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