Stroke, Cerebral Infarction

Essentials of Diagnosis

• Sudden onset of neurologic deficit of cerebrovascular origin

• History of hypertension, diabetes mellitus, tobacco use, atrial fibrillation, or atherosclerosis

• Distinctive neurologic signs reflect the region of the brain involved

General Considerations

• Stroke due to cerebral infarction is caused by thrombotic or embolic occlusion of a major vessel

• Causes are identical to the disorders predisposing to transient ischemic attacks

• The resulting deficit depends on the particular vessel involved and the extent of any collateral circulation

Symptoms and Signs

• Obstruction of carotid circulation

  • Ophthalmic artery or central retinal artery occlusion

    • Probably symptomless in most cases

    • Transient embolic obstruction can lead to transient monocular blindness (amaurosis fugax)

  • Anterior cerebral artery occlusion distal to its junction with the anterior communicating artery

    • Causes weakness and cortical sensory loss in the contralateral leg and sometimes mild weakness of the arm, especially proximally

    • A contralateral grasp reflex, paratonic rigidity, and abulia (lack of initiative) or frank confusion may be present

    • Urinary incontinence is not uncommon

    • Bilateral anterior cerebral infarction may cause marked behavioral changes and memory disturbances

    • Unilateral anterior cerebral artery occlusion proximal to the junction with the anterior communicating artery is generally well tolerated because of the collateral supply from the other side

  • Middle cerebral artery occlusion

    • Leads to contralateral hemiplegia, hemisensory loss, and homonymous hemianopia, with the eyes deviated to the side of the lesion

    • If the dominant hemisphere is involved, global aphasia is also present

    • In extreme cases, there may be considerable swelling of the hemisphere, leading to drowsiness, stupor, and coma

    • Anterior branch occlusion leads to an expressive dysphasia and to contralateral paralysis and loss of sensations in the arm, the face and, to a lesser extent, the leg

    • Posterior branch occlusion produces a receptive (Wernicke) aphasia and a homonymous visual field defect

    • With involvement of the nondominant hemisphere, speech and comprehension are preserved, but there may be a left hemispatial neglect syndrome or constructional and visuo-spatial deficits

• Obstruction of vertebrobasilar circulation

  • Posterior cerebral artery occlusion

    • May lead to a thalamic syndrome in which contralateral hemisensory disturbance occurs, followed by the development of spontaneous pain and hyperpathia

    • Often a macular-sparing homonymous hemianopia and sometimes a mild, usually temporary, hemiparesis occurs

  • Vertebral artery occlusion

    • May be clinically silent when occlusion is below the origin of the anterior spinal and posterior inferior cerebellar arteries because the circulation is maintained by the other vertebral artery

    • If the remaining vertebral artery is congenitally small or severely atherosclerotic, a deficit similar to that of basilar artery occlusion is seen unless there is good collateral circulation from the anterior circulation through the circle of Willis

    • With occlusion of the small paramedian arteries arising from the vertebral artery, contralateral hemiplegia and sensory deficit occur in association with an ipsilateral cranial nerve palsy at the level of the lesion

  • Posterior inferior cerebellar artery (PICA) or vertebral artery occlusion just before it branches to the PICA leads to

    • Ipsilateral spinothalamic sensory loss involving the face

    • Ninth and tenth cranial nerve lesions

    • Limb ataxia and numbness

    • Horner syndrome, combined with contralateral spinothalamic sensory loss involving the limbs

  • Bilateral vertebral artery or basilar artery occlusion leads to coma with pinpoint pupils, flaccid quadriplegia and sensory loss, and variable cranial nerve abnormalities

    • Partial basilar artery occlusion causes diplopia, visual loss, vertigo, dysarthria, ataxia, weakness or sensory disturbances in some or all of the limbs, and discrete cranial nerve palsies

    • Cerebellar artery occlusion produces vertigo, nausea, vomiting, nystagmus, ipsilateral limb ataxia, and contralateral spinothalamic sensory loss in the limbs

Laboratory Tests

• Complete blood count

• Blood glucose

• Serum total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides

• Serologic test for syphilis

• Blood cultures (if endocarditis suspected)

• If a hypercoagulable disorder is suspected or needs to be ruled out if PFO closure is under consideration, test for congenital or acquired hypercoagulable states (thrombophilia)

