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Clinical Evaluation of Stroke**(Contents borrowed from the original Up to Date article, “Overview of the Evaluation of Stroke” by Louis Caplan, 2012. Further details can be found in Dr Caplan’s article)The clinical evaluation of a patient with an acute stroke should be broken down into 4 separate steps1. Understanding the classification of stroke2. An initial quick evaluation to stabilize vital signs, determine if intracranial hemorrhage is present, and decide if thrombolytic therapy is warranted.3. Forming a hypothesis of stroke etiology based on history, physical examination and neuroimaging studies.4. Confirming the precise pathophysiological process with more directed diagnostic studies.I. Classification of cerebrovascular diseaseIschemic infarctions may be caused by pathological process intrinsic to the blood vessels (such as atherosclerosis, lipohyalinosis, inflammation, amyloid deposition, arterial dissection, developmental malformation, aneurysmal dilation or venous thrombosis).Ischemic infarctions may also originate remotely (such as when an embolus from the heart or extracranial circulation lodges in an intracranial vessel).Ischemic infarctions may also arise from inadequate blood flow due to decreased cerebral perfusion pressure.Intracranial hemorrhage accounts for 20% of cerebrovascular accidents and may arise from rupture of a vessel within the subarachnoid space or brain parenchyma.A. Transient Ischemic Attack (TIA)The definition of a TIA is “a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction”. This definition is tissue based and not just clinical and replaces the more arbitrary former definition of a reversible ischemic neurological event lasting less than 24 hours. TIA’s may progress to ischemic strokes, especially if other risk factors are present. An “ABCD” score may help to predict those at greatest risk.The ABCD score is calculated based on the following:Age (≥60 years = 1 point) Blood pressure elevation when first assessed after TIA (systolic ≥140 mmHg or diastolic ≥90 mmHg = 1 point)Clinical features (unilateral weakness = 2 points; isolated speech disturbance = 1 point; other = 0 points)Duration of TIA symptoms (≥60 minutes = 2 points; 10 to 59 minutes = 1 point; <10 minutes = 0 points)Diabetes (present = 1 point)The scoring system predicts risk of ischemic infarction within 2 days as follows:Score 6 to 7: High two-day stroke risk (8 percent)Score 4 to 5: Moderate two-day stroke risk (4 percent)Score 0 to 3: Low two-day stroke risk (1 percent)B. Intracerebral HemorrhageBleeding from arterioles directly into the brain results in a localized hematoma which spreads along white matter pathways. Neurological symptoms usually increase over minutes to a few hours. Causes of intracranial hemorrhage include hypertension, trauma, bleeding diatheses, amyloid angiopathy, sympathomimetic drug use (especially amphetamines and cocaine) and vascular malformations.C. Subarachnoid HemorrhageRupture of arterial aneurysms is the major cause of SAH. Following aneurysm rupture, blood is released directly into the subarachnoid CSF space, rapidly increasing intracranial pressure, resulting in coma or death if the bleeding continues. Bleeding generally only lasts a few seconds, but rebleeding is common. Symptoms of SAH begin abruptly and usually consist of a severe thunderclap headache (“the worst headache of my life”). The onset of headache may or may not be associated with a brief loss of consciousness, seizures, nausea, vomiting, and/or nuchal rigidity. There are usually no focal neurological signs at presentation.D. IschemiaThere are 3 major types of brain ischemia:ThrombosisEmbolismSystemic HypoperfusionThrombotic stroke is caused by thrombus formation within an artery that either reduces blood flow distally in the vessel or breaks of to cause an artery-to-artery embolus. Thrombotic stroke can further be divided into either large or small vessel disease. Large vessel thrombotic stroke can originate in either the extracranial or intracranial arterial system with atherosclerosis the most common cause. Intrinsic lesions in large extracranial and intracranial arteries cause symptoms by reducing blood flow beyond obstructive lesions, and by serving as the source of intra-arterial emboli. At times a combination of mechanisms is operant. Severe stenosis promotes the formation of thrombi which can break off and embolize, and the reduced blood flow caused by the vascular obstruction makes the circulation less competent at washing out and clearing these emboli. Pathologies