Stroke Syndromes Dr. Gerrard Uy 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 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 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 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 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 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 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 ISCHEMIC STROKE 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 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 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 Management of Acute Ischemic Stroke • 6 categories to improve clinical outcome – Medical support – Intravenous thrombolysis – Endovascular techniques – Antithrombotic treatment – Neuroprotection – rehabilitation 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 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 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 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 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 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 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 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 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 Causes of Ischemic Stroke 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 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 Cardioembolic Stroke causes: • • • • • nonrheumatic atrial fibrillation MI prosthetic valves rheumatic heart disease ischemic cardiomyopathy 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 Other causes of stroke • • • • • • • Intracranial Atherosclerosis Dissection of Internal Carotid Artery Hypercoagulability Venous sinus thrombosis Fibromuscular dysplasia Vasculitis Drugs (amphetamines, cocaine, phenylpropanolamine) 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 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 Transient Ischemic Attack (TIA) • Other risk factors: – Prior stroke or TIA – Certain cardiac conditions – Oral contraceptives – Hypertension – most significant risk factor 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 • 50-325 mg/day is recommended for stroke prevention 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 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) STROKE SYNDROMES Middle Cerebral Artery 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