Stroke

Definitions
Stroke (“brain attack”) is the sudden onset of a focal neurologic deficit(s) resulting from either infarction or hemorrhage within the brain.

*Transient ischemic attack (TIA) or “mini-stroke:” Stroke symptoms that resolve in <24 hours; Reversible ischemic neurological deficit (RIND): Stroke symptoms that last >24 hours but <1 week

Epidemiology
Incidence in the US: 150/100,000 per year
Prevalence in the US: 550/100,000
Risk increases >45 years and is highest in the 7th and 8th decades
Male > Female (3:1), but equalizes after menopause

Classification

Ischemic (80%)	blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. Causes: thrombptic, embolic, systemic hypoperfusion, vascular thrombosis.
Hemorrhagic (20%)	Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault.

Aetiology:

Thrombotic	blood clot usually forms around atherosclerotic plaques in the vessels. Types: Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis. Causes: atherosclerosis, vasoconstriction (tightening of the artery), aortic, carotid or vertebral artery dissection Inflammatory- Takayasu arteritis, giant cell arteritis, vasculitis vasculopathy-Moyamoya disease and fibromuscular dysplasia. Small vessel disease involves occlusion of the middle cerebral artery (MCA), the lenticulostriate arteries, or the penetrating branches of the circle of Willis, vertebral artery, or basilar artery. This is refered as lacunar stroke (20% of all ischaemic stroke). Causes: lipohyalinosis and fibroid degeneration Sickel cell anaemia  which can cause blood cells to clump up and block blood vessels, can also lead to stroke.
Embolic	blockage of an artery by an arterial embolus. To treat, the source must be identified. Causes: atrial fibrillation, deep vain thrombosis, sick sinus syndrome, atrial flutter, fat, air embolus, cancer cells or clumps of bacteria (eg. infective endocarditis)
Systemic hypoperfusion	reduction of blood flow to all parts of the body.  Causes cardiac pump failure from cardiac arrest or arrhythmias reduced cardiac output as a result of myocardial infarction, pulmonary embolism, pericardial effusion, or bleeding. May result in watershed stroke - condition of compromised blood supply to the border zone regions in the brain supplied by the major cerebral arteries. Blood flow to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur.(“last meadow" phenomenon)
Venous thrombosis	Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure.
Intracerebral hemorrhage	Causes :hypertension(commonest), intracranial vascular malformations cerebral amyloid angiopathy, or infarcts into which secondary haemorrhage has occurred. Others causes: trauma, bleeding disorders, illicit drug use (e.g. amphetamines or cocaine). ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid hemorrhage

Pathophysiology

Ischemic Stroke

Ischemic cascade The processes involved in stroke injury at the cellular level loss of glucose and oxygen delivery to neurons neuronal and glial injury produces edema in the ensuing hours to days after stroke. Ischemic penumbra Stroke produces heterogeneous regions of ischemia in the dependent vascular territory The core=Brain regions without significant flow, irreversible injury Ischemic penumbra=Zones of decreased or marginal perfusion, viable for few hours, reversible injury.

Haemorrhagic Stroke

causes tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can distort and injure tissue. the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, blood released appears to have direct toxic effects on brain tissue and vasculature

Presentation

• Acute hemiparesis or hemiplegia
• Complete or partial hemianopia, monocular or binocular visual loss, or diplopia
• Dysarthria or aphasia
• Ataxia, vertigo, or nystagmus
• Sudden decrease in consciousness

Proposed systems include FAST (stroke) (face, arm, speech, and time),
*Establishing the time the patient was last normal is especially critical when thrombolytic therapy is an option. If the patient awakens with the symptoms, then the time of onset is defined as the time the patient was last seen without symptoms

Ddx
Migraine
Focal seizure
Tumor
Subdural hematoma
Hypoglycemia; hyperglycemia; hypercalcemia

Investigation

CT	Noncontrast CT is very sensitive in excluding intracranial haemorrhage. Hemorrhage in the cerebellum (arrow) not very sensitive for early ischemia (<6 h), findings may suggest ischemic changes relatively early in the time course of stroke. Loss of the gray-white matter interface, loss of sulci, and loss of the insular ribbon are subtle signs of early ischemia.
MRI	MRI with diffusion-weighted imaging (DWI) remains the most powerful and accurate method for stroke identification, but access and cost make it prohibitive in most acute settings.
FBC	hemoglobin and hematocrit, platelet count, which is important in fibrinolytic candidates
Glucose, electrolyte test	exclude hypoglycaemia, electrolyte disorder
PT, PTT	Treatment decisions, such as thrombolytic use, require data on coagulation status. Consideration of hypercoagulable workup in younger patients
Cardiac enzymes. ECG	exclude MI
Transthoracic echocardiogram	in acute ischemic stroke with atrial fibrillation or suspicion of cardiac origin to emboli). If normal and a cardiac source is suspected, follow up with transesophageal
Holter monitor	Monitor for hypertension
Duplex carotid ultrasonography	in acute ischemic stroke where carotid stenosis is a consideration
EEG	if suspected seizure
Lumbar puncture	rule out meningitis or subarachnoid hemorrhage when the CT scan is negative but the clinical suspicion remains high.