affecting large extracranial vessels include atherosclerosis, arterial dissection, Takayasu arteritis, giant cell arteritis, and fibromuscular dysplasia. Pathologies affecting large intracranial vessels include atherosclerosis, arterial dissection, arteritis or vasculitis, noninflammatory vasculopathy (such as Moyamoya syndrome) and vasoconstriction.Small vessel disease refers to penetrating arteries that arise from the distal vertebral artery, the basilar artery, the MCA, and the circle of Willis arteries. These small arteries thrombose either due to a lipid hyaline buildup due to hypertension (‘lipohyalinosis”) or from artery-to-artery embolis of thrombus from more proximal large vessels. Small vessel disease results in small deep infarcts referred to as lacunes.Embolic stroke is caused by “debris” originating elsewhere that block arterial access to a particular brain region. Since the process is not localized as with thrombosis, local therapy only temporarily solves the problem and further events may occur if the source of the emboli is not identified and treated.There are four categories of embolic stroke:Known cardioembolic sourcesPossible cardiac or aortic arch sourceKnown arterial sourceTruly unknown source after an extensive diagnostic evaluationThe symptoms of an embolic stroke depend upon the region of brain rendered ischemic. The embolus suddenly blocks the recipient site so that the onset of symptoms is abrupt and usually maximal at the start. Unlike thrombosis, multiple sites within different vascular territories may be affected when the source is the heart. Cardioembolic strokes usually occur abruptly, although they occasionally present with stuttering, fluctuating symptoms. The symptoms may clear entirely since emboli can migrate and lyse, particularly those composed of thrombus. Causes of known cardioembolic stroke include atrial fibrillation and paroxysmal atrial fibrillation, rheumatic mitral or aortic valve disease, bioprosthetic and mechanical heart valves, atrial or ventricular thrombus, sick sinus syndrome, sustained atrial flutter, recent myocardial infarction (within one month), chronic myocardial infarction (together with ejection fraction <28 %), symptomatic congestive heart failure (with ejection fraction <30 %), dilated cardiomyopathy, fibrous nonbacterial endocarditis as found in patients with systemic lupus (ie, Libman-Sacks endocarditis), antiphospholipid syndrome, and cancer (marantic endocarditis), infective endocarditis, left atrial myxoma, coronary artery bypass graft (CABG) surgery.Causes of possible cardiac or aortic sources of Cardioembolic stroke include mitral annular calcification, patent foramen ovale (PFO) with or without atrial septal aneurysm, left ventricular aneurysm without thrombus, complex atheroma in the ascending aorta or proximal arch.Known arterial sources include intracranial and extracranial arterial dissections. Arterial dissections are a common cause of stroke in the young, but may occur at any age. Dissection occurs when structural integrity of the arterial wall is compromised, allowing blood to collect between layers as an intramural hematoma. Treatment recommendations will be discussed below, but depend on whether the dissection is intracranial or extracranial in origin as well as the amount of time from onset of stroke symptoms to treatment.Blood disorders — Blood and coagulation disorders are an uncommon primary cause of stroke and TIA, but they should be considered in patients younger than age 45, patients with a history of clotting dysfunction, and in patients with a history of cryptogenic stroke. The blood disorders associated with arterial cerebral infarction include:Sickle cell anemiaPolycythemia veraEssential thrombocytosisHeparin induced thrombocytopeniaProtein C or S deficiency, acquired or congenitalProthrombin gene mutationFactor V Leiden (resistance to activated protein C)Antithrombin III deficiencyAntiphospholipid syndromeHyperhomocysteinemiaFactor V Leiden mutation and prothrombin 20210 mutations are associated mostly with venous rather than arterial thrombosis. They can result in cerebral venous thrombosis or deep venous thrombosis with paradoxical emboli. Infectious and inflammatory disease such as pneumonia, urinary tract infections, Crohn's disease, ulcerative colitis, HIV/AIDS, and cancers result in a rise in acute phase reactants such as fibrinogen, C-reactive protein, and coagulation factors VII and VIII. In the presence of an endothelial cardiac or vascular lesion, this increase can promote active thrombosis and embolism.Systemic hypoperfusion is