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

2. Understand the pertinent history, clinical evaluation, and management.
Objectives
Recognize the most relevant clinical findings consistent with posterior circulation ischemic stroke syndromes
Understand the pertinent history, clinical evaluation, and management. 3

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

4. 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)
may be considered as transient ischemic attacks when occurring in combined fashion (simultaneously or successively) or with symptoms of probable vertebrobasilar transient ischemic attacks

5. 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

6. 4

7. 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.

8. Clinical profiles may be distinguished
Occlusion of the distal basilar artery is frequently embolic in origin, and produces signs of midbrain and thalamic ischemia, signs of occipital and temporal lobe ischemia, or both

9. 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

10. 6

11. 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

12. 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

13. 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

14. 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. 10

15. 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

16. 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

17. Conventional angiography confirmed occlusion of the basilar trunk.
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. 13

18. Despite reperfusion, the patient failed to improve neurologically.
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. 14

19. 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. 15

20. 16

21. 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. 17

22. Dolichoectasia of the basilar artery
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
Eventhought majority of cases are asymptomatic and this is usually a radiological of autopsy finding

24. 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
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 a maximal deficit may occur. Outcomes in some series suggest that about half of patients have severe or moderate residual deficits, an occasional patient has a fatal outcome, and the remainder show no or only mild impairment. 18

25. The top of the basilar syndrome
sudden loss of consciousness
sometimes preceded by acute vertigo
Ataxia
diplopia 19

26. 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

27. 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

28. Pontine infarction 22

29. 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. 23

30. Pontine Infarctions
Identification of paramedian pontine infarctions should prompt evaluation of the basilar artery, because they are often caused by atherothrombosis of this vessel. 24

31. 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. 26

32. 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

33. 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. 28

34. Vignette 5
32 year old male. Transient tinnitus right ear, then 10 minutes of right sided weakness. Resolved. CT negative. BP 160/90.
TIA ABCD2 score 3

35. 32 year old male. Transient tinnitus right ear, then 10 minutes of right sided weakness. Resolved.

36. 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

37. 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%).

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

39. 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 tPA, rescue endovascular embolectomy therapy should be considered

40. 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

41. 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.

42. 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

43. 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

44. Questions?