Basilar artery stroke …

Stroke & Vascular Disorders

Updated 02.26.2024
Released 10.28.1997
Expires For CME 02.26.2027

Basilar artery stroke

Authors: H Steven Block MD, Jose Biller MD

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Editor: Steven R Levine MD

Basilar artery stroke

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Introduction

Overview

Basilar artery brainstem infarctions are perhaps the most feared and devastating of all ischemic strokes. With the development of advanced high-resolution MRI wall imaging, our understanding of symptomatic intracranial atherosclerotic disease has expanded beyond the presence of luminal diameter stenosis. Basilar arterial wall remodeling and symptomatic non-stenosing intracranial atherosclerotic disease (and its significant contribution to embolic stroke of undetermined source) are presented. The latest basilar artery mechanical thrombectomy randomized controlled trial data, bridging intravenous thrombolysis prior to mechanical thrombectomy, intra-arterial thrombolysis, and basilar artery percutaneous angioplasty and stent randomized controlled trial evidence, are discussed.

Key points

	• Basilar artery stroke can be a grave condition.
	• Basilar artery stroke is most commonly caused by atherothrombosis and cardioembolism.
	• Patients with acute ischemic stroke in the basilar artery territory should receive intravenous thrombolytic therapy with tenecteplase or alteplase, even if mechanical thrombectomy is planned.
	• Mechanical thrombectomy has been proven to be beneficial in basilar artery thrombosis.
	• Current evidence does not support the use of percutaneous angioplasty and stent in the intracranial posterior circulation.
	• Arteriographic absence of arterial luminal imaging is no longer the “gold standard” in ruling out symptomatic intracranial atherosclerosis. Symptomatic non-stenosing intracranial atherosclerosis appears to play a substantial role in stroke.

Historical note and terminology

The first clinico-pathologic report of basilar artery occlusion appeared in 1868 by Hayem (80). In 1882, Leyden reviewed prior cases of basilar artery occlusion, reported two additional clinico-pathologic cases of his own, described aneurysmal dilation of the basilar artery, and discussed the differential diagnosis between atherosclerotic basilar artery disease and superimposed thrombosis, embolism to the basilar artery, and syphilitic basilar artery endarteritis with thrombosis (106). His discussion of three patients who presented with sudden (but nonfatal) bulbar signs, presumed to have basilar artery thrombosis, probably represents the first recorded instance of basilar artery stroke. Charles Dana, in an extensive review of infarctions and hemorrhages of the pons and medulla surveyed 39 autopsied cases of lower brainstem infarction and noted that many patients had prodromal transient attacks of hemiparesis, vertigo, dysarthria, and double vision during the months or years preceding their major strokes (43). He divided the clinical presentation into two major categories: (1) long tract motor and sensory dysfunction and (2) bulbar symptoms and signs. Foix and Hillemand published a detailed review of pontine infarcts and the anatomy of the basilar artery and its branches (63).

Kubik and Adams's classic report on basilar artery occlusion in 1946 shaped modern conceptions of pathology and pathogenesis of basilar artery steno-occlusive disease (96). They analyzed 18 necropsy cases, concluding that basilar artery occlusions are characterized by frequent early loss of consciousness, common bilateral involvement, and combinations of pupillary disturbance, ocular and other cranial nerve palsies, dysarthria, extensor plantar responses, hemiplegia or quadriplegia, and often a marked remission of symptoms. Biemond emphasized amnesia, hemianopsia, and other posterior cerebral artery manifestations of basilar artery distribution ischemia (23). Millikan and Siekert detailed vertebrobasilar transient ischemic attacks ("vertebrobasilar insufficiency") and advocated anticoagulants as therapy. Kemper and Romanul described a patient with the loss of the ability to communicate due to limb and bulbar paralysis, a condition later coined "locked-in syndrome." A public light was shed on this rare and devastating disorder with the 1997 publication and film of the same name in 2007, Le Scaphandre et le Papillon (The Diving Bell and The Butterfly) a moving, first-person account by Jean-Dominique Bauby, former Editor-in-Chief of the French magazine Elle and a victim of a basilar artery stroke. The locked-in syndrome had already been depicted in Alexandre Dumas’ novel The Count of Monte Cristo, when he created Monsieur Noirtier de Villefort. Dumas described his character as a “corpse with living eyes” (188). Caplan described the "top of the basilar syndrome” and attributed it to embolic occlusion of the distal basilar artery producing ischemia of the rostral brainstem and the posterior cerebral artery territories (35).

Clinical manifestations

Presentation and course

The clinical manifestations of basilar artery ischemia vary according to the site and nature of vascular compromise. Four broad clinical profiles may be distinguished.

Proximal and middle basilar artery occlusive disease. Stenosis or occlusion of the proximal or middle segments of the basilar artery is frequently atherosclerotic in origin. It produces unilateral or bilateral pontine dysfunction and less often cerebellar, midbrain, occipital, or mesial temporal lobe ischemia. The clinical profile of large vessel pontine ischemia is dominated by long tract motor dysfunction, frequent altered consciousness, and disordered horizontal eye movement.

Midbasilar artery stenosis (angiogram anteroposterior projection)

Angiogram anteroposterior projection showing midbasilar artery stenosis. (Contributed by Dr. Jeffrey Saver.)
Proximal and midbasilar artery stenosis (angiogram)

MR angiogram showing proximal and midbasilar artery stenosis. (Contributed by Dr. Jeffrey Saver.)
Midbasilar artery stenosis (angiogram)

MR angiogram showing midbasilar artery stenosis. (Contributed by Dr. Jeffrey Saver.)

The most characteristic motor manifestation is asymmetric quadriparesis, though hemiparesis, hemiplegia, and quadriplegia can occur. Weakness of bulbar musculature, including the face, pharynx, larynx, and tongue, is frequent and typically bilateral. A crossed pattern of motor deficit occasionally is encountered, for example, simultaneous lower motor neuron left facial weakness and upper motor neuron right arm and leg paresis. Bulbar symptoms include facial weakness, jaw weakness, dysarthria, dysphonia, and dysphagia. Impaired handling of secretions with aspiration is a common complication. The most extreme motor manifestation of pontine ischemia is the locked-in syndrome; this is characterized by complete loss of all voluntary limb and facial movement, with retained consciousness and preserved vertical gaze. Basilar artery thrombosis may also present as a transient locked-in syndrome (64).

Oculomotor signs include a sixth nerve palsy, horizontal gaze paresis, internuclear ophthalmoplegia, the one-and-a-half syndrome (ipsilateral horizontal gaze palsy in one direction of gaze and internuclear ophthalmoplegia in the other), ocular bobbing (rapid downward movement of the eyes with slow return to primary position), horizontal nystagmus, vertical nystagmus, ptosis, and skew deviation. Pupils are often spared, but pinpoint, reactive pupils may be seen in comatose patients with large pontine lesions.

Ocular bobbing

A 68-year-old woman presented with deep coma (E1, V1, and M2) of 2 days duration. On examination the patient had pinpoint sluggishly reacting pupils, absence of extraocular movements on oculocephalic maneuvers, ocular bobbing, ...

Acutely altered consciousness is present in up to half of patients with proximal-middle basilar artery occlusions. Findings range from mild somnolence to coma.

Less prominent manifestations of proximal-middle basilar artery territory ischemia include limb ataxia, pseudobulbar affect, somatosensory deficits, and hemianopsia. Limb ataxia occurs frequently, is often bilateral, and usually coexists with, but is disproportional to, homolateral weakness. Pathologic crying and laughing appears occasionally. Unilateral or bilateral somatosensory deficits are reported in one-fifth of patients. Occasionally, artery-to-artery embolism from the proximal basilar artery to the posterior cerebral artery produces homonymous hemianopsia, visual agnosia, memory dysfunction, and other features of occipital or mesial temporal lobe ischemia. Basilar artery ischemia can manifest as acute unilateral or, more rarely, bilateral sensorineural hearing loss (91) or rhythmic tonic movements of all the extremities, often mistaken as seizures (155; 189).

Transient vertebrobasilar circulation ischemic attacks precede stroke in about three fourths of infarcts due to proximal and middle basilar artery stenosis or occlusion. Often one or more transient ischemic attacks culminate in infarction over a 3- to 6-month time period. Occasional patients may have transient ischemic attacks alone, or incidental, asymptomatic disease. Infarcts often progress with a stuttering course of stepwise worsening over minutes, hours, or days, although abrupt onset of maximal deficit can occur.

Basilar artery thrombosis may cause auditory hallucinations. Galtrey evaluated a 60-year-old man with episodes of bilateral auditory hallucinations described as “white noise,” which were associated with basilar artery thrombosis and attributed to ischemia of the auditory pathways in the brainstem (65).

Distal basilar artery occlusive disease ("top of the basilar syndrome"). Occlusion of the distal basilar artery is frequently embolic in origin, and produces signs of midbrain and thalamic ischemia, occipital and mesial temporal lobe ischemia, or both.

Distal basilar artery occlusion (angiogram)

(A) Lateral projection of distal basilar artery occlusion. (B) Anteroposterior projection of distal basilar artery occlusion. (Contributed by Dr. Jeffrey Saver.)

Infarction of the rostral brainstem and cerebral hemispheres fed by the distal basilar artery causes a clinically recognizable syndrome characterized by visual, oculomotor, and behavioral abnormalities, often without significant motor dysfunction. Leading features of midbrain ischemia are abnormalities of oculomotor and pupillary function and alertness.

Somnolence, vivid hallucinations, and dreamlike behavior can also accompany rostral brainstem infarction. Temporal and occipital lobe infarctions frequently cause hemianopsia with distinctive characteristics, fragments of the Balint syndrome named for the Austro-Hungarian neurologist Rezso Balint in 1909 (a triad of optic ataxia, oculomotor apraxia, and simultanagnosia), amnesia, and agitated behavior. More than three fourths of patients exhibit disruption of voluntary and reflex vertical gaze, rarely selectively affecting upgaze or downgaze but more often disrupting both. Convergence abnormalities are common, most often esotropia at rest or convergence retraction nystagmus (quick phases that converge or retract the eye) on attempted vertical gaze. Bilateral eyelid ptosis and lid retraction occur. Pupils will be fixed and dilated if the third nerve nucleus is compromised. Hypersomnolence may be present at onset, and rarely can persist for months. Ataxia occurs frequently, but hemiparesis is rare. Visual hallucinations, vivid but generally nonthreatening, are infrequently observed ("peduncular hallucinosis") (35).

Encephalomalacia and gliosis secondary to prior ischemic insult (MRI)

This brain MRI shows bilateral hyperintense signal changes on fluid-attenuated inversion recovery (FLAIR) sequences in the parieto-occipital regions consistent with encephalomalacia and gliosis secondary to prior ischemic insult i...

When ischemia extends to the mesial or anterior thalamus, memory dysfunction, abulia, or both, may appear.

Occipital lobe infarction produces visual field defects, generally homonymous hemianopsia or homonymous quadrantanopsia. Alexia without agraphia may appear with dominant occipital lesions involving the splenium of the corpus callosum. Bilateral lesions may produce other higher visual function disturbances, including cortical blindness, prosopagnosia, visual object agnosia, and Balint syndrome. Mesial temporal lobe infarction can produce memory disturbance, especially if lesions are bilateral (135). Agitated delirium at onset can occur with dominant occipitotemporal infarcts.

Transient ischemic attacks commonly precede strokes when distal basilar artery disease is due to local and upstream atherosclerosis within the vertebrobasilar system, whereas embolism from the heart and ascending aorta usually produces sudden infarcts without warning.

Generalized tonic clonic seizures may rarely be the initial presentation of the top of the basilar syndrome (123).

In 1977, Archer and Horenstein elegantly documented the clinical symptomatology and angiographic findings of 20 patients with basilar occlusions at various sites along the artery and three patients with bilateral vertebral artery occlusions (13). Although the clinical symptoms have been separately discussed in this article, a review of this concise, clinical-radiographic correlation is a useful exercise.

Basilar branch disease. Basilar artery atherothrombosis may occlude the ostium of a penetrating vessel without compromising flow in the basilar artery itself, producing a fractionated ventral pontine clinical syndrome. Ataxia, hemiparesis, and dysarthria in various combinations are common, including syndromes of pure motor hemiparesis, ataxic-hemiparesis, and clumsy hand-dysarthria, which may occur in paramedian pontine perforator occlusions. Either vertigo or diplopia appears infrequently, accompanying mild, transient sensory loss. Occlusion of the thalamogeniculate branches arising from the posterior cerebral artery may produce contralateral subjective sensory symptoms and limb hemiataxia and hemichorea. Occlusion of the thalamoperforating artery branches may produce unilateral or bilateral thalamic infarctions, which may culminate in cognitive dysfunction, somnolence, and aphasia (34).

Basilar artery dolichoectasia (elongation and tortuosity). When the basilar artery becomes markedly widened, elongated, and tortuous, distinctive syndromes related to compression may arise in addition to ischemic syndromes related to abnormal laminar flow causing thrombosis and occasional distal embolism, torsion occluding the origins of small penetrating vessels, and associated intrinsic small vessel disease (45). Cranial nerve compressive signs are present in over half of symptomatic cases, most often hemifacial spasm and trigeminal neuralgia. It can also cause abducens nerve (CN VI) paralysis, and rarely compress the optic tract, accounting for optic atrophy and homonymous hemianopsia. Direct brainstem compression of the ventral pons may produce ataxia and hemiparesis, progressing over months to years. Hydrocephalus may arise and produce gait, bladder, and cognitive abnormalities. Headaches occur in 15%. Almost half of reported symptomatic cases have coexisting or isolated ischemic symptoms, affecting pontine, midbrain, cerebellar, thalamic, or occipitotemporal regions. Subarachnoid hemorrhage can occur infrequently. In younger people, dolichoectasia may be associated with acquired immune deficiency syndrome (AIDS), Marfan syndrome, Ehler-Danlos syndrome, sickle cell disease, autosomal dominant polycystic kidney disease, neurofibromatosis type I, pseudoxanthoma elasticum, tuberous sclerosis complex, Pompe disease, moyamoya disease, cavernous malformations, and Fabry disease (115; 45). Ischemic symptoms are often attributable to lacunar infarctions. Apart from symptomatic cases, dolichoectatic basilar arteries are often an asymptomatic finding at imaging or autopsy.

Elongated and tortuous basilar artery (angiograms)

(A) Lateral projection of elongated and tortuous basilar artery. (B) Anteroposterior projection of elongated and tortuous basilar artery. (Contributed by Dr. Jeffrey Saver.)
Enlarged basilar artery compression pons (CT)

Noncontrast CT showing enlarged basilar artery compression pons. (Contributed by Dr. Jeffrey Saver.)

Prognosis and complications

Series of patients diagnosed by noninvasive imaging suggest a less ominous prognosis than earlier autopsy and angiographic cohorts, but basilar artery stroke remains a grave condition. One review found that patients presenting with consciousness disorders or the combination of dysarthria, pupillary disorders, and lower cranial nerve involvement invariably had poor outcomes compared to only 11% of patients without these signs (49). In addition, patient age and comorbidity, the size of infarct, and whether the vascular lesion is stenotic or totally occlusive are major determinants of outcome.

Prospective data on acute outcome from basilar artery stroke are sparse. In the New England Medical Center Registry series of 87 patients with severe basilar artery occlusive disease, only 2.3% of patients died of their acute stroke. At hospital discharge 40% had no neurologic deficit, whereas residual deficits were minor in 31%, and severe in 26%. Predictors of poor outcome included distal territory involvement, embolism, occlusion, impaired consciousness, tetraparesis, and abnormal pupils. Similarly, in a series of 27 patients with top of the basilar stroke, only 4% died within the first 30 days (131).

The typical course of basilar artery occlusions is more devastating than basilar artery stenoses. Angiographic series have reported mortality in 80% to 90% of patients. (99; 78; 57). Other studies suggest a less grim prognosis, especially in patients with atherothrombotic occlusions of only a short basilar segment and good collateral supply (98; 29). Endovascular therapy may improve the outcome of acute basilar artery occlusion.

There is a paucity of long-term follow-up information regarding patients who suffer from locked-in syndrome. Five-year survival rates have been estimated to be 80%, and some patients have been reported to live for more than 20 years. In an attempt to further understand locked-in syndrome, 44 patients surviving an average of 62 months following onset of locked-in syndrome were surveyed (103). Attention level was described as good by 86%, and 77% were able to read. A majority (85%) characterized themselves as being more emotional than before their stroke, and 48% reported a good mood. Although communication is difficult for patients with locked-in syndrome, 66% could communicate without technical aids using a system of eye movements and blinking, and 78% were capable of emitting sounds. This survey highlights the importance of multidisciplinary treatment of patients with locked-in syndrome in order to maximize their abilities. In another study of 67 patients with locked-in syndrome for a median of 7 years, including 51 due to stroke, self-reported quality of life survey results were relatively satisfactory compared to those with other severe conditions. Satisfaction persisted during a 6-year follow-up interval. However, those whose communication was limited to yes-no code rather than an electronic communication device reported lower satisfaction (152).

Patients with basilar artery embolism with spontaneous dissolution may fare better than those with persistent occlusion. In a study of patients with presumed basilar artery embolism without occlusion, 42% had no or only mild neurologic deficits 8 to 12 weeks after stroke onset, and 18% died (161).

The long-term risk of recurrent transient ischemic attack or stroke after first ischemic presentation of basilar artery disease is poorly defined. Anecdotal clinical experience suggests that intrinsic atherothrombotic disease is attended by frequent subsequent transient ischemic attacks or recurrent strokes. In the Oxford Vascular Study, the 90-day risk of recurrent stroke or transient ischemic attack was 46% for patients with greater than or equal to 50% basilar or vertebral artery stenosis (122). Distal basilar artery low flow status as measured by quantitative MRA in patients with at least 50% symptomatic stenosis of the vertebral or basilar arteries within the preceding 60 days is strongly associated with subsequent stroke risk (10). Moreover, despite the overall increased stroke risk with higher blood pressure in patients with intracranial stenosis, blood pressure 140/90 mm Hg or lower may increase the stroke risk in patients with symptomatic vertebrobasilar stenosis and low-flow status (11). Advancements in intracranial high-resolution MRI arterial wall imaging can demonstrate “active” culprit plaques that have been symptomatic with recent infarction as well as presymptomatic active plaques.