a generalized circulatory problem manifesting itself in the brain as well as in other organs (elevated levels of transaminases, elevation of BUN and creatinine, oliguria, lactic acidosis, and elevated CPK may be useful markers). Reduced blood flow to the CNS is more global in patients with systemic hypoperfusion and does not affect isolated regions. The reduced perfusion can be due to cardiac pump failure caused by cardiac arrest or arrhythmia, or to reduced cardiac output related to acute myocardial ischemia, pulmonary embolism, pericardial effusion, or bleeding. Hypoxemia may further reduce the amount of oxygen carried to the brain.Symptoms of brain dysfunction typically are diffuse and nonfocal in contrast to the other two categories of ischemia. Most affected patients have other evidence of circulatory compromise and hypotension such as pallor, sweating, tachycardia or severe bradycardia, and low blood pressure. The neurologic signs are typically bilateral, although they may be asymmetric when there is preexisting asymmetrical craniocerebral vascular occlusive disease.The most severe ischemia may occur in border zone (watershed) regions between the major cerebral supply arteries since these areas are most vulnerable to systemic hypoperfusion. The signs that may occur with border zone infarction include cortical blindness, or at least bilateral visual loss; stupor; and weakness of the shoulders and thighs with sparing of the face, hands, and feet (a pattern likened to a "man-in-a-barrel").II. A. Initial General AssessmentSudden loss of brain function is the core feature present at the onset of ischemic stroke. Patients may have other conditions which can mimic stroke and these should be considered as well. A partial list includes: Post-ictal Todd’s paresis; Metastatic brain tumors; Demyelinating diseases; Head trauma; Intracerebral hemorrhage; Systemic infections; Toxic-metabolic disorders; and Conversion disorders. In addition, patients with ischemic stroke may present concurrently with other serious medical conditions, such as myocardial infarction, or diabetic ketoacidosis, dehydration, etc. Thus the initial evaluation must be broadly based but rapidly performed. Goals should include:Insuring medical stabilityQuickly reversing conditions contributing to the patient’s problemMoving toward uncovering the pathophysiological basis of the patient’s neurological symptomsQuickly diagnosing intracerebral or subarachnoid hemorrhage by CT scanning can be lifesaving, however it is important to assess vital signs before moving the patient to the imaging department. Vital parameters of particular importance include blood pressure, breathing, and temperature.Blood pressure: The mean arterial blood pressure (MAP) is usually elevated in patients following an acute stroke. This can be due to chronic hypertension (which is an independent risk factor for both ischemic and hemorrhagic stroke) or part of a physiological response originating in the CNS to maintain adequate cerebral perfusion pressure (CPP). The goal of blood pressure management is to maintain adequate perfusion to the ischemic brain tissue. The pharmacological lowering of blood pressure in the setting of acute ischemic stroke may be associated with clinical deterioration. For ischemic stroke, it is recommended that hypertension not be treated acutely unless systolic BP >220mmHg or diastolic BP>120mmHg, or if the patient has active ischemic coronary disease, heart failure, aortic dissection, hypertensive encephalopathy, acute renal failure or eclampsia. Blood pressure medications should be held and restarted 24 hours after the onset of stroke in neurologically stable patients with preexisting hypertension. Exceptions to this rule include patients with intracranial or extracranial arterial stenosis who may need to maintain higher blood pressures for as long as 7 to 10 days after infarction. Also, patients who are considered candidates for thrombolytic therapy need to achieve blood pressures lower than 185/105 mmHg during infusion of tPA as well as for the next 24 hours.For patients with intracranial hemorrhage (intracerebral hemorrhage or subarachnoid hemorrhage), one must weigh risks of further bleeding with risks of reducing cerebral perfusion. In addition, patients with intracranial hemorrhage may develop increased intracranial pressure (ICP) due to blood within the cranium. Raised ICP may reduce CPP unless MAP is increased (recall that CPP=MAP – ICP). Directly measuring ICP directly allows blood pressure to be reduced as low as possible while still maintaining CPP above 