial Stenosis
Lacunar strokes (small vessel disease)
Afib (atrial fibrillation)
Cryptogenic strokes and atrial cardiopathy
Patent foramen ovale (PFO) closure
Hyperlipidemia and Hypertriglyceridemia
Post-stroke depression, motor recovery, and role of SSRI
As described above initial revascularization followed by secondary prevention should be performed in BAO patients.
The most significant side effects of thrombolysis and mechanical thrombectomy are intracranial hemorrhagic transformation, groin/femoral artery perforation/bleeding complications, death, and disability. Prognosis and outcomes should be discussed in urgency with the family while administering alteplase and wheeling patients for thrombectomy.
Prognosis of BAO depends on the severity of the stroke, time to LKN, the treatment offered, successful recanalization, and access to tertiary care hospital and comprehensive stroke center. Overall, mortality is very high in this population, in patients with successful recanalization after thrombectomy has a lower mortality rate of 33 to 50%, versus 74 to 100% in patients without thrombectomy or failed reperfusion. With early arrival and appropriate management, as described above, the outcome may be good, with minimum deficits. But late arrival and failure of revascularisation of BAO invariably result in poor outcomes, including severe neurological deficits and very high mortality in these patients.
An interprofessional team approach, including emergency department, neurology (stroke), neurosurgery, neurocritical teams, as well as nursing, physical therapy, occupational therapy, and speech therapy collaboration, is essential and the key to good outcomes in patients with basilar artery occlusion.
Counsel the patient and family regarding stroke that the risk of a stroke can be decreased by appropriately treating diabetes, hypertension, high cholesterol, cardiac diseases, obesity, and by quitting smoking, reducing alcohol intake, and staying physically active. Time is of the essence. Discuss the BE-FAST (balance loss, eyesight, facial droop, arm weakness, slurry speech, time) symptoms awareness on all the media and public education channels and campaigns.
The risk of a stroke can be decreased by treating hypertension, high cholesterol, diabetes, heart disease, and obesity and by quitting smoking, limiting alcohol, and staying physically active. Time is of the essence. It is essential to seek treatment within 3 to 4.5 hours of the start of symptoms because, during that time, thrombolytic drugs are an option. Even if one does not know when symptoms began, get treatment as soon as possible. After the 4.5-hour window has passed, treatment may include rest, oxygen, intravenous (IV) fluids, and medicines to thin the blood (anticoagulants). Treatment of stroke depends on the duration, severity, and cause of one's symptoms. Medications and diet may be used to address diabetes, high blood pressure, and other risk factors. Physical, speech, and occupational therapists will assess and work to improve any functions impaired by the stroke. Measures will be taken to prevent short-term and long-term complications, including infection from breathing foreign material into the lungs (aspiration pneumonia ), blood clots in the legs, bedsores, and falls. Rarely, surgery may be needed to remove large blood clots or to open up blocked arteries.
Measures should be taken to prevent short-term and long-term complications, including infection from breathing foreign material into the lungs (aspiration pneumonia), UTI, DVT, PE, bedsores, dysphonia, dysphagia, and falls. Aggressive physical and occupational therapies should treat post-stroke complications like contractures, follow-up in the neurology clinic, and consideration of botox injection may help with recovery from contractures. Rarely, surgery may be needed to remove large blood clots or to open up blocked arteries. Another significant complication is post-stroke depression; we should be treated by citalopram or fluoxetine, which has been proved beneficial and recent studies for post-stroke depression and motor recovery after stroke.
There is a lot of high-quality evidence regarding the prevention and management of stroke, as described in any organized and comprehensive stroke guidelines in 2018. Here is is the summary of stroke prevention and management with the corresponding class of recommendation (COR=strength of study) and level of evidence (LOE=quality of study):
An interprofessional team approach is necessary for improving outcomes in patients with basilar strokes. In addition to the various clinical specialties already covered, a pharmacist should consult for thrombolytic therapy; this may well be a cardiac board-certified pharmacist. Stroke-certified nursing staff is an invaluable resource, irrespective of which direction therapy takes; they can help in evaluating the patient, assist during procedures, and monitor the patient's condition following interventions, charting, and reporting their findings for the clinician staff. These types of interprofessional actions enhance patient outcomes in basilar artery occlusion and other types of strokes. [Level 5]
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