Overview 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). Stroke symptoms lasting < 1 h are termed a transient ischemic attack (TIA). Strokes damage brain tissue; TIAs often do not, and when damage occurs, it is less extensive than that due to strokes. In Western countries, stroke is the 3rd most common cause of death and the most common cause of neurologic disability.
Strokes involve the arteries of the brain (see Fig. 1: Stroke (CVA): 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).
Arteries of the brain.
The anterior cerebral artery supplies the medial portions of the frontal and parietal lobes and corpus callosum. The middle cerebral artery supplies large portions of the frontal, parietal, and temporal lobe surfaces. Branches of the anterior and middle cerebral arteries (lenticulostriate arteries) supply the basal ganglia and anterior limb of the internal capsule.
The vertebral and basilar arteries supply the brain stem, cerebellum, posterior cerebral cortex, and medial temporal lobe. The posterior cerebral arteries bifurcate from the basilar artery to supply the medial temporal (including the hippocampus) and occipital lobes, thalamus, and mammillary and geniculate bodies.
Anterior circulation and posterior circulation communicate in the circle of Willis.
Risk factors: Risk factors include the following:
Family history of stroke
Use of certain drugs (eg, cocaine, amphetamines)
Certain risk factors predispose to a particular type of stroke (eg, hypercoagulability predisposes to thrombotic stroke, atrial fibrillation to embolic stroke, and intracranial aneurysms to subarachnoid hemorrhage).
Symptoms and Signs
Initial symptoms occur suddenly. Generally, they include numbness, weakness, or paralysis of the contralateral limbs and the face; aphasia; confusion; visual disturbances in one or both eyes (eg, transient monocular blindness); dizziness or loss of balance and coordination; and headache.
Neurologic deficits reflect the area of brain involved (see Table 1: Stroke (CVA): Selected Stroke Syndromes). Anterior circulation stroke typically causes unilateral symptoms. Posterior circulation stroke can cause unilateral or bilateral deficits and is more likely to affect consciousness, especially when the basilar artery is involved.
Selected Stroke Syndromes
Symptoms and Signs
Contralateral hemiparesis (maximal in the leg), urinary incontinence, apathy, confusion, poor judgment, mutism, grasp reflex, gait apraxia
Anterior cerebral artery (uncommon)
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)
Middle cerebral artery (common)
Contralateral homonymous hemianopia, unilateral cortical blindness, memory loss, unilateral 3rd cranial nerve palsy, hemiballismus
Posterior cerebral artery
Monocular loss of vision (amaurosis)
Ophthalmic artery (a branch of the middle cerebral artery)
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
Absence of cortical deficits plus one of the following:
Pure motor hemiparesis
Pure sensory hemianesthesia
Dysarthria–clumsy hand syndrome
*Ipsilateral facial sensory loss or motor weakness with contralateral body hemianesthesia or hemiparesis indicates a lesion at the pons or medulla.
Other manifestations, rather than neurologic deficits, often suggest the type of stroke. For example, sudden, severe headache suggests subarachnoid hemorrhage. Impaired consciousness or coma, often accompanied by headache, nausea, and vomiting, suggests increased intracranial pressure (see Intracranial and Spinal Tumors: Symptoms and Signs), which can occur 48 to 72 h after large ischemic strokes and earlier with many hemorrhagic strokes; fatal brain herniation may result (see Coma and Impaired Consciousness: Pathophysiology).
Complications: Stroke complications can include sleep problems, confusion, depression, incontinence, atelectasis, pneumonia, and swallowing dysfunction, which can lead to aspiration, dehydration, or undernutrition. Immobility can lead to thromboembolic disease, deconditioning, sarcopenia, UTIs, pressure ulcers, and contractures. Daily functioning (including the ability to walk, see, feel, remember, think, and speak) may be decreased.
Evaluation aims to establish whether stroke has occurred, whether it is ischemic or hemorrhagic, and whether immediate treatment is required.
