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 Understand the pertinent history, clinical evaluation, and management.

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Clinical manifestations

► Posterior circulation infarcts comprise approximately 20% to 25% of all ischemic strokes (Kumral et al 2004) ► Vertebrobasilar ischemic stroke homogenous entity  is not a Duration of transient ischemic attacks varies considerably   Symptoms vary from mild to extreme Frequency may vary from a solitary attack to many per day

Symptoms of vertebrobasilar transient ischemic attacks are complex!

► ► Unilateral or bilateral motor or sensory symptoms involving the face or limbs and unilateral or bilateral visual field defects  Vertigo    Diplopia Dysarthria, dyphagia loss of balance isolated sensory symptoms  may be considered as transient ischemic attacks when occurring in combined fashion (simultaneously or successively) (Albucher et al 2005)

Clinical manifestations

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

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Etiology

► In situ atherosclerosis and cardioembolism are the most common causes of basilar artery strokes ► Less frequent etiologies include cervicocephalic arterial dissection, migraine , dolichoectasia , vasculitis , and paradoxical embolism .

Clinical profiles may be distinguished

Vignette 1

A 68-year-old woman with a history of atrial fibrillation on chronic anticoagulation presented to the hospital with acute behavioral changes, visual disturbances, and right hemiparesis. On examination, she was somnolent, had poor short term recollection, dense right hemianopia, mild right hemiparesis, and profound right hypoesthesia. 5

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POSTERIOR CEREBRAL ARTERY OCCLUSION MRI of her brain showed a large left PCA infarction and MRA disclosed proximal occlusion of this vessel. Despite some functional recovery over the following 6 months, her visual and cognitive disturbances remained disabling 7

POSTERIOR CEREBRAL ARTERY OCCLUSION The PCAs supply the midbrain, thalami, lateral geniculate bodies, posterior portion of the choroid plexus, occipital lobes, inferior and medial aspects of the temporal lobes, and posterior-inferior areas of the parietal lobes. 8

Proximal occlusion of a PCA may produce:

 decreased level of consciousness  profound disturbances of visual perception  antegrade amnesia  ophthalmoparesis (from damage to the upper midbrain)  hemiplegia (typically from peduncular ischemia)  hemihypoesthesia  hemianopia. 9

Patients with left PCA infarctions may experience incapacitating neurocognitive disorders:

     Alexia without agraphia (corpus callosum) alexia with agraphia (corpus callosusm + angular gyrus). Anomic aphasia may be produced by left temporo occipital strokes. Severe memory impairment can be caused by ischemia of the mesial temporal structures or the thalamus. Left PCA stroke may be responsible for single stroke dementia.

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POSTERIOR CEREBRAL ARTERY OCCLUSION Midbrain ischemia may express with ipsilateral or bilateral ophthalmoparesis (III nerve palsy, abnormal vertical eye movements). Embolism from a cardiac or an arterial (aortic arch, vertebral artery origin) source is the most common mechanism of PCA stroke. 11

Vignette 2

A 64-year-old woman was found unresponsive in her bathroom by her husband. She was intubated by EMS and transported to our emergency department.

On arrival, she was comatose and breathing at a rate of 40 to 45 per minute. She was tachycardic and hypertensive. Her pupils were slightly anisocoric (3.5 mm on the left and 3 mm on the right), and responses to light were minimal on the left and absent on the right. Corneal and oculocephalic reflexes were preserved. Best motor responses to pain were in the form of withdrawal. 12

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

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

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VERTEBROBASILAR DISEASE Occlusion of the basilar artery represents the most dreaded form of ischemic stroke. At its worst, it causes massive fatal infarction involving the brainstem, cerebellum, the occipital and posterior temporal lobes, and the thalami.

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

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VERTEBROBASILAR DISEASE Infarctions at different levels are caused by different mechanisms:  ♦ Proximal territory infarctions (i.e., involving the medulla and lower cerebellum) are caused by embolism from the heart or atherosclerosis of the extracranial vertebral arteries or by hypoperfusion related to severe intracranial vertebral occlusive lesions.

♦ Middle territory infarctions (i.e., involving pons and anterior cerebellum) are typically due to intrinsic basilar artery disease.

♦ Distal territory infarctions (i.e., involving midbrain, superior cerebellum and posterior cerebral artery territories) are mostly embolic from cardiac or vertebral artery sources.

