introduction
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).
Intracerebral hemorrhage
Intracerebral hemorrhage is focal bleeding from a blood vessel in the brain parenchyma. The cause is usually hypertension. Typical symptoms include focal neurologic deficits, often with abrupt onset of headache, nausea, and impairment of consciousness. Diagnosis is by CT or MRI. Treatment includes BP control, supportive measures, and, for some patients, surgical evacuation.
Most intracerebral hemorrhages occur in the basal ganglia, cerebral lobes, cerebellum, or pons. Intracerebral hemorrhage may also occur in other parts of the brain stem or in the midbrain.
Etiology and Pathophysiology
Intracerebral hemorrhage usually results from rupture of an arteriosclerotic small artery that has been weakened, primarily by chronic arterial hypertension. Such hemorrhages are usually large, single, and catastrophic. Use of cocaine or, occasionally, other sympathomimetic drugs can cause transient severe hypertension leading to hemorrhage. Less often, intracerebral hemorrhage results from congenital aneurysm, arteriovenous or other vascular malformation trauma, mycotic aneurysm, brain infarct (hemorrhagic infarction), primary or metastatic brain tumor, excessive anticoagulation, blood dyscrasia, or a bleeding or vasculitic disorder.
Vascular Lesions in the Brain
Common brain vascular lesions include arteriovenous malformations and aneurysms.
Arteriovenous malformations (AVMs): AVMs are tangled, dilated blood vessels in which arteries flow directly into veins. AVMs occur most often at the junction of cerebral arteries, usually within the parenchyma of the frontal-parietal region, frontal lobe, lateral cerebellum, or overlying occipital lobe. AVMs can bleed or directly compress brain tissue; seizures or ischemia may result.
Neuroimaging may detect them incidentally; contrast or noncontrast CT can usually detect AVMs > 1 cm, but the diagnosis is confirmed with MRI. Occasionally, a cranial bruit suggests an AVM. Conventional angiography is required for definitive diagnosis and determination of whether the lesion is operable.
Superficial AVMs > 3 cm in diameter are usually obliterated by a combination of microsurgery, radiosurgery, and endovascular surgery. AVMs that are deep or < style="font-weight: bold;">Aneurysms: Aneurysms are focal dilations in arteries. They occur in about 5% of people. Common contributing factors may include arteriosclerosis, hypertension, and hereditary connective tissue disorders (eg, Ehlers-Danlos syndrome, pseudoxanthoma elasticum, autosomal dominant polycystic kidney syndrome). Occasionally, septic emboli cause mycotic aneurysms. Brain aneurysms are most often <> 3 cm in diameter may cause midline shift or herniation. Herniation, midbrain or pontine hemorrhage, intraventricular hemorrhage, acute hydrocephalus, or dissection into the brain stem can impair consciousness and cause coma and death.
Symptoms and Signs
Symptoms typically begin with sudden headache, often during activity. However, headache may be mild or absent in the elderly. Loss of consciousness is common, often within seconds or a few minutes. Nausea, vomiting, delirium, and focal or generalized seizures are also common. Neurologic deficits are usually sudden and progressive. Large hemorrhages, when located in the hemispheres, cause hemiparesis; when located in the posterior fossa, they cause cerebellar or brain stem deficits (eg, conjugate eye deviation or ophthalmoplegia, stertorous breathing, pinpoint pupils, coma). Large hemorrhages are fatal within a few days in about ½ of patients. In survivors, consciousness returns and neurologic deficits gradually diminish to various degrees as the extravasated blood is resorbed. Some patients have surprisingly few neurologic deficits because hemorrhage is less destructive to brain tissue than infarction.
Small hemorrhages may cause focal deficits without impairment of consciousness and with minimal or no headache and nausea. Small hemorrhages may mimic ischemic stroke.
Diagnosis and Treatment
Diagnosis is suggested by sudden onset of headache, focal neurologic deficits, and impaired consciousness, particularly in patients with risk factors. Intracerebral hemorrhage must be distinguished from ischemic stroke, subarachnoid hemorrhage, and other causes of acute neurologic deficits (eg, seizure, hypoglycemia).
Immediate CT or MRI and bedside blood glucose measurement are necessary. Neuroimaging is usually diagnostic. If neuroimaging shows no hemorrhage but subarachnoid hemorrhage is suspected clinically, lumbar puncture is necessary.
Treatment includes supportive measures and control of general medical risk factors. Anticoagulants and antiplatelet drugs are contraindicated. If patients have used anticoagulants, the effects are reversed when possible by giving fresh frozen plasma, vitamin K, or platelet transfusions as indicated. Hypertension should be treated only if mean arterial pressure is > 130 mm Hg or systolic BP is > 185 mm Hg. Nicardipine Some Trade Names
CARDENE
2.5 mg/h IV is given initially; dose is increased by 2.5 mg/h q 5 min to a maximum of 15 mg/h as needed to decrease systolic BP by 10 to 15%. Cerebellar hemisphere hematomas that are > 3 cm in diameter may cause midline shift or herniation, so surgical evacuation is often lifesaving. Early evacuation of large lobar cerebral hematomas may also be lifesaving, but rebleeding occurs frequently, sometimes increasing neurologic deficits. Early evacuation of deep cerebral hematomas is seldom indicated because surgical mortality is high and neurologic deficits are usually severe.