Nearly half of patients with basilar artery dolichoectasia deteriorate clinically over 5-years (194). Infarction (18%), transient ischemic attack (10%), compressive symptoms (10%), intracerebral and subarachnoid hemorrhage (6%), and hydrocephalus (3%) account for the clinical deterioration (45). Those with large, bilateral pontine infarcts related to basilar artery occlusion almost uniformly experience poor outcomes. Those with smaller, unilateral pontine infarcts, likely due to obstruction of the origin of a pontine penetrator or associated intrinsic small vessel disease, have a more favorable early outcome. The long-term course is poor, with up to one third of patients dying within 5 years, often from recurrent stroke (125). Symptomatic initial presentation, dolichoectasia severity at diagnosis, worsening angioarchitecture during follow-up and mural thrombus, contribute to delayed morbidity. Radiographic progression occurs in 42%.

Complications of basilar artery stroke include aspiration, dysphagia requiring G-tube or J-tube placement, urinary tract infection, pressure ulcers, and venous thromboembolism.

Clinical vignette

Vignette 1. A 65-year-old man with arterial hypertension, hypercholesterolemia, and coronary artery disease, was admitted with transient dysphagia, dysarthria, binocular diplopia, and impaired consciousness from which he markedly improved on arrival to the emergency room. He had mild dysarthria on examination at 1 hour after fluid resuscitation and blood pressure support for hypotension, which was thought to be responsible for his presentation.

A code was called later the first night of admission (12:34 am) at which time he was found unresponsive and profoundly hypertensive, tachycardic, and tachypneic.

The patient was intubated and transferred to the intensive care unit on intravenous antihypertensive agents. Evaluations for cardiac etiology and pulmonary embolism were unremarkable. Neurology consultation was obtained when patient examination did not improve by the morning. MRI of the brain demonstrated restricted diffusion in the pons. MRA demonstrated thrombus in the mid-basilar artery. Endovascular treatment was unsuccessful. The patient remained in a “locked-in” state and mechanical ventilation was eventually withdrawn at his own wish.

Basilar artery stroke in 65-year-old man (MRI/MRA)

65-year-old male with basilar artery stroke. MRI of the brain with diffusion-weighted sequences demonstrated subacute infarct in the pons. MRA demonstrated thrombus in the mid-basilar artery. (Contributed by Dr. José Biller.)

Vignette 2. A 65-year-old woman presented with acute onset ataxia, headaches, bilateral arm numbness, and binocular diplopia. Examination was remarkable for decreased alertness, bilateral sixth nerve palsies, and bilateral upper limb dysmetria. Further deterioration in her level of consciousness prompted an acute CT without contrast, which was normal. MRI showed restricted diffusion in bilateral thalamic, bilateral cerebellar, and right midbrain regions. Presentation after 3 hours prompted catheter cerebral angiography where basilar artery thrombus superior to the anterior inferior cerebellar artery branches was demonstrated. Intraarterial tissue plasminogen activator (tPA) in combination with MERCI (Mechanical Embolectomy Retrieval in Cerebral Ischemia) retriever restored flow to the remainder of posterior circulation with good clinical outcome. (Courtesy of Dr. Tim Malisch and Dr. José Biller.)

Basilar artery stroke in 65-year-old woman (1)

A 65-year-old woman presented with acute onset ataxia, headaches, bilateral arm numbness, and binocular diplopia. Examination was remarkable for decreased alertness, bilateral sixth nerve palsies, and bilateral upper limb dysmetri...
Basilar artery stroke in 65-year-old woman (2)

A 65-year-old woman presented with acute onset ataxia, headaches, bilateral arm numbness, and binocular diplopia. Examination was remarkable for decreased alertness, bilateral sixth nerve palsies, and bilateral upper limb dysmetri...

Vignette 3. An 81-year-old woman with arterial hypertension and a left middle cerebral artery bifurcation aneurysm was evaluated at an outside hospital for nausea, dysarthria, headache, and dizziness. She was intubated after exhibiting decreased alertness in the emergency department. Gaze-evoked nystagmus, decreased arousal, and inability to follow commands were noted on examination prior to intubation. She was transferred to our institution for further evaluation and management. MRI and MRA showed right cerebellar, midbrain, bilateral occipital, and pontine tegmentum infarcts from proximal basilar artery thrombosis. (Courtesy of Dr. José Biller.)

Basilar artery stroke in 81-year-old woman

An 81-year-old woman admitted with arterial hypertension and a left middle cerebral artery bifurcation aneurysm was evaluated at an outside hospital for nausea, dysarthria, headache, and dizziness. She was intubated after exhibiti...

Vignette 4. A 51-year-old man was evaluated for transient quadriparesis and dysarthria. At the time of examination, the patient was asymptomatic with unremarkable neurologic exam. He had a history of prior transient right hemiparesis. Diffusion-weighted MRI showed no acute lesion. MRA demonstrated moderate to severe midbasilar artery stenosis. Catheter cerebral angiography showed a 65% to 70% midbasilar stenosis with poststenotic dilatation above the level of the anterior inferior cerebellar artery and below the labyrinthine arteries. (Courtesy of Dr. José Biller.) The patient was placed on antiplatelet and statin therapy.

Basilar artery stroke in 51-year-old man

A 51-year-old man was evaluated for transient quadriparesis and dysarthria. At the time of examination, the patient was clinically asymptomatic but had a history much like the one described in C. Miller Fisher’s classic observatio...

Vignette 5. A 69-year-old man with diabetes mellitus, arterial hypertension, and a previous stroke was found unconscious at home. He was last known to be well 8 hours before. His trachea was intubated on the scene by Emergency Medical Services and he was taken to the emergency department. Initial neurologic exam was confounded by residual pharmacologic paralysis and sedation used for intubation. Emergent CT showed a midbasilar hyperdensity suggesting thrombus and MRI demonstrated restricted diffusion in bilateral cerebellar, bilateral thalamic, and bilateral occipital regions. Follow-up examination showed impaired consciousness, bilateral decerebrate posturing, bilateral nonreactive pupillary reflex, bilateral absent corneal reflex, absent eye movements with oculovestibular reflex testing, and preserved gag reflex.

Basilar artery stroke in a 69-year-old man

A 69-year-old man with diabetes mellitus, arterial hypertension, and a previous stroke was found unconscious at home. He was last known to be well 8 hours before. His trachea was intubated on the scene by Emergency Medical Service...

Vignette 6. A 70-year-old man with a past history of trigeminal neuralgia awoke with dysarthria, left hemiplegia, and nausea. Examination also revealed horizontal and vertical nystagmus, skew deviation, and hoarse voice. Noncontrast brain CT showed hyperdensity anterior to the pons consistent with dolichoectasia of the basilar artery with acute or chronic thrombus. CT angiography demonstrated dolichoectasia of the basilar artery with occlusion of bilateral vertebral arteries and proximal basilar artery. MRI showed displacement of the brainstem with restricted diffusion in the right pons consistent with paramedian pontine small vessel distribution infarction. Motor examination initially improved to antigravity strength in the left arm and leg. Non-bolus intravenous heparin nomogram was started on hospital day 1 with target aPTT 50 to 70. He was transitioned to subcutaneous enoxaparin 1 mg/kg twice daily on hospital day 2, and warfarin was initiated. On hospital day 4, he became acutely unresponsive, apneic, bradycardic, and pulseless. A code was called, trachea was intubated, and return of spontaneous circulation was achieved. Noncontrast brain CT demonstrated diffuse subarachnoid hemorrhage. Neurologic examination did not recover, and death was subsequently declared by neurologic criteria.

Dolichoectasia of the basilar artery with thrombus (CT)

Noncontrast brain CT shows hyperdensity anterior to the pons consistent with dolichoectasia of the basilar artery with acute or chronic thrombus. (Contributed by Dr. Sean Ruland and Dr. Adam Schnitz.)
Dolichoectasia of the basilar artery with occlusion of bilateral vertebral arteries and proximal basilar artery (CTA)

CT angiography demonstrates dolichoectasia of the basilar artery with occlusion of bilateral vertebral arteries and proximal basilar artery. (Contributed by Dr. Sean Ruland and Dr. Adam Schnitz.)
Paramedian pontine small vessel distribution infarction (MRI)

MRI shows displacement of the brainstem with restricted diffusion in the right pons consistent with paramedian pontine small vessel distribution infarction. (Contributed by Dr. Sean Ruland and Dr. Adam Schnitz.)
Diffuse subarachnoid hemorrhage (CT)

Noncontrast brain CT demonstrates diffuse subarachnoid hemorrhage. (Contributed by Dr. Sean Ruland and Dr. Adam Schnitz.)

Biological basis

Etiology and pathogenesis

Atherothrombosis and cardioembolism are the most common causes of basilar artery territory infarctions. Less frequent etiologies include cervicocephalic vertebral artery dissection, migraine, dolichoectasia, hematologic disorders (eg, sickle cell disease, hypercoagulable states), vasculitis, meningovascular syphilis, and paradoxical embolism (124; 196).

Anatomy

The vertebral arteries unite to form the basilar artery at the base of the pons. The vertebral arteries arise from their respective subclavian arteries medial to the anterior scalene muscle. After originating (ie, V1 or first segment) from the subclavian arteries, the vertebral artery traverses the foramina transversaria from C6 to C2 (ie, V2 or second segment), loops around the atlanto-occipital joint (ie, V3 or third segment), and finally pierces the dura passing through the foramen magnum to enter the intracranial cavity (ie, V4 or fourth segment) to join the other vertebral artery at the pontomedullary junction. The V2 segment is further subdivided into proximal V2 segment (C6), mid V2 segment (C2-5), and distal V2 segment (C1-2). The basilar artery ascends in a shallow groove on the anterior surface of the pons, with an average length of 32 mm and width of 2.6 mm to 3.5 mm (157). In most patients, the artery is curved, whereas in one fourth of patients it follows a straight-line rostral course. The basilar artery ends by dividing into the two posterior cerebral arteries in 80% of the population at the level of the interpeduncular cistern. Many variations can occur, including fetal origin of one or both posterior cerebral arteries, a vertebral artery ending as a posterior inferior cerebellar artery, and a persistent trigeminal artery. Thalamoperforating arteries arise near the basilar artery bifurcation and perfuse the medial and anterolateral thalamus. Thalamogeniculate arteries arise from the posterior cerebral artery and perfuse the lateral thalamus. Asymmetric vertebral arteries are found in over two thirds of cases. Throughout its rostral course in the middle third, the basilar artery gives off approximately 14 small paramedian branches that penetrate directly into the ventral pons and lower midbrain, and 14 small circumferential arteries that loop around the pons and midbrain to give off lateral basal and lateral tegmental penetrators (153; 133).

Normal posterior circulation (angiograms)

(A) Lateral projection of normal posterior circulation. (B) Anteroposterior projection of normal posterior circulation. Posterior cerebral artery = curved blue arrows, superior cerebellar artery = green arrows, basilar artery = re...

The major branches of the posterior circulation include the paired posterior inferior cerebellar arteries, which arise from the V4 segment and can have intra- or extradural origins in some cases. Paired anterior inferior cerebellar arteries arise next from the more proximal basilar artery. Distal paired superior cerebellar arteries arise last, prior to the basilar artery termination into bilateral posterior cerebral arteries, and serve the superior cerebellum. Clinically, superior cerebellar artery territory infarcts can potentially interrupt Mollaret’s triangle and cause palatal tremor (myoclonus).

The pons is a knob-like process measuring approximately 2 cm in length. It is organized into white matter tracts that travel transversely whereas most other fibers in the brainstem travel rostral and caudal. The posterior surface of the pons forms the anterior wall of the fourth ventricle. The pons may be further subdivided into the basis pontis and pontine tegmentum.

The basis pontis or anterior portion of the pons houses the corticospinal tracts and the nuclei of cranial nerves V, VI, VII, and VIII. The mid-pons houses the motor nucleus and chief sensory nucleus of cranial nerve V. The lower pons houses the cranial nerve nuclei VI, VII, and VIII. Corticopontine fibers carry signals from the primary motor cortex to the ipsilateral pontine nuclei in the anterior pons. Pontocerebellar fibers then relay information to the contralateral cerebellar hemispheres, allowing action modification and correction in complex motor activities. The pons also controls arousal and regulates respiration. The pontine tegmentum located more posteriorly is involved in sleep and wakefulness and is postulated to be involved in initiation of REM sleep. It contains the richly serotonergic raphe nucleus and locus coeruleus, a norepinephrine-producing area involved in stress response and anxiety. Tegmental lesions in various models can reduce or eliminate REM sleep and dreaming.

Basilar artery fenestration (BAF), considered an anatomic variant, has been reported in association with arteriovenous malformations and developmental arterial anomalies (16). Basilar artery fenestration has a reported prevalence of 1.5% and may play a role in basilar aneurysmal formation and basilar artery thrombosis (20).

Atherosclerosis

Atherothrombotic disease is the most common cause of basilar artery strokes. In a series of 87 consecutive cases of basilar artery ischemia, atherothrombotic disease accounted for approximately 86% (184). Among intracranial vessels, the basilar artery is a frequent site of atherosclerotic change. The middle and proximal thirds of the basilar artery are more susceptible than the distal segment, but the difference is slight. In a review of 412 reported cases of basilar artery atherostenosis, the middle portion was involved in 56%, the proximal in 48%, and the distal in 40% (36). Patterns of vessel injury included atherosclerosis confined to the basilar artery, complex plaques arising in a distal intracranial vertebral artery extending into the basilar artery, and diffuse, disseminated vertebral and basilar artery atherosclerosis.

Atherosclerotic basilar artery with stenosis throughout (MR angiogram)

MR angiogram showing atherosclerotic basilar artery with stenosis throughout. (Contributed by Dr. Jeffrey Saver.)
Atherosclerotic basilar artery (angiograms)

(A) Lateral projection of atherosclerotic basilar artery. (B) Anteroposterior projection of atherosclerotic basilar artery. (Contributed by Dr. Jeffrey Saver.)

Symptomatic non-stenosing intracranial atherosclerosis and arterial wall remodeling

The 1991 TOAST criteria classified ischemic stroke as due to intracranial atherosclerosis if the luminal diameter stenosis was greater than 50% and without other causes. Following advances in high-resolution MRI vessel wall imaging, clinically significant non-stenosing atherosclerotic plaque can rupture, producing artery-to-artery embolization. This has been increasingly observed and is currently considered to be one of the major causes of embolic stroke of undetermined source (ESUS) (51).

Symptomatic non-stenosing intracranial atherosclerosis is considered one of the most significant etiologies for ESUS. Recurrent transient ischemic attack or acute ischemic stroke in the same vascular territory should raise suspicion of a symptomatic intracranial atherosclerotic plaque. Stroke recurrence with intracranial atherosclerosis is estimated to be 15% in 1 year. When including non-stenosing intracranial atherosclerosis, it increases to 25% in 1 year. This emphasizes the need to determine the risk of artery-to-artery embolization by assessing high-risk plaque features (44).

Vessel wall remodeling. Intracranial arteries with atherosclerosis may develop luminal narrowing without enlargement of the atherosclerotic lesions. Many vessel wall plaque segments display compensatory enlargement, which may or may not prevent luminal narrowing. Two forms of vessel wall remodeling have been described. Positive remodeling is consistent with vessel enlargement. Negative remodeling produces vessel and luminal narrowing. Positive remodeling is associated with increased lipid-rich plaque, which increases the risk for plaque rupture (120).

The basilar artery has a greater capacity for positive remodeling, with increasing plaque burden in comparison to the anterior circulation. Suspected mechanisms include the markedly slower blood flow in the basilar artery compared to the anterior circulation, which may impose different endothelial stress on the vessel wall. The relatively sparse sympathetic innervation in the vertebral and basilar arteries in comparison to the anterior circulation make autoregulation less robust, with the potential for arterial dilatation and remodeling (145).

Many of the studies imaging intracranial atherosclerosis using high-resolution MRI vessel walls compared the suspected culprit plaque with an adjacent reference area of vessel appearing to be normal. One of the few studies to longitudinally follow the same intracranial atherosclerotic plaque segment over time revealed that diabetes and wall contrast enhancement were significantly associated with advancing plaque progression, almost 11% in 1 year (75). This produced a 6.6% decrease in luminal area and 6.7% increase in wall thickness.

Radiographic biomarkers of symptomatic intracranial atherosclerotic disease

Plaque enhancement, intraplaque hemorrhage, plaque surface irregularity, degree of stenosis, plaque burden, and positive vessel remodeling were predictors of symptomatic intracranial atherosclerosis. Plaque enhancement was the most significant of all the biomarkers for demonstrating culprit plaque in downstream infarctions (167; 84).

Morphologic and radiographic characteristics of high-risk atherosclerotic plaque

Plaque enhancement. Abnormal plaque MRI contrast enhancement is considered a high-risk marker for future stroke in the same vascular territory, both with and without hemodynamically significant luminal diameter stenosis. Although most intracranial arteries do not have a vasa vasorum, neovascularization of inflammatory atherosclerotic plaque may produce gadolinium leakage and enhancement. A 2016 meta-analysis of predominantly anterior circulation infarctions performed high-resolution vessel wall MR-detected plaque enhancement in the intracranial internal carotid artery or middle cerebral artery within 30 days of the index stroke (76). Plaque enhancement was strongly associated with downstream acute infarction. An infarction was 10 times more likely in tissue supplied by the enhancing artery than a non-enhancing artery.

Significance of the atherosclerotic plaque location within the basilar artery wall. High-resolution MRI wall imaging of the basilar artery within 48 hours of symptom onset in patients with normal-appearing basilar artery on MRA revealed that 60% of the vessels demonstrated non-stenosing atherosclerotic wall plaque; 58.3% of those plaques were located along the dorsal or dorsolateral surface of the basilar artery in the expected location of the origin of penetrating branch arterioles, on the same side and axial image as the acute infarction (41). These findings were significant for branch vessel atheromatous disease and were associated with neurologic deterioration and worsened functional outcome.