60mmHg.Intravenous Labetolol is the first line drug of choice for lowering blood pressure in the setting of stroke since it allows for rapid upward and downward titration of blood pressure. Other agents include Nitroglycerin Paste and intravenous Nicardipine.Airway and Breathing: Patients with increased ICP due to intracranial hemorrhage, vertebrobasilar ischemia, or diffuse cerebral edema can present with a reduced respiratory drive and/or upper airway obstruction. In addition, hypoventilation may lead to cerebral vasodilation which further increases ICP. Intubation may be necessary to maintain airway control and regulate ventilation. Patients who are hypoxic should also receive supplemental oxygen. Oxygen administration in patients who are not hypoxic is not indicated.Position of Head: During the acute phase of stroke, the patients head should be midline and elevated to 30° for patients who have or are at risk for the following conditions:Increased ICP (due to large ischemic stroke, intracranial hemorrhage, hydrocephalus, space occupying lesion, etc)Aspiration (patients with dysphagia or diminished consciousness)Cardiopulmonary decomensation or oxygen desaturationOtherwise it is recommended to keep the head of the bed flat for all other patients.Fever Management: Patients with acute stroke may develop due to central mechanisms or part of an infectious disease process. Infectious workup should be initiated and empiric antibiotics may need to be administered until results are in. Regardless of the cause, fever can worsen brain ischemia and normothermia should be maintained.Glucose Management: Both hyper and hypoglycemia can increase neurological injury in the setting of stroke. Hyperglycemia (defined as a blood glucose >126mg/dl) is common in acute stroke and associated with a poor functional outcome. Hyperglycemia is most commonly caused by a physiological stress response, though newly diagnosed diabetes may also be a factor. It is recommended to treat hyperglycemia with insulin possibly for glucose concentrations >140mg/dl and certainly for >180mg/dl. Hypoglycemia can cause focal neurological deficits mimicking stroke. Measuring blood glucose should be part of the initial vital sign evaluation (ABCD’s, Airway, Breathing, Cardiovascular, Dextrose).History, Physical and Neurological Examinations: The purpose here is to exclude stroke from stroke mimickers and to quickly establish a baseline neurological examination. Seizures, syncope, migraine, and hypoglycemia can all mimic stroke. Establishing stroke as the underlying etiology of the patient’s neurological condition can be challenging in patients with depressed levels of consciousness and focal neurological findings.II. B. Urgent neuroimaging to exclude intracranial hemorrhageNon-contrasted CT should be performed as soon as the patient is medically stable. CT detection of early ischemic stroke (< 6 hours) findings is about 60% with improved sensitivity developing over the first 24 hours. The presence of early CT ischemic changes also portends a worse neurological outcome. Diagnosing an intracerebral hemorrhage or subarachnoid hemorrhage quickly can be lifesaving.II. C. Determining if the patient is a candidate for acute thrombolysis therapy.Once it has been determined that the patient has an acute ischemic stroke, consideration should be given for thrombolysis. Whenever possible, vascular imaging studies (MRA, CTA, Doppler ultrasound) should confirm a large vessel thromboembolism. Without a large vessel occlusion, there is no apparent target for recanalization and many of these patients improve spontaneously. Also, some patients presenting too late for rTPA may still be candidates for intravenous or intra-arterial thrombolysis if imaging studies show a significant “at-risk” brain that is underperfused but not infarcted. With that being said, it is still reasonable to treat with rTPA eligible patients if neurovascular imaging is not readily available or would delay treatment.