Cerebrovascular Disease

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Cerebrovascular Disease

• J. B. Handler, M.D.
• University of New England
• Physician Assistant Program

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Abbreviations

• BP- blood pressure
• MI- myocardial infarction
• VHD- valvular heart disease
• Sx- symptoms
• CV- cardiovascular
• CBC- complete blood count
• Plts- platelets
• PT- prothrombin time
• INR- international normalized ratio
• PTT- partial thromboplastin time
• ECG-electrocardiogram
• CxR- chest x-ray
• PAD- peripheral arterial disease

• MRI-magnetic resonance imaging
• MRA-magnetic resonance arteriography
• CHD- coronary heart disease
• Afib-atrial fibrillation
• DM- diabetes mellitus
• t-PA- tissue specific plasminogen activator
• AVM-arteriovenous malformation
• Dx- diagnosis
• Rx-treatment
• S/S-signs and symptoms
• ESR- erythrocyte sedimentation rate
• LVH- left ventricular hypertrophy

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Objectives

• Define the stroke syndromes comparing
  ischemia/infarct to hemorrhage
• Understand the risk factors for strokes and
  prevention
• Understand the pathology involved in the most
  common stroke syndromes
• Recognize common presentations
• Understand appropriate diagnostic testing
• Understand treatment options and planning for
  short and long term care

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Case

• A 61 y/o man presents to the ED after developing
  sudden onset of weakness/numbness of the right
  arm accompanied by difficulty with speech.
  Symptoms started 30 minutes ago and have resolved
  by the time he reaches the ED.
• Neuro exam normal
• What is the diagnosis?

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• Stroke
• Cerebrovascular accident
• Transient ischemic attack
• Lacunar infarct
• Intracerebral hemorrhage

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Definitions-I

• Stroke (Brain Attack) The sudden or rapid
  onset of a neurologic deficit in the distribution
  of a vascular territory lasting gt 24 hours.
• TIA The sudden or rapid onset of a neurologic
  deficit in the distribution of a vascular
  territory lasting lt 24 hours. Most last lt 30
  minutes. Reversible ischemic insult to brain
  cells that recover but ?s risk of subsequent
  stroke. ?frequency of TIAs a bad sign.
• Brain ischemia vs infarction.

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Definitions II

• Stroke-in-evolution (progressive stroke)
  worsening signs or symptoms over time.
• Ischemia/Infarct (85) vs hemorrhage (15) as
  stroke etiologies.
• CVA Cerebrovascular accident- outdated term Do
  not use.

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Epidemiology

• 3rd leading cause of death in the U.S.
• gt200,000 deaths per year
• Perception of elderly
• Incidence has declined due to prevention. Why?
• Men 1.3x gt women (MI men 3x gt women).
• Blacks 1.3x gt whites.
• Most common cause of death in patients with
  cerebrovascular disease is myocardial infarction.

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Risk Factors

• Hypertension most powerful risk factor,
  especially systolic BP (goallt140/90 for most)
• Smoking 2-4x increase risk
• Atherosclerosis elsewhere (CHD, PAD)
• Diabetes Mellitus 3x increase risk for stroke
• Atrial fibrillation Cardiac Emboli
• Others male gender, oral contraceptives, ETOH in
  excess, hyperlipidemia.

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Etiology Pathogenesis

• Atherosclerosis Large vessels often involved
  Involved in 50 of all ischemic strokes
  (infarcts)Thrombus-in-situ vs artery to artery
  embolus Base of aorta, carotid
  bifurcation, origin of internal carotid,
  external carotid, vertebral/basilar arteries
• Pathological outcomes depend on
• Adequacy of collateral circulation
• Development of Circle of Willis
• Duration of insult/restoration of blood flow.

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Carotid Disease
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Stable Stenosis vs Unstable Placque
Unstable Placque
Stable Stenosis
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Etiology Pathogenesis

• Lacunar infarcts (aka lipohyalinosis) Small
  vessel disease- deep penetrating arterioles
  thrombose.
• ? 20 of ischemic strokes.
• Major risk factor HTN
• lipids, DM contribute.
• Very small strokes. Defect lt1.5 cm (most are
  lt5mm) on CT or MRI.
• May be without symptoms- detected by CT scan as
  incidental finding.