Basilar artery tortuosity may be associated with atherosclerotic plaque, which tends to form on the inner arc of the tortuous vessel and is more likely to produce positive vascular remodeling of the artery, greater plaque burden, and plaque enhancement (203).

A systematic review of 21 studies of patients with acute and subacute ischemic infarction found that although there was no MRA evidence of hemodynamically significant stenosis as defined by either no stenosis or less than 50% arterial luminal diameter stenosis, MRI arterial wall imaging demonstrated that over half of these patients had atherosclerotic plaque without significant luminal stenosis in the vascular distribution of the infarction (186). Furthermore, radiographic markers that these were active, culprit plaques included intra-plaque hemorrhage, positive arterial wall remodeling, and plaque surface irregularity. Intraplaque hemorrhage was the strongest independent marker of a symptomatic state, with an odds ratio of 27.5. The prevalence of intraplaque hemorrhage did not significantly differ between low- and high-grade stenotic plaque. Low-degree stenosis in the basilar artery was more prevalent than in the middle cerebral artery (63.1% versus 45.4%, respectively) due to the greater capacity for positive (ie, outward) remodeling of the basilar artery wall from atherosclerosis and decreased sympathetic innervation. Suspected infarction mechanisms include artery-to-artery embolization from plaque rupture and plaque-related occlusion of arterial branch vessels.

MRI vessel wall imaging may assist in detecting response to treatment and predict stroke recurrence following intracranial atherosclerotic-mediated stroke.

Song and colleagues demonstrated a combination of atherosclerotic culprit plaque enhancement at the time of the index stroke, and the magnitude of collateral vessels was associated with a higher incidence of stroke recurrence (20% of 60 study patients, p < 0.05) (168).

In a small retrospective study of 29 patients (reduced from 40 patients following exclusion criteria) 3D MR vessel wall imaging was performed within 8 weeks of ischemic stroke onset and subsequently repeated 3 to 18 months after stroke onset (193). Arterial luminal stenosis greater than 50% of the major intracranial artery in the ischemic territory and at least two atherosclerotic risk factors were required. Patients were divided into recurrent and nonrecurrent stroke groups. All were treated with antiplatelet and intensive lipid-lowering therapy. There was no significant difference in the plaque features in baseline scans between the two groups. Of the plaque morphological features analyzed (degree of stenosis, plaque burden, intraplaque hemorrhage, and plaque enhancement ratio), patients with no stroke recurrence had improvement in all of the aforementioned parameters. In patients with recurrent stroke in the same vascular territory, there were statistically significant increases in the plaque wall contrast enhancement, the maximal ratio of wall area to vessel area, and the magnitude of plaque enhancement. The radiographic differences between patients without and with recurrent stroke in this small study demonstrated that MR vessel wall imaging may lead to the identification of patients who may not be responsive to a prescribed medical therapy, which may lead to modification of treatment type or duration.

Lv and colleagues found the risk of stroke recurrence to be significantly increased with increasing plaque burden, degree of stenosis, and contrast enhancement (119).

Additional advanced imaging techniques

Stroke mechanism cannot be accurately assessed without visualization of the intracranial arterial walls and characterization of plaque properties (186). Approximately half of acute and subacute ischemic stroke patients with non-stenotic intracranial MRA have identified plaques on vessel wall MRI. Approximately half of acute and subacute ischemic stroke patients with clinical intracranial atherosclerosis have less than 50% stenosis on MRA. Intracranial high-risk plaque with zero or a mild degree of stenosis is associated with ischemic stroke and multiple unfavorable outcomes. Vessel wall MRI can identify the high-risk plaque features and better risk stratify stroke patients.

MRI techniques. 3D black-blood variable-flip-angle intracranial vessel wall MRI can perform whole-brain vessel imaging with higher spatial resolution, greater signal-to-noise ratio, and the ability to reformat in multiple planes. It is superior to conventional 3D time-of-flight MRA and contrast-based CTA in detecting symptomatic plaque, active inflammatory plaque, and plaque length, especially in the posterior circulation. There is greater sensitivity to detect culprit plaque not seen with other conventional imaging as well as plaque showing contrast enhancement consistent with active inflammation, which increases the likelihood of a recurrent infarction (176).

MRA techniques. 3D 5T time-of-flight MRA is superior to demonstrating small intracranial branch arteries in comparison to 3T time-of-flight, with comparable image quality to 7T (162).

Digital subtraction angiography (DSA) techniques. 4D-DSA applies a reconstruction algorithm to three-dimensional time-resolved digital subtraction angiography, which allows significantly greater small vessel spatial resolution, can be reconstructed in any plane, and allows quantification of vascular flow. In addition to providing significant presurgical detail for the management of intracranial arteriovenous malformations and fistulas and intracranial aneurysm, there is potential utility for the evaluation of basilar artery occlusive disease and assessment of perforating and collateral vessels (56).

Radiomics in the assessment of symptomatic intracranial atherosclerotic plaque. With advances in computer processing power and the development of artificial intelligence modeling, early research in the emerging field of radiomics has demonstrated enhanced ability to detect culprit intracranial atherosclerotic plaque likely responsible for acute ischemic stroke and vulnerable unstable plaque (especially in non-stenotic vessels) for personalized prediction of stroke recurrence. Radiomics in high-resolution MRI vessel wall imaging analyzes features of signal intensity, texture, and spatial orientation within a specified field-of-view. These quantitative high-dimensional mineable features use machine learning to process complex relationships amongst a large number of variables. Radiomics has the potential to enhance detection of abnormalities and differentiate between symptomatic and asymptomatic intracranial arterial plaque beyond the thresholds detected by human direct visualization. Beyond the qualitative detection of the aforementioned parameters that current radiographic interpretation provides, radiomics has the benefit of identifying quantitative variables to enhance accuracy. Three circumstances in which machine learning of signal quantification may provide benefit are establishment of prognosis, future infarction risk, and tailored therapies. Intraplaque hemorrhage signal changes can quantify volume, shape, signal intensity, and proximity to the arterial wall. Secondly, pre-contrast T1 wall hyperintensity may represent intraplaque hemorrhage, and low T1 pre-contrast signal may represent lipid core. Post-contrast T1 hyperintensity may be caused by contrast enhancement of the fibrous cap or vasa vasorum. Thirdly, machine learning analysis of combined radiographic and clinical data can predict preoperatively poor functional outcome following basilar artery thrombectomy. Machine prediction models exceeded traditional scoring systems, such as Brain Stem Score, pc-ASPECTS, and NIHSS (41; 164; 203; 108; 174; 117).

Basilar perforator origin occlusion

In 1971, C Miller Fisher and Louis Caplan were the first to report their autopsy findings of atheromatous plaque in the basilar trunk, which occluded the ostia of a dorsal wall paramedian perforating arteriole producing a deep pontine infarction (60). The concept was further discussed by Caplan in 1989 (34). These observations expanded the etiology of deep pontine infarctions beyond hypertensive-mediated lipohyalinosis and may also be responsible for some occlusions of the thalamogeniculate, thalamoperforating, and short circumferential basilar artery branches.

Hemodynamically significant atherosclerotic stenosis of the basilar artery lumen is not needed to occlude the ostia of penetrating arteries. Basilar perforating artery origin occlusion should be suspected if there are no vascular risk factors for lacunar disease, especially hypertension.

In 2005, Klein and colleagues reported the first high-resolution MRI vessel wall imaging of basilar artery atherosclerotic plaque in the context of a normal appearing basilar artery lumen. Over 75% of their patients demonstrated non-stenosis plaque (93). Their technique was further refined in 2010 using black blood imaging sequences for high-resolution MRI vessel wall imaging, proving that small deep pontine infarctions not reaching the pial surface originally considered to be lacunar may also be caused by branch vessel occlusive disease from non-stenosing basilar artery plaque (94). Further discussion of intracerebral high-resolution MRI while vessel imaging is described in the Diagnostic Workup section.

Embolism

Embolism to the basilar artery is the second most common cause of basilar artery territory strokes, responsible for 14% of cases in one series (184). Emboli lodging in the basilar artery generally produce acute occlusion rather than stenosis. Origins for the emboli include the heart, atherosclerotic lesions of proximal extracranial and intracranial vertebral arteries, proximal subclavian arteries, the aortic arch, and vertebral artery dissection. Because the width of the basilar artery narrows as it courses distal, most emboli small enough to pass through the vertebral arteries will traverse the proximal basilar segment and occlude the middle or distal segments.

High-resolution cerebral MRI wall vessel imaging has demonstrated unstable active, inflammatory atherosclerotic plaque that does not have to demonstrate significant luminal diameter stenosis to become symptomatic with plaque rupture and embolization. High-risk MRI features include lipid-rich necrotic core, intraplaque hemorrhage, gadolinium contrast enhancement that may be consistent with neovascularization and vessel leakage, thin fibrous cap, and ulcerations. Embolization from an active non-stenotic cerebral atherosclerotic plaque is considered one of several major causes of embolic stroke of undetermined source (51).

Cervical spine surgical interventions including reduction of cervical spondylolisthesis can rarely result in distal vertebrobasilar embolization (179).

Dolichoectasia

The basilar artery and the distal vertebral arteries, along with the internal carotid arteries, are particularly susceptible to a dilatative arteriopathy, producing vertebrobasilar dolichoectasia (dolichos meaning “long”, ectasia meaning “distended”), also called “fusiform aneurysm” (115). Its prevalence ranges between 0.05% and 18%. Various theories for the development of basilar and carotid dolichoectasia have been advanced, including congenital defects of the media or fragmentation of the internal elastic laminae; and unrecognized preceding arterial dissection with formation of dissecting aneurysms (12). Some or all of these mechanisms likely operate together to account for most cases. Although atherosclerosis can be found within dolichoectatic vessels, atherosclerosis is associated but not primarily causative. Both conditions can coexist. However, data from high-resolution MRI vessel wall imaging in 34 patients with vertebrobasilar dolichoectasia (22 with stroke, 12 without) demonstrated that stroke occurs more commonly in vertebrobasilar dolichoectasia with an associated atherosclerotic plaque (54.5% versus 8.3% in patients without stroke). The degree of basilar artery luminal diameter stenosis and arterial wall remodeling were lower in the stroke group, suggesting that hemodynamic insufficiency is not a cause for stroke. Rather, infarction was suspected due to occlusion of the ostia of perforating arterioles and plaque vulnerability with artery-to-artery embolization. Slow flow within the dilated segment may result in intraluminal thrombus (190). In a study of 719 consecutive patients evaluated for stroke, 238 (33%) demonstrated basilar artery dolichosis, of which 12 (1.7%) patients demonstrated basilar artery dolichoectasia (33). There was increased incidence of stroke in the dolichoectatic versus dolichosis population. Diabetes and smoking, risk factors for intracranial atherosclerosis, are also observed in basilar artery dolichosis. This may exacerbate the development of coexisting atherosclerosis and increase stroke risk. Arterial wall remodeling can occur. Direct compression on the pons and cranial nerves may occur. On rare occasion, there may be vessel rupture producing subarachnoid hemorrhage.

Basilar artery (MRIs)

(A) T1-weighted MRI image of enlarged and thickened basilar artery. (B) T1-weighted MRI coronal view image of elongated and tortuous basilar artery. (C) T2-weighted MRI image of enlarged and tortuous basilar artery displacing medu...

Bow hunter syndrome

Bow hunter syndrome is a rare condition whereby lateral head rotation produces symptoms of vertebrobasilar ischemia by mechanical compression of a vertebral artery. The term was coined by Sorensen in 1978, who described a patient who developed a Wallenberg syndrome during archery practice (169). Symptoms include syncope or presyncope, vertigo, diplopia, nystagmus, hemiparesis, paresthesias, nausea and vomiting, Horner syndrome, dysphagia, and headache. Symptoms may be transient or persistent due to ischemic stroke in cases of sufficient hemodynamic compromise or formation of thromboembolism.

A case series of 11 patients diagnosed by dynamic catheter-directed vertebral angiography over 14 years at a tertiary referral center reported that the level of vertebral artery compression was most commonly C1-2 and C5-7, with a slight predilection for the left vertebral artery (200). In the same study, the direction of head rotation did not predict the laterality of the compressed artery; 55% of patients had compression contralateral to head rotation, whereas 45% had ipsilateral symptoms. Surgical decompression may be beneficial in alleviating symptoms, although clinical trial data are lacking.

Cerebral vasculitis and other miscellaneous etiologies

Rare causes of basilar artery thrombosis include meningovascular syphilis, Behçet disease, antiphospholipid syndrome, meningitis, giant cell arteritis, and neuroborreliosis. Back and colleagues reported 11 patients with neuroborreliosis-associated cerebral vasculitis (17). Eight cases involved the vertebrobasilar circulation, and two had basilar artery thrombosis.

Epidemiology

Posterior circulation infarcts represent 12% to 27% of all strokes in hospital-based registries, and basilar artery disease accounts for a substantial proportion of these (26; 27). Among 520 consecutive patients with posterior circulation ischemia in three series, basilar artery stenosis or occlusion was responsible for 20% (25; 36). These data suggest that basilar artery stenosis or occlusion is responsible for approximately 4% of all infarcts.

Well-established systemic vascular risk factors strongly influence the development of atherosclerotic change. In the New England Medical Center series of 66 consecutive patients with basilar artery atherostenosis, hypertension was present in 64%, diabetes in 36%, tobacco use in 35%, hyperlipidemia in 35%, coronary artery disease in 45%, and peripheral vascular disease in 20%. Affected individuals tend to be over the age of 50, and more men are reported than women. People of African descent, and possibly those with Asian ancestry, have a predilection to stenosis in more distal segments of the basilar artery, whereas Caucasians are predisposed to stenosis in more proximal segments (72; 36).

Atrial fibrillation was previously considered to be the most common risk factor for cardioembolism to the basilar artery. Currently, artery-to-artery embolization from ruptured non-stenosing intracranial atherosclerotic plaque may play an even more significant role. Valvular disease, left ventricular dysfunction, and patent foramen ovale are also important. Acute basilar artery occlusion is an infrequent complication of cardiac papillary fibroelastoma (113; 51). Other cardioembolic sources include myxoma, papillary fibroblastoma, mural cardiac thrombi, and both infectious and nonbacterial thrombotic endocarditis.

Dolichoectasia of the basilar artery is increasingly encountered. Older autopsy and angiographic series of consecutive cases estimated an incidence greater than 0.1% (83; 81; 198). An MRI study identified dolichoectatic vertebrobasilar arteries in 0.9% of 1416 consecutive patients (160). However, in clinical series of patients with posterior circulation ischemia, vertebrobasilar dolichoectasia is present in 3% to 14% of cases (25; 36). In a population-based study of patients with first ischemic stroke, 2.5% had a dolichoectatic basilar artery (87). In a multiethnic study of stroke-free patients older than 55 years, at least one dolichoectatic intracranial artery was found in 19% (77). Risk factors for dolichoectasia of the basilar artery include increasing age and male sex, with an average age at diagnosis of 59 years, and men accounting for approximately 70% of reported cases (105). Risk factors for stroke occurrence include more severe ectasia and vertical elongation and superimposed atherosclerosis (139).

Differential diagnosis

Confusing conditions

Basilar artery disease is most closely mimicked by other illnesses that cause brainstem pontine dysfunction. These include brainstem encephalitis, demyelinating disease, central pontine myelinolysis (osmotic demyelination syndrome), and basilar migraine.

Basilar artery stroke can also mimic a host of other conditions, leading to a missed diagnosis of basilar artery stroke. These include other causes of acute coma or depressed levels of consciousness. Distal basilar artery occlusion may result in top of the basilar syndrome, which can present with acute neuropsychiatric abnormalities, including visual disturbances and hallucinations that may be confused with psychiatric disease. Basilar artery occlusion may present with rhythmic movements of the extremities mimicking convulsive seizures (189). Clues to basilar artery ischemia include abrupt onset, the presence of a Parinaud syndrome, Collier sign (retraction and elevation of the eyelids), pupillary abnormalities indicating midbrain involvement, and vertical gaze paresis.

Infectious rhombencephalitides tend to have slower onset over hours to days, be accompanied by fever, follow infectious exposures, and have a marked cerebrospinal fluid pleocytosis. Multiple sclerosis tends to have slower onset over hours, history of prior lesions disseminated in time and space, lesions confined to white matter, and cerebrospinal fluid positive for oligoclonal bands, and elevations in IgG synthesis and index ratio. The clinical differentiation of both disorders from basilar artery ischemia is sometimes challenging as basilar artery atherosclerotic disease produces abrupt, maximal onset of deficits less often than ischemia at other sites, and a stuttering, progressive course over hours to days is not unusual. Central pontine myelinolysis tends to follow episodes of rapid correction of hyponatremia or other systemic illness and produces bilateral tegmental lesions not fully respecting vascular territory boundaries. Migraine with brainstem aura (previously known as basilar-type migraine) tends to occur in younger adults, often children, and usually produces transient episodes of posterior circulation territory dysfunction (dysarthria, vertigo, diplopia, ataxia, tinnitus, visual symptoms, simultaneous bilateral paresthesias, decreased level of consciousness, etc.) lasting 20 to 30 minutes. The diagnostic picture can be mixed as migraine can rarely be associated with basilar artery stroke, and ischemia related to basilar artery disease can precipitate headaches.

Acute peripheral nerve demyelination and neuromuscular junction defects, such as Miller Fisher syndrome, botulism, and myasthenic crisis, respectively, can mimic symptoms of basilar artery occlusion (114).

Occasional patients with bilateral intracranial vertebral artery stenosis will experience pontine ischemia due to hemodynamic impairment or artery-to-artery emboli, mimicking intrinsic basilar artery disease.

Additionally, a number of other metabolic or systemic etiologies for basilar stroke must be considered. These include trauma leading to vertebral or basilar pseudoaneurysm or dissection with subsequent thrombus formation, cardioembolic sources, vasculitides, hypercoagulable states, Fabry disease, and sickle cell disease. Screening may involve rheumatologic investigation including sedimentation rate, C-reactive protein, antiphospholipid syndrome panel, antinuclear antibodies, rheumatoid factor, ANCA, CSF analysis, or more detailed hypercoagulable studies.