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Dolichoectasia of the basilar artery

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Basilar artery becomes markedly widened, elongated, and tortuous

Compression due to mass effect may arise in addition to ischemic syndromes  Cranial nerve compressive signs are present in over half of symptomatic cases, most often

hemifacial spasm

and trigeminal neuralgia      Direct brainstem compression of the ventral pons may produce slowly progressive ataxia and hemiparesis

Hydrocephalus

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

Headaches occur in 15% Almost one half of reported symptomatic cases have coexisting or isolated ischemic symptoms, affecting pontine, midbrain, cerebellar, thalamic, or occipitotemporal regions

Subarachnoid hemorrhage

occurs infrequently

VERTEBROBASILAR DISEASE Early signs of vertebrobasilar ischemia can be subtle and possibly

deceiving Fluctuations with remissions and relapses

of symptoms may precede frank progression and irreversible development of severe deficits Diagnostic imaging modalities other than angiography have limited value in the acute setting 18

The top of the basilar syndrome

sudden loss of consciousness sometimes preceded by acute vertigo Ataxia diplopia

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Signs suspicious for basilar artery occlusion Combination of ophthalmoplegia with motor, sensory, or coordination deficits Crossed motor or sensory findings Acute ataxia with inability to walk Sequential appearance of bilateral Babinski signs Sequential appearance of bilateral weakness Acute reduction in the level of consciousness 20

Vignette 3

A 63-year-old man developed acute onset of slurred speech, gait imbalance, left-sided weakness, and horizontal diplopia. On examination, he had mild dysarthria, right abducens palsy, right facial weakness, left arm and leg weakness, and mild axial and right appendicular ataxia. 21

Pontine infarction

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Pontine Infarctions

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

Vestibular disorder ipsilateral to the infarction may also occur. Dysarthria may be extremely disabling.

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

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Vignette 4

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

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Wallenberg's Syndrome

DWI demonstrated a left lateral medullary infarction with associated ischemia of the left cerebellum. The PICA was not seen on noninvasive angiogram and considered to be occluded. 27

Wallenberg's Syndrome

The triad of Horner's syndrome, ipsilateral ataxia, and contralateral hypolgesia The ipsilateral vertebral artery must be investigated because occlusion of this vessel is often responsible for the infarction. Vertebral atherothrombosis is by far the most common mechanism.

Vertebral dissection has been found responsible in some cases.

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Vignette 5

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

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TIA ABCD2 score 3

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

Cervical Artery Dissections Dissections represent one of the most common causes of ischemic stroke in the young (under age 45) They should be suspected in trauma patients presenting with focal neurological symptoms or Horner's sign Majority are due occur with trivial activity 29

Differential Diagnosis

► Analysis of clinical features of patients who present with posterior circulation ischemic disease or stroke show commonality with:  unilateral limb weakness (81.9%)    central facial palsy (61.1%) dysarthria (46.3%) dizziness (33.8%) (Shi 2008) . ► The incidence of crossed paralysis was relatively low (2.8%).

Differential Diagnosis

► Basilar artery disease is most closely mimicked by other illnesses that cause acute pontine dysfunction  brainstem encephalitis    demyelinating disease central pontine myelinolysis demyelination syndrome) basilar-type migraine (osmotic

Management VB ischemia

► General precepts of acute stroke treatment fully apply to basilar artery stroke  IV rTPA for patients < 3 hours-4.5 hours  For patients presenting within 3 hours who fail to recanalize with intravenous considered tPA , rescue endovascular embolectomy therapy should be

Management of VB ischemia

► The common occurrence of a slowly progressive or stuttering course suggests that borderline hypoperfusion is a frequent feature of basilar artery ischemia ► Regulating intravascular volume and blood pressure to maximize blood flow is an accordingly critical aspect of acute care

The Basilar Artery International Cooperation Study (BASICS) ► ► ► ► ► ► ► ► ► The largest prospective observational registry available to date 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 outcomes Exclusion was due to the lack of administration of any type of acute antithrombotic or thrombolytic therapy 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 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), primarily immediate intravenous thrombolysis, and immediate intraarterial thrombolysis. Intravenous thrombolysis included patients treated with and without additional intraarterial thrombolysis. Intraarterial thrombolysis comprised intraarterial tPA only, mechanical thrombectomy, stenting, or a combination of these approaches Thirty-one percent received antithrombotic therapy, 30% intravenous tPA only, 14% intravenous tPA only, 13% intra-arterial tPA and thrombectomy, 5% mechanical thrombectomy only, and 7% received intra arterial and intravenous r-tPA. 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 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 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 superiority of interventional procedures over other therapies. Randomized control trials comparing current guidelines of acute stroke management against intraarterial thrombolysis in patients with basilar artery occlusion are necessary.

BASICS

► ► ► ► 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 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).

BASICS study does not confirm or reject one specific therapeutic intervention Randomized control trials comparing current guidelines of acute stroke management against in patients with basilar artery occlusion are necessary

Key points

► A posterior circulation infarct may be preceded by a transient ischemic attack in one fourth of patients ► Same precepts of acute stroke treatment fully apply to vertobro-basilar artery stroke ► Clinical suspicion is important to identify these patients

Questions?