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Ischemic Posterior Circulation Stroke Christopher Lewandowski, M. D

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1 Ischemic Posterior Circulation Stroke Christopher Lewandowski, M. D
Ischemic Posterior Circulation Stroke Christopher Lewandowski, M.D. Residency Program Director Department of Emergency Medicine Henry Ford Hospital, Detroit, MI Sunitha Santhakumar, M.D. Department of Emergency Medicine Henry Ford Hospital, Detroit, MI 54 1 54

2 Case Study HPI: The patient is 41 y.o. male, with a past history of alcohol abuse, hypertension who presents to the ED with a chief complaint of right -sided weakness, slurred speech, and loss of balance. The symptoms began 90 minutes prior to arrival.

3 Case Study PMHx: Medications Social Hx
Alcohol Abuse, quit for 3 years Hypertension Seizures, Generalized, none for past 7 years Medications Dyazide Social Hx Smoking- 2 pack per day ROS: Mild dizzy spells for the past 2 weeks, each lasting 5-10 minutes

4 Case Study Physical Exam: BP- 149/79, P-100, RR-18, T-36.9
A&Ox3 on presentation, later became stuporous CN: dysarthria, pupils: R 3.5/ L 3.0 reactive L facial droop, gaze palsy to the L Motor: R arm and R leg weakness (3/5) Sensory: Decreased to light touch and pinprick on R Coordination: dysmetria on R (not out of proportion to weakness) NIH Stroke Scale score = 14

5 What does this patient have?
Differential Diagnosis Stroke Intracerebral Hemorrhage Tumor VBI Migraine Seizure

6 Epidemiology Stroke - leading cause of adult disability in the USA
20% of strokes involve the vertebrobasilar arteries 20% of global cerebral blood flow is vertebrobasilar Vertebrobasilar ischemia ranges from intermittent vascular insufficiency (VBI) to total basilar artery occlusion (BAO) 20% - 60% with unfavorable outcome Overall mortality 4%, BAO - 90% mortality

7 Risk Factors: Uncontrollable
Age Stroke risk doubles for every decade over 55 Gender, Males x Males have a higher risk, but females live longer, therefore there are more female stroke survivors Heredity African Americans - 2x Family History Previous stroke or TIA - 10x Diabetes - 3x (even if well controlled)

8 Risk Factors: Controllable
Hypertension - 6x (consistently >140/90) Atrial Fibrillation - 6x Smoking - 2x Hypercholesterolemia > 200 Heart Disease - 2x Alcohol, (> 4oz/day) Obesity BMI > 30 35 inch waist in women, 40 inches in men

9 Risk Factors Vertebrobasilar Ischemia
Risk factors for the Posterior circulation are the same as for the anterior circulation Hypertension, diabetes mellitus, hyperlipidemia, and tobacco are especially important for the posterior circulation

10 Posterior Circulation Stroke: Anatomy

11 Posterior Circulation Stroke: Anatomy

12 Pathology Atherosclerosis In situ thrombosis Often complete occlusion
90% mortality Embolization (20%-50%) Heart or proximal vessels May cause VBI Good prognosis Subclavian steal syndrome Symptoms brought on by arm exercise Trauma Especially in the young Vertebral artery dissection Lacunar (small vessel disease)

13 Emergency Department Presentation
Prodrome very common 60 % of patients with Basilar artery thrombosis Stuttering or progressive onset of symptoms 2 weeks prior to ED presentation

14 Emergency Department Presentation
Prodromal Symptoms (in order of frequency) Vertigo and Nausea (30%) Headache, Neckache (20%) Hemiparesis (10%) Dysarthria, Diplopia (10%) Hemianopia ( 6%) Ferbert, Stroke 1990

15 Emergency Department Presentation
Clinical Findings: Depends on the syndrome Range: asymptomatic to comatose The 5 Ds: Dizziness, Diplopia, Dysarthria, Dysphagia, Dystaxia Hallmarks: Crossed findings Cranial nerve deficits - Ipsilateral Motor / Sensory deficits - Contralateral

16 Vertigo Hallucination of movement of the patient or the environment, not associated with loss of consciousness Visual, proprioceptive, and vestibular systems maintain position (Romberg test) Semicircular canals connect to the vestibular nuclei in the brainstem via CN VIII Vestibular nuclei connect to the cerebellum, MLF (eye movement) and the vestibulospinal tract