Ischemic stroke
Ischemic stroke is focal brain infarction that produces sudden neurologic deficits persisting > 1 h. Common causes are (from most to least common) nonthrombotic occlusion of small, deep cortical arteries (lacunar infarction); cardiogenic embolism; arterial thrombosis that decreases cerebral blood flow; and artery-to-artery embolism. Diagnosis is clinical, but CT or MRI is done to exclude hemorrhage and confirm the presence and extent of stroke. Thrombolytic therapy may be useful acutely in certain patients. Depending on the cause of stroke, carotid endarterectomy, antiplatelet drugs, or warfarin may help reduce risk of subsequent strokes.
Etiology
Ischemia usually results from thrombi or emboli. Even infarcts classified as lacunar based on clinical criteria (morphology, size, and location) often involve small thrombi or emboli.
Thrombosis: 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. Partial or complete thrombotic occlusion occurs most often at the main trunk of the middle cerebral artery and its branches but is also common in the large arteries at the base of the brain, in deep perforating arteries, and in small cortical branches. The basilar artery and the segment of the internal carotid artery between the cavernous sinus and supraclinoid process are often occluded.
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, moyamoya disease, Binswanger's disease). Older oral contraceptive formulations increase risk of thrombosis.
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). Rarely, thrombosis of the subclavian artery results in embolic stroke in the vertebral artery or its branches.
Lacunar infarcts: Ischemic stroke can also result from 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: Less commonly, ischemic stroke results from vasospasm (eg, during migraine, after subarachnoid hemorrhage, after use of sympathomimetic drugs such as cocaine or amphetamines) or venous sinus thrombosis (eg, during intracranial infection, postoperatively, peripartum, secondary to a hypercoagulation disorder).
Pathophysiology
Inadequate blood flow in a single brain artery can often be compensated for by an efficient collateral system, particularly between the carotid and vertebral arteries via anastomoses at the circle of Willis and, to a lesser extent, between major arteries supplying the cerebral hemispheres. However, normal variations in the circle of Willis and in the caliber of various collateral vessels, atherosclerosis, and other acquired arterial lesions can interfere with collateral flow, increasing the chance that blockage of one artery will cause brain ischemia.
Some neurons die when perfusion is <> 5 min; however, the extent of damage depends on the severity of ischemia. If it is mild, damage proceeds slowly; thus, even if perfusion is 40% of normal, 3 to 6 h may elapse before brain tissue is completely lost. However, if severe ischemia (ie, decrease in perfusion) persists > 15 to 30 min, all of the affected tissue dies (infarction). Damage occurs more rapidly during hyperthermia and more slowly during hypothermia. If tissues are ischemic but not yet irreversibly damaged, promptly restoring blood flow may reduce or reverse injury. For example, intervention may be able to salvage the moderately ischemic areas (penumbras) that often surround areas of severe ischemia (these areas exist because of collateral flow).
Mechanisms of ischemic injury include edema, microvascular thrombosis, programmed cell death (apoptosis), and infarction with cell necrosis. Inflammatory mediators (eg, IL-1B, tumor necrosis factor-α) contribute to edema and microvascular thrombosis. Edema, if severe or extensive, can increase intracranial pressure. Many factors may contribute to necrotic cell death; they include loss of ATP stores, loss of ionic homeostasis (including intracellular Ca accumulation), lipid peroxidative damage to cell membranes by free radicals (an iron-mediated process), excitatory neurotoxins (eg, glutamate), and intracellular acidosis due to accumulation of lactate.
Symptoms and Signs
Symptoms and signs depend on the part of brain affected. Patterns of neurologic deficits often suggest the affected artery but correlation is often inexact.
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 thrombotic 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. A stroke is considered submaximal when, after it is complete, there is residual function in the affected area, suggesting viable tissue at risk of damage.
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. Lacunar infarcts may produce one of the classic lacunar syndromes (eg, pure motor hemiparesis, pure sensory hemianesthesia, ataxic hemiparesis, dysarthria–clumsy hand syndrome); signs of cortical dysfunction (eg, aphasia) are absent. Multiple lacunar infarcts may result in multi-infarct dementia.
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
Diagnosis is suggested by sudden neurologic deficits referable to a specific arterial territory. Ischemic stroke must be distinguished from other causes of similar focal deficits (eg, hypoglycemia; postictal [Todd's] paralysis; hemorrhagic stroke; rarely, migraine). Headache, coma or stupor, and vomiting are more likely with hemorrhagic stroke.
Although diagnosis is clinical, neuroimaging and bedside glucose testing are mandatory. 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 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. After 24 h of ischemia, medium-sized to large infarcts are usually 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 CT initial neuroimaging.