(For treatment indications and contraindications, see “Thrombolysis Guidelines” handout)III. Forming a Hypothesis of the Stroke EtiologyHistoryThe clinical course of symptom progression may be useful in determining the type of stroke that the patient has suffered from. For example, embolic strokes usually have an abrupt onset with maximal neurological deficit at onset. A rapid recovery also supports embolic stroke. Thrombotic strokes have fluctuating symptoms with a stuttering course. Penetrating artery occlusions (lacunar strokes) often cause symptoms evolving over hours or days whereas large vessel ischemia often evolves over a longer period of time. Intracerebral hemorrhage does not improve in the early phase and tends to be progressive over minutes to hours. Aneurysmal SAH has a very abrupt onset and focal neurological deficits are uncommon.Patient demographics can influence the likelihood of specific etiologies for stroke. For example, most thrombotic and embolic strokes occurring in older individuals are caused by atherosclerosis. In younger individuals (under 40 years), arteriosclerosis is less common unless there are multiple risk factors, such as smoking, diabetes, hypertension, hyperlipidemia, or a strong family history. Hypertensive ICH is more common among African American and Asian individuals than among Caucasians. Caucasians have a higher incidence of occlusive disease of the extracranial carotid circulation and vertebral arteries than do other ethnicities.Hypertension is the most common and important risk factor for stroke with increasing incidence of both coronary artery disease and stroke with blood pressures that rise above 110/75. Previous TIA, especially in the same territory as the stroke favors the possibility of a local arterial thrombosis. Attacks in more than one vascular territory favor embolism from the heart or aortic arch.Smoking increases the likelihood of extracranial occlusive vascular disease and more than doubles the risk of stroke. Smoking cessation results in reduction of stroke risk over time. Diabetes increases the risk of small vessel occlusive disease. Amphetamine use increases the risk for both ICH and SAH but not ischemic stroke. Cocaine causes strokes that are often hemorrhagic, often affecting the posterior circulation intracranial arteries. Heart disease (such as cardiac valvular disease, prior MI, atrial fibrillation, and endocarditis) increases the risk for embolic stroke. Stroke during the puerperium increases the risk of stroke due to venous or arterial thrombosis. Anticoagulants or bleeding diatheses can increases the risk of ICH. The use of birth control pills is much less of a risk factor with low-dose estrogen containing pills. Vigorous physical activity or sexual intercourse can be associated with ICH or SAH and not usually thrombotic stroke. A history of recent head or neck trauma increases the probability of arterial dissection.Associated symptomsFever raises the possibility of endocarditis. Infectious illness can also raise the levels of acute phase reactants which may predispose to thrombosis. Headache, seizures, and/or nausea and vomiting are common with ICH or SAH. Nausea and vomiting may also be a sign of posterior circulation strokes. Reduced level of consciousness favors SAH or large ischemic strokes with edema and subfalcine herniation.Physical ExaminationThe purpose of the general physical examination is to look for possible underlying causes of stroke in the patient. Absent pulses (lower extremity, radial or carotid) favors a diagnosis of atherosclerosis with thrombosis, though a sudden-onset cold, blue limb favors embolism. An occlusion of the common carotid may be picked up by the absence of a carotid pulse. The presence of a neck bruit also favors partial common carotid or vertebral artery occlusion. Facial pulses may be lost if there is an ipsilateral common carotid artery occlusion or even increased if there is an internal carotid artery occlusion (suggesting more blood being shunted to the external carotid artery circulation).Cardiac findings such as atrial fibrillation, murmurs and cardiomegaly may suggest a cardioembolic source.Fundoscopic examination may reveal cholesterol crystals, white intravascular occlusions (fibrin-platelet embolus), or red clot emboli. Subhyaloid hemorrhage suggests SAH. Ischemia to the retina may occur with internal carotid artery occlusion affecting the central retinal artery.Neurological ExaminationTime is of the essence in the hyperacute evaluation of stroke patient as the window of intervention for thrombolysis is less than 4 ? hours. The neurological examination should attempt to confirm the findings from the history and provide a quantifiable measurement of any neurological deficits that can be followed over time. A quantifiable and validated scoring system for rating the severity of stroke is the NIH Stroke Scale, which is composed of 11 items adding to a total score of 0 to 42. The NIHSS has been shown to correlate with functional outcome for stroke. (See “NIHSS” document in the Stroke Resources Folder).Certain constellations of neurological deficits will constitute specific stroke syndromes based on the vascular territories