17 Nystagmus Nystagmus means “nodding” off (as in sleeping during this lecture, slow sleep phase with rapid correction) Nystagmus is named for its fast component Medial longitudinal fasciculus coordinates the ipsilateral medial rectus (CN III) and the contralateral lateral rectus (CN VI) Inner ear provides symmetric resting discharge

18 Nystagmus Loss of input from one side leaves the other side unopposed
Unopposed stimulation causes a slow drift toward the diseased side Cerebral cortex corrects for slow drift with a very rapid return toward a more normal position The brainstem can compensate for asymmetric peripheral inputs leading to latency, fatigue, and habituation

19 Vertebrobasilar Ischemia: Syndromes
VBI Common term for TIAs of the vertebrobasilar system Patients often asymptomatic in ED Frequent episodes, especially as prodromal sx Requires evaluation of etiology Very rare to present as vertigo alone Difficult to distinguish from other causes of dizziness

20 Was this Patient’s Dizziness Central or Peripheral
Central Peripheral Intensity Mild Severe Tinnitis Rare Common CN findings Frequent None Nystagmus: Visual fixation No inhibition Inhibits Horizontorotary Rare Common Latency None sec Fatigue None yes

21 Posterior Circulation Stroke: Syndromes
VBI, brainstem TIAs: Occur over days-weeks Intermittent fluctuating brainstem sx Dizziness plus cranial nerve symptoms Rarely dizziness alone

22 Vertebrobasilar Ischemia: Syndromes
Branch artery occlusions Produce a specific stroke syndrome for each artery Longer and circumfrential arteries Small penetrating branches supplying midline structures and causing lacunar syndromes Characterized by the 5Ds and crossed findings The severity of the stroke depends on the collateral blood flow and the location of the occlusion

23 Posterior Circulation Stroke: Syndromes

24 Vertebrobasilar Ischemia: Syndromes
Basilar artery occlusion 75% with prodromal symptoms 63% with gradual and progressive onset Can produce a locked-in syndrome Awake, quadriplegia, bilateral facial and oropharyngeal palsy, preserved vertical gaze May present comatose if reticular activating system is involved

25 Emergency Department Diagnosis
History Prodrome Dizziness Physical Exam, Blood pressure in both arms Diagnostic Studies Blood tests,CXR, EKG Imaging

26 Emergency Department Diagnosis
Confirm the Diagnosis (Emergent) CT Scan MRI, MRA, DWI TCD Angiography (DSA) Evaluation of Stroke Etiology (Inpatient) MRA / Angiography Echo / TEE TCD Carotid Doppler

27 Emergency Department Evaluation
CT scan - head, noncontrast Necessary to rule out intracerebral hemorrhage Most sensitive test for ICH Poor for posterior fossa visualization Bone artifact Can pick up Basilar artery thrombosis Highly specific sign, very low sensitivity CT Angiography (spiral CT) Reliably assesses basilar artery patency, inconclusive in patients with advanced arterial calcification

28 Case Study: CT Scan

29 Baseline CT scan

30 Emergency Department Evaluation
MRI - long scan times, unavailable, access to patient is poor Standard MRI, not reliable for ICH in first hours Major advantage is Posterior Fossa imaging MR Angiography -reliable evaluation of arteries for VBI, BAO DWI - Diffusion weighted imaging demonstrates infarcted tissue, this is not a contraindication to thrombolysis

31 MRI-DWI in the posterior fossa

32 Emergency Department Evaluation
TCD Assesses flow through Vertebrobasilar system Limited in BAO Patient anatomy, penetration to distal BA difficult Brandt: TCD diagnostic in 7 of 19 patients with suspected BAO, 2 of 19 false negatives Low sensitivity for BAO, not useful in ED

33 Emergency Department Evaluation
Digital subtraction angiography Gold Standard for diagnosis of BAO Time consuming, expensive, invasive Requires patient cooperation, anesthesia Allows for intra-arterial intervention Thrombolysis, angioplasty