Stroke is suspected in patients with any of the following:
Sudden neurologic deficits compatible with brain damage in an arterial territory
A particularly sudden, severe headache
Sudden, unexplained coma
Sudden impairment of consciousness
If stroke is suspected, immediate neuroimaging is required to differentiate hemorrhagic from ischemic stroke and to detect signs of increased intracranial pressure. CT is sensitive for intracranial blood but may be normal or show only subtle changes during the first hours of symptoms after anterior circulation ischemic stroke. CT also misses some small posterior circulation strokes and up to 3% of subarachnoid hemorrhages. MRI is sensitive for intracranial blood and may detect signs of ischemic stroke missed by CT, but CT can usually be done more rapidly. If CT does not confirm clinically suspected stroke, diffusion-weighted MRI can usually detect ischemic stroke (see Stroke (CVA): Ischemic Stroke). If consciousness is impaired and lateralizing signs are absent or equivocal, further tests to check for other causes are done (see Coma and Impaired Consciousness).
After the stroke is identified as ischemic or hemorrhagic, tests are done to determine the cause. Patients are also evaluated for coexisting acute general disorders (eg, infection, dehydration, hypoxia, hyperglycemia, hypertension). Patients are asked about depression, which commonly occurs after stroke. A dysphagia team evaluates swallowing; sometimes a barium swallow study is necessary.
Supportive measures and treatment of complications
Stabilization may need to precede complete evaluation. Comatose or obtunded patients (eg, Glasgow Coma Score ≤ 8) may require airway support (see Respiratory Failure and Mechanical Ventilation). If increased intracranial pressure is suspected, intracranial pressure monitoring (see Approach to the Critically Ill Patient: Intracranial Pressure Monitoring) and measures to reduce cerebral edema (see Traumatic Brain Injury (TBI): Increased intracranial pressure) may be necessary. Specific acute treatments vary by type of stroke.
Strategies to Prevent and Treat Stroke Complications
Applying tight elastic or air-filled support stockings and providing frequent active and passive leg exercises
Turning bedridden patients frequently, with special attention to pressure sites
Passively moving limbs at risk of contractures and placing them in the appropriate resting positions, using splints if necessary
Ensuring adequate fluid intake and nutrition, including evaluating patients for swallowing difficulties and providing nutritional support as necessary
Giving small doses of heparin
(5000 U) sc
q 12 h or an equivalent amount of low molecular weight heparin
heparinoid, when not contraindicated, to prevent deep venous thrombosis and pulmonary embolism
Encouraging early ambulation (as soon as vital signs are normal), with close monitoring
Maximizing lung function (eg, smoking cessation, deep breathing exercises, respiratory therapy, measures to prevent aspiration in patients with dysphagia)
Looking for and treating infections early, especially pneumonia, UTIs, and skin infections
Managing urinary bladder problems in bedbound patients, preferably without using an indwelling catheter
Promoting risk factor modification (eg, smoking cessation, weight loss, healthful diet)
Prescribing early rehabilitation (eg, active and passive exercises, range-of-motion exercises)
Compassionately discussing residual function, prognosis for recovery, and strategies to compensate for lost function with the patient
Encouraging maximum independence through rehabilitation
Encouraging the patient and family members to contact stroke support groups for social and psychologic support
Providing supportive care, correcting coexisting abnormalities (eg, fever, hypoxia, dehydration, hyperglycemia, sometimes hypertension), and preventing and treating complications are vital during the acute phase and convalescence (see Table 2: Stroke (CVA): Strategies to Prevent and Treat Stroke Complications); these measures clearly improve clinical outcomes. During convalescence, measures to prevent aspiration, deep venous thrombosis, UTIs, pressure ulcers, and undernutrition may be necessary. Passive exercises, particularly of paralyzed limbs, and breathing exercises are started early to prevent contractures, atelectasis, and pneumonia. Most patients require occupational and physical therapy (see Rehabilitation: Stroke Rehabilitation) to maximize functional recovery. Some need additional therapies (eg, speech therapy, feeding restrictions). Depression after stroke may require antidepressants; many patients benefit from counseling. For rehabilitation, an interdisciplinary approach is best. Modifying risk factors through lifestyle changes (eg, stopping cigarette smoking) and drug therapy (eg, for hypertension) can help delay or prevent subsequent strokes.