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Stroke Syndromes Dr. Gerrard Uy
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Cerebrovascular Disease
ischemic stroke hemorrhagic stroke cerebrovascular anomalies such as intracranial aneurysms and arteriovenous malformations (AVMs) Cause 200,000 deaths each year in the U.S. Incidence increases with age
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Stroke Most strokes manifest by the abrupt onset of a focal neurologic deficit Like patients were “struck by the hand of God” Definition: abrupt onset of a neurologic deficit that is attributable to a focal vascular cause
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Definition of terms Thrombosis: inappropriate clotting
Embolism: migration of clots Ischemia: loss of blood supply in a tissue due to impeded arterial flow or reduced venous drainage Infarction: cell death
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Definition of Terms Cerebral ischemia is caused by a reduction in blood flow that lasts longer than several seconds infarction - death of brain tissue transient ischemic attack (TIA) - all neurologic signs and symptoms resolve within 24 h regardless of whether there is imaging evidence of new permanent brain injury
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Hemorrhagic Stroke Bleeding into subdural and epidural spaces is principally produced by trauma SAHs are produced by trauma and rupture of intracranial aneurysms Hemorrhage are classified by location Often identified by CT scan
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Approach to the patient
Rapid evaluation is essential for use of time sensitive treatments such as thrombolysis Most patients with acute stroke do not seek medical attention because they are rarely in pain and they experience anosagnosia Important clues pointing to stroke: Hemiparesis Changes in vision Changes in gait Disturbance in the ability to speak or understand Sudden severe headache
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Approach to the patient
Migraine can mimic stroke The sensory and motor deficit tend to migrate slowly across a limb over minutes rather than seconds as with stroke Once diagnosis of stroke is made, brain imaging study is necessary to determine the cause of the stroke whether ischemic or hemorrhagic CT imaging is the standard imaging procedure
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ISCHEMIC STROKE
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Ischemic Stroke Acute occlusion of an intracranial vessel causing reduction in blood flow to the brain region The magnitude of flow reduction is a function of collateral blood flow INFARCTION results when: Cerebral blood flow of 0 (zero) in 4 – 10 mins CBF <16-18 ml/ 100g tissue per min in 1 hour CBF <20ml/100g tissue per min = ischemia The tissue surrounding the infarction is ischemic and is called the ischemic penumbra
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Pathophysiology Ischemia produces necrosis by starving neurons of glucose No glucose means no ATP production No ATP, the neurons start to depolarize which in turn increases intracellular calcium levels to rise and glutamate to accumulate Free radicals produced in this process will result in cellular dysfunction and death
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Management of Acute Ischemic Stroke
First goal is to prevent or reverse brain injury Check ABCs and treat hypoglycemia or hyperglycemia Brain imaging to determine whether stroke is ischemic or hemorrhagic
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Management of Acute Ischemic Stroke
6 categories to improve clinical outcome Medical support Intravenous thrombolysis Endovascular techniques Antithrombotic treatment Neuroprotection rehabilitation
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Management of Acute Ischemic Stroke
Medical Support Immediate goal is to optimize cerebral perfusion Prevent complications such as infections, DVT, and bedsores Maintain euglycemia Treat fever Manage hypertension Use of IV Mannitol to raise serum osmolarity and prevent brain edema
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Management of Acute Ischemic Stroke
Intravenous Thrombolysis: NINDS rTPA stoke study showed benefit for IV rTPA in selected patients with acute stroke Golden period is within 3 hrs of the onset of ischemic stroke (0.9 mg/kg – 10% as bolus and remainder over 1 hr) The time of onset of stroke is defined as the time patient’s symptoms began or the time the patient was last seen normal
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Management of Acute Ischemic Stroke
Indications for rTPA Clinical diagnosis of stroke Onset < 3 hrs CT scan shows no hemorrhage or edema of > 1/3 of the MCA territory Age > 18 yrs of age consent
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Management of Acute Ischemic Stroke
Contraindications Sustained BP > 185/110 despite treatment Plt < 100,000, hct < 25%, glucose <50 or >400 mg/dl Use of heparin within 48 hrs, prolonged PTT, or elevated INR Rapidly improving symptoms Prior stroke or head injury within 3 months Major surgery in preceding 14 days Minor stroke symptoms GI bleeding in preceding 21 days Recent MI Coma or Stupor
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Management of Acute Ischemic Stroke
Endovascular Techniques Usually done in occlusions of large vessels such as MCA, internal carotid artery, and basilar artery Procedure is done intraarterially Mechanical thrombectomy is an alternative
