posterior circulation syndromes the non focal presentation

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2 Posterior Circulation Posterior Circulation Syndromes Syndromes The Non Focal Presentation The Non Focal Presentation Victoria Parada MD Victoria Parada MD Valley Baptist Neuroscience Valley Baptist Neuroscience Department Department UTHSCSA RAHC Harlingen UTHSCSA RAHC Harlingen

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Posterior Circulation Syndromes The Non Focal Presentation. Victoria Parada MD Valley Baptist Neuroscience Department UTHSCSA RAHC Harlingen. 2. Objectives. Recognize the most relevant clinical findings consistent with posterior circulation ischemic stroke syndromes - PowerPoint PPT Presentation

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Page 1: Posterior Circulation Syndromes The Non Focal Presentation

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Posterior Circulation Posterior Circulation SyndromesSyndromes

The Non Focal PresentationThe Non Focal Presentation

Victoria Parada MDVictoria Parada MDValley Baptist Neuroscience DepartmentValley Baptist Neuroscience Department

UTHSCSA RAHC HarlingenUTHSCSA RAHC Harlingen

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ObjectivesObjectives

Recognize the most relevant clinical Recognize the most relevant clinical findings consistent with posterior findings consistent with posterior circulation ischemic stroke syndromes circulation ischemic stroke syndromes Understand the pertinent history, clinical Understand the pertinent history, clinical evaluation, and management.evaluation, and management.

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Clinical manifestations Clinical manifestations ►Posterior circulation infarcts comprise Posterior circulation infarcts comprise

approximately 20% to 25% of all approximately 20% to 25% of all ischemic strokes ischemic strokes (Kumral et al 2004)

► Vertebrobasilar ischemic Vertebrobasilar ischemic stroke is not is not a homogenous entity a homogenous entity Duration of transient ischemic attacks varies Duration of transient ischemic attacks varies

considerably considerably Symptoms vary from mild to extreme Symptoms vary from mild to extreme Frequency may vary from a solitary attack to Frequency may vary from a solitary attack to

many per day many per day

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Symptoms of vertebrobasilar Symptoms of vertebrobasilar transient ischemic attacks are transient ischemic attacks are

complex!complex! ► Unilateral or bilateral motor or sensory Unilateral or bilateral motor or sensory

symptoms involving the face or limbs and symptoms involving the face or limbs and unilateral or bilateral visual field defects unilateral or bilateral visual field defects VertigoVertigo DiplopiaDiplopia Dysarthria, dyphagiaDysarthria, dyphagia loss of balanceloss of balance isolated sensory symptoms isolated sensory symptoms

► may be considered as transient ischemic may be considered as transient ischemic attacks when occurring in combined fashion attacks when occurring in combined fashion (simultaneously or successively) (simultaneously or successively)

(Albucher et al 2005)

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Clinical manifestations Clinical manifestations

►The clinical manifestations of The clinical manifestations of vertebral basilar occlusive disease vertebral basilar occlusive disease vary according to the site and nature vary according to the site and nature of vascular compromise and the of vascular compromise and the location of resultant neural ischemialocation of resultant neural ischemia

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EtiologyEtiology

► In situ atherosclerosis and In situ atherosclerosis and cardioembolism are the most common cardioembolism are the most common causes of basilar artery strokescauses of basilar artery strokes

►Less frequent etiologies include Less frequent etiologies include cervicocephalic arterial dissection, cervicocephalic arterial dissection, migraine, , dolichoectasia, , vasculitis, , and paradoxical and paradoxical embolism. .

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Clinical profiles may be Clinical profiles may be distinguished distinguished

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Vignette 1Vignette 1

A 68-year-old woman with a history of atrial fibrillation A 68-year-old woman with a history of atrial fibrillation on chronic anticoagulation presented to the hospital on chronic anticoagulation presented to the hospital with acute behavioral changes, visual disturbances, with acute behavioral changes, visual disturbances, and right hemiparesis. and right hemiparesis.

On examination, she was somnolent, had poor short-On examination, she was somnolent, had poor short-term recollection, dense right hemianopia, mild right term recollection, dense right hemianopia, mild right hemiparesis, and profound right hypoesthesia. hemiparesis, and profound right hypoesthesia.