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Cerebral Emboli

• Embolism from heart or artery to brain.
• Important role in pathology of strokes and TIAs
• Blood clot breaks off, occludes more
  distant/distal vessel.
• Cardiac emboli often lodge in medium sized
  vessels (MCA, ACA, etc.).
• Artery to artery emboli also occur. Often cause
  TIAs (lodge, then break up) or small neuro
  deficits.
• Frequent source Carotid bifurcation or internal
  carotid
• Often small emboli Platelets/fibrin/RBCs

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Cardioembolism

• Etiology of ? 20 of ischemic strokes
• Atrial Fibrillation-very common, both idiopathic
  or combined with other cardiac pathology.
  Importance of prevention with anticoagulation.
• MI with mural thrombus 35 incidence post large
  anterior wall MI. 40 will embolize if left
  untreated.
• Dilated cardiomyopathy
• VHD- rheumatic and otherwise less common
  compared to other etiologies.

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Other Etiologies Interest Only

• Vasculitis, Temporal Arteritis, others
• Hematologic abnormalities- Sickle cell disease,
  hyperviscosity syndromes
• Drug abuse cocaine, amphetamines, others
• Sympathomimetic agents- ephedrine,
  phenylpropanolamine, etc.

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Stroke Signs and Symptoms

• Abrupt onset of non-convulsive focal defect in a
  vascular territory.
• 80-90 no warning symptoms.
• 10-20 have warning (TIA).
• Variable course stabilize, improve or worsen.
  Essential to make dx early.

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Brain Circulation
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Stroke Syndromes

• Middle cerebral artery (MCA)
• Contralateral hemiparesis or hemisensory loss
• Hemianopsia- visual field defect
• If dominant hemisphere- Aphasia
• If non-dominant- Speech and comprehension
  preserved may develop anosognosia
  (denial/neglect of deficit) or a confusional
  state.

Ref http//www.ebrsr.com/modules/module2.pdf
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Stroke Syndromes

• Anterior cerebral artery (ACA) - less common- Sx
  more pronounced in leg, associated language, gait
  disturbance.
• Posterior circulation (least common)
• Vertebral artery (Branch of subclavian artery)
• Crossed contralateral dysfunction (motor/sensory)
  plus ipsilateral bulbar/cerebellar signs
  vertigo, dizziness, gait disturbance, diplopia,
  facial palsy, dysarthria, etc.

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Stroke Syndromes

• Lacunar strokes/infarcts
• Hypertension
• Deep penetrating arterioles
• Small infarcts up to 1.5cm on CT/MRI
• Clinical syndrome depending on where infarct is
  may also present as TIA. Examples contralateral
  motor/sensory deficit (infarct of anterior limb
  of internal capsule). Prognosis usually good.
• Amaurosis fugax (carotid disease present)
• Transient monocular blindness
• Embolism to ophthalmic artery (off of carotid)

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Evaluation

• History Precise onset of Sx, neuro deficit.
• Physical exam detailed neuro, CV exam.
• Blood pressure- often elevated- caution.
• Lab- CBC, Plts, Glucose, INR, PTT, Lipids, ESR,
  Creatinine/BUN.
• ECG- atrial fib/other arrhythmias, MI or LVH?
• CxR- cardiomegaly or aortic calcification?

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CT Scan

• R/O hemorrhage
• Better than MRI in 1st 48 hrs after intracranial
  hemorrhage.
• Detection of infarcts limited to size and timing-
  only 5 visible in 1st 12 hrs, gt90 visible at
  one week.
• More readily available than MRI and less
  expensive. Does not require contrast.

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CT Ischemic Stroke
Cecil
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MRI/MRA

• Magnetic resonance imaging/angiogram.
• Changes of infarct may be seen as early as one
  hour- usually not available or needed emergently.
  
• Provides better detail than CT for small lesions
  and other pathology.
• Better for imaging posterior fossa.
• MRA- Non invasive with excellent resolution of
  large vessels replaces need for arteriogram in
  some patients may be difficult to differentiate
  complete vs near complete occlusions.

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MRI Stroke
Cecil
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Ultrasound

• Carotid Doppler Ultrasound (Duplex)- Screening
  tool for evaluating common carotid and origin of
  internal carotid artery.
• Combines B mode with doppler ultrasound
• May be difficult to differentiate complete vs
  near complete occlusions.
• Non-invasive but limited capability.