Insular Ribbon Loss
Distinction between lacunar, embolic, and thrombotic stroke based on history, examination, and neuroimaging is not always reliable, so tests to identify common or treatable causes and risk factors for all of these types of strokes are routinely done. These tests typically include carotid duplex ultrasonography, ECG, transesophageal echocardiography, and various blood tests (CBC, platelet count, PT/PTT, fasting blood glucose, lipid profile, homocysteine, ESR, and, for at-risk patients, syphilis serology). Troponin I level is measured to detect concomitant MI. Magnetic resonance or CT angiography is also often done. Other tests (eg, antiphospholipid antibodies) are done if certain disorders are suspected clinically.
Prognosis
Stroke severity and progression are often assessed using standardized measures such as the National Institutes of Health 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.
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. Complete neurologic recovery occurs in about 10%. 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 aging.
Treatment
Acute: Guidelines for early management of stroke are available from the. 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 situations:
• 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 tissue plasminogen activator (tPA) is likely.
If indicated, nicardipine Some Trade Names
CARDENE
2.5 mg/h IV is given initially; dose is increased by 2.5 mg/h q 5 min to a maximum of 15 mg/h as needed to decrease systolic BP by 10 to 15%. Alternatively, IV labetalol Some Trade Names
NORMODYNE
TRANDATE
can be used.
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 Some Trade Names
BUFFERIN
ECOTRIN
GENACOTE
325 mg po) when they are admitted to the hospital. Contraindications to antiplatelet drugs include aspirin- or NSAID-induced asthma or urticaria, other hypersensitivity to aspirin or to tartrazine, acute GI bleeding, G6PD deficiency, and use of warfarin Some Trade Names
COUMADIN
.Recombinant tPA is used for patients with acute ischemic stroke of <> 1⁄3 of the territory supplied by the middle cerebral artery) on CT scan
Rapidly decreasing symptoms
Presentation suggesting subarachnoid hemorrhage even if CT is negative
History of intracranial hemorrhage, AVM, aneurysm, or brain tumor
History of stroke or head trauma within the past 3 mo
Systolic BP > 185 mm Hg or diastolic BP > 110 mm Hg after antihypertensive treatment
Arterial puncture at noncompressible site or lumbar puncture in the past 7 days
Major surgery or serious trauma in the past 14 days
GI or urinary tract hemorrhage in the past 21 days
Platelet count <> 1.7, or PT > 15
Seizure at onset of stroke
Blood glucose <> 400 mg/dL (<> 22.2 mmol/L)
Bacterial endocarditis or suspected pericarditis
AVM = arteriovenous malformation.
Thrombolysis-in-situ (angiographically directed intra-arterial thrombolysis) of a thrombus or embolus can sometimes be used for major strokes if symptoms have begun > 3 h but < style="font-weight: bold;">Etiology
Most TIAs are caused by emboli, usually from carotid or vertebral arteries, although most of the causes of ischemic stroke can also result in TIAs. Uncommonly, TIAs result from impaired perfusion due to severe hypoxemia, reduced O2-carrying capacity of blood (eg, profound anemia, carbon monoxide poisoning), or increased blood viscosity (eg, severe polycythemia), particularly in brain arteries with preexisting stenosis. Systemic hypotension does not usually cause cerebral ischemia unless it is severe or arterial stenosis preexists because autoregulation maintains brain blood flow at near normal levels over a wide range of systemic BPs.
In 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.
Occasionally, TIAs occur in children with a severe cardiovascular disorder that produces emboli or a very high Hct.
Symptoms and Signs
Neurologic deficits are similar to those of strokes Transient monocular blindness (amaurosis fugax), which usually lasts <>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, including tests for carotid stenosis, cardiac sources of emboli, atrial fibrillation, and hematologic abnormalities and screening for stroke risk factors. Because risk of subsequent ischemic stroke is high and immediate, evaluation proceeds rapidly, usually on an inpatient basis. It is not clear which patients, if any, can be safely discharged from the emergency department.
Treatment is aimed at preventing strokes; antiplatelet drugs 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. Warfarin Some Trade Names
COUMADIN
is indicated if cardiac sources of emboli are present. Modifying stroke risk factors, when possible, may prevent stroke.
Subarachnoid hemorrhage(SAH)
Subarachnoid hemorrhage is sudden bleeding into the subarachnoid space. The most common cause of spontaneous bleeding is a ruptured aneurysm. Symptoms include sudden, severe headache, usually with loss or impairment of consciousness. Secondary vasospasm (causing focal brain ischemia), meningismus, and hydrocephalus (causing persistent headache and obtundation) are common. Diagnosis is by CT or MRI; if neuroimaging is normal, diagnosis is by CSF analysis. Treatment is with supportive measures and neurosurgery or endovascular measures, preferably in a referral center.
Etiology and Pathophysiology
Subarachnoid hemorrhage is bleeding between the arachnoid and pia mater. In general, head trauma is the most common cause, but traumatic subarachnoid hemorrhage is usually considered a separate disorder. Spontaneous (primary) subarachnoid hemorrhage usually results from ruptured aneurysms. A congenital intracranial saccular or berry aneurysm is the cause in about 85% of patients. Bleeding may stop spontaneously. Aneurysmal hemorrhage may occur at any age but is most common from age 40 to 65. Less common causes are mycotic aneurysms, arteriovenous malformations, and bleeding disorders.