Associated or underlying disorders

Analysis of clinical features of patients who present with posterior circulation ischemia show commonality with unilateral limb weakness (81.9%), central facial palsy (61.1%), dysarthria (46.3%), and dizziness (33.8%) (163). The incidence of crossed paralysis was relatively low (2.8%).

Pontine syndromes as rare as inappropriate laughter or “fou rire prodromique” have been described, as well as anosognosia for hemiplegia, blepharospasm, brief jerking movements, jaw dystonia, bilateral deafness, trunk ataxia without limb ataxia, hypoesthesias, painful Horner syndrome, sleep disturbances, and trigeminal neuralgia (30).

Table 1. Symptoms of Vertebrobasilar (Posterior Circulation) Stroke and Transient Ischemic Attacks

Symptoms and signs	Vertebrobasilar artery territory
Motor deficits	Unilateral, bilateral, or shifting limb weakness; limb clumsiness or paralysis; ataxia, imbalance, or disequilibrium with or without vertigo
Sensory deficits	Unilateral, bilateral, or shifting limb numbness, sensory loss, or paresthesias
Speech deficits	Dysarthria*
Visual deficits	Binocular diplopia, partial or complete blindness in both homonymous visual fields
*Dysarthria may occur with stroke and transient ischemic attacks in either the vertebrobasilar or carotid distribution. Adapted from: (30)

Diagnostic workup

Diagnostic evaluation is directed toward imaging the brainstem, cerebellum, and occipitotemporal regions to characterize the size and territory of the infarct, exclude stroke mimics, determine the vascular mechanism, and guide therapy.

MRI is the preferred modality for imaging posterior fossa structures. CT can be compromised by beam-hardening artifacts from the skull base. In candidates for treatment with intravenous tPA, CT can be helpful in promptly ruling out an intracerebral hemorrhage. MRI infarct patterns particularly suggestive of proximal-middle large artery basilar disease, rather than penetrator disease, are bilateral infarction in the basal or tegmentobasal pons; bilateral infarction in the brachium pontis (anterior inferior cerebellar artery territory); and upper pontine or midbrain infarction, plus anterior inferior cerebellar artery territory cerebellar or brachium pontis infarction. In patients with top of the basilar lesions, upper pontine or midbrain infarcts may coexist with unilateral or bilateral thalamic and hemispheric posterior cerebral artery infarcts. Diffusion or perfusion MRI sequences can be especially helpful in the first few hours after onset of ischemia, when findings on standard T2-weighted MR studies may be absent or subtle.

The posterior circulation Acute Stroke Prognosis Early CT score (pc-ASPECT) has been proposed as a measurement of vertebrobasilar ischemia severity. A pc-ASPECT score of 10 is normal. One point is subtracted for left or right ischemic changes in the thalamus, cerebellar hemisphere, or posterior cerebral artery territory, and 2 points are subtracted if any part of the midbrain or pons is involved (144). A pc-ASPECT score of less than 8 is considered severe. DWI-pc-ASPECTS imaging may provide a more sensitive assessment then CT-based imaging. It has been reported that even with a score of 6 or less, good 90-day clinical outcomes (mRS < 2) were achieved in almost 25% of patients after endovascular reperfusion (92).

MRI can also help distinguish basilar branch infarcts from small artery strokes (61; 177; 19). Basilar branch infarcts tend to produce unilateral ventral pontine infarcts, often larger than 1.5 cm, that extend to the pontine surface. Small artery disease tends to produce small, unilateral tegmental or ventral infarcts that do not reach the surface of the pons. Diffusion weighted MR sequences are helpful in differentiating lesions of recent onset from prior pontine lacunae or leukoaraiosis, as they can appear similar on T2-weighted sequences.

Basilar branch infarction (T2-weighted MRI)

T2-weighted MRI image of the basilar branch infarction. (Contributed by Dr. Jeffrey Saver.)
Acute pontine infarction due to basilar branch occlusion (DWI)

Diffusion-weighted image of acute pontine infarction due to basilar branch occlusion. (Contributed by Dr. Jeffrey Saver.)

Clues to the status of the basilar artery and related vasculature can be gleaned from standard CT and MR imaging. Calcification of the basilar artery may be seen on CT but does not correlate well with the degree of associated atherosclerosis. Unenhanced CT may show a hyperdense basilar artery before a brainstem infarct is visualized. The presence of a hyperdense basilar artery often is a strong predictor of basilar artery thrombosis if no similar intra-arterial hyperdense changes are seen in the supraclinoid carotid arteries. (71). Absence of normal basilar artery flow voids on MR may indicate occlusion or slow flow, but also may arise from other causes such as in-plane flow effects in a tortuous, but open basilar artery. In addition, a FLAIR-hyperintense basilar artery is a strong marker of occlusion and a predictor of poor outcome (67). Dolichoectasia of the basilar artery may generally be demonstrated on both standard CT and MRI axial images. The MR will show an enlarged vessel often with inhomogeneous intraluminal signal, reflecting in situ thrombus, sometimes compressing the ventral surface of the pons.

Basilar artery sign

Unenhanced head CT showing hyperdense basilar artery sign (white arrow). (Contributed by Dr. José Biller.)
Flow void in basilar artery (T2-weighted MRIs)

(A) T2-weighted MRI of pontomedullary infarction with normal flow void in basilar artery (B) T2-weighted MRI of abnormal flow void in basilar artery with pontine infarction. (C) T2-weighted MRI showing a return to normal flow void...
Absence of flow void in basilar artery (T1-weighted MRI)

T1-weighted MRI showing absence of flow void in basilar artery. (Contributed by Dr. Jeffrey Saver.)

Vessel imaging studies are crucial to characterize the status of the basilar artery as, in contrast to the anterior circulation, clinical measures such as the NIH Stroke Scale have been shown to be poor predictors of vascular occlusion in the posterior circulation (82). However, this has significantly improved following high-resolution MRI vessel wall imaging, 5T MRA, and 4D DSA. Other options include magnetic resonance angiography, transcranial Doppler sonography, CT angiography, and catheter angiography. Intracranial magnetic resonance angiography centered on the circle of Willis will demonstrate the basilar artery in its entirety, as well as the distal portions of the feeding vertebral arteries and the initial segments of the exiting posterior cerebral arteries. Magnetic resonance angiography generally correlates well with angiographic findings but has a tendency to overestimate degree of stenosis. However, basilar artery occlusive disease appears to be more accurately characterized on MRA than vertebral occlusive disease (22). CT angiography can rapidly image the basilar, vertebral, and posterior cerebral arteries and is less susceptible to stenosis overestimation (183). Transcranial Doppler can be a useful adjunctive study to confirm magnetic resonance or computerized tomography angiography findings, or to provide some noninvasive test information in patients intolerant of MR or iodinated contrast. The depth and tortuosity of the basilar artery can make insonation difficult, and false-positive and false-negative findings can occur, limiting its utility. Transcranial Doppler is most reliable in characterizing the proximal two thirds of the basilar artery (47; 159). Administration of IV contrast agent during transcranial Doppler sonography enhances insonation of the basilar tip and increases the total length of the basilar artery identified (86; 95; 170).

Although management decisions are often based on noninvasive MRA, CTA, and transcranial Doppler studies alone, functional imaging modalities allow real-time physiologic assessment. These include CT and MR perfusion in which cerebral blood flow, cerebral blood volume, and contrast transit-time are compared to distinguish ischemic versus likely infarcted brain tissue. CT and MR perfusion studies have been well-validated in the anterior circulation. However, their utility in the posterior circulation remains uncertain. The pc-ASPECTS score applied to CT perfusion imaging demonstrated improved performance compared to use of noncontrast CT or CTA source images and may be useful in selecting patients who may benefit from endovascular thrombectomy (182). Catheter cerebral angiography continues to play a crucial diagnostic role in a selective number of patients.

ECG and echocardiography allow screening for sources of cardioembolism. For patients in whom an embolic mechanism is clinically suspected, such as those with top of the basilar syndrome, but in whom no cardioembolic source is confirmed by ECG or transthoracic echocardiography, transesophageal echocardiography with contrast may be considered. Prolonged mobile outpatient cardiac telemetry should be considered in patients with suspected atrial fibrillation, although the duration of such monitoring is a subject of controversy.

Management

	• Acute basilar artery stroke is a medical emergency.
	• Early recognition and diagnosis are crucial for the implementation of time-sensitive treatment.
	• Acute treatment strategies include intravenous thrombolysis and endovascular thrombectomy.
	• Management of secondary complications is crucial and may require intensive care unit monitoring.

General principles of acute stroke treatment fully apply to basilar artery stroke. Acute supportive care includes correction of severe hyperglycemia and hyperthermia, administration of supplemental oxygen as needed to maintain normal oxygen saturation, intubation if the airway is threatened by bulbar weakness or altered sensorium, assessing swallowing function before oral intake is instituted, and administration of isotonic crystalloids to maintain euvolemia (142; 143).

The common occurrence of a slowly progressive or stuttering course suggests that hemodynamic failure may be contributing to basilar artery ischemia. Regulating intravascular volume and blood pressure to improve blood flow may be useful. In general, blood pressure should not be lowered unless it exceeds a systolic pressure of 220 mm Hg or a diastolic pressure of 120 mm Hg; the patient is to be treated by an intravenous thrombolytic agent (< 185/110); or permissive hypertension acutely threatens an existing co-morbidity (eg, heart failure or concomitant myocardial infarction) (142). In select cases with a progressive or fluctuating course, cautious blood pressure augmentation, although not well established, may be beneficial, theoretically taking advantage of collateral pathways. However, the coexistence of active cardiovascular dysfunction (eg, left ventricular failure) may render such patients intolerant of this strategy. Admission to an intensive care unit is often warranted in the setting of profound or unstable neurologic deficits, decreased level of consciousness, hemodynamic instability, or cardiac or respiratory failure.

The natural history of basilar artery occlusion carries such a poor prognosis that acute reperfusion constitutes an important goal for the urgent management of these patients, increasing 2- to 4-fold the odds for a favorable neurologic outcome (110; 97; 74). Studies have demonstrated that failure of basilar artery recanalization is associated with a dismal prospect for favorable outcome (110). Presently, clinical and investigative strategies include intravenous thrombolysis and endovascular rescue techniques (ie, intraarterial thrombolysis, endovascular thrombectomy, and angioplasty with or without stenting combined with best medical management).

Intravenous thrombolytics should be offered to all patients with basilar artery stroke who present within 4.5 hours of onset and who qualify for such treatment based on accepted criteria, even in older children and adolescents (24; 142). However, the reported rates of basilar artery recanalization following intravenous tPA following this approach approximate 40% to 50%, and only 20% to 40% of patients achieve a favorable neurologic outcome (110; 154; 127). Moreover, it is evident that clot burden negatively influences the effectiveness of intravenous thrombolysis. Smaller clots more commonly result in distal basilar artery occlusion and relatively better outcomes (173).

Bridging thrombolytics before endovascular thrombectomy. Multiple randomized trials have demonstrated improved functional outcomes after bridging intravenous thrombolytics prior to endovascular thrombectomy versus direct thrombectomy alone, including the DIRECT-SAFE (126) and SWIFT DIRECT trials (59). Although not FDA approved for use in ischemic stroke, tenecteplase has shown promise for achieving higher rates of recanalization in basilar artery occlusion before endovascular thrombectomy when compared to alteplase (reperfusion > 50%; TNK 26% vs. tPA 7%) based on retrospective observational data (05). EXTEND-IA TNK parts I and II have demonstrated a similar benefit overall; however, the number of basilar artery occlusions in these studies were low (32; 31). Randomized trials are needed to confirm that the recanalization benefit can also be consistently achieved in the basilar artery. The use of intravenous thrombolytics (unless contraindicated in an individual patient) before endovascular thrombectomy is recommended in both the most recent guidelines from the American Stroke Association and European Stroke Organisation (32; 31; 181).

Technological advances have proven the benefit of mechanical thrombectomy in the anterior circulation. There is robust evidence of its utility in the treatment of acute internal carotid artery and middle cerebral artery occlusion, leading to American Heart Association and European Stroke Association guideline recommendations in the treatment of these patients (142).

Only four of 414 patients randomized in the mechanical thrombectomy after intravenous alteplase versus alteplase alone after stroke (THRombectomie des Artères CErebrales [THRACE]) trial and six of 202 patients randomized in the Tenecteplase versus Alteplase before Endovascular Therapy for Ischemic Stroke (EXTEND-IA TNK) trial had basilar artery occlusion (31). Although registry series and retrospective studies have demonstrated the benefit of endovascular thrombectomy in basilar artery occlusion, improving recanalization defined as thrombolysis in cerebral infarction (TICI, score = 2b–3) and favorable neurologic outcome defined as modified Rankin scale of 0 to 2 while reducing 90-day mortality, the first two randomized controlled studies demonstrated neutral outcomes without statistically significant superiority over medical therapy.

The first of two neutral randomized controlled studies, the Basilar Artery Occlusion Endovascular Intervention versus Standard Medical Treatment (BEST) trial, was a multicenter, randomized, open-label trial conducted between 2015 and 2017 (112). It randomized 131 patients with basilar artery occlusion within 8 hours of symptom onset to endovascular thrombectomy plus standard medical therapy (n=66) or standard medical therapy alone (n=65). The primary outcome was a modified Rankin scale score of 3 or lower at 90 days. The trial was terminated early due to poor recruitment and a high crossover rate. In the intention-to-treat analysis, there was no statistically significant difference in the primary outcome (42% in the intervention group vs. 32% in the control group; OR 1.74; 95% CI 0.81 to 3.74), but there was a trend towards favorable outcome in the group utilizing best medical management. The primary safety outcome was 90-day mortality and did not differ between groups. The trial was underpowered due to its early termination.

The second neutral randomized controlled trial, the Basilar Artery International Cooperative Study (BASICS) trial, was a prospective randomized trial of endovascular thrombectomy within 6 hours of symptom onset for stroke due to basilar artery occlusion (101). The trial was conducted between 2011 and 2019 in 23 centers in seven countries and randomized 300 patients to standard medical care or endovascular thrombectomy. Most patients in each group received IV thrombolysis. The primary outcome was a modified Rankin Scale score of 0-3 at 90 days and occurred in 44.2% in the endovascular thrombectomy group and in 37.7% in the medical care group, a difference that was not statistically significant (RR 1.18; 95% CI 0.92 to 1.50). Symptomatic intracranial hemorrhage occurred in 4.5% in the endovascular thrombectomy group and in 0.7% in the medical therapy group (RR 6.9; 95% CI 0.9 to 53.0).

There are multiple reasons why these two initial trials failed to demonstrate superiority of endovascular thrombectomy. In both trials, results may have been confounded by the loss of equipoise over the course of the trial period due to positive results from thrombectomy trials in the anterior circulation. This likely led to selection bias, with patients more likely to benefit from endovascular thrombectomy receiving treatment outside of the trial. This resulted in low recruitment and high crossover between groups. For example, of the 424 eligible patients screened in BASICS, 29% (n=124) were not enrolled and were treated outside of the trial; 79% (n=98) of these patients received endovascular thrombectomy. The outcomes in these patients are not known (101). The BEST trial had limited enrollment and a high crossover of patients treated with endovascular thrombectomy (06). The BASICS trial demonstrated slow recruitment, taking 8 years to enroll 300 patients across 23 centers. Initially using an entry criteria NIHSS greater than 10, the slow recruitment rate forced enrollment of less severely affected patients experiencing transient ischemic attack and minor symptoms, which diluted the treatment effect. The substantially high use of intravenous alteplase in BASICS and a greater number of patients randomized to the endovascular thrombectomy group experiencing atrial fibrillation (29%) also reduced the interventional treatment group benefit. Sudden basilar artery occlusion from atrial fibrillation–induced cardiogenic embolization may fare worse after endovascular thrombectomy in comparison to atherosclerotic basilar artery occlusion due to the latter having more time to develop collateral vessels. The BEST trial used first-generation endovascular thrombectomy devices, which were inferior to subsequent devices.

Taken together, these two early studies utilizing endovascular thrombectomy for basilar artery occlusion were inconclusive. However, they demonstrated that arterial recanalization could be successfully achieved by endovascular thrombectomy (75% to 80%) and result in lower mortality (25% to 48%) and better neurologic outcome (ie, mRS 0-2 in approximately 33% to 43%) (97; 73).

Following improvements in patient selection and study design, two randomized control trials in 2022 demonstrated that basilar artery endovascular thrombectomy was superior to best medical management, with good functional outcomes at 90 days with lower mortality.

The Endovascular Treatment for Acute Basilar Artery Occlusion (ATTENTION) trial enrolled patients within 12 hours of estimated time of stroke onset utilizing an NIHSS of greater than 10 and pc-ASPECTS score of less than 6 if younger than 80 years old and less than 8 if older than 80 years old (175). The median pc-ASPECTS score was 9 in the thrombectomy group and 10 in the control group. There was a low crossover rate. Endovascular thrombectomy demonstrated better 90-day functional outcome (mRS 0–3) than the best medical management group, 46% versus 23%, respectively (p < 0.001). Similar to thrombectomy in the anterior circulation, the number needed to treat to achieve an ambulatory outcome was four. The endovascular thrombectomy group was more likely to have a patent basilar artery at 4 hours. Forty percent of the endovascular thrombectomy group experienced basilar artery atherosclerosis requiring angioplasty and stent placement, which prolonged procedure time and increased risk. The symptomatic intracranial hemorrhage rate was 5.3% in the endovascular thrombectomy group versus none in the best medically managed group, counterbalanced against a statistically significant lower mortality in the thrombectomy group (37% vs. 55%, p < 0.001).