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Carotid Ultrasound
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Arteriography

• Most accurate- invasive- gold standard for
  extra and intracranial disease.
• Complications contrast reaction, kidney failure,
  placque rupture, stroke.
• Use of non-ionic contrast has reduced
  complication rate.

Images.google.com
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Prevention

• CHD (and stroke) prevention
• Risk factor modification aggressive control of
  blood pressure, lipids, diabetes smoking
  cessation, exercise, diet, etc.
• Atrial Fibrillation and embolization
• Full anticoagulation for most patients
• Warfarin (Coumadin) therapy long term

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TIAs

• Abrubt onset of symptoms with transient focal
  neuro deficit dependent on involved anatomy
  (anterior, posterior circulation). Sx may vary
  during episodes. Exam between episodes is normal.
  Warning for subsequent stroke.
• Etiology likely
• Embolic from carotid stenosis/placque or
• Embolic from cardiac source
• Severe carotid stenosis with transient
  hypotension
• Small vessel occlusion Lacunar infarcts may mimic

Important to listen with stethoscope for bruit
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Carotid TIA/Incomplete Stroke Surgical Rx

• Carotid Endarterectomy Remove plaque
• Best results if symptomatic blockage and gt70
  stenosis. Significantly reduces risk of
  subsequent ipsilateral stroke.
• Selected patients with symptoms and 50-70
  stenosis
• Risks Stroke and complications of surgery
• Carotid angioplasty/stenting a promising
  alternative, but long term data is lacking
  option in poor surgical candidates.

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Carotid TIAs-Medical Rx

• Patients Poor operative risk, lt70 stenosis or
  asymptomatic carotid disease.
• Risk factor modification HTN, smoking, lipids,
  DM.
• Aggressive BP control.

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Carotid TIAs-Medical Rx

• Anti-platelet agents indicated for all patients
  with lt 70 stenosis and TIA symptoms, diffuse
  cerebrovascular disease, patients who are poor
  operative candidates, and patients with
  asymptomatic carotid disease. These agents
  prevent platelet aggregation and release of
  vasoactive substances like thromboxane A2.

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Aspirin

• Inhibits cyclooxygenase.
• Inhibits synthesis of thromboxane A2, decreasing
  both platelet aggregation and vasoconstriction.
• Permanent, life of platelet (about 8 days).
• 325 mg/daily GI side effects and bleeding.
• Decreases frequency of TIAs and risk of
  subsequent stroke. Also applies to patient with
  prior stroke- ?incidence of recurrence.

ASA 25 mg dipyridamole ER 200mg- orally 2x/D-
alternative to ASA alone with likely improved
protection at a cost
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Clopidogrel (Plavix)

• 75mg/day
• Inhibits platelet aggregation and prevents
  activation of glycoprotein IIb/IIIa (a fibrinogen
  binder).
• Decreases atherosclerotic events
• Slightly better outcomes compared to ASA alone
  but expensive- alternative to ASA in patients
  with recurrent TIAs or ASA intolerance/allergy.
• Diarrhea, rash

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Lacunar Infarcts Treatment

• Small lesion infarct in distribution of
  penetrating arterioles. Small infarcts with
  discreet symptoms (TIA or stroke) related to
  distribution may be incidental finding in
  asymptomatic patient.
• Usually good prognosis for recovery over 4-6
  weeks.
• Treatment supportive measures plus ASA or
  Clopidogrel. Aggressive long term Rx of BP and
  lipids.

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Stroke Treatment

• Hospitalize all stroke patients most TIA (1st
  episode) patients.
• HTN-Avoid rapid BP reduction-decreases perfusion-
  brain will auto regulate perfusion.
• BP often elevated during strokes- leave as is
  unless BP markedly elevated (gt200/100) wait 2
  wks for oral meds if possible.
• Supportive (IV fluids, etc.)
• Consider thrombolytic therapy- see below
• When to anticoagulate?

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Cerebral Infarct

• Thrombotic or embolic occlusion of major vessel.
  Treatment dependent on timing.
• 1st Obtain head CT to r/o hemorrhage.
• If onset of symptoms lt3 hours, thrombolytic
  therapy with t-PA (bolus/infusion up to 90 mgs)
  over 1 hr.
• No benefit for thrombolytics after 3 hours from
  onset of symptoms.