Blood in the subarachnoid space causes a chemical meningitis that commonly increases intracranial pressure for days or a few weeks. Secondary vasospasm may cause focal brain ischemia; about 25% of patients develop signs of a TIA or ischemic stroke. Brain edema is maximal and risk of vasospasm and subsequent infarction (called angry brain) is highest between 72 h and 10 days. Secondary acute hydrocephalus is also common. A 2nd rupture (rebleeding) sometimes occurs, most often within about 7 days.
Symptoms and Signs
Headache is usually severe, peaking within seconds. Loss of consciousness may follow, usually immediately but sometimes not for several hours. Severe neurologic deficits may develop and become irreversible within minutes or a few hours. Sensorium may be impaired, and patients may become restless. Seizures are possible. Usually, the neck is not stiff initially unless the cerebellar tonsils herniate. However, within 24 h, chemical meningitis causes moderate to marked meningismus, vomiting, and sometimes bilateral extensor plantar responses. Heart or respiratory rate is often abnormal. Fever, continued headaches, and confusion are common during the first 5 to 10 days. Secondary hydrocephalus may cause headache, obtundation, and motor deficits that persist for weeks. Rebleeding may cause recurrent or new symptoms.
Diagnosis
Diagnosis is suggested by characteristic symptoms. Testing should proceed as rapidly as possible, before damage becomes irreversible. Noncontrast CT is > 90% sensitive. MRI is comparably sensitive but less likely to be immediately available. False-negative results occur if volume of blood is small. If subarachnoid hemorrhage is suspected clinically but not identified on neuroimaging or if neuroimaging is not immediately available, lumbar puncture is done. Lumbar puncture is contraindicated if increased intracranial pressure is suspected because the sudden decrease in CSF pressure may lessen the tamponade of a clot on the ruptured aneurysm, causing further bleeding.
CSF findings suggesting subarachnoid hemorrhage include numerous RBCs, xanthochromia, and increased pressure. RBCs in CSF may also be caused by traumatic lumbar puncture. Traumatic lumbar puncture is suspected if the RBC count decreases in tubes of CSF drawn sequentially during the same lumbar puncture About 6 h or more after a subarachnoid hemorrhage, RBCs become crenated and lyse, resulting in a xanthochromic CSF supernatant and visible crenated RBCs (noted during microscopic CSF examination); these findings usually indicate that subarachnoid hemorrhage preceded the lumbar puncture. If there is still doubt, hemorrhage should be assumed, or the lumbar puncture should be repeated in 8 to 12 h. In patients with subarachnoid hemorrhage, conventional cerebral angiography is done as soon as possible after the initial bleeding episode; alternatives include magnetic resonance angiography and CT angiography. All 4 arteries (2 carotid and 2 vertebral arteries) should be injected because up to 20% of patients (mostly women) have multiple aneurysms.
On ECG, subarachnoid hemorrhage may produce ST-segment elevation or depression. It can cause syncope, mimicking MI. Other possible ECG abnormalities include prolongation of the QRS or QT intervals and peaking or deep, symmetric inversion of T waves.
Prognosis and Treatment
About 35% of patients die after the first aneurysmal subarachnoid hemorrhage; another 15% die within a few weeks because of a subsequent rupture. After 6 mo, a 2nd rupture occurs at a rate of about 3%/yr. In general, prognosis is grave with an aneurysm, better with an arteriovenous malformation, and best when 4-vessel angiography does not detect a lesion, presumably because the bleeding source is small and has sealed itself. Among survivors, neurologic damage is common, even when treatment is optimal.
Patients with subarachnoid hemorrhage should be treated in referral centers whenever possible. Hypertension should be treated only if mean arterial pressure is > 130 mm Hg; euvolemia is maintained, and IV nicardipine Some Trade Names
CARDENE
is titrated as for intracerebral hemorrhage Bed rest is mandatory. Restlessness and headache are treated symptomatically. Stool softeners are given to prevent constipation, which can lead to straining. Anticoagulants and antiplatelet drugs are contraindicated.
Nimodipine Some Trade Names
NIMOTOP
60 mg po q 4 h is given for 21 days to prevent vasospasm, but BP needs to be maintained in the desirable range (usually considered to be a mean arterial pressure of 70 to 130 mm Hg and a systolic pressure of 120 to 185 mm Hg). If clinical signs of acute hydrocephalus occur, ventricular drainage should be considered.
Occlusion of the aneurysm reduces risk of rebleeding. Detachable endovascular coils can be inserted during angiography to occlude the aneurysm. Alternatively, if the aneurysm is accessible, surgery to clip the aneurysm or bypass its blood flow can be done, especially for patients with an evacuable hematoma or acute hydrocephalus. If patients are arousable, most vascular neurosurgeons operate within the first 24 h to minimize risk of rebleeding and risks due to angry brain. If > 24 h have elapsed, some neurosurgeons delay surgery until 10 days have passed; this approach decreases risks due to angry brain but increases risk of rebleeding and overall mortality.