The Basilar Artery Occlusion Chinese Endovascular (BAOCHE) trial also demonstrated benefit of mechanical thrombectomy, this time within a 6- to 24-hour window in patients between the ages of 18 to 80 years (88). Entry criteria included pc-ASPECTS greater than 6, pons-midbrain index greater than 2, and evaluating three subgroups of severity with an NIHSS of 6 to 9, 10 to 20, and greater than 20 points. There was a low crossover rate. The study was stopped early after interim analysis demonstrated that nearly double the patients in the thrombectomy group achieved good functional outcome in comparison to the medically managed group. Outcomes were mRS of 0 to 3 at 90 days and sICH producing at least 4-point NIHSS deterioration. At 90 days, mRS of 0 to 3 was found in 46% of the endovascular thrombectomy group versus 24% of the control group, and mRS of 0 to 2 in 39% versus 14%, respectively. Successful TICI 2b or 3 recanalization occurred in 92% of the thrombectomy group versus 19% of the control group. There was dramatic neurologic improvement of 25% in the endovascular thrombectomy group versus 10% in the control group and patency of the basilar artery at 24 hours in 92% of the endovascular thrombectomy group versus 19% of controls. Subgroup analysis demonstrated response in both male and female patients and in those both younger and older than 70 years. Additionally, there was benefit from treating patients in a 6- to 12-hour window as well as in the 12- to 24-hour timeframe, albeit with better results when treated earlier. As seen in other studies, the endovascular thrombectomy group demonstrated a higher sICH rate of 5.9% versus 1.1%, again counterbalanced against lower mortality in the thrombectomy group (31% vs. 42%). Neither were statistically significant. Like both the ATTENTION trial and the anterior circulation endovascular thrombectomy trials, the number needed to treat for an ambulatory outcome was 4.5.

A meta-analysis of the aforementioned four randomized controlled trials confirmed a statistically significant ambulatory functional outcome benefit of endovascular thrombectomy over medical therapy and reduced 90-day mortality rate despite sICH (68).

The benefit of endovascular thrombectomy for basilar artery occlusion appears to be similar to treatment of anterior circulation large vessel occlusions. Both the ATTENTION and BAOCHE trials also demonstrated a potential mortality benefit. There appears to be limited benefit of basilar artery endovascular thrombectomy in patients with mild stroke with an NIHSS of less than 10, and this deserves further study. Conceivably, this could be due to less severe symptoms from better collateral flow, smaller clot burden, or more distal basilar artery thrombus. As such, one author suggested that milder strokes could potentially be treated with therapeutic anticoagulation and careful observation for clinical deterioration that might necessitate further intervention (06). Additional areas deserving of further study include how to identify patients that may not benefit from endovascular thrombectomy, the safety and benefit of bridging intravenous thrombolytic administration prior to endovascular thrombectomy during an extended time window, and how to identify potential subgroups that may benefit from angioplasty and stent, which has not yet been proven to be beneficial (01; 141). As most of the trials were performed in China, generalizability to other ethnicities needs to be confirmed.

Percutaneous transluminal angioplasty and stenting. Intracranial atherosclerotic disease (ICAD) represents a major etiology of initial and recurrent strokes, especially with severe stenosis (70% to 99%). Various retrospective and registry trials have reported safety and treatment benefits of percutaneous transluminal angioplasty and stenting (PTAS), yet the findings may have been influenced by non-standardized selection criteria that included treating lesser degrees of stenosis (50% to 70%) and early versus late treatment (ie, before or after 2 to 3 weeks of symptom onset, for transient ischemic attack and minor stroke, etc) (137).

Three subsequent randomized controlled trials have not demonstrated superiority of PTAS over medical management. Nonetheless, it is important to discuss salient features of these three trials to serve as a basis for future study as their data and methodology provide insight that may benefit carefully selected groups of patients.

Stenting versus aggressive medical therapy for intracranial arterial stenosis (SAMMPRIS), published in 2011, randomized 451 patients who experienced transient ischemic attack or stroke to a Wingspan stent and aggressive medical management versus aggressive medical management alone for the treatment of intracranial atherosclerosis of 70% to 90% with primary endpoints of stroke and death (40). Within 30 days, the stented group demonstrated both significantly greater ischemic strokes in the qualifying artery territory as well as a significantly increased incidence of cerebral hemorrhage in comparison to the medically managed group. Most of the complications occurred within the first 30 days. This prompted early discontinuation of the trial. Between 30 days and 1 year, endpoints were similar. Baseline data demonstrated a similar number of patients with basilar artery stenosis in the medical and procedural groups.

In 2014, after 3 years of follow-up of SAMMPRIS patients, the benefit of the aggressively medically managed group demonstrated a stable absolute risk reduction of 8.9% beginning at 30 days and remained a stable 9% at 3 years (48). The long-term probability of any stroke and major hemorrhage was greater in the PTAS group. For basilar artery territory strokes, the 2-year probability of stroke or death in the PTAS group was 25% versus 10% in the medical management group. The authors concluded that aggressive medical treatment was superior to PTAS in both early and late phases up to 3 years but noted that there were still high-risk subgroups of patients that might benefit from new treatments to lower stroke risk.

There were similar findings of poor outcome in patients receiving a balloon-expandable stent in comparison to medical management. An increased risk of stroke, transient ischemic attack, intracerebral hemorrhage, and worsening of baseline modified Rankin scale were observed in the VISSIT trial (199). This study was prematurely discontinued before full enrollment following the futility of the SAMMPRIS trial. After 1 year, there was a lower risk of symptomatic atherosclerotic plaque, possibly due to plaque stabilization or collateral development.

Following the significantly elevated SAMMPRIS periprocedural complication rate of 14.7% (stroke, cerebral hemorrhage, and death), an FDA review panel revised criteria for the stent in March 2012, increasing the degree of stenosis from more than 50% to more than 70%, and required patients to have two strokes in the vascular territory of the stenotic artery. The FDA-mandated WEAVE trial published in 2019 and the 1-year follow-up WOVEN trial published in 2021 were safety studies using the revised criteria. There were significant improvements in safety at 72 hours following Wingspan stent placement, with only 2.6% (4/152 consecutive patients) periprocedural stroke, cerebral hemorrhage, and death, down from 14.7% in SAMPRISS. At 1 year there were seven strokes and no deaths. Eighteen of the 129 patients at 1 year experienced vessel restenosis (> 70%), of which 61% were asymptomatic. Regarding the basilar artery, only one out of the 20 patients with basilar artery atherosclerotic disease experienced a delayed stroke (5%) (07; 08).

CASSISS, the third randomized controlled trial, demonstrated non-superiority of Wingspan stenting for atherosclerotic stenosis between 70% to 99% over medical management (66). Over 28% of the patients had basilar artery stenosis. There was no significant difference in stroke or death between the stenting and medical therapy groups. The poor performance of the stent group was significantly influenced by procedural complications. Stenting of patients within 3 weeks of the index event confers a higher procedural risk of stroke and hemorrhage, in part suspected to be caused by plaque instability. In the first 30 days, the stenting group experienced five ischemic and four hemorrhagic strokes. The medically managed group experienced four ischemic strokes and no hemorrhage. Regarding the etiology of early hemorrhage, the stent group experienced four hemorrhagic strokes, two of which were related to guidewire perforation and two related to reperfusion. None were observed in the medically managed group.

In a subsequent post hoc analysis, no specific intracranial artery was more responsive than any other to PTAS (191).

Concerns about the CASSISS trial design include entrance criteria that created a lower risk study population in comparison to SAMMPRIS. Specifically, patients with perforating artery territory infarcts as the qualifying event were excluded due to concern that angioplasty would occlude the origin of the perforating arterioles. Additionally, both the medical and surgical groups were felt to be a lower risk population in comparison to SAMMPRIS as their 1-year stroke and death rates were significantly lower in CASSISS; enrolled CASSISS patients did not have a history of stroke in the territory of the index artery counter to the FDA revised guidelines; and differences in median timing of event to randomization were longer in CASSISS versus SAMMPRIS and VISSIT due to concern of poor outcome from treatment earlier than 3 weeks, which might predispose to plaque rupture (201; 180).

A meta-analysis combined the data of the 921 patients enrolled in the aforementioned three randomized controlled trials (195). Stenting within the first 3 weeks carries considerable risk due to plaque instability and reperfusion injury. Medical therapy alone had a lower risk of stroke and death in the first 30 days than stenting plus medical therapy, with no statistically significant long-term differences between the two groups between 1 and 3 years. Subgroup analyses showed that if additional stenting was needed after 3 weeks, there would be no effect on stroke or death within 30 days and 1 year. There was a higher risk of stroke and death within 1 year using a balloon-expandable stent in comparison to medical therapy. The long-term effect of stent plus medical therapy on the risk of stroke and death was not inferior to medical therapy alone. In comparison to Wingspan stents, balloon-expandable stents are more rigid and may have contributed to perforator artery occlusion.

The current randomized controlled data favor aggressive vascular risk factor medical management over PTAS. However, given the relatively small sample size and partial heterogeneity of trial design in only three randomized controlled trials, the long-term (1 to 3 years) non-inferiority of stenting and medical therapy over medical therapy alone suggests that further study is indicated, especially for patients who have failed maximal medical therapy, which increases the risk of devastating stroke. This includes refinement of patient selection criteria and development of new stents for tortuous, angulated, and small caliber vessels that may enhance flow while reducing radial forces that may produce plaque or vessel wall rupture as well as identification of specific basilar artery high-grade degrees of stenosis that may have a lower procedural PTAS risk than maximal medical management in patients who experience recurring transient ischemic attack and stroke. Best medical management refinements may include new strategies for atherosclerotic plaque stabilization and regression. There is also need for the development of a standardized, rapidly and easily performed imaging approach to assess basilar artery hemodynamics, radiographic visualization of basilar artery perforator anatomy (including anastomoses that may contribute to collateral flow), and identification of high-risk basilar artery plaque location and composition.

Role of reduced basilar artery blood flow in PTAS planning

Prior to the VERiTAS study group trial, hemodynamic insufficiency as a cause of posterior circulation stroke was suspected, but there were insufficient data to support this mechanism. It was subsequently proven that patients with symptomatic vertebrobasilar stenosis or occlusion with decreased blood flow on large-vessel phase contrast quantitative 3T MRA are at a higher risk of subsequent posterior circulation stroke (10). Study patients were symptomatic for less than 60 days and had more than 50% stenosis by conventional DSA or CTA. Distal flow status was designated as low or normal based on an algorithm of more than 20% reduction below normative vessel-specific flow. Primary endpoint was fatal and nonfatal ischemic stroke in the vertebrobasilar territory. Seventy-two patients were followed for 5 years; 18 of 72 patients (25%) met criteria for distal low flow status. Five of the 18 patients (28%) had low distal flow and five of the 54 patients (9%) had normal distal flow. The event-free survival rates in the low flow group were 78% at 12 months and 70% at 24 months versus 96% at 12 months and 87% at 24 months in the normal flow group. The authors concluded that distal posterior circulation is robust in patients with symptomatic atherosclerotic vertebrobasilar occlusive disease. They suggest that patients with low flow states are at high risk and may represent a candidate population for future endovascular intervention trials. Those with normal distal flow in three quarters of the patient population were at low risk of subsequent stroke on medical therapy and should not undergo intervention. The authors acknowledged that the etiology of posterior circulation stroke may be due to thromboembolism, small vessel occlusive disease, or hypoperfusion, and compromised distal flow may reduce washout of emboli.

The role of perforator anatomy in basilar artery stroke in PTAS planning

Perforating branch arterioles arising from the basilar artery may be easily occluded by either overlying plaque, plaque rupture and compression of the ostia by angioplasty, and stent (snowplow effect). There are three main groups of basilar artery perforators:

(1) Caudal: two to five vessels that produce terminal branches as well as branching off the pond to medullary artery, pyramidal vessels, and hypoglossal branches

(2) Middle: five to nine vessels that arise from the basilar artery and basilar artery collateral branches

(3) Rostral: one to five vessels that arise from the terminal basilar artery, superior cerebellar artery, and posterior lateral artery

Anastomoses between perforators occur in 41.6% to 66.6% (121). These small perforating arteries were visualized in a proof-of-concept study revealing circumferential vessels and anastomotic pial networks using high field strength 3D rotational angiographic datasets with CT-like reconstruction (104). This technique produced resolution greater than conventional biplane angiography. There is almost no segment of the basilar artery free from perforators that may be occluded with angioplasty and stent placement. Identifying the location of these perforators and advances in stent design may reduce perforator occlusion.

This imaging technique was further refined with reconstruction of fully time-resolved vascular volumes obtained from projections of the 3D-DSA acquisition, otherwise known as 4D-DSA (56). Superior to CTA or MRA, visualization of smaller vessels with enhanced imaging resolution can be viewed in any phase of the contrast cycle. This can be useful for identifying stent and balloon sizes, reconstructing the location and anatomy of perforating arterioles. It can also quantify blood flow through the vessel. Other uses for this technology include preoperative anatomic evaluation of arteriovenous malformations, AV fistulas, and intracranial aneurysms.

Small basilar artery perforating arteries can also be visualized with 3D 5T time-of-flight MRA, which was significantly superior to 3T time-of-flight MRA and comparable to the image quality of 7T imaging (202).

Clinical relevance of plaque distribution in PTAS planning

The basilar artery is the main artery of the posterior circulation and has the highest risk for postoperative complications following endovascular treatment amongst the intracranial arteries. The basilar artery is more capable of plaque burden due to low blood flow and less sympathetic innervation and overlies the ostia of a significant number of perforating arteries. Anatomically, 65.3% of penetrating arteries originate from the lateral aspect of the basilar artery, and 34.7% originate from the dorsal side.

More anastomosis from basilar artery penetrators originates from its dorsal than lateral walls. The relatively lower number of lateral wall penetrators with anastomotic branches makes the brainstem perfused by these vessels more vulnerable to infarction from lateral wall penetrator occlusion. In a study, high-resolution MR vessel wall imaging followed by digital subtraction angiography before endovascular intervention produced axial images that were divided into dorsal, ventral, and lateral quadrants (118). The anterior inferior cerebellar artery was used as a dividing line between inferior and superior aspects of the basilar artery. Large plaques were found to span more than one quadrant. Of 140 patients, 5% were treated with primary angioplasty and 81.5% were treated with stent. There was an 11.4% complication rate (transient ischemic attack 18.75%; perforating infarctions 25%; artery-to-artery embolization 43%; mixed mechanism 12.5%). Plaque localizable to the dorsal and lateral walls of the basilar artery and above the anterior inferior cerebellar artery was most common in post-procedural complications. Independent risk factors for postoperative ischemic events included large plaque burden and plaques in the lateral wall and across the level of the anterior inferior cerebellar artery.

Potential adjunctive and rescue recanalization strategies following endovascular thrombectomy

Intra-arterial thrombolytics administered following endovascular thrombectomy as both a rescue strategy for incomplete recanalization and in an attempt to improve functional outcome has been studied, predominantly in the anterior circulation. Posterior circulation randomized trial data have been miniscule to date. Thus far, the findings have been inconclusive due to variable results, with only some anterior circulation studies demonstrating favorable outcomes and safety profiles of endovascular thrombectomy and intra-arterial thrombolysis in comparison to endovascular thrombectomy alone. Additionally, these early anterior circulation findings may not be generalizable to basilar artery occlusion due to its substantially greater number of perforating arteries. Following the BAOCHE and ATTENTION trials, only 46% of patients achieved favorable functional improvement (mRS 0-3) at 90 days. A Chinese prospective multicenter registry of 1672 patients with stroke from basilar artery occlusion treated with either stent retriever or thromboaspiration administered intra-arterial urokinase or alteplase in 126 patients (7.5%) (38). There was unresolved equipoise with no functional improvement between the groups. There were no safety differences between the groups for intracerebral hemorrhage and 90-day all-cause mortality. As a registry study, there were no preselected criteria for type or dose of intra-arterial thrombolytic nor endovascular thrombectomy method. In an attempt to resolve this question, the prospective, randomized, open-label, blinded-endpoint multicenter study INSIST-IT trial will test the functional efficacy and safety of intra-arterial tenecteplase following successful endovascular thrombectomy recanalization of the basilar artery (149; 55; 111; 129; 146; 178).

Antithrombotic agents may increase the efficacy of attempted recanalization. Argatroban, a direct thrombin inhibitor; eptifatide and tirofiban, both platelet glycoprotein IIb/IIIa inhibitors; and glenzocimab, a platelet glycoprotein VI antibody, are currently being evaluated as adjuvant treatments (178).

Outcomes

Several factors have been studied as predictors of the outcome of therapeutic recanalization of basilar artery occlusion, including: (a) clinical severity, (b) topography of basilar artery occlusion, (c) angioarchitecture, (d) concurrent tandem vertebral artery occlusive pathology, (e) underlying in situ basilar artery atherostenosis, (f) clot burden, (g) recanalization technique, and (h) time to treatment.

Clinical severity. Patients with tandem proximal dominant vertebral artery occlusive lesions more commonly present with higher NIHSS scores and impaired consciousness (37). A more severe presenting syndrome has been consistently associated with worse outcomes, even in patients who undergo successful recanalization (15; 89; 52; 85; 28; 107). In particular, coma on presentation has been implicated in worse outcome (136; 85; 192).

Topography of basilar artery occlusion. Traditionally, basilar artery occlusion has been categorized into three distinct locations: proximal, middle, and distal. These categories correspond to a span of approximately one third the basilar artery length. Patients with distal basilar artery occlusion have been reported to have better prognosis following intraarterial thrombolysis or thrombectomy than patients with proximal or mid-basilar occlusion (42; 187). At least in part, this may be due to distal basilar artery occlusion more commonly resulting from embolism than in situ atherosclerosis.

Angioarchitecture. The most common anatomic variable is collateral circulation, which has been independently shown to positively influence both recanalization and outcomes when present (147; 166). However, in a series of 38 patients treated with first-generation thrombectomy devices, there was no demonstrable effect of unilateral hypoplasia of either the vertebral or posterior communicating arteries (79).

Tandem vertebral artery pathology. Concurrent tandem stenosis or occlusion of the dominant vertebral artery negatively influences outcomes in patients with basilar artery occlusion by reducing the chances of recanalization possibly related to prolonged procedural time and increased complexity (37). However, successful endovascular reconstruction of vertebral artery occlusion prior to basilar artery thrombectomy has been reported, with 66% of patients having favorable outcomes (54).