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Thrombolytic Therapy

• Thrombolytic therapy requires team approach- best
  done in large treatment centers.
• Neurologic outcome improved at 3 mos and 1 yr
  with decrease in expected deficit and reduction
  of initial deficit.
• Increases the chances of a favorable outcome by
  50.

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Thrombolytic Therapy

• Ideal scenario is large referral hospital with
  consultants available.
• ? Management in small community hospitals.
• Risks of t-PA Cerebral hemorrhage- 6 to 7
  incidence, half will die.
• Contraindications recent bleeding, prior stroke,
  BPgt185/110, recent major surgery.

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Full Anticoagulation

• Indications includeEmbolus from heart (stroke
  or TIA) Atrial fibrillation gt 72 hours
• Risk is cerebral hemorrhage.
• Must do CT to r/o hemorrhage before use.

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Anticoagulants-Heparin

• Unfractionated Heparin Bolus and continuous
  infusion per hour based on weight and PTT.
• 2-10 bleed risk
• Low molecular weight heparin
• Enoxaparin (and other LMW heparins) given
  subcutaneous every 12-24 hours
• Heparin preparations are used for immediate and
  short term anticoagulation (days). They work
  (simplistically) by inhibiting the action of
  clotting factors to be covered in detail during
  pharmacology course.

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Anticoagulants - Warfarin

• Long term oral anticoagulation (aka Coumadin)
  Inhibits production of clotting factors in liver.
• Stroke or TIA from cardiac embolism- proven by 2
  large randomized studies- ?subsequent stroke
  risk.
• Chronic Atrial Fibrillation ?s stroke risk.
• Monitored by INR (2-3x control) and requires
  frequent follow-up for dosing.

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Post Stroke Management

• Prevention of complications
• Avoid prolonged bed rest (UTIs, skin
  infection/ulcers, PE)
• Physical therapy, occupation therapy, speech
  therapy very important.

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Hemorrhagic Stroke

• Intracerebral (HTN, AVM, and Trauma)
• Subarachnoid space (Aneurysm, AVM)
• CT scan is usually diagnostic
• Spinal tap if CT is negative to R/O SAH.

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Intracerebral Hemorrhage

• Rupture of small arteries or microaneurysms of
  the perforating vessels.
• Hypertension major risk factor.
• Hematologic and bleeding disorders (leukemia,
  thrombocytopenia, hemophilia).
• Trauma
• Anticoagulant therapy, liver disease

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Intracerebral Hemorrhage

• Rapid evolution of neuro deficit often
  progressing to hemiparesis, hemiplegia or
  hemisensory loss 50 mortality.
• Focal signs and symptoms dependent on location of
  the hemorrhage.
• Loss of or impaired consciousness develops in
  50.
• Vomiting and headache are common.

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Intracerebral Hemorrhage
Cecil
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Hemorrhagic Stroke Treatment

• Cautious BP reduction where applicable.
• Treatment conservative and supportive some
  patients will benefit from surgical evacuation of
  the hematoma.
• Surgery Decompression- limited usefulness
• Best in cerebellar bleeds- improves outcomes
• Bleeding AVM

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Subarachnoid Bleeds

• Most due to bleeding from saccular aneurysms
• Present in 3-4 population, usually without
  symptoms
• 2-3 risk bleed per year
• Highest risk if gt6mm
• Sudden onset of severe headache followed by N
  V, impaired or loss of consciousness /- neuro
  deficit. Meningeal signs often present
• Kernigs and Brudzinski signs

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Subarachnoid Hemorrhage
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Subarachnoid Dx and Rx

• CT identifies blood in subarachnoid space.
• If suspected and CT negative do CSF tap and look
  for blood or xanthochromia.
• Treatment If patient is conscious- bed rest,
  symptomatic and supportive care with cautious
  reduction of B.P.
• Angiography once patient stable- aneurysym
• Surgery or coil placement to prevent re-bleeding
  where applicable.

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Aneurysm
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Arterial Venous Malformations (AVMs)

• Most common vascular malformation of CNS often
  involving MCA and branches.
• Tangled web of arteries connected directly to
  veins- congenital up to 70 bleed, often by age
  40.
• MalesgtFemales, some familial trends
• 2-3 risk bleed per year
• S/S hemorrhage (30-60), headache (5-25),
  recurrent seizure (20-40), focal deficits.
• CT may confirm hemorrhage angiography necessary
  for diagnosis.
• Treatment surgery if lesion is accessible.

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AVM
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