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).
Intracerebral hemorrhage
Intracerebral hemorrhage is focal bleeding from a blood vessel in the brain parenchyma. The cause is usually hypertension. Typical symptoms include focal neurologic deficits, often with abrupt onset of headache, nausea, and impairment of consciousness. Diagnosis is by CT or MRI. Treatment includes BP control, supportive measures, and, for some patients, surgical evacuation.
Most intracerebral hemorrhages occur in the basal ganglia, cerebral lobes, cerebellum, or pons. Intracerebral hemorrhage may also occur in other parts of the brain stem or in the midbrain.
Etiology and Pathophysiology
Intracerebral hemorrhage usually results from rupture of an arteriosclerotic small artery that has been weakened, primarily by chronic arterial hypertension. Such hemorrhages are usually large, single, and catastrophic. Use of cocaine or, occasionally, other sympathomimetic drugs can cause transient severe hypertension leading to hemorrhage. Less often, intracerebral hemorrhage results from congenital aneurysm, arteriovenous or other vascular malformation trauma, mycotic aneurysm, brain infarct (hemorrhagic infarction), primary or metastatic brain tumor, excessive anticoagulation, blood dyscrasia, or a bleeding or vasculitic disorder.
Vascular Lesions in the Brain
Common brain vascular lesions include arteriovenous malformations and aneurysms.
Arteriovenous malformations (AVMs): AVMs are tangled, dilated blood vessels in which arteries flow directly into veins. AVMs occur most often at the junction of cerebral arteries, usually within the parenchyma of the frontal-parietal region, frontal lobe, lateral cerebellum, or overlying occipital lobe. AVMs can bleed or directly compress brain tissue; seizures or ischemia may result.
Neuroimaging may detect them incidentally; contrast or noncontrast CT can usually detect AVMs > 1 cm, but the diagnosis is confirmed with MRI. Occasionally, a cranial bruit suggests an AVM. Conventional angiography is required for definitive diagnosis and determination of whether the lesion is operable.
Superficial AVMs > 3 cm in diameter are usually obliterated by a combination of microsurgery, radiosurgery, and endovascular surgery. AVMs that are deep or < style="font-weight: bold;">Aneurysms: Aneurysms are focal dilations in arteries. They occur in about 5% of people. Common contributing factors may include arteriosclerosis, hypertension, and hereditary connective tissue disorders (eg, Ehlers-Danlos syndrome, pseudoxanthoma elasticum, autosomal dominant polycystic kidney syndrome). Occasionally, septic emboli cause mycotic aneurysms. Brain aneurysms are most often <> 3 cm in diameter may cause midline shift or herniation. Herniation, midbrain or pontine hemorrhage, intraventricular hemorrhage, acute hydrocephalus, or dissection into the brain stem can impair consciousness and cause coma and death.
Symptoms and Signs
Symptoms typically begin with sudden headache, often during activity. However, headache may be mild or absent in the elderly. Loss of consciousness is common, often within seconds or a few minutes. Nausea, vomiting, delirium, and focal or generalized seizures are also common. Neurologic deficits are usually sudden and progressive. Large hemorrhages, when located in the hemispheres, cause hemiparesis; when located in the posterior fossa, they cause cerebellar or brain stem deficits (eg, conjugate eye deviation or ophthalmoplegia, stertorous breathing, pinpoint pupils, coma). Large hemorrhages are fatal within a few days in about ½ of patients. In survivors, consciousness returns and neurologic deficits gradually diminish to various degrees as the extravasated blood is resorbed. Some patients have surprisingly few neurologic deficits because hemorrhage is less destructive to brain tissue than infarction.
Small hemorrhages may cause focal deficits without impairment of consciousness and with minimal or no headache and nausea. Small hemorrhages may mimic ischemic stroke.
Diagnosis and Treatment
Diagnosis is suggested by sudden onset of headache, focal neurologic deficits, and impaired consciousness, particularly in patients with risk factors. Intracerebral hemorrhage must be distinguished from ischemic stroke, subarachnoid hemorrhage, and other causes of acute neurologic deficits (eg, seizure, hypoglycemia).
Immediate CT or MRI and bedside blood glucose measurement are necessary. Neuroimaging is usually diagnostic. If neuroimaging shows no hemorrhage but subarachnoid hemorrhage is suspected clinically, lumbar puncture is necessary.
Treatment includes supportive measures and control of general medical risk factors. Anticoagulants and antiplatelet drugs are contraindicated. If patients have used anticoagulants, the effects are reversed when possible by giving fresh frozen plasma, vitamin K, or platelet transfusions as indicated. Hypertension should be treated only if mean arterial pressure is > 130 mm Hg or systolic BP is > 185 mm Hg. Nicardipine Some Trade Names
CARDENE
2.5 mg/h IV is given initially; dose is increased by 2.5 mg/h q 5 min to a maximum of 15 mg/h as needed to decrease systolic BP by 10 to 15%. Cerebellar hemisphere hematomas that are > 3 cm in diameter may cause midline shift or herniation, so surgical evacuation is often lifesaving. Early evacuation of large lobar cerebral hematomas may also be lifesaving, but rebleeding occurs frequently, sometimes increasing neurologic deficits. Early evacuation of deep cerebral hematomas is seldom indicated because surgical mortality is high and neurologic deficits are usually severe.