Management

Pre-hospital	ABCs, stroke patient evaluation and, if eligible, fibrinolytic therapy should be administered within 1 hour from presentation
Early admission	Admit to Stroke unit. Treat hypo/hyperglycaemia, monitor BP/ECG, IV fluid, oral intake, Oxygen, control temperature
Medication	IV tissue plasminogen activator (tPA): 0.9 mg/kg in highly selected cases within 3 hours of ischemic stroke symptom onset Enteric-coated aspirin: 50–325 mg/d or Dipyridamole-aspirin (Aggrenox): Extended-release, 200 mg/25 mg capsule p.o. b.i.d.; more efficacious than aspirin or dipyridamole alone for prevention of recurrence Clopidogrel (Plavix): 75 mg/d; fewer side effects than dipyridamole; approximately equivalent to dipyridamole-aspirin in prevention of recurrent stroke or TIA Warfarin: INR adjusted dose 2–4 for patients with atrial fibrillation and cardioembolic stroke has shown decreased risk of recurrent stroke compared to ASA 300 mg/d at 2.3 years Contraindications: Enteric-coated aspirin: Active peptic ulcer disease, hypersensitivity to aspirin, patients who had bronchospastic reaction to aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs). Clopidogrel may also cause severe gastrointestinal (GI) bleeding. Warfarin: Intolerance or allergy, dementia, liver disease, active bleeding, pregnancy, recent head injury Precautions: Enteric-coated aspirin: May aggravate preexisting peptic ulcer disease, may worsen symptoms in some patients with asthma Clopidogrel: Thrombotic thrombocytopenic purpura can occur. Warfarin: age >80, poor balance (given fall risk), alcohol/drug abuse
General measures	Maintain oxygenation. Monitor cardiac rhythm for 48 hours. Control hyperglycemia (keep glucose <220 mg/dL [12.1 mmol/L]). Treat blood pressure (BP) >185/110 in patients who receive tPA. Otherwise, do not treat elevated BP unless acute end-organ dysfunction (encephalopathy, myocardial ischemia, aortic dissection, acute renal failure) is suspected. Prevent hyperthermia. Subcutaneous heparin 5,000 units SC q.12h. or other deep vein thrombosis (DVT) prophylaxis (compression cuffs) Smoking cessation counseling, if indicated Physical, occupational, and speech therapy as appropriate
Surgery	Surgical therapy for patients with carotid disease: Carotid endarterectomy is indicated for stenosis of >70% on side ipsilateral to stroke in medically fit patients with nondisabling stroke. For stenosis of 50–69%, treatment depends on risk factors. For <50% stenosis, medical not surgical therapy . Selected patients with either hemorrhagic transformation or intracerebral hemorrhage after thrombolytic therapy may benefit from surgical evacuation of the hematoma.
Further out-patient care	Begin efforts to restore neurologic function through rehabilitation or other techniques. This includes occupational, physical, and speech therapy. Medication Aspirin, taken daily in low-to-medium doses (50-325 mg), is an effective and inexpensive first-choice agent for reducing recurrent stroke risk. Newer antiplatelet agents, such as clopidogrel (Plavix) and aspirin/dipyridamole combinations (Aggrenox) are also effective in reducing recurrent stroke rate but may cause adverse effects that must be monitored. Initiating long-term anticoagulation (eg, warfarin) reduces the risk of recurrent stroke in patients at risk for cardioembolic stroke. INR for A fib(2-3) for prosthetic valve (2-3.5)
Follow-up	Follow the patient q.3mo for the 1st year, then yearly Alert with no dysphagia: Regular diet (no added salt if hypertensive) Alert with dysphagia: Pureed dysphagia diet or nasogastric feeding tube if indicated Enteral feeding via G- or J-tube is controversial with suboptimal outcomes

Complications
Postfibrinolytic complications center around a bleeding issue.
Hyperextension knee injury
Sympathetic dystrophy
Acute: Pneumonia, seizures, GI bleeding, myocardial infarction (MI)
Chronic: Shoulder subluxation, falls and fractures, depression (100%), pain (central and peripheral)

Prognosis
Variable, depending on severity of stroke
Patients with posterior circulation strokes have a higher acute mortality rate, but generally make a better functional recovery than do those with hemispheric strokes.
mortality rate at 30 days after stroke was 28%. The mortality rate at 30 days after ischemic stroke was 19%. The 1-year survival rate for patients with ischemic stroke in the Framingham study was 77%.
31% needed help caring for themselves, 20% needed help when walking, and 71% had impaired vocational capacity in long-term follow-up.