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POSTERIOR CEREBRAL ARTERY POSTERIOR CEREBRAL ARTERY OCCLUSIONOCCLUSION

MRI of her brain showed a large left PCA MRI of her brain showed a large left PCA infarction and MRA disclosed proximal infarction and MRA disclosed proximal occlusion of this vessel. occlusion of this vessel.

Despite some functional recovery over the Despite some functional recovery over the following 6 months, her visual and cognitive following 6 months, her visual and cognitive disturbances remained disablingdisturbances remained disabling

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POSTERIOR CEREBRAL ARTERY POSTERIOR CEREBRAL ARTERY OCCLUSION OCCLUSION

The PCAs supply the midbrain, thalami, The PCAs supply the midbrain, thalami, lateral geniculate bodies, posterior portion lateral geniculate bodies, posterior portion of the choroid plexus, occipital lobes, of the choroid plexus, occipital lobes, inferior and medial aspects of the temporal inferior and medial aspects of the temporal lobes, and posterior-inferior areas of the lobes, and posterior-inferior areas of the parietal lobes. parietal lobes.

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Proximal occlusion of a PCA may Proximal occlusion of a PCA may produce: produce: decreased level of consciousness decreased level of consciousness profound disturbances of visual perceptionprofound disturbances of visual perception antegrade amnesiaantegrade amnesia ophthalmoparesis (from damage to the upper ophthalmoparesis (from damage to the upper

midbrain) midbrain) hemiplegia (typically from peduncular ischemia) hemiplegia (typically from peduncular ischemia) hemihypoesthesia hemihypoesthesia hemianopia. hemianopia.

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Patients with left PCA infarctions may Patients with left PCA infarctions may experience incapacitating neurocognitive experience incapacitating neurocognitive disorders:disorders: Alexia without agraphia (corpus callosum) Alexia without agraphia (corpus callosum) alexia with agraphia (corpus callosusm + angular alexia with agraphia (corpus callosusm + angular

gyrus). gyrus). Anomic aphasia may be produced by left temporo-Anomic aphasia may be produced by left temporo-

occipital strokes. occipital strokes. Severe memory impairment can be caused by Severe memory impairment can be caused by

ischemia of the mesial temporal structures or the ischemia of the mesial temporal structures or the thalamus. thalamus.

Left PCA stroke may be responsible for single Left PCA stroke may be responsible for single stroke dementia.stroke dementia.

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POSTERIOR CEREBRAL ARTERY POSTERIOR CEREBRAL ARTERY OCCLUSIONOCCLUSION

Midbrain ischemia may express with Midbrain ischemia may express with ipsilateral or bilateral ophthalmoparesis (III ipsilateral or bilateral ophthalmoparesis (III nerve palsy, abnormal vertical eye nerve palsy, abnormal vertical eye movements). movements).

Embolism from a cardiac or an arterial Embolism from a cardiac or an arterial (aortic arch, vertebral artery origin) source (aortic arch, vertebral artery origin) source is the most common mechanism of PCA is the most common mechanism of PCA stroke. stroke.

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Vignette 2Vignette 2

A 64-year-old woman was found unresponsive in her A 64-year-old woman was found unresponsive in her bathroom by her husband. bathroom by her husband. She was intubated by EMS and transported to our She was intubated by EMS and transported to our emergency department.emergency department. On arrival, she was comatose and breathing at a rate On arrival, she was comatose and breathing at a rate of 40 to 45 per minute. She was tachycardic and of 40 to 45 per minute. She was tachycardic and hypertensive. Her pupils were slightly anisocoric (3.5 hypertensive. Her pupils were slightly anisocoric (3.5 mm on the left and 3 mm on the right), and responses mm on the left and 3 mm on the right), and responses to light were minimal on the left and absent on the to light were minimal on the left and absent on the right. Corneal and oculocephalic reflexes were right. Corneal and oculocephalic reflexes were preserved. Best motor responses to pain were in the preserved. Best motor responses to pain were in the form of withdrawal. form of withdrawal.

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DWI showed DWI showed restricted diffusion in restricted diffusion in the midcerebellum the midcerebellum and mesencephalon. and mesencephalon. A hyperintense signal A hyperintense signal in the basilar artery in the basilar artery indicative of acute indicative of acute thrombosis was thrombosis was visualized on FLAIR. visualized on FLAIR. Conventional Conventional angiography angiography confirmed occlusion of confirmed occlusion of the basilar trunk.the basilar trunk.