Ischemic stroke
Ischemic stroke is focal brain infarction that produces sudden neurologic deficits persisting > 1 h. Common causes are (from most to least common) nonthrombotic occlusion of small, deep cortical arteries (lacunar infarction); cardiogenic embolism; arterial thrombosis that decreases cerebral blood flow; and artery-to-artery embolism. Diagnosis is clinical, but CT or MRI is done to exclude hemorrhage and confirm the presence and extent of stroke. Thrombolytic therapy may be useful acutely in certain patients. Depending on the cause of stroke, carotid endarterectomy, antiplatelet drugs, or warfarin may help reduce risk of subsequent strokes.
Etiology
Ischemia usually results from thrombi or emboli. Even infarcts classified as lacunar based on clinical criteria (morphology, size, and location) often involve small thrombi or emboli.
Thrombosis: 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. Partial or complete thrombotic occlusion occurs most often at the main trunk of the middle cerebral artery and its branches but is also common in the large arteries at the base of the brain, in deep perforating arteries, and in small cortical branches. The basilar artery and the segment of the internal carotid artery between the cavernous sinus and supraclinoid process are often occluded.
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, moyamoya disease, Binswanger's disease). Older oral contraceptive formulations increase risk of thrombosis.
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). Rarely, thrombosis of the subclavian artery results in embolic stroke in the vertebral artery or its branches.
Lacunar infarcts: Ischemic stroke can also result from 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: Less commonly, ischemic stroke results from vasospasm (eg, during migraine, after subarachnoid hemorrhage, after use of sympathomimetic drugs such as cocaine or amphetamines) or venous sinus thrombosis (eg, during intracranial infection, postoperatively, peripartum, secondary to a hypercoagulation disorder).
Pathophysiology
Inadequate blood flow in a single brain artery can often be compensated for by an efficient collateral system, particularly between the carotid and vertebral arteries via anastomoses at the circle of Willis and, to a lesser extent, between major arteries supplying the cerebral hemispheres. However, normal variations in the circle of Willis and in the caliber of various collateral vessels, atherosclerosis, and other acquired arterial lesions can interfere with collateral flow, increasing the chance that blockage of one artery will cause brain ischemia.
Some neurons die when perfusion is <> 5 min; however, the extent of damage depends on the severity of ischemia. If it is mild, damage proceeds slowly; thus, even if perfusion is 40% of normal, 3 to 6 h may elapse before brain tissue is completely lost. However, if severe ischemia (ie, decrease in perfusion) persists > 15 to 30 min, all of the affected tissue dies (infarction). Damage occurs more rapidly during hyperthermia and more slowly during hypothermia. If tissues are ischemic but not yet irreversibly damaged, promptly restoring blood flow may reduce or reverse injury. For example, intervention may be able to salvage the moderately ischemic areas (penumbras) that often surround areas of severe ischemia (these areas exist because of collateral flow).
Mechanisms of ischemic injury include edema, microvascular thrombosis, programmed cell death (apoptosis), and infarction with cell necrosis. Inflammatory mediators (eg, IL-1B, tumor necrosis factor-α) contribute to edema and microvascular thrombosis. Edema, if severe or extensive, can increase intracranial pressure. Many factors may contribute to necrotic cell death; they include loss of ATP stores, loss of ionic homeostasis (including intracellular Ca accumulation), lipid peroxidative damage to cell membranes by free radicals (an iron-mediated process), excitatory neurotoxins (eg, glutamate), and intracellular acidosis due to accumulation of lactate.
Symptoms and Signs
Symptoms and signs depend on the part of brain affected. Patterns of neurologic deficits often suggest the affected artery but correlation is often inexact.
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 thrombotic 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. A stroke is considered submaximal when, after it is complete, there is residual function in the affected area, suggesting viable tissue at risk of damage.
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. Lacunar infarcts may produce one of the classic lacunar syndromes (eg, pure motor hemiparesis, pure sensory hemianesthesia, ataxic hemiparesis, dysarthria–clumsy hand syndrome); signs of cortical dysfunction (eg, aphasia) are absent. Multiple lacunar infarcts may result in multi-infarct dementia.
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
Diagnosis is suggested by sudden neurologic deficits referable to a specific arterial territory. Ischemic stroke must be distinguished from other causes of similar focal deficits (eg, hypoglycemia; postictal [Todd's] paralysis; hemorrhagic stroke; rarely, migraine). Headache, coma or stupor, and vomiting are more likely with hemorrhagic stroke.
Although diagnosis is clinical, neuroimaging and bedside glucose testing are mandatory. 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 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. After 24 h of ischemia, medium-sized to large infarcts are usually 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 CT initial neuroimaging.
