Stroke

د. بشار باطنية الاثنين30/10/2017
STROKEOverview of Stroke
Strokes are a heterogeneous group of disorders involving sudden, focal interruption of cerebral blood flow that causes neurologic deficit. Strokes can be ischemic (80%), typically resulting from thrombosis or embolism, or hemorrhagic (20%), resulting from vascular rupture (eg, subarachnoid or intracerebral hemorrhage).
Transient stroke symptoms (typically lasting < 1 h) without evidence of acute cerebral infarction (based on diffusion-weighted MRI) are termed a transient ischemic attack (TIA).
In the US, stroke is the 4th most common cause of death and the most common cause of neurologic disability in adults.
Strokes involve the arteries of the brain, either the anterior circulation (branches of the internal carotid artery) or the posterior circulation (branches of the vertebral and basilar arteries).

Ischemic Stroke

sudden neurologic deficits that result from focal cerebral ischemia associated with permanent brain infarction (eg, positive results on diffusion-weighted MRI).
Common causes are (from most to least common) atherothrombotic occlusion of large arteries; cerebral embolism (embolic infarction); nonthrombotic occlusion of small, deep cerebral arteries (lacunar infarction); and proximal arterial stenosis with hypotension that decreases cerebral blood flow in arterial watershed zones (hemodynamic stroke).
Etiology
Modifiable risk factors that contribute the most to increased risk of ischemic stroke:
Hypertension
Cigarette smoking
Dyslipidemia
Diabetes
Abdominal obesity
Alcoholism
Lack of physical activity
High-risk diet (eg, high in saturated fats, trans fats, and calories)
Psychosocial stress (eg, depression)
Heart disorders (particularly disorders that predispose to emboli, such as acute MI, infective endocarditis, and atrial fibrillation)
Use of certain drugs (eg, cocaine, amphetamines)
Hypercoagulability
Vasculitis
Unmodifiable risk factors
Prior stroke
Older age
Family history of stroke
Male sex
Ischemia usually results from thrombi or emboli
Thrombosis
Atherothrombotic occlusion of large arteries (thrombus superimposed on an atherosclerotic artery) is the most common cause of ischemic stroke.
Atheromas, particularly if ulcerated, predispose to thrombi. Atheromas can occur in any major cerebral artery and are common at areas of turbulent flow, particularly at the carotid bifurcation.
Less common causes of thrombosis include vascular inflammation secondary to disorders such as acute or chronic meningitis, vasculitic disorders, and syphilis; dissection of intracranial arteries or the aorta; hypercoagulability disorders (eg, antiphospholipid syndrome, hyperhomocysteinemia); hyperviscosity disorders (eg, polycythemia, thrombocytosis, hemoglobinopathies, plasma cell disorders); and rare disorders (eg, fibromuscular dysplasia, moyamoya disease).Older oral contraceptive formulations increase risk of thrombosis. In children, sickle cell disease is a common cause of ischemic stroke.
Embolism
Emboli may lodge anywhere in the cerebral arterial tree
Emboli may originate as cardiac thrombi, especially in the following conditions
Atrial fibrillation
Rheumatic heart disease (usually mitral stenosis)
Post-MI
Vegetations on heart valves in bacterial or marantic endocarditis
Prosthetic heart valves
Other sources include clots that form after open-heart surgery and atheromas in neck arteries or in the aortic arch. Rarely, emboli consist of fat (from fractured long bones), air (in decompression sickness), or venous clots that pass from the right to the left side of the heart through a patent foramen ovale with shunt (paradoxical emboli). Emboli may dislodge spontaneously or after invasive cardiovascular procedures (eg, catheterization).
Lacunar infarcts
These small (≤ 1.5 cm) infarcts result from nonatherothrombotic obstruction of small, perforating arteries that supply deep cortical structures; the usual cause is lipohyalinosis (degeneration of the media of small arteries and replacement by lipids and collagen). Whether emboli cause lacunar infarcts is controversial. Lacunar infarcts tend to occur in elderly patients with diabetes or poorly controlled hypertension.