Underlying in situ basilar artery atherostenosis. The presence of an underlying atherosclerotic stenosis has been reported in 20% to 80% of patients with basilar artery occlusion (128; 85; 102), particularly in the proximal segment, but it does not seem to negatively affect either outcome or rate success rate of recanalization (102). However, it commonly requires angioplasty with or without stenting (128; 85; 102).

Clot burden. Treatment with intravenous thrombolytics may be hampered by increased clot burden (173). However, reports regarding the impact of clot burden on endovascular treatment effectiveness have been conflicting (69; 165).

Time to treatment. Elapsing time to recanalization likely adversely impacts patients with basilar artery occlusion as it does in other vascular territories. Although earlier recanalization has been associated with good outcome (15; 138; 18; 52; 85), this finding is not uniform across the literature (107). This is not surprising, considering the results of multicenter studies showing benefit of mechanical thrombectomy in selected patients with internal carotid or middle cerebral artery occlusion despite prolonged therapeutic windows (04; 132). There is evidence that patients who present without early radiographic evidence of extensive ischemic injury (eg, pc-ASPECTS score of 8 or higher), can be successfully treated up to 48 hours after onset (172). Conversely, radiographic evidence of extensive infarction constitutes a poor prognostic sign (172; 197). Moreover, studies employing multimodal MRI have shown salvage of diffusion-perfusion mismatch zones following intraarterial thrombolysis for acute basilar artery occlusion (134). Good outcomes were reported in eight of nine patients with prolonged basilar artery occlusion (median = 31 hours) selected for endovascular treatment on the basis of clinical-diffusion mismatch when the latter did not involve the dorsal pons, midbrain, or thalamus (109).

In addition, higher mortality or worse neurologic outcome have been associated with older age (89), male sex (136), diabetes mellitus (89), and tobacco smoking (28).

The optimal antithrombotic medication regimen for patients with basilar artery occlusion largely depends on the urgent recanalization strategy utilized and its outcome. In general, all antithrombotic medication should be avoided for 24 hours following treatment with intravenous tPA (142). However, patients treated with mechanical thrombectomy only have no restrictions to immediate postprocedural antithrombotic agents. Patients whose urgent recanalization treatment included stenting of an underlying atherosclerotic lesion constitute a subset whose treatment must include dual antiplatelet therapy to prevent in-stent thrombosis. The optimal duration of this treatment may be device-specific per manufacturer recommendations.

In patients with high-risk sources of recurrent embolism (eg, atrial fibrillation, left apical thrombus, left atrial thrombus), anticoagulation should be considered to reduce the risk of additional cerebral embolization. However, anticoagulation may need to be delayed in situations where imaging shows evidence of hemorrhagic transformation or a large infarct volume (90).

Stroke progression due to in situ atherosclerosis may result from clot propagation occluding ostia of additional basilar artery branches or downstream embolism. In this setting, anticoagulation is often utilized although its effectiveness has not been established. Optimal antithrombotic medication selection for long-term secondary prevention therapy after initial basilar artery stroke is beyond the scope of the present review.

Neurosurgical intervention by posterior fossa decompression can be lifesaving when basilar artery strokes produce large cerebellar infarcts with mass effect that lead to obstructive hydrocephalus and cerebellar herniation, with or without brainstem compression (24).

Management of dolichoectasia of the basilar artery is challenging. On one hand, long-term antithrombotic therapy is theoretically attractive as a means to prevent progressive thrombosis in low-flow regions within patulous vessels (53). On the other, extreme caution regarding anticoagulation is urged by occasional observations of fatal subarachnoid hemorrhage (140; 21). Surgical treatments carry considerable risk because of the vulnerability of small pontine penetrators to injury but should be considered when the vessel is compressing brainstem and cranial nerve structures. Surgical techniques include proximal vessel occlusion, or direct thrombectomy and reconstruction of the vessel lumen with clips (12).

Special considerations

Basilar artery stroke in children. Non-neonatal pediatric ischemic stroke has been estimated to occur in 1.3 per 100,000 person-years (03). Given the infrequency and atypical presentations depending on the child’s developmental age, stroke diagnosis is often delayed. Initial misdiagnosis as migraine or seizures is common. Additionally, stroke etiologic factors commonly found in adults such as atherosclerosis and atrial fibrillation are unlikely causes of childhood stroke, and the differential etiologic diagnosis is diverse. Cervicocephalic arterial dissection, congenital and acquired heart and vascular disorders, prothrombotic states, infections, and metabolic disorders must be considered.

Compared with adults, children with basilar artery strokes with basilar artery occlusion may have better long-term outcomes than adults with and without acute recanalization treatment (100; 39). Unfortunately, the Thrombolysis in Pediatric Stroke (TIPS) trial, an international, multicenter, phase 1, dose-finding study of intravenous tissue plasminogen activator in children 2 to 17 years of age terminated early due to slow recruitment (09). Similarly, limited patient volumes will make it impossible to recruit a significant number of patients for randomized endovascular trials to achieve any level of statistical significance. Case reports and small series have shown successful recanalization and neurologic outcome in children with basilar artery thrombosis treated with intravenous tPA (185; 150; 148) and endovascular strategies, including intravenous bridging, intra-arterial thrombolysis, mechanical thrombectomy with both stent retrievers, and thromboaspiration achieving high levels of recanalization and low modified Rankin scores (58; 156). Endovascular therapy with both stent retrievers and thromboaspiration has been used successfully in children as young as 14 hours after birth (130; 171).

Craniovertebral junction abnormalities, including atlantoaxial dislocation and instability with or without basilar invagination, Chiari malformation type I, bow hunter syndrome and skeletal dysplastic syndromes, may produce posterior circulation infarctions. Cough-induced headache may be present. Craniovertebral junction abnormalities are underrecognized as a cause of posterior circulation infarction in children and should be considered, especially if the patient has short stature, short neck, torticollis, or flat occiput. Flexion-extension plane cervical radiographs and dynamic vascular imaging may help establish the diagnosis (14).

A congenital basilar artery fenestration was discovered in a 12-year-old boy following diplopia, tinnitus, headache, dysarthria, imbalance, and mild right hemiparesis. MRI imaging demonstrated bilateral cerebellar infarctions. Although there was no thrombus or aneurysm detected during catheter angiography, there was increased flow through the fenestration that may have predisposed to thrombus. Basilar artery fenestration is a developmental malformation due to abnormal fusion of the primitive longitudinal neural arteries in the fifth week of gestation. Although visualized on conventional angiography, MRA of the basilar artery may not detect it. There is the potential for aneurysm formation due to turbulent flow at the site of fenestration (70).

Pregnancy

No information specifically addresses the risk of basilar artery stroke in pregnancy or its treatment. Presumably, the risk is slightly increased as for ischemic stroke in general. Exclusion of pregnant women from trials of acute stroke treatments limits therapeutic decision-making. However, given the potential morbidity and mortality from acute basilar artery occlusion in pregnant women, risks and benefits of acute reperfusion therapies pose medical and ethical considerations. On the basis of clinical trial protocols leading to intravenous tPA approval, guidelines previously listed pregnancy as a relative contraindication. However, available case series demonstrate clinical improvement after intravenous tPA use in pregnancy and continuance of pregnancy to normal gestation (46). Therefore, current guidelines state that intravenous tPA may be considered for stroke during pregnancy when the anticipated benefits outweigh the potential risks to the fetus (142).

Data on thrombectomy in pregnancy are extrapolated from patients with anterior circulation large-vessel occlusion. An analysis of 4590 patients from the National Inpatient Sample who received mechanical thrombectomy between 2015 and 2018 found that thrombectomy was safe and efficacious, with pregnant patients experiencing low rates of intracerebral hemorrhage and lower likelihoods of poor functional outcome (50). Potential short- and long-term effects on the fetus from ionizing radiation and contrast exposure are uncertain.

Anesthesia

Although previous retrospective and post hoc analyses have reported an association between general anesthesia and worse clinical outcomes compared to conscious sedation in patients undergoing mechanical thrombectomy (02), several small single-center randomized controlled trials have failed to confirm this finding (158; 116). Individualization of anesthetic modality is reasonable in lieu of additional trial data (142).