Insular Ribbon Loss
Distinction between lacunar, embolic, and thrombotic stroke based on history, examination, and neuroimaging is not always reliable, so tests to identify common or treatable causes and risk factors for all of these types of strokes are routinely done. These tests typically include carotid duplex ultrasonography, ECG, transesophageal echocardiography, and various blood tests (CBC, platelet count, PT/PTT, fasting blood glucose, lipid profile, homocysteine, ESR, and, for at-risk patients, syphilis serology). Troponin I level is measured to detect concomitant MI. Magnetic resonance or CT angiography is also often done. Other tests (eg, antiphospholipid antibodies) are done if certain disorders are suspected clinically.
Prognosis
Stroke severity and progression are often assessed using standardized measures such as the National Institutes of Health 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.
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. Complete neurologic recovery occurs in about 10%. 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 aging.
Treatment
Acute: Guidelines for early management of stroke are available from the. 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 situations:
• 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 tissue plasminogen activator (tPA) is likely.
If indicated, nicardipine Some Trade Names
CARDENE
2.5 mg/h IV is given initially; dose is increased by 2.5 mg/h q 5 min to a maximum of 15 mg/h as needed to decrease systolic BP by 10 to 15%. Alternatively, IV labetalol Some Trade Names
NORMODYNE
TRANDATE
can be used.
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 Some Trade Names
BUFFERIN
ECOTRIN
GENACOTE
325 mg po) when they are admitted to the hospital. Contraindications to antiplatelet drugs include aspirin- or NSAID-induced asthma or urticaria, other hypersensitivity to aspirin or to tartrazine, acute GI bleeding, G6PD deficiency, and use of warfarin Some Trade Names
COUMADIN
.Recombinant tPA is used for patients with acute ischemic stroke of <> 1⁄3 of the territory supplied by the middle cerebral artery) on CT scan
Rapidly decreasing symptoms
Presentation suggesting subarachnoid hemorrhage even if CT is negative
History of intracranial hemorrhage, AVM, aneurysm, or brain tumor
History of stroke or head trauma within the past 3 mo
Systolic BP > 185 mm Hg or diastolic BP > 110 mm Hg after antihypertensive treatment
Arterial puncture at noncompressible site or lumbar puncture in the past 7 days
Major surgery or serious trauma in the past 14 days
GI or urinary tract hemorrhage in the past 21 days
Platelet count <> 1.7, or PT > 15
Seizure at onset of stroke
Blood glucose <> 400 mg/dL (<> 22.2 mmol/L)
Bacterial endocarditis or suspected pericarditis
AVM = arteriovenous malformation.
Thrombolysis-in-situ (angiographically directed intra-arterial thrombolysis) of a thrombus or embolus can sometimes be used for major strokes if symptoms have begun > 3 h but < style="font-weight: bold;">Etiology
Most TIAs are caused by emboli, usually from carotid or vertebral arteries, although most of the causes of ischemic stroke can also result in TIAs. Uncommonly, TIAs result from impaired perfusion due to severe hypoxemia, reduced O2-carrying capacity of blood (eg, profound anemia, carbon monoxide poisoning), or increased blood viscosity (eg, severe polycythemia), particularly in brain arteries with preexisting stenosis. Systemic hypotension does not usually cause cerebral ischemia unless it is severe or arterial stenosis preexists because autoregulation maintains brain blood flow at near normal levels over a wide range of systemic BPs.
In 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.
Occasionally, TIAs occur in children with a severe cardiovascular disorder that produces emboli or a very high Hct.
Symptoms and Signs
Neurologic deficits are similar to those of strokes Transient monocular blindness (amaurosis fugax), which usually lasts <>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, including tests for carotid stenosis, cardiac sources of emboli, atrial fibrillation, and hematologic abnormalities and screening for stroke risk factors. Because risk of subsequent ischemic stroke is high and immediate, evaluation proceeds rapidly, usually on an inpatient basis. It is not clear which patients, if any, can be safely discharged from the emergency department.
Treatment is aimed at preventing strokes; antiplatelet drugs 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. Warfarin Some Trade Names
COUMADIN
is indicated if cardiac sources of emboli are present. Modifying stroke risk factors, when possible, may prevent stroke.
Subarachnoid hemorrhage(SAH)
Subarachnoid hemorrhage is sudden bleeding into the subarachnoid space. The most common cause of spontaneous bleeding is a ruptured aneurysm. Symptoms include sudden, severe headache, usually with loss or impairment of consciousness. Secondary vasospasm (causing focal brain ischemia), meningismus, and hydrocephalus (causing persistent headache and obtundation) are common. Diagnosis is by CT or MRI; if neuroimaging is normal, diagnosis is by CSF analysis. Treatment is with supportive measures and neurosurgery or endovascular measures, preferably in a referral center.
Etiology and Pathophysiology
Subarachnoid hemorrhage is bleeding between the arachnoid and pia mater. In general, head trauma is the most common cause, but traumatic subarachnoid hemorrhage is usually considered a separate disorder. Spontaneous (primary) subarachnoid hemorrhage usually results from ruptured aneurysms. A congenital intracranial saccular or berry aneurysm is the cause in about 85% of patients. Bleeding may stop spontaneously. Aneurysmal hemorrhage may occur at any age but is most common from age 40 to 65. Less common causes are mycotic aneurysms, arteriovenous malformations, and bleeding disorders.