Other causes
Any factor that impairs systemic perfusion (eg, carbon monoxide toxicity, severe anemia or hypoxia, polycythemia, hypotension) increases risk of all types of ischemic strokes. A stroke may occur along the borders between territories of arteries (watershed areas); in such areas, blood supply is normally low, particularly if patients have hypotension and/or if major cerebral arteries are stenotic.
Symptoms and Signs
Symptoms and signs depend on the part of brain affected. Patterns of neurologic deficits often suggest the affected artery


Anterior cerebral artery (uncommon)
Contralateral hemiparesis (maximal in the leg), urinary incontinence, apathy, confusion, poor judgment, mutism, grasp reflex, gait apraxia
Middle cerebral artery (common)
Contralateral hemiparesis (worse in the arm and face than in the leg), dysarthria, hemianesthesia, contralateral homonymous hemianopia, aphasia (if the dominant hemisphere is affected) or apraxia and sensory neglect (if the nondominant hemisphere is affected)
Posterior cerebral artery
Contralateral homonymous hemianopia, unilateral cortical blindness, memory loss, unilateral 3rd cranial nerve palsy, hemiballismus
Ophthalmic artery (a branch of the middle cerebral artery)
Monocular loss of vision (amaurosis)
Vertebrobasilar system
Unilateral or bilateral cranial nerve deficits (eg, nystagmus, vertigo, dysphagia, dysarthria, diplopia, blindness), truncal or limb ataxia, spastic paresis, crossed sensory and motor deficits, impaired consciousness, coma, death (if basilar artery occlusion is complete), tachycardia, labile BP
Lacunar infarcts
Absence of cortical deficits plus one of the following:
Pure motor hemiparesis
Pure sensory hemianesthesia
Ataxic hemiparesis
Dysarthria–clumsy hand syndrome
Deficits may become maximal within several minutes of onset, typically in embolic stroke. Less often, deficits evolve slowly, usually over 24 to 48 h (called evolving stroke or stroke in evolution), typically in atherothrombotic stroke. In most evolving strokes, unilateral neurologic dysfunction (often beginning in one arm, then spreading ipsilaterally) extends without causing headache, pain, or fever.
Progression is usually stepwise, interrupted by periods of stability.
Embolic strokes often occur during the day; headache may precede neurologic deficits. Thrombi tend to occur during the night and thus are first noticed on awakening.
A seizure may occur at stroke onset, more often with embolic than thrombotic stroke. Seizures may also occur months to years later; late seizures result from scarring or hemosiderin deposition at the site of ischemia
Deterioration during the first 48 to 72 h after onset of symptoms, particularly progressively impaired consciousness, results more often from cerebral edema than from extension of the infarct.
Unless the infarct is large or extensive, function commonly improves within the first few days; further improvement occurs gradually for up to 1 yr.
Diagnosis
Primarily clinical evaluation
Neuroimaging and bedside glucose testing
Evaluation to identify the cause
Sudden neurologic deficits referable to a specific arterial territoryHeadache, coma or stupor, and vomiting are more likely with hemorrhagic stroke
Stroke mimics
CT is done first to exclude intracerebral hemorrhage, subdural or epidural hematoma, and a rapidly growing, bleeding, or suddenly symptomatic tumor. CT evidence of even a large anterior circulation ischemic stroke may be subtle during the first few hours; changes may include effacement of sulci or the insular cortical ribbon, loss of the gray-white junction between cortex and white matter, and a dense middle cerebral artery sign.
Within 6 to 12 h of ischemia, medium-sized to large infarcts start to become visible as hypodensities
Small infarcts (eg, lacunar infarcts) may be visible only with MRI. Diffusion-weighted MRI (highly sensitive for early ischemia) can be done immediately after initial CT neuroimaging
Cardiac causes
ECG, telemetry or Holter monitoring, serum troponin, and transthoracic or transesophageal echocardiography
Vascular causes
Magnetic resonance angiography (MRA), CT angiography (CTA), carotid and transcranial duplex ultrasonography, and conventional angiography
Blood-related causes
blood tests are done to assess their contribution and that of other causes. Routine testing typically includes CBC, platelet count, PT/PTT, fasting blood glucose, and lipid profile.