Media

References

01: Abdalkader M, Hu W. Endovascular therapy for stroke due to basilar artery occlusion: challenges and opportunities. J Neuroradiol 2023;50:42-3. PMID 36528085
02: Abou-Chebl A, Lin R, Hussain MS, et al. Conscious sedation versus general anesthesia during endovascular therapy for acute anterior circulation stroke preliminary results from a retrospective, multicenter study. Stroke 2010;41(6):1175-9. PMID 20395617
03: Agarwal N, Johnston SC, Wu YW, Sidney S, Fullerton HJ. Imaging data reveal higher pediatric stroke incidence than prior US estimates. Stroke 2009;40(11):3415-21. PMID 19762687
04: Albers GW, Marks MP, Kemp S, et al. Thrombectomy for stroke at 6 to 16 hours with selection by perfusion imaging. N Engl J Med 2018;378(8):708-18. PMID 29364767
05: Alemseged F, Ng FC, Williams C, et al. Tenecteplase vs alteplase before endovascular therapy in basilar artery occlusion. Neurology 2021;96(9):e1272-7. PMID 33408145
06: Alemseged F, Nguyen TN, Alverne F, Liu X, Schonewille WJ, Nogueira RG. Endovascular therapy for basilar artery occlusion. Stroke 2023;54(4):1127-37. PMID 36722343
07: Alexander MJ, Zauner A, Chaloupka J, et al. WEAVE Trial: final results in 152 on-label patients. Stroke 2019;50(4):889-94. PMID 31125298
08: Alexander MJ, Zauner A, Gupta R, et al. The WOVEN trial: wingspan one-year vascular events and neurological outcomes. J Neurointerv Surg 2021;13(4):307-10. PMID 32561658
09: Amelie-Lefond C. Thrombolysis in Pediatric Stroke (TIPS). Available at: https://clinicaltrials.gov/ct2/show/NCT01591096. Accessed December 31, 2014.
10: Amin-Hanjani S, Pandey DK, Rose-Finnell L, et al. Effect of hemodynamics on stroke risk in symptomatic atherosclerotic vertebrobasilar occlusive disease. JAMA Neurol 2016;73(2):178-85. PMID 26720181
11: Amin-Hanjani S, Turan TN, Due X, et al. Higher stroke risk with lower blood pressure in hemodynamic vertebrobasilar disease: analysis from the VERiTAS study. J Stroke Cerebrovasc Dis 2017;26(2):403-10. PMID 28029608
12: Anson JA, Lawton MT, Spetzler RF. Characteristics and surgical treatment of dolichoectatic and fusiform aneurysms. J Neurosurg 1996;84:185-93. PMID 8592220
13: Archer C, Horenstein S. Basilar artery occlusion: clinical and radiographic correlation. Stroke 1977;8(3):383-90. PMID 860293
14: Aripirala P, Reddy N, Lingappa L, Konanki R, Varma DR, Raju S. Cryptogenic posterior circulation stroke in children. Dev Med Child Neurol 2023;65(6):847-54. PMID 36380707
15: Arnold M, Nedeltchev K, Schroth G, et al. Clinical and radiological predictors of recanalisation and outcome of 40 patients with acute basilar artery occlusion treated with intra-arterial thrombolysis. J Neurol Neurosurg Psychiatry 2004;75(6):857-62. PMID 15146000
16: Arraez-Aybar LA, Villar-Martin A, Poyatos-Ruiperez C, Rodriguez-Boto G, Arrazola Garcia J. Prevalence of fenestrated basilar artery with magnetic resonance angiography: a transversal study. Surg Radiol Anat 2013;35(6):487-93. PMID 23250566
17: Back T, Grünig S, Winter Y, Bodechtel U, Guthke K, Khati D, von Kummer R. Neuroborreliosis-associated cerebral vasculitis: long-term outcome and health-related quality of life. J Neurol 2013;260(6):1569-75. PMID 23329377
18: Baek JM, Yoon W, Kim SK, et al. Acute basilar artery occlusion: outcome of mechanical thrombectomy with Solitaire stent within 8 hours of stroke onset. AJNR Am J Neuroradiol 2014;35(5):989-93. PMID 24335542
19: Bassetti C, Bogousslavsky J, Barth A, Regli F. Isolated infarcts of the pons. Neurology 1996;46:165-75. PMID 8559368
20: Berry AD 3rd, Kepes JJ, Wetzel MD. Segmental duplication of the basilar artery with thrombosis. Stroke 1988;19(2):256-60. PMID 3344542
21: Besson G, Bogousslavsky J, Moulin T, Hommel M. Vertebrobasilar infarcts in patients with dolichoectatic basilar artery. Acta Neurol Scand 1995;91:37-42. PMID 7732772
22: Bhadelia RA, Bengoa F, Gesner L, et al. Efficacy of MR angiography in the detection and characterization of occlusive disease in the vertebrobasilar system. J Comput Assist Tomogr 2001;25(3):458-65. PMID 11351199
23: Biemond A. Thrombosis of the basilar artery and the vascularization of the brain stem. Brain 1951;74:300-17. PMID 14869537
24: Biller J, Ferro JM. Evidence-Based Management of Stroke. London, UK: TFM Publishing Limited, Castel Hill Barns, 2011.**
25: Bogousslavsky J, Regli F, Maeder P, Meuli R, Nader J. The etiology of posterior circulation infarcts. Neurology 1993;43:1528-33. PMID 8351006
26: Bogousslavsky J, Van Melle G, Regli F. The Lausanne Stroke Registry: analysis of 1,000 consecutive patients with first stroke. Stroke 1988;19:1083-92. PMID 3413804
27: Bornstein N, Aronovich BD, Karepov VG, et al. The Tel Aviv Stroke Registry: 3600 consecutive patients. Stroke 1996;27:1770-3. PMID 8841327
28: Bouslama M, Haussen DC, Aghaebrahim A, et al. Predictors of good outcome after endovascular therapy for vertebrobasilar occlusion stroke. Stroke 2017;48(12):3252-7. PMID 29089457
29: Brandt T, Pessin MS, Kwan ES, Caplan LR. Survival with basilar artery occlusion. Cerebrovasc Dis 1995;5:182-7.
30: Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 6th ed. Wolters Kluwer. Lippincott Williams & Wilkins, 2011.
31: Campbell BC, Mitchell PJ, Churilov L, et al. Effect of intravenous tenecteplase dose on cerebral reperfusion before thrombectomy in patients with large vessel occlusion ischemic stroke: the EXTEND-IA TNK Part 2 Randomized Clinical Trial. JAMA 2020;323(13):1257-65. PMID 32078683
32: Campbell BCV, Mitchell PJ, Churilov L, et al. Tenecteplase versus alteplase before thrombectomy for ischemic stroke. N Engl J Med 2018;378(17):1573-82. PMID 29694815
33: Cao S, Zhai M, He J, et al. Prevalence and associated factors of basilar artery dolichosis in patients with acute cerebral infarction. Front Med (Lausanne) 2023;10:832878. PMID 36910498
34: Caplan LR. Intracranial branch atheromatous disease: a neglected under-studied and underused concept. Neurology 1989;39(9):1246-50. PMID 2671793
35: Caplan LR. "Top of the basilar" syndrome. Neurology 1980;30(1):72-9. PMID 7188637
36: Caplan LR. Posterior circulation disease: clinical findings, diagnosis, and management. Cambridge: Blackwell Science, 1996.
37: Chang JY, Jung S, Jung C, Bae HJ, Kwon O, Han MK. Dominant vertebral artery status and functional outcome after endovascular therapy of symptomatic basilar artery occlusion. J Neuroradiol 2017;44(2):151-7. PMID 28131432
38: Chang Y, Li YZ, Xue L. Adjuvant intra-arterial thrombolysis during mechanical thrombectomy is an effective means of improving outcomes for patients with large vessel occlusion stroke: a systematic review and meta-analysis. Clin Neurol Neurosurg 2023;232:107898. PMID 37473487
39: Chikkannaiah M, Lo WD. Childhood basilar artery occlusion: a report of 5 cases and review of the literature. J Child Neurol 2014;29(5):633-45. PMID 23670249
40: Chimowitz MI, Lynn MJ, Derdeyn CP, et al. Stenting versus aggressive medical therapy for intracranial arterial stenosis. N Engl J Med 2011;365(11):993-1003. PMID 21899409
41: Cho HJ, Kim KH, Kim EJ, et al. Clinical implications of basilar artery plaques in the pontine infarction with normal basilar angiogram: a high-resolution magnetic resonance imaging study. J Stroke Cerebrovasc Dis 2018;27(12):3591-8. PMID 30219629
42: Cross DT, Moran CJ, Akins PT, et al. Relationship between clot location and outcome after basilar artery thrombolysis. Am J Neuroradiol 1997;18:1221-8. PMID 9282845
43: Dana CL. Acute bulbar paralysis due to hemorrhage and softening of the pons and medulla. Med Record 1903;64:361-74.
44: Del Bello B, Rognone E, Pichiecchio A, Cavallini A, Mazzacane F. Vessel wall MRI in the diagnosis and follow-up of nonstenosing intracranial atherosclerotic lesions in acute stroke. Stroke 2024;55(2):e35-8. PMID 38126182
45: Del Brutto VJ, Ortiz JG, Biller J. Intracranial arterial dolichoectasia. Front Neurol 2017;8:344.** PMID 28769872
46: Demaerschalk BM, Kleindorfer DO, Adeoye OM, et al. Scientific rationale for the inclusion and exclusion criteria for intravenous alteplase in acute ischemic stroke a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2016;47:1-59. PMID 26696642
47: Demchuk AM, Christou I, Wein TH, et al. Accuracy and criteria for localizing arterial occlusion with transcranial Doppler. J Neuroimaging 2000;10(1):1-12. PMID 10666975
48: Derdeyn CP, Chimowitz MI, Lynn MJ, et al. Aggressive medical treatment with or without stenting in high-risk patients with intracranial artery stenosis (SAMMPRIS): the final results of a randomised trial. Lancet 2014;383(9914):333-41. PMID 24168957
49: Devuyst G, Bogousslavsky J, Meuli R, Moncayo J, de Freitas G, van Melle G. Stroke or transient ischemic attacks with basilar artery stenosis or occlusion: clinical patterns and outcome. Arch Neurol 2002;59(4):567-73. PMID 11939891
50: Dicpinigaitis AJ, Sursal T, Morse CA, et al. Endovascular thrombectomy for treatment of acute ischemic stroke during pregnancy and the early postpartum period. Stroke 2021;52(12):3796-804. PMID 34538088
51: Diener HC, Easton JD, Hart RG, Kasner S, Kamel H, Ntaios G. Review and update of the concept of embolic stroke of undetermined source. Nat Rev Neurol 2022;18(8):455-65. PMID 35538232
52: Dornak T, Herzig R, Kuliha M, et al. Endovascular treatment of acute basilar artery occlusion: time to treatment is crucial. Clin Radiol 2015;70(5):e20-7. PMID 25703459
53: Echiverri HC, Rubino FA, Gupta SR, Gujrati M. Fusiform aneurysm of the vertebrobasilar arterial system. Stroke 1989;20:1741-7. PMID 2595737
54: Ecker RD, Tsujiura CA, Baker CB, Cushing D. Endovascular reconstruction of vertebral artery occlusion prior to basilar thrombectomy in a series of six patients presenting with acute symptomatic basilar thrombosis. J Neurointerv Surg 2014;6(5):379-83. PMID 23737492
55: Elfil M, Ghozy S, Elmashad A, et al. Effect of intra-arterial thrombolysis following successful endovascular thrombectomy on functional outcomes in patients with large vessel occlusion acute ischemic stroke: a post-CHOICE meta-analysis. J Stroke Cerebrovasc Dis 2023;32(8):107194. PMID 37216750
56: Falk KL, Schafer S, Speidel M, Strother C. 4D-DSA: development and current neurovascular applications. AJNR Am J Neuroradiol 2021;42(2):214-20. PMID 33243899
57: Ferbert A, Bruckmann H, Drummen R. Clinical features of proven basilar artery occlusion. Stroke 1990;21:1135-42. PMID 2389292
58: Fink J, Sonnenborg L, Larsen LL, Born AP, Holtmannspötter M, Kondziella D. Basilar artery thrombosis in a child treated with intravenous tissue plasminogen activator and endovascular mechanical thrombectomy. J Child Neurol 2013;28(11):1521-6. PMID 23034976
59: Fischer U, Kaesmacher J, Strbian D, et al. Thrombectomy alone versus intravenous alteplase plus thrombectomy in patients with stroke: an open-label, blinded-outcome, randomized noninferiority trial. Lancet 2022;400:104-15. PMID 35810756
60: Fisher CM, Caplan LR. Basilar artery branch occlusion: a cause of pontine infarction. Neurology 1971;21(9):900-5. PMID 5106254
61: Fisher CM. Bilateral occlusion of the basilar artery branches. J Neurol Neurosurg Psychiatry 1977;40:1182-9. PMID 591986
62: Fisher CM. The herald hemiparesis of basilar artery occlusion. Arch Neurol 1988;45(12):1301-3. PMID 3196188
63: Foix C, Hillemand P. Contribution a l'etude des ramollisements protuberentiels. Rev Med 1926;43:278-305.
64: Fujimoto Y, Ohnishi YI, Wakayama A, Yoshimine T. Transient total mesencephalic locked-in syndrome after bilateral ptosis due to basilar artery thrombosis. J Stroke Cerebrovasc Dis 2012;21(8):909. PMID 22177934
65: Galtrey CM, MacKinnon AD, Pereira AC. Localization of bilateral auditory hallucinations and correlation to imaging in posterior circulation stroke. Neurologist 2012;18(6):418-22. PMID 23114681
66: Gao P, Wang T, Wang D, et al. Effect of stenting plus medical therapy vs medical therapy alone on risk of stroke and death in patients with symptomatic intracranial stenosis: the CASSISS randomized clinical trial. JAMA 2022;328(6):534-42. PMID 35943472
67: Gawlitza M, Quaschling V, Hobohm C, et al. Hyperintense basilar artery on FLAIR MR imaging: diagnostic accuracy and clinical impact in patients with acute brainstem stroke. Am J Neuroradiol 2014;35(8):1520-6. PMID 24812014
68: Ghozy S, El-Qushayri A, Elfil M, et al. Endovascular treatment for basilar artery occlusion: revisiting evidence from randomized clinical trials. Stroke Vasc Interv Neurol 2023;00:e000655.
69: Gilberti N, Gamba M, Premi E, et al. Endovascular mechanical thrombectomy in basilar artery occlusion: variables affecting recanalization and outcome. J Neurol 2016;263(4):707-13. PMID 26872664
70: Gold JJ, Crawford JR. An unusual cause of pediatric stroke secondary to congenital basilar artery fenestration. Case Rep Crit Care 2013;2013:627972. PMID 24804123
71: Goldmakher GV, Camargo EC, Furie KL, et al. Hyperdense basilar artery sign on unenhanced CT predicts thrombus and outcome in acute posterior circulation stroke. Stroke 2009;40(1):134-9. PMID 19038918
72: Gorelick PB, Caplan LR, Hier DB, et al. Racial differences in the distribution of posterior circulation occlusive disease. Stroke 1985;16:785-9. PMID 4049442
73: Gory B, Mazighi M, Blanc R, et al. Mechanical thrombectomy in basilar artery occlusion: influence of reperfusion on clinical outcome and impact of the first-line strategy (ADAPT vs stent retriever). J Neurosurg 2018a:1-10. PMID 29327997
74: Gory B, Mazighi M, Labreuche J, et al. Predictors for mortality after mechanical thrombectomy of acute basilar artery occlusion. Cerebrovasc Dis 2018b;45(1-2):61-7. PMID 29393092
75: Guo Y, Canton G, Baylam Geleri D, et al. Plaque evolution and vessel wall remodeling of intracranial arteries: a prospective, longitudinal vessel wall MRI study. J Magn Reson Imaging 2023. [Epub ahead of print] PMID 38131254
76: Gupta A, Baradaran H, Al-Dasuqi K, et al. Gadolinium enhancement in intracranial atherosclerotic plaque and ischemic stroke: a systematic review and meta-analysis. J Am Heart Assoc 2016;5:e003816. PMID 27528408
77: Gutierrez J, Bagci A, Gardener H, et al. Dolichoectasia diagnostic methods in a multi-ethnic, stroke-free cohort: results from the northern Manhattan study. J Neuroimaging 2014;24(3):226-31. PMID 23317292
78: Hacke W, Zeumer H, Ferbert A, Bruckmann H, del Zoppo GJ. Intra-arterial thrombolytic therapy improves outcome in patients with acute vertebrobasilar occlusive disease. Stroke 1988;19:1216-22. PMID 3176080
79: Haussen DC, Dharmadhikari SS, Snelling B, et al. Posterior communicating and vertebral artery configuration and outcome in endovascular treatment of acute basilar artery occlusion. J Neurointerv Surg 2015;7(12):864-7. PMID 25230838
80: Hayem MG. Sur la thrombose par arterite du tronc basilaire. Comme cause du mort rapide. Arch Physiol Norm Pathol 1868;1:270-89.
81: Hayes WT, Bernhardt H, Young JM. Fusiform arteriosclerotic aneurysm of the basilar artery. Vasc Surg 1967;1:171-8. PMID 5299951
82: Heldner MR, Zubler C, Mattle HP, et al. National Institutes of Health stroke scale score and vessel occlusion in 2152 patients with acute ischemic stroke. Stroke 2013;44(4):1153-7. PMID 23471266
83: Housepian EM, Pool JL. A systematic analysis of intracranial aneurysms from the autopsy file of the Presbyterian Hospital, 1914-1956. J Neuropathol Exp Neurol 1958;17:409-23. PMID 13564252
84: Huang LX, Wu XB, Liu YA, et al. Qualitative and quantitative plaque enhancement on high-resolution vessel wall imaging predicts symptomatic intracranial atherosclerotic stenosis. Brain Behav 2023;13(6):e3032. PMID 37128149
85: Huo X, Gao F, Sun X, et al. Endovascular mechanical thrombectomy with the solitaire device for the treatment of acute basilar artery occlusion. World Neurosurg 2016;89:301-8. PMID 26875658
86: Iglseder B, Huemer M, Staffen W, Ladurner G. Imaging the basilar artery by contrast-enhanced color-coded ultrasound. J Neuroimaging 2000;10:195-9. PMID 11147396
87: Ince B, Petty GW, Brown RD, et al. Dolichoectasia of the intracranial arteries in patients with first ischemic stroke: a population based study. Neurology 1998;50:1694-8. PMID 9633713
88: Jovin TG, Li C, Wu L, et al. Trial of thrombectomy 6 to 24 hours after stroke due to basilar-artery occlusion. N Engl J Med 2022;387(15):1373-84. PMID 36239645
89: Jung S, Mono ML, Fischer U, et al. Three-month and long-term outcomes and their predictors in acute basilar artery occlusion treated with intra-arterial thrombolysis. Stroke 2011;42(7):1946-51. PMID 21546481
90: Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the prevention of stroke in patients with stroke and transient ischemic attack: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2014;45(7):2160-236. PMID 24788967
91: Kim E, Son MK, Kang CK, Lee YB. Vertebrobasilar occlusion presenting as sudden isolated bilateral sensorineural hearing loss: case report. J Cerebrovasc Endovasc Neurosurg 2013;15(3):225-8. PMID 24167804
92: Kim JG, Lee D, Choi J, Song Y, Lee DH, Suh DC. DWI-pc-ASPECT score in basilar artery occlusion: is 6 points or less always indicative of a bad outcome? Interv Neuroradiol 2019;25(4):371-9. PMID 30803336
93: Klein IF, Lavallee PC, Schouman-Claeys E, Amarenco P. High-resolution MRI identifies basilar artery plaques in paramedian pontine infarct. Neurology 2005;64(3):551-2. PMID 15699395
94: Klein IF, Lavallée PC, Mazighi M, Schouman-Claeys E, Labreuche J, Amarenco P. Basilar artery atherosclerotic plaques in paramedian and lacunar pontine infarctions: a high-resolution MRI study. Stroke 2010;41(7):1405-9. PMID 20538696
95: Koga M, Kimura K, Minematsu K, Yamaguchi T. Relationship between findings of conventional and contrast-enhanced transcranial color-coded real-time sonography and angiography in patients with basilar artery occlusion. AJNR 2002;23(4):568-71. PMID 11950645
96: Kubik CS, Adams RD. Occlusion of the basilar artery: a clinical and pathological study. Brain 1946;69:6-121. PMID 20274363
97: Kumar G, Shahripour RB, Alexandrov AV. Recanalization of acute basilar artery occlusion improves outcomes: a meta-analysis. J Neurointerv Surg 2015;7(12):868-74. PMID 25271064
98: Labauge R, Pages M, Blard JM. Survie prolongee apres occlusion du tronc basilaire. Rev Neurol 1989;145:789-94. PMID 2595168
99: Labauge R, Pages M, Marty-Double C, et al. Occlusion du tronc basilaire. Rev Neurol 1981;137:545-71. PMID 7034122
100: Lagman-Bartolome AM, Pontigon AM, Moharir M, et al. Basilar artery strokes in children: good outcomes with conservative medical treatment. Dev Med Child Neurol 2013;55(5):434-9. PMID 23398238
101: Langezaal LCM, van der Hoeven EJRJ, Mont’Alverne FJA, et al. Endovascular therapy for stroke due to basilar-artery occlusion. N Engl J Med 2021;384(20):1910-20. PMID 34010530
102: Lee WJ, Jung KH, Ryu YJ, et al. Utility of digital subtraction angiography-based collateral evaluation in medically treated acute symptomatic basilar artery stenosis. Eur J Neurol 2017a;24(9):1148-55. PMID 28707434
103: Leon-Carrion J, van Eeckhout P, Dominguex-Morales R, et al. The locked-in syndrome: a syndrome looking for a therapy. Brain Inj 2002;16:571-82. PMID 12119076
104: Lescher S, Samaan T, Berkefeld J. Evaluation of the pontine perforators of the basilar artery using digital subtraction angiography in high resolution and 3D rotation technique. AJNR Am J Neuroradiol 2014;35(10):1942-7. PMID 24904054
105: Levine RL, Turski PA, Grist TM. Basilar artery dolichoectasia: review of the literature and six patients studied with magnetic resonance angiography. J Neuroimag 1995;5(3):164-70. PMID 7626824
106: Leyden E. Ueber die thrombose der basilar arterie. Zeitscrift Klin Med 1882;5:165-85.
107: Li C, Zhao W, Wu C, et al. Outcome of endovascular treatment for acute basilar artery occlusion in the modern era: a single institution experience. Neuroradiology 2018;60(6):651-9. PMID 29651500
108: Li H, Liu J, Dong Z, et al. Identification of high-risk intracranial plaques with 3D high-resolution magnetic resonance imaging-based radiomics and machine learning. J Neurol 2022;269(12):6494-503. PMID 35951103
109: Lian X, Xu D, Wu J, et al. Endovascular recanalization therapy for prolonged basilar artery occlusion based on clinical-diffusion MRI mismatch. Clin Neurol Neurosurg 2013;115(7):915-9. PMID 23021202
110: Lindsberg PJ, Mattle HP. Therapy of basilar artery occlusion: a systematic analysis comparing intra-arterial and intravenous thrombolysis. Stroke 2006;37(3):922-8. PMID 16439705
111: Liu L, Li W, Qiu J, et al. Improving neurological outcome for acute basilar artery occlusion with sufficient recanalization after thrombectomy by intraarterial tenecteplase (INSIST-IT): Rationale and design. Eur Stroke J 2023;8(2):591-7. PMID 37231688
112: Liu X, Dai Q, Ye R, et al. Endovascular treatment versus standard medical treatment for vertebrobasilar artery occlusion (BEST): an open-label, randomised controlled trial. Lancet Neurol 2020;19(2):115-22. PMID 31831388
113: Ljevak J, Mismas A, Bazima A, et al. An infrequent type of stroke with an unusual cause and successful therapy basilar artery occlusion caused b y a cardiac papillary fibroblastoma recanalized 12 hours after onset. Intern Med 2013;52(2):277-9. PMID 23318863
114: Lobbous M, Williams S, Rashid S. Child neurology: childhood basilar artery occlusion and stroke. Neurology 2017;89(7):e68-70. PMID 28808172
115: Lou M, Caplan LR. Vertebrobasilar dilatative arteriopathy (dolichoectasia). Ann NY Acad Sci 2010;1184:121-33. PMID 20146694
116: Lowhagen HP, Rentzos A, Karlsson JE, et al. General anesthesia versus conscious sedation for endovascular treatment of acute ischemic stroke: the AnStroke trial (Anesthesia During Stroke). Stroke 2017;48:1601-7. PMID 28522637
117: Luo J, Bai X, Huang K, et al. Clinical relevance of plaque distribution for basilar artery stenosis. AJNR Am J Neuroradiol 2023a;44(5):530-5. PMID 37024307
118: Luo YL, Sun X, Kong X, et al. A DWI-based radiomics-clinical machine learning model to preoperatively predict the futile recanalization after endovascular treatment of acute basilar artery occlusion patients. Eur J Radiol 2023b;161:110731. PMID 36804312
119: Lv Y, Ma X, Zhao W, et al. Association of plaque characteristics with long-term stroke recurrence in patients with intracranial atherosclerotic disease: a 3D high-resolution MRI-based cohort study. Eur Radiol 2023. [Epub ahead of print] PMID 37870623
120: Ma N, Jiang W, Lou X, et al. Arterial remodeling of advanced basilar atherosclerosis: a 3-tesla MRI study. Neurology 2010;75(3):253-8. PMID 20644151
121: Marinkovic SV, Gibo H. The surgical anatomy of perforating branches of the basilar artery. Neurosurgery 1993;33(1):80-7. PMID 8355851
122: Marquardt L, Kuker W, Chandratheva A, Geraghty O, Rothwell PM. Incidence and prognosis of > or = 50% symptomatic vertebral or basilar artery stenosis: prospective population-based study. Brain 2009;132(Pt 4):982-8. PMID 19293244
123: Matsuo K, Fujii C, Fuse I, Nakajima M, Takada M, Miyata K. Top of the basilar syndrome in a young adult initially presenting with a convulsive seizure. Intern Med 2011;50(13):1425-8. PMID 21720064
124: Merwick A, Werring D. Posterior circulation ischaemic stroke. BMJ 2014;348:g3175. PMID 24842277
125: Milandre L, Bonnefoi B, Pestre P, et al. Dolichoectasies arterielles vertebrobasilaires: complications et prognostic. Rev Neurol 1991;147:714-22. PMID 1775825
126: Mitchell PJ, Yan B, Churilov L, et al. Endovascular thrombectomy versus standard bridging thrombolytic with endovascular thrombectomy within 4·5 h of stroke onset: an open-label, blinded-endpoint, randomised non-inferiority trial. Lancet 2022;400(10346):116-25. PMID 35810757
127: Miyagi T, Koga M, Shiokawa Y, et al. Intravenous alteplase at 0.6 mg/kg for acute stroke patients with basilar artery occlusion: the stroke acute management with urgent risk factor assessment and improvement (SAMURAI) Recombinant tissue plasminogen activator registry. J Stroke Cerebrovasc Dis 2013;22(7):1098-106. PMID 23063059
128: Mordasini P, Brekenfeld C, Byrne JV, et al. Technical feasibility and application of mechanical thrombectomy with the Solitaire FR Revascularization Device in acute basilar artery occlusion. AJNR Am J Neuroradiol 2013;34(1):159-63. PMID 22723058
129: Mujanovic A, Kurmann C, Serrllach B, et al. Intra-arterial thrombolysis is associated with delayed reperfusion of remaining vessel occlusions following incomplete thrombectomy. AJNR Am J Neuroradiol 2023;44(9):1050-6. PMID 37500281
130: Mukherjee S, McCullagh H, Goddard T, Patankar T. Delayed mid-basilar artery stenosis following paediatric acute mechanical thrombectomy: a rare complication from a rare case. BMJ Case Rep 2019;12(8):e216876. PMID 31377714
131: Nadeau S, Jordan J, Mishra S. Clinical presentation as a guide to early prognosis in vertebrobasilar stroke. Stroke 1992;23:165-70. PMID 1561642
132: Nogueira RG, Jadhav AP, Haussen DC, et al. Thrombectomy 6 to 24 hours after stroke with a mismatch between deficit and infarct. N Engl J Med 2018;378(1):11-21. PMID 29129157
133: Nouh A, Remke J, Ruland S. Ischemic posterior circulation stroke: a review of anatomy, clinical presentations, diagnosis, and current management. Front Neurol 2014;5:30.** PMID 24778625
134: Ostrem JL, Saver JL, Alger JR, et al. Acute basilar artery occlusion: diffusion-perfusion MRI characterization of tissue salvage in patients receiving intra-arterial stroke therapies. Stroke 2004;35(2):e30-4. PMID 14739412
135: Ott B, Saver JL. Unilateral amnesic stroke: six new cases and a review of the literature. Stroke 1993;24:1033-42. PMID 8322379
136: Ottomeyer C, Zeller J, Fesl G, et al. Multimodal recanalization therapy in acute basilar artery occlusion: long-term functional outcome and quality of life. Stroke 2012;43(8):2130-5. PMID 22569932
137: Palmisciano P, Hoz SS, Algburi HA, et al. Percutaneous transluminal angioplasty and/or stenting for the treatment of basilar artery stenosis: a systematic review and meta-analysis. Neuroradiology 2023;65(6):985-1000. PMID 36881121
138: Park BS, Kang CW, Kwon HJ, et al. Endovascular mechanical thrombectomy in basilar artery occlusion: initial experience. J Cerebrovasc Endovasc Neurosurg 2013;15(3):137-44. PMID 24167791
139: Passero S, Filosomi G. Posterior circulation infarcts in patients with vertebrobasilar dolichoectasia. Stroke 1998;29:653-9. PMID 9506608
140: Pessin MS, Chimowitz MI, Levine SR, et al. Stroke in patients with fusiform vertebrobasilar aneurysms. Neurology 1989;39:16-21. PMID 2909908
141: Puetz V, Lutsep H, Nguyen T. Endovascular therapy border basilar artery occlusion: among the first to conceptualize, last to prove. Stroke 2023;54(3):905-8. PMID 36688315
142: Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2018;49(3):e46-110.** PMID 29367334
143: Powers WJ, Rabinstein AA, Ackerson T, et al. 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;50(12):e344-418. PMID 31662037
144: Puetz V, Bodechtel U, Gerber JC, et al. Reliability of brain evaluation by stroke neurologists in telemedicine. Neurology 2013;80(4):332-8. PMID 23255831
145: Qiao Y, Anwar Z, Intrapiromkul J, et al. Patterns and implications of intracranial arterial remodeling in stroke patients. Stroke 2016;47(2):434-40. PMID 26742795
146: Qureshi A, Lodhi A, Ma X, et al. Intraarterial thrombolytics as an adjunct to mechanical thrombectomy in patients with basilar artery occlusion. J Neuroimaging 2023;33(3):415-21. PMID 36797047
147: Raphaeli G, Eichel R, Ben-Hur T, Leker RR, Cohen JE. Multimodal reperfusion therapy in patients with acute basilar artery occlusion. Neurosurgery 2009;65(3):548-52; discussion 52-3. PMID 19687700
148: Rego Sousa P, Vasconcellos R. Paediatric acute basilar thrombosis successfully treated with intravenous alteplase. BMJ Case Rep 2012;2012. PMID 22605850
149: Renu A, Millan M, Roman L, et al. Effect of intra-arterial alteplase vs placebo following successful thrombectomy on functional outcomes in patients with large vessel occlusion acute ischemic stroke. The CHOICE randomized clinical trial. JAMA 2022;327(9):826-35. PMID 35143603
150: Roach ES, Golomb MR, Adams R, et al. Management of stroke in infants and children: a scientific statement from a Special Writing Group of the American Heart Association Stroke Council and the Council on Cardiovascular Disease in the Young. Stroke 2008;39(9):2644-91. PMID 18635845
151: Rosa A, Moudi M, Mizone JP. Typical and atypical ocular bobbing: pathology through five case reports. Neuro-Ophthalmol 1987;7:285-90.
152: Rousseau MC, Baumstarck K, Alessandrini M, et al. Quality of life in patients with locked-in syndrome: evolution over a 6-year period. Orphanet J Rare Dis 2015;10:88. PMID 26187655
153: Saeki N, Rhoton AL. Microsurgical anatomy of the upper basilar artery and the posterior circle of Willis. J Neurosurg 1977;46:563-78. PMID 845644
154: Sairanen T, Strbian D, Soinne L, et al. Intravenous thrombolysis of basilar artery occlusion: predictors of recanalization and outcome. Stroke 2011;42(8):2175-9. PMID 21737807
155: Saposnik G, Caplan LR. [Ischemia of the vertebrobasilar territory: mechanisms and practical considerations]. Rev Neurol 2001;33(9):854-64. PMID 11784989
156: Satti S, Chen J, Sivapatham T, Jayaraman M, Orbach D. Mechanical thrombectomy for pediatric acute ischemic stroke: review of the literature. J Neurointerv Surg 2017;9(8):732-7. PMID 27448827
157: Saver JL, Feldmann E. The basic transcranial Doppler examination: technique and anatomy. In: Babikian VL, Wechsler L, editors. Transcranial Doppler sonography: clinical and research applications. Philadelphia: B.C. Decker, 1992.
158: Schonenberger S, Uhlmann L, Hacke W, et al. Effect of conscious sedation vs general anesthesia on early neurological improvement among patients with ischemic stroke undergoing endovascular thrombectomy: a randomized clinical trial. JAMA 2016;316(19):1986-96. PMID 27785516
159: Schulte-Altedorneburg G, Droste DW, Popa V, et al. Visualization of the basilar artery by transcranial color-coded duplex sonography: comparison with postmortem results. Stroke 2000;31(5):1123-7. PMID 10797175
160: Schwartz A, Rautenberg W, Hennerici M. Dolichoectatic intracranial arteries: review of selected aspects. Cerebrovasc Dis 1993;3:273-9.
161: Schwarz S, Egelhof T, Schwab S, et al. Basilar artery embolism. Clinical syndrome and neuroradiologic patterns in patients without permanent occlusion of the basilar artery. Neurology 1997;49:1346-52. PMID 9371920
162: Shi A, Zhao X, Zhu S, et al. Time-of-flight intracranial MRA at 3T versus 5T versus 7T: visualization of distal small cerebral arteries. Radiology 2023;306(1):207-17. PMID 36040333
163: Shi GW, Xiong XL, Lin Y, Li YS. The clinical characteristics of patients with posterior circulation ischemic stroke. [Article in Chinese] Zhonghua Nei Ke Za Zhi 2008;47(5):393-6. PMID 18953949
164: Shi Z, Zhu C, Degnan A, et al. Identification of high-risk plaque features in intracranial atherosclerosis: initial experience using a radiomic approach. Eur Radiol 2018;28(9):3912-21. PMID 29633002
165: Shu L, Riedel C, Meyne J, Jansen O, Jensen-Kondering U. Successful recanalization in acute basilar artery occlusion treated with endovascular therapy is independent of thrombus length. J Neurointerv Surg 2017;9(11):1047-52. PMID 27789788
166: Singer OC, Berkefeld J, Nolte CH, et al. Mechanical recanalization in basilar artery occlusion: the ENDOSTROKE study. Ann Neurol 2015;77(3):415-24. PMID 25516154
167: Song JW, Pavlou A, Xiao J, Kasner SE, Fan Z, Messe SR. Vessel wall magnetic resonance imaging biomarkers of symptomatic intracranial atherosclerosis: a meta-analysis. Stroke 2021;52(1):193-202. PMID 33370193
168: Song X, Zhao X, Liebeskind D, et al. Incremental value of plaque enhancement in predicting stroke recurrence in symptomatic intracranial atherosclerosis. Neuroradiology 2020;62(9):1123-31. PMID 32300828
169: Sorensen BF. Bow hunter’s stroke. Neurosurgery 1978;2(3):259-61. PMID 732978
170: Stolz E, Nuckel M, Mendes I, et al. Vertebrobasilar transcranial color-coded duplex ultrasonography: improvement with echo enhancement. AJNR 2002;23:1051-4. PMID 12063240
171: Stracke CP, Meyer L, Schwindt W, Ranft A, Straeter R. Case report: successful mechanical thrombectomy in a newborn with basilar artery occlusion. Front Neurol 2022;12:790486. PMID 35273551
172: Strbian D, Sairanen T, Silvennoinen H, Salonen O, Kaste M, Lindsberg PJ. Thrombolysis of basilar artery occlusion: Impact of baseline ischemia and time. Ann Neurol 2013;73(6):688-94. PMID 23536323
173: Strbian D, Sairanen T, Silvennoinen H, Salonen O, Lindsberg PJ. Intravenous thrombolysis of basilar artery occlusion: thrombus length versus recanalization success. Stroke 2014;45(6):1733-8. PMID 24781081
174: Tang M, Gao J, Ma N, et al. Radiomics nomogram for predicting stroke recurrence in symptomatic intracranial atherosclerotic stenosis. Front Neurosci 2022;16:851353. PMID 35495035
175: Tao C, Nogueria R, Zhu Y, et al. Trial of endovascular treatment of acute basilar artery occlusion. N Engl J Med 2022;387(15):1361-72. PMID 36239644
176: Tian X, Tian B, Shi Z, et al. Assessment of intracranial atherosclerotic plaque using 3D lack-blood MRI: comparison with 3D time-of-flight MRA and DSA. J Magn Reson Imaging 2021;53(2):469-78. PMID 32864816
177: Toyoda K, Saku Y, Ibayashi S, et al. Pontine infarction extending to the basal surface. Stroke 1994;25:2171-8. PMID 7974541
178: Tsivgoulis G, Katsanos A, Sandset C, et al. Thrombolysis for acute ischemic stroke: current status and future perspectives. Lancet Neurol 2023;22(5):418-29. PMID 36907201
179: Tumialan LM, Theodore N. Basilar artery thrombosis after reduction of cervical spondyloptosis: a cautionary report. J Neurosurg Spine 2012;16(5):492-6. PMID 22385083
180: Turan T, Psychogios MN. The CASSISS randomized clinical trial. Stroke 2023;54(1):286-9. PMID 36367102
181: Turc G, Bhogal P, Fischer U, et al. European Stroke Organisation (ESO)- European Society for Minimally Invasive Neurological Therapy (ESMINT) guidelines on mechanical thrombectomy in acute ischemic stroke. J Neurointerv Surg 2019;11(6):535-8. PMID 31152058
182: van der Hoeven EJ, Dandbaar JW, Algra A, et al. Additional diagnostic value of computed tomography perfusion for detection of acute ischemic stroke in the posterior circulation. Stroke 2015;46(4):1113-15. PMID 25744516
183: Vieco PT, Maurin EE, Gross CE. Vertebrobasilar dolichoectasia: evaluation with CT angiography. Am J Neuroradiol 1997;18:1385-8. PMID 9282873
184: Voetsch B, DeWitt D, Pessin MS, Caplan LR. Basilar artery occlusive disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol 2004;61:496-504. PMID 15096396
185: Wang M, Hays T, Balasa V, et al. Low-dose tissue plasminogen activator thrombolysis in children. Pediatr Hematol Oncol 2003;(5):379-86. PMID 1275962
186: Wang Y, Liu X, Wu X, Degnana AJ, Malhotra A, Zhu C. Culprit intracranial plaque without substantial stenosis in acute ischemic stroke on vessel MRI: a systematic review. Atherosclerosis 2019;287:112-21. PMID 31254918
187: Wen WL, Li ZF, Zhang YW, et al. Effect of baseline characteristics on the outcome of stent retriever-based thrombectomy in acute basilar artery occlusions: a single-center experience and pooled data analysis. World Neurosurg 2017;104:1-8. PMID 28427984
188: Williams AN. Cerebrovascular disease in Dumas’s The Count of Monte Cristo. JR Soc Med 2003;96(8):412-4. PMID 12893866
189: Wilson LK, Benavente OR, Woolfenden AR, Asdaghi N. Spontaneous limb movements and posturing secondary to acute basilar artery occlusion: a potentially devastating seizure mimic. Pract Neurol 2014;14(1):42-4. PMID 24046437
190: Wu F, Zhang M, Qi Z, Ma Q, Yu Z, Lu J. Imaging features of vertebrobasilar dolichoectasia combined with posterior circulation ischemic stroke: a vessel wall magnetic resonance imaging study. Eur J Radiol 2023a;166:110971. PMID 37506476
191: Wu Q, Wang J, Zheng B, et al. Impact of qualifying artery on the efficacy of stenting plus medical therapy versus medical therapy alone in patients with symptomatic intracranial stenosis: a post-hoc analysis of the CASSISS trial. J Neurointerv Surg 2023b. [Epub ahead of print] PMID 37438104
192: Xianxian Z, Chengsong Y, Qiang M, et al. The efficiency analysis of thrombolytic rt-PA combined with intravascular interventional therapy in patients with acute basilar artery occlusion. Int J Biol Sci 2017;13(1):57-64. PMID 28123346
193: Xiao J, Song SS, Schlick KH, et al. Disparate trends of atherosclerotic plaque evolution in stroke patients under 18-month follow-up: a 3D whole-brain magnetic resonance vessel wall imaging study. Neuroradiol J 2022;35(1):42-52. PMID 34159814
194: Xu DS, Levitt MR, Kalani MY, et al. Dolichoectatic aneurysms of the vertebrobasilar system: clinical and radiographic factors that predict poor outcomes. J Neurosurg 2018;128:560-6. PMID 28387624
195: Xue F, Yun HJ, Peng L, Wu C. Where are we heading in post-China angioplasty and stenting for symptomatic intracranial severe stenosis era? Brain Circ 2023;9(1):3-5. PMID 37151789
196: Yin-Dan Y, Wen-Ke H, Li-Fey G. Meningovascular syphilis with basilar artery occlusion: case report and literature review. Neurol India 2014;62(2):213-4. PMID 24823745
197: Yoon W, Kim SK, Heo TW, Baek BH, Lee YY, Kang HK. Predictors of good outcome after stent-retriever thrombectomy in acute basilar artery occlusion. Stroke 2015;46(10):2972-5. PMID 26330448
198: Yu YL, Moseley IF, Pullicino P, et al. The clinical picture of ectasia of the intracerebral arteries. J Neurol Neurosurg Psychiat 1982;45:29-36. PMID 7062068
199: Zaidat O, Fitzsimmons BF, Woodward B, et al. Effect of a balloon-expandable intracranial stent vs medical therapy on risk of stroke in patients with symptomatic intracranial stenosis. the VISSIT randomized clinical trial. JAMA 2015;313(12):1240-8. PMID 25803346
200: Zaidi HA, Albuquerque FC, Chowdhry SA, Zabramski JM, Ducruet AF, Spetzler RF. Diagnosis and management of bow hunter’s syndrome: 15-year experience at Barrow Neurological Institute. World Neurosurg 2014;82(5):733-8. PMID 24549025
201: Zedde M, Pascarella R. Stenting plus medical therapy and risk of stroke and death in patients with symptomatic intracranial stenosis. JAMA 2022;328(24):2455-6. PMID 36573985
202: Zhang S, Zhao X, Zhu S, et al. Time-of-flight intracranial MRA at 3 T versus 5 T versus 7 T: visualization of distal small cerebral arteries. Radiology 2023;306(1):207-17. PMID 36040333
203: Zhou L, Yan Y, Du H, et al. Plaque features and vascular geometry in basilar artery atherosclerosis. Medicine 2020;99:18(e19742).