Blood in the subarachnoid space causes a chemical meningitis that commonly increases intracranial pressure for days or a few weeks. Secondary vasospasm may cause focal brain ischemia; about 25% of patients develop signs of a TIA or ischemic stroke. Brain edema is maximal and risk of vasospasm and subsequent infarction (called angry brain) is highest between 72 h and 10 days. Secondary acute hydrocephalus is also common. A 2nd rupture (rebleeding) sometimes occurs, most often within about 7 days.
Symptoms and Signs
Headache is usually severe, peaking within seconds. Loss of consciousness may follow, usually immediately but sometimes not for several hours. Severe neurologic deficits may develop and become irreversible within minutes or a few hours. Sensorium may be impaired, and patients may become restless. Seizures are possible. Usually, the neck is not stiff initially unless the cerebellar tonsils herniate. However, within 24 h, chemical meningitis causes moderate to marked meningismus, vomiting, and sometimes bilateral extensor plantar responses. Heart or respiratory rate is often abnormal. Fever, continued headaches, and confusion are common during the first 5 to 10 days. Secondary hydrocephalus may cause headache, obtundation, and motor deficits that persist for weeks. Rebleeding may cause recurrent or new symptoms.
Diagnosis
Diagnosis is suggested by characteristic symptoms. Testing should proceed as rapidly as possible, before damage becomes irreversible. Noncontrast CT is > 90% sensitive. MRI is comparably sensitive but less likely to be immediately available. False-negative results occur if volume of blood is small. If subarachnoid hemorrhage is suspected clinically but not identified on neuroimaging or if neuroimaging is not immediately available, lumbar puncture is done. Lumbar puncture is contraindicated if increased intracranial pressure is suspected because the sudden decrease in CSF pressure may lessen the tamponade of a clot on the ruptured aneurysm, causing further bleeding.
CSF findings suggesting subarachnoid hemorrhage include numerous RBCs, xanthochromia, and increased pressure. RBCs in CSF may also be caused by traumatic lumbar puncture. Traumatic lumbar puncture is suspected if the RBC count decreases in tubes of CSF drawn sequentially during the same lumbar puncture About 6 h or more after a subarachnoid hemorrhage, RBCs become crenated and lyse, resulting in a xanthochromic CSF supernatant and visible crenated RBCs (noted during microscopic CSF examination); these findings usually indicate that subarachnoid hemorrhage preceded the lumbar puncture. If there is still doubt, hemorrhage should be assumed, or the lumbar puncture should be repeated in 8 to 12 h. In patients with subarachnoid hemorrhage, conventional cerebral angiography is done as soon as possible after the initial bleeding episode; alternatives include magnetic resonance angiography and CT angiography. All 4 arteries (2 carotid and 2 vertebral arteries) should be injected because up to 20% of patients (mostly women) have multiple aneurysms.
On ECG, subarachnoid hemorrhage may produce ST-segment elevation or depression. It can cause syncope, mimicking MI. Other possible ECG abnormalities include prolongation of the QRS or QT intervals and peaking or deep, symmetric inversion of T waves.
Prognosis and Treatment
About 35% of patients die after the first aneurysmal subarachnoid hemorrhage; another 15% die within a few weeks because of a subsequent rupture. After 6 mo, a 2nd rupture occurs at a rate of about 3%/yr. In general, prognosis is grave with an aneurysm, better with an arteriovenous malformation, and best when 4-vessel angiography does not detect a lesion, presumably because the bleeding source is small and has sealed itself. Among survivors, neurologic damage is common, even when treatment is optimal.
Patients with subarachnoid hemorrhage should be treated in referral centers whenever possible. Hypertension should be treated only if mean arterial pressure is > 130 mm Hg; euvolemia is maintained, and IV nicardipine Some Trade Names
CARDENE
is titrated as for intracerebral hemorrhage Bed rest is mandatory. Restlessness and headache are treated symptomatically. Stool softeners are given to prevent constipation, which can lead to straining. Anticoagulants and antiplatelet drugs are contraindicated.
Nimodipine Some Trade Names
NIMOTOP
60 mg po q 4 h is given for 21 days to prevent vasospasm, but BP needs to be maintained in the desirable range (usually considered to be a mean arterial pressure of 70 to 130 mm Hg and a systolic pressure of 120 to 185 mm Hg). If clinical signs of acute hydrocephalus occur, ventricular drainage should be considered.
Occlusion of the aneurysm reduces risk of rebleeding. Detachable endovascular coils can be inserted during angiography to occlude the aneurysm. Alternatively, if the aneurysm is accessible, surgery to clip the aneurysm or bypass its blood flow can be done, especially for patients with an evacuable hematoma or acute hydrocephalus. If patients are arousable, most vascular neurosurgeons operate within the first 24 h to minimize risk of rebleeding and risks due to angry brain. If > 24 h have elapsed, some neurosurgeons delay surgery until 10 days have passed; this approach decreases risks due to angry brain but increases risk of rebleeding and overall mortality.
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