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She underwent successful She underwent successful basilar recanalization by basilar recanalization by intra-arterial thrombolysis intra-arterial thrombolysis combined with mechanical combined with mechanical disruption of the clot. disruption of the clot. Despite reperfusion, the Despite reperfusion, the patient failed to improve patient failed to improve neurologically. neurologically. Repeat MRI showed Repeat MRI showed established infarction established infarction throughout the midbrain. throughout the midbrain. Patient expired shortly after Patient expired shortly after her family requested her family requested withdrawal ofwithdrawal of artificial life artificial life support.support.

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VERTEBROBASILAR DISEASE VERTEBROBASILAR DISEASE

Occlusion of the basilar artery represents Occlusion of the basilar artery represents the most dreaded form of ischemic stroke. the most dreaded form of ischemic stroke.

At its worst, it causes massive fatal At its worst, it causes massive fatal infarction involving the brainstem, infarction involving the brainstem, cerebellum, the occipital and posterior cerebellum, the occipital and posterior temporal lobes, and the thalami.temporal lobes, and the thalami.

Catastrophic results may at times be Catastrophic results may at times be avoided by prompt recognition of early signs avoided by prompt recognition of early signs of vertebrobasilar ischemia.of vertebrobasilar ischemia.

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VERTEBROBASILAR DISEASEVERTEBROBASILAR DISEASE

Infarctions at different levels are caused by Infarctions at different levels are caused by different mechanisms:different mechanisms: ♦    ♦    Proximal territory infarctions (i.e., involving the medulla and Proximal territory infarctions (i.e., involving the medulla and

lower cerebellum) are caused by embolism from the heart or lower cerebellum) are caused by embolism from the heart or atherosclerosis of the extracranial vertebral arteries or by atherosclerosis of the extracranial vertebral arteries or by hypoperfusion related to severe intracranial vertebral occlusive hypoperfusion related to severe intracranial vertebral occlusive lesions.lesions.  ♦    Middle territory infarctions (i.e., involving pons and   ♦    Middle territory infarctions (i.e., involving pons and anterior cerebellum) are typically due to intrinsic basilar artery anterior cerebellum) are typically due to intrinsic basilar artery disease.disease.  ♦    Distal territory infarctions (i.e., involving midbrain, superior   ♦    Distal territory infarctions (i.e., involving midbrain, superior cerebellum and posterior cerebral artery territories) are mostly cerebellum and posterior cerebral artery territories) are mostly embolic from cardiac or vertebral artery sources.embolic from cardiac or vertebral artery sources.

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Dolichoectasia of the basilar Dolichoectasia of the basilar arteryartery

► Basilar artery becomes markedly widened, elongated, Basilar artery becomes markedly widened, elongated, and tortuousand tortuous

► Compression due to mass effect may arise in addition to Compression due to mass effect may arise in addition to ischemic syndromesischemic syndromes Cranial nerve compressive signs are present in over half of Cranial nerve compressive signs are present in over half of

symptomatic cases, most often symptomatic cases, most often hemifacial spasm and trigeminal and trigeminal neuralgianeuralgia

Direct brainstem compression of the ventral pons may produce slowly Direct brainstem compression of the ventral pons may produce slowly progressive ataxia and hemiparesisprogressive ataxia and hemiparesis

Hydrocephalus may arise and produce gait, bladder, and cognitive may arise and produce gait, bladder, and cognitive abnormalities.abnormalities.

Headaches occur in 15%Headaches occur in 15% Almost one half of reported symptomatic cases have coexisting or Almost one half of reported symptomatic cases have coexisting or

isolated ischemic symptoms, affecting pontine, midbrain, cerebellar, isolated ischemic symptoms, affecting pontine, midbrain, cerebellar, thalamic, or occipitotemporal regionsthalamic, or occipitotemporal regions