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Authors

H Steven Block MD

Dr. Block of the Stritch School of Medicine at Loyola University in Chicago has no relevant financial relationships to disclose.
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Jose Biller MD

Dr. Biller of the Stritch School of Medicine at Loyola University of Chicago has no relevant financial relationships to disclose.
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Editor

Steven R Levine MD

Dr. Levine of the SUNY Health Science Center at Brooklyn has no relevant financial relationships to disclose.
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Former Authors

Sean Ruland DO
Cara Joyce PhD
Camilo R Gomez MD
Michael Teitcher MD
Jeffrey L Saver MD (original author), Brian H Buck MD, Mary A Kalafut MD, John M Whapham MD, Sarkis Morales-Vidal MD, and Murray Flaster MD PhD

Patient Profile

Age range of presentation: 0 month to 65+ years
Sex preponderance: male>female, >1:1
Heredity: heredity may be a factor
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-9: Occlusion and stenosis of precerebral arteries, basilar artery: 433.0

Cerebral thrombosis: 434.0

Cerebral embolism: 434.1

Transient cerebral ischemia, Basilar artery syndrome: 435.0

Transient cerebral ischemia, Vertebrobasilar artery syndrome: 435.3

Basilar artery stroke

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Anatomy

Atherosclerosis

Symptomatic non-stenosing intracranial atherosclerosis and arterial wall remodeling

Radiographic biomarkers of symptomatic intracranial atherosclerotic disease

Morphologic and radiographic characteristics of high-risk atherosclerotic plaque

Additional advanced imaging techniques

Basilar perforator origin occlusion

Embolism

Dolichoectasia

Bow hunter syndrome

Cerebral vasculitis and other miscellaneous etiologies

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Table 1. Symptoms of Vertebrobasilar (Posterior Circulation) Stroke and Transient Ischemic Attacks

Diagnostic workup

Management

Role of reduced basilar artery blood flow in PTAS planning

The role of perforator anatomy in basilar artery stroke in PTAS planning

Clinical relevance of plaque distribution in PTAS planning

Potential adjunctive and rescue recanalization strategies following endovascular thrombectomy

Outcomes

Special considerations

Pregnancy

Anesthesia

Media

References

Contributors

Authors

Editor

Former Authors

Patient Profile

ICD & OMIM codes