Additional tests may include
Measurement of homocysteine
Testing for thrombotic disorders (antiphospholipid antibodies, protein S, protein C, antithrombin III, factor V)
Testing for rheumatic disorders (eg, antinuclear antibodies, rheumatoid factor, ESR)
Syphilis serologic testing
Hb electrophoresis
Urine drug screen for cocaine and amphetamines.
A cause cannot be identified for some strokes (cryptogenic strokes)
Prognosis
Stroke severity and progression are often assessed using standardized measures such as the National Institutes of Health (NIH) Stroke Scale (the score on this scale correlates with extent of functional impairment and prognosis
During the first days, progression and outcome can be difficult to predict
Older age, impaired consciousness, aphasia, and brain stem signs suggest a poor prognosis.
Early improvement and younger age suggest a favorable prognosis.
Complete neurologic recovery occurs in about 10%
About 50% of patients with moderate or severe hemiplegia and most with milder deficits have a clear sensorium and eventually can take care of their basic needs and walk adequately
Use of the affected limb is usually limited, and most deficits that remain after 12 mo are permanent
Subsequent strokes often occur, and each tends to worsen neurologic function
About 20% of patients die in the hospital; mortality rate increases with age
Treatment
General stroke treatments
Acute antihypertensive therapy only in certain circumstances
Antiplatelet therapy
Occasionally for acute treatment, reperfusion (eg, recombinant tissue plasminogen activator [tPA] or thrombolysis-in-situ)
Sometimes anticoagulation
Long-term control of risk factors
Sometimes carotid endarterectomy or stenting
Patients with acute ischemic strokes are usually hospitalized. Supportive measures may be needed during initial evaluation and stabilization
Perfusion of an ischemic brain area may require a high BP because autoregulation is lost; thus, BP should not be decreased except in the following cases
BP is > 220 mm Hg systolic or > 120 mm Hg diastolic on 2 successive readings >15 min apart.
There are signs of other end-organ damage (eg, aortic dissection, acute MI, pulmonary edema, hypertensive encephalopathy, retinal hemorrhages, acute renal failure).
Use of recombinant tPA is likely.
Patients with presumed thrombi or emboli may be treated with tPA, thrombolysis-in-situ, antiplatelet drugs, and/or anticoagulants.
Most patients are not candidates for thrombolytic therapy; they should be given an antiplatelet drug (usually aspirin 325 mg po) when they are admitted to the hospital
Recombinant tPA
Used for patients with acute ischemic stroke up to 4.5 h after symptom onset if they have no contraindications to tPA.
Although tPA can cause fatal or other symptomatic brain hemorrhage, patients treated with tPA strictly according to protocols still have a higher likelihood of functional neurologic recovery
Before treatment with tPA, brain hemorrhage must be excluded by CT, systolic BP must be < 185 mm Hg, and diastolic BP must be < 110 mm Hg
Dose of tPA is 0.9 mg/kg IV (maximum dose 90 mg); 10% is given by rapid IV injection, and the remainder by constant infusion over 60 min. Vital signs are closely monitored for 24 h after treatment, and BP is maintained below 185 mm Hg systolic and 110 mm Hg diastolic.
Any bleeding complications are aggressively managed.
Anticoagulants and antiplatelet drugs are not used within 24 h of treatment with tPA.
Thrombolysis-in-situ (angiographically directed intra-arterial thrombolysis).
Sometimes used for major strokes if symptoms began >3 h but < 6 h ago, particularly for strokes due to large occlusions in the middle cerebral artery.
Clots in the basilar artery may be intra-arterially lysed up to 12 h after stroke onset, sometimes even later depending on the clinical circumstances
Mechanical thrombectomy (angiographically directed intra-arterial removal of a thrombus or embolus by a device)
Often used as rescue treatment for patients who have had a severe stroke and have an NIH stroke score ≥ 8 when IV and/or intra-arterial thrombolysis has been ineffective; it must be done within 8 h of symptom onset
Anticoagulation
Used for stroke caused by cerebral venous thrombosis and is sometimes used for emboli due to atrial fibrillation and for stroke due to presumed progressive thrombosis if it continues to evolve despite use of antiplatelet drugs and cannot be treated any other way (eg, with tPA or invasive methods).
Warfarin is begun simultaneously with heparin. Before anticoagulation, hemorrhage must be excluded by CT.