Subarachnoid hemorrhage occurs infrequently occurs infrequently

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VERTEBROBASILAR DISEASEVERTEBROBASILAR DISEASE

Early signs of vertebrobasilar ischemia can Early signs of vertebrobasilar ischemia can be subtle and possibly be subtle and possibly deceivingdeceiving Fluctuations with remissions and Fluctuations with remissions and relapsesrelapses of symptoms may precede frank of symptoms may precede frank progression and irreversible development of progression and irreversible development of severe deficitssevere deficitsDiagnostic imaging modalities other than Diagnostic imaging modalities other than angiography have limited value in the acute angiography have limited value in the acute setting setting

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The top of the basilar syndrome The top of the basilar syndrome

sudden loss of sudden loss of consciousnessconsciousnesssometimes sometimes preceded by acute preceded by acute vertigovertigoAtaxiaAtaxiadiplopiadiplopia

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Signs suspicious for basilar artery occlusion Signs suspicious for basilar artery occlusion

  Combination of ophthalmoplegia with motor, Combination of ophthalmoplegia with motor, sensory, or coordination deficitssensory, or coordination deficits

Crossed motor or sensory findingsCrossed motor or sensory findings

Acute ataxia with inability to walkAcute ataxia with inability to walk

Sequential appearance of bilateral Babinski Sequential appearance of bilateral Babinski signssigns

Sequential appearance of bilateral weaknessSequential appearance of bilateral weakness

Acute reduction in the level of consciousnessAcute reduction in the level of consciousness

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Vignette 3Vignette 3

A 63-year-old man developed acute onset of slurred A 63-year-old man developed acute onset of slurred speech, gait imbalance, left-sided weakness, and speech, gait imbalance, left-sided weakness, and horizontal diplopia. horizontal diplopia.

On examination, he had mild dysarthria, right On examination, he had mild dysarthria, right abducens palsy, right facial weakness, left arm and abducens palsy, right facial weakness, left arm and leg weakness, and mild axial and right appendicular leg weakness, and mild axial and right appendicular ataxia. ataxia.

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Pontine infarctionPontine infarction

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Pontine InfarctionsPontine Infarctions

Clinical manifestations of pontine infarctions Clinical manifestations of pontine infarctions include oculomotor palsy, contralateral motor include oculomotor palsy, contralateral motor and sensory deficits, and ataxia.and sensory deficits, and ataxia.

Vestibular disorder ipsilateral to the infarction Vestibular disorder ipsilateral to the infarction may also occur. may also occur.

Dysarthria may be extremely disabling.Dysarthria may be extremely disabling.

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Pontine InfarctionsPontine Infarctions

Identification of paramedian Identification of paramedian pontine infarctions should prompt pontine infarctions should prompt evaluation of the basilar artery, evaluation of the basilar artery, because they are often caused by because they are often caused by atherothrombosis of this vessel.atherothrombosis of this vessel.

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Vignette 4Vignette 4

A 75-year-old man was admitted with sudden A 75-year-old man was admitted with sudden onset of dysphagia, dysarthria, and gait onset of dysphagia, dysarthria, and gait imbalance. imbalance. He had long-standing history of hypertension He had long-standing history of hypertension and poorly controlled type 2 diabetes. and poorly controlled type 2 diabetes. On examination, he had left miosis and ptosis, On examination, he had left miosis and ptosis, dysarthria, difficulty swallowing his saliva, left dysarthria, difficulty swallowing his saliva, left ataxia, and decreased sensation to pain and ataxia, and decreased sensation to pain and temperature on the right side. temperature on the right side. He developed uncontrollable hiccups in the He developed uncontrollable hiccups in the emergency department. emergency department. CT scan was not informative.CT scan was not informative.

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Wallenberg's Syndrome Wallenberg's Syndrome

DWI demonstrated a left lateral DWI demonstrated a left lateral medullary infarction with medullary infarction with associated ischemia of the left associated ischemia of the left cerebellum. cerebellum. The PICA was not seen on The PICA was not seen on noninvasive angiogram and noninvasive angiogram and considered to be occluded. considered to be occluded.

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Wallenberg's SyndromeWallenberg's Syndrome

The triad of Horner's syndrome, ipsilateral The triad of Horner's syndrome, ipsilateral ataxia, and contralateral hypolgesia ataxia, and contralateral hypolgesia

The ipsilateral vertebral artery must be The ipsilateral vertebral artery must be investigated because occlusion of this investigated because occlusion of this vessel is often responsible for the infarction. vessel is often responsible for the infarction.