  • Antiphospholipid antibody syndrome (lupus anticoagulant, anticardiolipin and anti-β₂-glycoprotein antibodies)

  • Activated protein C resistance/Factor V Leiden

  • Protein C, protein S deficiency

  • Antithrombin deficiency

  • Hyperprothrombinemia (prothrombin gene G20210A mutation)

  • Increased Factor VIII activity

  • Hyperhomocysteinemia

Imaging Studies

• CT scan of the head (non-contrast)

  • Should be performed immediately, before administration of aspirin or other antithrombotic agents (Table 24–3)

  • Relatively insensitive to acute ischemic stroke within the first 6–12 hours

• MRI with diffusion-weighted sequences to

  • Define distribution and extent of infarction

  • Exclude other differential diagnoses

• CT angiography of the head and neck should be performed within 6 hours of stroke onset to identify large vessel occlusions potentially amenable to endovascular therapy

• Imaging of the cervical vasculature is indicated as part of a search to identify the source of the stroke

• In patients with a patent foramen ovale (PFO) and otherwise cryptogenic stroke, the intracranial vasculature must be imaged to rule out large vessel atherosclerosis before PFO closure can be considered

Diagnostic Studies

• Electrocardiogram or continuous cardiac monitoring for 24 hours to exclude myocardial infarction or arrhythmia

• Echocardiography (bubble contrast study) to exclude valvular heart disease or PFO

• Cerebrospinal fluid examination

  • Useful for suspected cerebral vasculitis or other inflammatory or infectious cause

  • Should be delayed until after CT or MRI to exclude risk of herniation from mass effect

Medications

• Intravenous labetalol or nicardipine should be used to lower blood pressure to < 185/110 mm Hg so that recombinant tissue plasminogen activator (rtPA) may be administered

• Intravenous thrombolytic therapy with rtPA

  • Dosage: 0.9 mg/kg to a maximum of 90 mg (10% given as a bolus over 1 minute, the remainder over 1 hour)

  • Treatment should be initiated as soon as possible; outcome is directly related to the time from stroke onset to treatment

  • Due to the risk of hemorrhage, rtPA should not be used beyond 4.5 hours, or in other situations where it is medically contraindicated

  • However, some evidence suggests patients with ischemic but not infarcted tissue identified by automated perfusion imaging or MRI may be treated up to 9 hours after onset or upon awakening with stroke symptoms

• Elevated intracranial pressure is managed by head elevation and osmotic agents such as mannitol

• Elevated systemic BP

  • Avoid antihypertensive therapy during acute phase (ie, within 72 hours, since there is loss of cerebral autoregulation

  • If systolic BP exceeds 220 mm Hg, it can be lowered to 170–200 mm Hg using intravenous labetalol or nicardipine with continuous monitoring

  • After 72 hours, systolic BP can be reduced further to < 140/90 mm Hg

• Antiplatelet therapy

  • Aspirin, 325 mg orally once daily, beginning immediately is indicated in patients not eligible for thrombolytic therapy and without CT evidence of intracranial hemorrhage

  • Discontinue aspirin therapy after achieving therapeutic anticoagulation because of an increased risk of hemorrhage

• Dual antiplatelet therapy should be used for 21 days in patients with minor stroke (National Institutes of Health Stroke Scale of 3 or less)

• Anticoagulant drugs are started when indicated

Therapeutic Procedures

• Endovascular mechanical embolectomy: eligible patients include

  • Those with large vessel occlusion (about 20% of patients with acute ischemic stroke) in whom treatment can be initiated within 6 hours of stroke onset

  • Those who present between 6 and 24 hours and also have a large ischemic penumbra identified by perfusion CT, perfusion MRI, or diffusion-weighted MRI

• Early decompressive hemicraniectomy (within 48 hours of stroke onset) for malignant middle cerebral artery infarctions reduces mortality and improves functional outcome

Follow-Up

• Early mobilization and active rehabilitation

• Leg brace, toe spring, frame, or cane, as needed

Prognosis

• Survival after cerebral infarction is better than after cerebral or subarachnoid hemorrhage

• Patients receiving rtPA are at least 30% more likely to have minimal or no disability at 3 months than otherwise

• Loss of consciousness after a cerebral infarct implies a poorer prognosis than otherwise

• Patients with massive strokes from which meaningful recovery is unlikely should receive palliative care

When to Refer

• All patients with new ischemic stroke

When to Admit

• All patients with new ischemic stroke