affected. Common stroke syndromes that may be encountered include:MCA territory stroke. If involving the dominant hemisphere, aphasia will be present (receptive, expressive or often both). Contralateral motor and sensory deficit (face, arm>leg>foot). Complete contralateral hemiplegia if internal capsule involved. Homonymous hemianopsia. Embolic > atherothrombolic etiology.ACA territory stroke. Motor and/or sensory deficit (foot >>face, arm). Grasp and sucking reflexes. Abulia, paratonic rigidity, gait apraxia. Embolic > atherothrombotic etiology.ICA territory stroke. Combined features of MCA and ACA strokes. Also ipsilateral amarosis fugax symptoms from central retinal artery involvement. Atherothrombotic > embolic etiology.PCA territory stroke. Homonymous hemianopsia; alexia without agraphia (dominant hemisphere); visual hallucinations; visual perseverations (calcarine cortex); sensory loss or spontaneous pain (thalamus); III nerve palsy (cerebral peduncle); upgaze paresis(midbrain); motor deficit (cerebral peduncle). Embolic > atherothrombotic etiology.Vertebrobasilar territory stroke. Various cranial nerve palsies with crossed sensory deficits (e.g. decreased pinprick and temperature sensation to ipsilateral face and contralateral arms and legs); diplopia; vertigo; nausea and vomiting; dysarthria; dysphagia; pathological hiccups; limb and gait ataxia; motor deficit; impaired LOC (from the reticular activating system). Bilateral signs suggest basilar artery involvement. Embolic = atherothrombolic for etiology.Penetrating vessel (Lacunar) strokes. Pure motor deficit; pure sensory deficit; pure motor and sensory deficit; hemiparesis and homolateral ataxia; dysarthria and clumsy hand. Small artery (Lacunar) infarction.(for a more complete listing of stroke syndromes, see “Stroke Syndromes” document in the Stroke Resources folder)3756660-99060Vascular supply to the brainCoronal section00Vascular supply to the brainCoronal sectionACA Territory Vascular Supply MCA Territory Vascular Supply716280-415925PCA Territory Vascular Supply4000020000PCA Territory Vascular Supply2034540193675Medial Inferior Pontine Syndrome (occlusion of a paramedian branch of the Basilar artery)Lateral Inferior Pontine Syndrome (occlusion of the anterior inferior cerebellar artery)00Medial Inferior Pontine Syndrome (occlusion of a paramedian branch of the Basilar artery)Lateral Inferior Pontine Syndrome (occlusion of the anterior inferior cerebellar artery)4130040486410Medial Midpontine Syndrome (occlusion of a paramedian branch of the mid-Basilar arteryLateral Midpontine Syndrome (occlusion of a short circumferential artery)400000Medial Midpontine Syndrome (occlusion of a paramedian branch of the mid-Basilar arteryLateral Midpontine Syndrome (occlusion of a short circumferential artery)71628092710Medial Medullary Syndrome (occlusion of Vertebral artery or branch of Vertebral or lower Basilar artery)Lateral Medullary Syndrome (occlusion of either Vertebral artery, Posterior Inferior Cerebellar Artery, or Superior, Middle or Lateral Medullary arteries)00Medial Medullary Syndrome (occlusion of Vertebral artery or branch of Vertebral or lower Basilar artery)Lateral Medullary Syndrome (occlusion of either Vertebral artery, Posterior Inferior Cerebellar Artery, or Superior, Middle or Lateral Medullary arteries)IV. Confirming the Diagnosis of StrokeThe previous assessment should allow for a presumptive diagnosis of the underlying stroke pathophysiology. The next phase of the evaluation is to confirm this hypothesis with diagnostic testing.A. Embolic StrokeEmbolism is likely in the following circumstances:The neurological deficit is sudden in onset and maximal in severity from the beginningThe region of infarction and degree of deficit are largeThere is a known cardiac or large artery lesion presentThe infarct becomes hemorrhagic on CT or MRIThere are multiple cortical and/or subcortical infarctions in different vascular territoriesClinical findings improve quicklyPosterior circulation strokesCardioembolic StrokeCardiac evaluation should be performed in all patients with suspected embolic stroke, especially in those under the age of 45 whether or not they are known to have pre-existing cardiac disease. Cardiac evaluation should also be considered in patients with occlusive cerebrovascular disease due to the possible co-occurrence of coronary heart disease and stroke. The initial evaluation should focus on the presence of cardiac ischemia and arrhythmias and should include a careful cardiac physical examination and an EKG. Cardiac Monitoring with an electrocardiogram