Vertebral atherothrombosis is by far the Vertebral atherothrombosis is by far the most common mechanism.most common mechanism.

Vertebral dissection has been found Vertebral dissection has been found responsible in some cases.responsible in some cases.

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•32 year old male. Transient 32 year old male. Transient tinnitus right ear, then 10 minutes tinnitus right ear, then 10 minutes of right sided weakness. of right sided weakness. Resolved. CT negative. BP Resolved. CT negative. BP 160/90. 160/90.

•TIA ABCD2 score 3TIA ABCD2 score 3

Vignette 5Vignette 5

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32 year old male. Transient tinnitus right ear, then 10 minutes of right sided weakness. Resolved.

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Cervical Artery DissectionsCervical Artery Dissections

Dissections represent one of the most common Dissections represent one of the most common causes of ischemic stroke in the young (under causes of ischemic stroke in the young (under age 45) age 45) 

They should be suspected in trauma patients They should be suspected in trauma patients presenting with focal neurological symptoms or presenting with focal neurological symptoms or Horner's signHorner's sign

Majority are due occur with trivial activityMajority are due occur with trivial activity

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Differential DiagnosisDifferential Diagnosis

►Analysis of clinical features of patients Analysis of clinical features of patients who present with posterior circulation who present with posterior circulation ischemic disease or stroke show ischemic disease or stroke show commonality with:commonality with: unilateral limb weakness (81.9%)unilateral limb weakness (81.9%) central facial palsy (61.1%)central facial palsy (61.1%) dysarthria (46.3%)dysarthria (46.3%) dizziness (33.8%) (Shi 2008). dizziness (33.8%) (Shi 2008).

►The incidence of crossed paralysis was relatively The incidence of crossed paralysis was relatively low (2.8%). low (2.8%).

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Differential DiagnosisDifferential Diagnosis

►Basilar artery disease is most closely Basilar artery disease is most closely mimicked by other illnesses that mimicked by other illnesses that cause acute pontine dysfunctioncause acute pontine dysfunction brainstem encephalitisbrainstem encephalitis demyelinating diseasedemyelinating disease central pontine myelinolysis (osmotic central pontine myelinolysis (osmotic

demyelination syndrome)demyelination syndrome) basilar-type migraine basilar-type migraine

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Management VB ischemiaManagement VB ischemia

►General precepts of acute stroke General precepts of acute stroke treatment fully apply to basilar artery treatment fully apply to basilar artery stroke stroke IV rTPA for patients < 3 hours-4.5 hoursIV rTPA for patients < 3 hours-4.5 hours For patients presenting within 3 hours For patients presenting within 3 hours

who fail to recanalize with intravenous who fail to recanalize with intravenous tPA, rescue endovascular embolectomy tPA, rescue endovascular embolectomy therapy should be consideredtherapy should be considered

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Management of VB ischemiaManagement of VB ischemia

►The common occurrence of a slowly The common occurrence of a slowly progressive or stuttering course progressive or stuttering course suggests that borderline suggests that borderline hypoperfusion is a frequent feature of hypoperfusion is a frequent feature of basilar artery ischemiabasilar artery ischemia

►Regulating intravascular volume and Regulating intravascular volume and blood pressure to maximize blood flow blood pressure to maximize blood flow is an accordingly critical aspect of is an accordingly critical aspect of acute care acute care

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The Basilar Artery International Cooperation The Basilar Artery International Cooperation Study (BASICS)Study (BASICS)

► The largest prospective observational registry available to dateThe largest prospective observational registry available to date► enrolled 592 patients with basilar artery occlusion confirmed by conventional angiography enrolled 592 patients with basilar artery occlusion confirmed by conventional angiography ► 619 patients entered in the registry of 27 patients who were excluded all had fatal outcomes619 patients entered in the registry of 27 patients who were excluded all had fatal outcomes► Exclusion was due to the lack of administration of any type of acute antithrombotic or Exclusion was due to the lack of administration of any type of acute antithrombotic or

thrombolytic therapythrombolytic therapy► Severe deficit was defined as coma, tetraplegia, or locked-in state. Mild to moderate deficit was Severe deficit was defined as coma, tetraplegia, or locked-in state. Mild to moderate deficit was

defined as anything less than coma, tetraplegia, or locked-in-state. Poor outcome, evaluated at defined as anything less than coma, tetraplegia, or locked-in-state. Poor outcome, evaluated at 1 month follow up, was defined as a modified Rankin scale (mRS) score of 4 or higher.1 month follow up, was defined as a modified Rankin scale (mRS) score of 4 or higher.