34 Emergency Department Management
Stabilization Ensure oxygenation and ventilation Optimize cerebral blood flow by managing the blood pressure and hydration carefully, as autoregulation lost, ischemic areas become perfusion dependant Avoid glucose, avoid hypotension, treat fevers aggressively Evaluate for anticoagulation or thrombolysis

35 Emergency Department Management
Conservative Treatment Antiplatelet and Antithrombotic Thrombolytic Treatment Intravenous: within 3 hours symptom onset and the patient meets all treatment criteria Intra-Arterial Therapy: infusion of thrombolytic agent into vessel or clot within 24 hours of onset of symptoms

36 Posterior Circulation Stroke: Treatment
Conservative Treatment Antiplatelet and Anti thrombotic Therapy Uncontrolled, Retrospective Studies , 1950s & 1960s Compared to historical controls, patients treated with heparin had lower mortality (8-15% vs %) Stopped progression of VBI to infarction TOAST Trial No evidence to support heparinization in acute stroke

37 Posterior Circulation Stroke: Treatment
Intravenous Thrombolysis NINDS rt-PA Acute Stroke Trial t-PA approved within 3 hours of symptom onset Few posterior circulation strokes

38 Posterior Circulation Stroke: Treatment
Intra-arterial Thrombolysis No randomized controlled trials completed Multiple small series and reports Results (Over 200 patients treated) Mortality % , assoc. with lack of recanalization Favorable outcomes in 25%-60% ICH rate low, 0-15%

39 Posterior Circulation Stroke Future Treatment
Intra-arterial Thrombolysis Superselective approach, micro-catheters Angioplasty Angio-jet

40 What is the prognosis for this patient ?
All Posterior Circulation Strokes New England Medical Center Posterior Circulation Stroke Registry: Mortality = 4% Minor or no Disability = 79% Locked In Syndrome (Basilar artery occlusion) Mortality > 90% How do you know if a patient will progress to locked-in syndrome ? Observation

41 Case Study: Outcome The patient mental status deteriorated, repeat NIH-SS score was 22 He received intravenous thrombolysis He had significant early improvement but without complete resolution of symptoms On day 4, the NIH - SS score was 10 MRA : L sup. cerebellar art. and R&L Ant-Inf cerebellar arteries were non-visualized, Cardiac evaluation was negative He was discharged on Coumadin to Rehab

42 Case Study: MRI - DWI <12 Hours 4 Days

43 Summary Posterior Circulation Strokes are characterized by the 5D’s and crossed findings Maintain a high index of suspicion for prodromal symptoms - vertigo with CN sx The locked-in syndrome consists of quadriplegia, bilateral facial and oropharyngeal palsy; but preservation of cortical function and vertical gaze

44 Summary The prognosis for vertebrobasilar ischemia is generally good, except for locked-in syndrome (basilar artery occlusion) Treatment consists of conservative therapy (aspirin and heparin) or IV thrombolysis (<3 hrs) or IA thrombolysis (up to 24 hours)

45 Question 1 All of the following are posterior circulation syndromes except: Ipsilateral CN III palsy with contralateral hemiplegia B) Ipsolateral facial palsy with contralateral C) Hemiaplegia and hemisensory loss of the face arm and leg on one side of the body D) Ipsilateral ataxia and Horner”s with contralateral loss of pain and temperature sensation

46 Question 2 Locked-in Syndrome consists of: A) Coma with quadriplegia
B) Bilateral upper extremity weakness greater than lower extremity weakness C) Quadriplegia, bilateral facial and oropharyngeal palsy but preservation of cortical function and vertical gaze D) cranial nerve findings contralateral to motor and sensory findings

47 Question 3 Vertigo of central origin is:
A)Generally severe and sudden in onset B) Is a very common isolated prodromal symptom of VBI C) Is often associated with tinnitus D) Fatigues easily E)Is generally associated with cranial nerve findings

48 Question 4 Proven therapy for posterior circulation stroke includes:
A) Heparin B) Low molecular weight heparin C) IV thrombolysis D) Intra-arterial regional thrombolysis E) Intra-arterial local thrombolysis

49 Question 5 Overall mortality for posterior circulation strokes is:
B) 20% C) 40% D) 70% E) > 90%

50 Question 6 Mortality for Locked-in Syndrome is: A) < 5% B) 20%

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