followed by telemetry or a Holter monitor for 24 hours after ischemic stroke can identify many patients with atrial fibrillation. A normal sinus rhythm does not exclude atrial fibrillation in all patients as this arrhythmia may be intermittent.Echocardiography should be performed in all patients with suspected embolic stroke. Echocardiography should strongly be considered especially in younger patients without obvious cerebrovascular atherosclerotic disease. The initial study of choice is generally transthoracic echocardiography (TTE). If the preliminary cardiac evaluation, vascular studies, and TTE fail to reveal a source for the ischemic stroke, then transesophageal echocardiography (TEE) should be considered. TEE has advantages of being able to examine the aorta, the atria, and the atrial septum. It is also the best study to identify clot in the left atrial appendage. The main disadvantage of TEE is its invasiveness compared to TTE. TTE may be better able to locate left ventricular thrombi in patients with congestive heart failure or prior myocardial infarction.Artery-to-Artery Embolic StrokeThe distinction between artery-to-artery and cardioembolic sources of embolism can be difficult. Suspicion of artery-to-artery embolism arises when pathology in a large vessel is identified with noninvasive testing. Repetitive ischemic attacks within a single vascular territory and/or a normal echocardiogram (especially with TEE) also raise suspicion.B. Large Vessel Atherothrombotic StrokeLarge vessel occlusive strokes are often preceded by TIA’s in the same vascular territory. The onset of symptoms may or may not be abrupt and the clinical course often fluctuates. The region of cerebral infarction is often large and includes both cortical and subcortical territories. The usual source of atherothrombotic stroke is intracranial artery occlusion.Patients with large vessel atherothrombotic stroke should have both intracranial and extra-cranial vascular imaging (see “Neuroimaging of the Acute Stroke Patient” below).C. Small Vessel (Lacunar) StrokeMost patients with Lacunar infarctions have risk factors for penetrating artery disease such as hypertension, diabetes mellitus, or polycythemia. Clinical findings on neurological examination typically conform to one of the well-recognized lacunar stroke syndromes:Pure Motor HemiparesisPure Sensory StrokeDysarthria-Clumsy Hand SyndromeAtaxia-Hemiparesis(For more information about these stroke syndromes, see the “Stroke Syndromes”document in the Stroke Resources folder)While most patients with lacunar infarctions with known risk factors won’t have other identifiable cardiac or large vessel sources, some will have large vessel disease, especially in patients of Asian ethnicity. Vascular imaging (CTA or MRA) performed at the same time as brain imaging (CT or MRI) to exclude localized occlusion of a feeding artery, a condition mimicking lacunar infarction. It is especially important to perform intracranial vascular imaging in Asians and African Americans as people with these ethnicities commonly have intracranial large vessel occlusive disease.Neuroimaging of the Acute Stroke PatientNeuroimaging studies in the acute stroke setting should be used to rule out hemorrhagic stroke, assess the degree of brain injury, and to identify the vascular lesion responsible for the ischemic puted Tomography has several advantages for imaging in the setting of acute stroke. CT is widely available and has a high rate of speed of acquisition. In the hyperacute phase of stroke, CT is highly sensitive for confirming or excluding intracranial hemorrhage. Vascular imaging studies may help define if there is a large vessel thrombus that may be amenable to systemic intravenous thrombolytic therapy or localized intra-arterial thrombolysis. Vascular imaging of any sort however should never delay treatment using intravenous tPA for eligible patients. Non-contrasted CT should be performed as soon as the patient is medically stable. CT detection of early (<6 hours) ischemic stroke findings is about 60% with improved sensitivity developing over the first 24 hours. The presence of early CT findings also portends a worse neurological outcome. Early signs on CT include:Hypodensity involving the MCA territoryObscuration of the lentiform nuclei (basal ganglia)Cortical sulcal effacementFocal parenchymal hypodensityLoss of the insular ribbon or obscuration of the Sylvian fissureHyperdensity of large vessels (“hyperdense MCA sign”, suggesting a thrombus within the MCA)Loss of grey-white matter differentiation in the basal gangliaCT Angiography (CTA) is performed by administering a rapid bolus of contrast during image acquisition of the brain. The procedure requires a large bore peripheral IV, but only requires an addition 5 to 10 minutes of acquisition time. CTA is very useful for detecting thrombus or embolus within large intracranial or extracranial arteries, which may guide therapy for intra-arterial vs intravenous thrombolysis. Using the source images from CTA, one may be able to detect reduced perfusion to a region of the brain based on reduced uptake of contrast within the microvasculature of the affected region (a “poor man’s” CT perfusion study).CT Perfusion studies (CTP) also uses a bolus of contrast which can be done by continuing to image after a CTA or by giving another separate bolus. CTP requires repeat scanning of select parts of the brain over and over to track the progress of the contrast bolus through the vasculature.Magnetic Resonance Imaging may allow further sub classification of acute stroke patients to guide intravenous thrombolysis or interventional vascular treatments. Brain MRI that combines T1, T2, T2 FLAIR, Diffusion-Weighted Imaging (DWI), Perfusion-Weighted Imaging (PWI), and Gradient Echo (GRE) sequences allows for differentiation of ischemic stroke from intracranial hemorrhage. GRE sequences picks up acute hemorrhage as well as CT and chronic hemorrhage even better. In centers with ultrafast MRI imaging protocols, acquisition times may be as short as 5 minutes, compared to the usual 15 – 20 minutes with conventional MRI.Diffusion-Weighted Imaging (DWI) measures a signal related to the movement of water molecules between two closely spaced radiofrequency pulses. In acute stroke, swelling of ischemic parenchymal cells follows failure of the Na+/K+ ATPase pumps leading to an increased ratio of intracellular to extracellular volume fractions. DWI picks up signal changes due to cytotoxic edema as well as T2 signal change from vasogenic edema or gliosis. In order to account for the “T2 shine-through”, Apparent Diffusion Coeficient (ADC) mapping can be created by “subtracting” the T2 shine-through from the bright signal on DWI images to leave behind a darkened signal reflecting pure signal changes from cytotoxic edema. DWI is a sensitive and specific indicator of acute stroke within 6 hours of symptom onset. In the setting of TIA’s, DWI may show signal changes predictive of future TIA’s or ischemic stroke in the same vascular region.Perfusion-Weighted Imaging (PWI) uses fast MRI techniques to quantify the amount of contrast agent reaching the brain following a bolus infusion. The course of contrast arrival and washout allows the construction of regional areas of reduced perfusion (the ischemic penumbra). While some patients may show a clearly defined area of irreversible infarction on DWI and surrounding reduced perfusion on PWI, this is not always the case with lots of exceptions.MR Angiography using time of flight technique is generally adequate for visualizing the intracranial portions of both the anterior and posterior circulations. These studies do not show the aortic arch or vertebral artery origins however. For these arteries, contrast bolus MRA may show vessel patency through these regions. Alternatively duplex and color-flow Doppler can be used to visualize the origins of the vertebral arteries as well as the extracranial portions of the carotid arteries.Carotid Duplex Ultrasound and Transcranial Doppler flow studies are non-invasive methods to evaluate flow and patency of the extracranial and large intracranial vessels. In some centers, when combined, they can be just as useful as conventional angiography in determining arterial lesions amenable to interventional treatment. Carotid Doppler ultrasound occasionally finds the source of an arterial-to-arterial embolus, but more often it is used as a staging risk factor for large vessel extracranial carotid artery stenosis. Patients with >70% stenosis ipsilateral to a anterior circulation large vessel thrombotic stroke may benefit from carotid endarterectomy.Conventional Angiography remains the gold standard for evaluating the cerebral vessels. It can determine the degree of arterial stenosis, the presence of dissection, vasculopathy, vasculitis, or vascular malformations. It can also provide information about collateral flow and perfusion status. In large vessel occlusion, angiography is more sensitive than non-invasive imaging techniques and allow for potential “in-situ” treatment, such as intra-arterial thrombolysis. ................
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