Long term
Supportive care is continued during convalescence.
Controlling hyperglycemia and fever can limit brain damage after stroke, leading to better functional outcomes.
Long-term management also focuses on prevention of recurrent stroke (secondary prevention)
Modifiable risk factors (eg, hypertension, diabetes, smoking, alcoholism, dyslipidemia, obesity) are treated.
Reducing systolic BP may be more effective when the target BP is < 120 mm Hg rather than the typical level (< 140 mm Hg).
Extracranial carotid endarterectomy or stenting
Extracranial vertebral angioplasty and/or stenting
Intracranial major artery angioplasty and/or stenting
Oral antiplatelet drugs
Used to prevent subsequent noncardioembolic (atherothrombotic, lacunar, cryptogenic) strokes (secondary prevention).
Aspirin 81 or 325 mg once/day, clopidogrel 75 mg once/day, or the combination product aspirin 25 mg/extended-release dipyridamole 200 mg bid may be used.
Ticlopidine 250 mg bid
Oral anticoagulants
For secondary prevention of cardioembolic strokes (as well as primary prevention). Adjusted-dose warfarin (a vitamin K antagonist) with a target INR of 2 to 3 is used for certain patients with nonvalvular or valvular atrial fibrillation.
A target INR of 2.5 to 3.5 is used if patients have a mechanical prosthetic cardiac valve.
Statins
Used to prevent recurrent strokes; lipid levels must be decreased by substantial amounts.
Atorvastatin 80 mg once/day is recommended for patients with evidence of atherosclerotic stroke and LDL (low-density lipoprotein) cholesterol ≥ 100 mg/dL.
A reasonable LDL cholesterol target is a 50% reduction or a level of < 70 mg/dL.
Other statins (eg, simvastatin, pravastatin) may be also used.
Transient Ischemic Attack (TIA)
Focal brain ischemia that causes sudden, transient neurologic deficits and is not accompanied by permanent brain infarction (eg, negative results on diffusion-weighted MRI).
TIA is similar to ischemic stroke except that symptoms usually last < 1 h; most TIAs last < 5 min. Infarction is very unlikely if deficits resolve within 1 h
As shown by diffusion-weighted MRI and other studies, deficits that resolve spontaneously within 1 to 24 h are often accompanied by infarction and are thus no longer considered TIAs
TIAs are most common among the middle-aged and elderly.
TIAs markedly increase risk of stroke, beginning in the first 24 h.
Etiology
Risk factors for TIA are the same as those for ischemic stroke.
Most TIAs are caused by emboli, although most of the causes of ischemic stroke can also result in TIAs
Subclavian steal syndrome
A subclavian artery stenosed proximal to the origin of the vertebral artery “steals” blood from the vertebral artery (in which blood flow reverses) to supply the arm during exertion, causing signs of vertebrobasilar ischemia.
Symptoms and SignsNeurologic deficits are similar to those of strokes.
Transient monocular blindness (amaurosisfugax), which usually lasts < 5 min, may occur when the ophthalmic artery is affected
Diagnosis
Resolution of strokelike symptoms within 1 h
Neuroimaging
Evaluation to identify the cause
Diagnosis is made retrospectively when sudden neurologic deficits referable to ischemia in an arterial territory resolve within 1 h.
Isolated peripheral facial nerve palsy, loss of consciousness, or impaired consciousness does not suggest TIA.
Because an infarct, a small hemorrhage, and even a mass lesion cannot be excluded clinically, neuroimaging is required.
Usually, CT is the study most likely to be immediately available. However, CT may not identify infarcts for > 24 h.
MRI usually detects evolving infarction within hours.
Diffusion-weighted MRI is the most accurate imaging test to rule out an infarct in patients with presumed TIA but is not always available.
The cause of a TIA is sought as for that of ischemic strokes
TreatmentPrevention of strokesAntiplatelet drugs and statins are used.
Carotid endarterectomy or arterial angioplasty plus stenting can be useful for some patients, particularly those who have no neurologic deficits but who are at high risk of stroke. Anticoagulation is indicated if cardiac sources of emboli are present.
Modifying stroke risk factors, when possible, may prevent stroke.