► Therapeutic interventions were divided into antithrombotic therapies (either aspirin or heparin), Therapeutic interventions were divided into antithrombotic therapies (either aspirin or heparin), primarily immediate intravenous thrombolysis, and immediate intraarterial thrombolysis. primarily immediate intravenous thrombolysis, and immediate intraarterial thrombolysis. Intravenous thrombolysis included patients treated with and without additional intraarterial Intravenous thrombolysis included patients treated with and without additional intraarterial thrombolysis. Intraarterial thrombolysis comprised intraarterial tPA only, mechanical thrombolysis. Intraarterial thrombolysis comprised intraarterial tPA only, mechanical thrombectomy, stenting, or a combination of these approachesthrombectomy, stenting, or a combination of these approaches

► Thirty-one percent received antithrombotic therapy, 30% intravenous tPA only, 14% Thirty-one percent received antithrombotic therapy, 30% intravenous tPA only, 14% intravenous tPA only, 13% intra-arterial tPA and thrombectomy, 5% mechanical thrombectomy intravenous tPA only, 13% intra-arterial tPA and thrombectomy, 5% mechanical thrombectomy only, and 7% received intra-arterial and intravenous r-tPA. only, and 7% received intra-arterial and intravenous r-tPA.

► There was no statistically significant superiority among the different therapeutic interventions.There was no statistically significant superiority among the different therapeutic interventions.►     At one month follow up, one third of patients were dead and one third were dependent on At one month follow up, one third of patients were dead and one third were dependent on

activities of daily living. Severe deficit at initial presentation predicted poor outcome. Patients activities of daily living. Severe deficit at initial presentation predicted poor outcome. Patients with moderate deficits at presentation had worse outcome after intraarterial thrombolysis as with moderate deficits at presentation had worse outcome after intraarterial thrombolysis as compared to intravenous thrombolysis (adjusted RR 1.49, 1.00 to 2.23). Although the BASICS compared to intravenous thrombolysis (adjusted RR 1.49, 1.00 to 2.23). Although the BASICS study does not confirm or reject one specific therapeutic intervention, it questions the alleged study does not confirm or reject one specific therapeutic intervention, it questions the alleged superiority of interventional procedures over other therapies. Randomized control trials superiority of interventional procedures over other therapies. Randomized control trials comparing current guidelines of acute stroke management against intraarterial thrombolysis in comparing current guidelines of acute stroke management against intraarterial thrombolysis in patients with basilar artery occlusion are necessary.patients with basilar artery occlusion are necessary.

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BASICSBASICS► At one month follow up, one third of patients were At one month follow up, one third of patients were

dead and one third were dependent on activities of dead and one third were dependent on activities of daily living. Severe deficit at initial presentation daily living. Severe deficit at initial presentation predicted poor outcome. predicted poor outcome.

► Patients with moderate deficits at presentation had Patients with moderate deficits at presentation had worse outcome after intraarterial thrombolysis as worse outcome after intraarterial thrombolysis as compared to intravenous thrombolysis (adjusted RR compared to intravenous thrombolysis (adjusted RR 1.49, 1.00 to 2.23).1.49, 1.00 to 2.23).

► BASICS study does not confirm or reject one specific BASICS study does not confirm or reject one specific therapeutic intervention therapeutic intervention

► Randomized control trials comparing current Randomized control trials comparing current guidelines of acute stroke management against in guidelines of acute stroke management against in patients with basilar artery occlusion are necessarypatients with basilar artery occlusion are necessary

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Key points Key points

►A posterior circulation infarct may be A posterior circulation infarct may be preceded by a transient ischemic preceded by a transient ischemic attack in one fourth of patients attack in one fourth of patients

►Same precepts of acute stroke Same precepts of acute stroke treatment fully apply to vertobro-treatment fully apply to vertobro-basilar artery stroke basilar artery stroke

►Clinical suspicion is important to Clinical suspicion is important to identify these patientsidentify these patients

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Questions?Questions?