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Management of Acute Ischemic Stroke
Antithrombotic Treatment Platelet inhibition Aspirin is the only antiplatelet agent that has been proven effective for the acute treatment of ischemic stroke Usually given within 48 hrs of stroke onset Anticoagulation Has shown no benefit in the primary treatment of atherothrombotic cerebral ischemia
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Management of Acute Ischemic Stroke
Neuroprotection To provide a treatment that prolongs the brain’s tolerance to ischemia Most common neuroprotective drug: Citicoline – reduces the rate of death and disability
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Management of Acute Ischemic Stroke
Rehabilitation to improve neurologic outcomes and reduce mortality Directed towards educating the patient and family about the patient’s neurologic deficit, preventing complications of immobility and providing encouragement and instruction in overcoming the deficit Goal is to return the patient home and to maximize recovery
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Causes of Ischemic Stroke
establishing a cause is essential in reducing the risk of recurrence 30% of strokes remain unexplained despite extensive evaluation Focus on: atrial fibrillation and carotid atherosclerosis
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Causes of Ischemic Stroke
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Cardioembolic Stroke Responsible for 20% of all ischemic strokes
embolism of thrombotic material forming on the atrial or ventricular wall or the left heart valves thrombi then detach and embolize into the arterial circulation Embolic strokes tend to be sudden in onset, with maximum neurologic deficit at once
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Cardioembolic Stroke Emboli from the heart most often lodge in the MCA, PCA, and infrequently ACA Nonrheumatic atrial fibrillation is the most common cause of cerebral embolism overall Patient’s with atrial fibrillation have an average annual risk of 5% Left atrial enlargement and CHF are additional risk factors for the formation of atrial thrombi
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Cardioembolic Stroke causes:
nonrheumatic atrial fibrillation MI prosthetic valves rheumatic heart disease ischemic cardiomyopathy
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Carotid Atherosclerosis
10% of all ischemic strokes frequently within the common carotid bifurcation and proximal internal carotid artery RISK FACTORS: Male gender, older age, smoking, hypertension, diabetes, and hypercholesterolemia
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Other causes of stroke Intracranial Atherosclerosis
Dissection of Internal Carotid Artery Hypercoagulability Venous sinus thrombosis Fibromuscular dysplasia Vasculitis Drugs (amphetamines, cocaine, phenylpropanolamine)
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Transient Ischemic Attack (TIA)
Episodes of stroke symptoms that last briefly Duration < 24 hrs May arise from emboli to the brain or from in situ thrombosis Amaurosis fugax – transient monocular blindness occurs from emboli to the central retinal artery of the eye
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Transient Ischemic Attack (TIA)
Risk of stroke after a TIA is ~10-15% in the first 3 months with most events occurring in the first 2 days Acute antiplatelet therapy is effective and recommended Atherosclerotic risk factors: Old age Family history of thrombotic stroke DM Tobacco smoking dyslipidemia
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Transient Ischemic Attack (TIA)
Other risk factors: Prior stroke or TIA Certain cardiac conditions Oral contraceptives Hypertension – most significant risk factor
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Transient Ischemic Attack (TIA) Treatment
Antiplatelet agents Aspirin: Can prevent platelet aggregation Acetylates cyclooxygenase whicg irreversibly inhibits the formation in platelets of thromboxane A2 Effect is permament and lasts for the usual 8-day life of the platelet Also inhibits endothelial prostacyclin, and antiaggregating and vasodilating prostaglandin mg/day is recommended for stroke prevention
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Transient Ischemic Attack (TIA) Treatment
Antiplatelet agents Clopidogrel: Blocks the ADP receptor on platelets blocking the platelet aggregation Dypiridamole: Inhibits the uptake of adenosine by a variety of cells Adenosine = inhibitor of aggregation Also potentiates the anti aggregatory effects of prostacyclin and nitric oxide by inhibiting platelet phosphodiesterase Prinicpal side effect is headache
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Transient Ischemic Attack (TIA) Treatment
Anticoagulation therapies The decision to use anticoagulation for primary prevention is based on risk factors (rheumatic heart disease, atrial fibrillation, and prosthetic valve implantation)
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STROKE SYNDROMES
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Middle Cerebral Artery
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Middle Cerebral Artery
entire MCA is occluded at its origin : contralateral hemiplegia, hemianesthesia, homonymous hemianopia, and a day or two of gaze preference to the ipsilateral side Dysarthria is common because of facial weakness global aphasia anosognosia, constructional apraxia, and neglect
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