Acute Cerebral Infarct Case File

Acute Cerebral Infarct Case File

Eugene C. Toy, MD, Ericka Simpson, MD, Pedro Mancias, MD, Erin E. Furr-Stimming, MD

CASE 11

A 68-year-old right-handed woman was brought to the emergency room 30 minutes after suddenly developing speech difficulty and weakness of the right arm and leg. She was found by her family members to be mute and slumped down in her chair. Her past medical history is significant for hypertension and angina, for which she takes atenolol and amlodipine. The patient’s temperature is 36.6°C (98°F); heart rate is 115 beats/min; and blood pressure is 172/86 mm Hg. Her physical examination reveals no carotid bruit, but she has an irregularly irregular cardiac rhythm. Neurologic examination reveals a lethargic but arousable patient who is able to follow some simple commands but has severe impairment of word fluency, naming, and repetition. There is a left gaze deviation and right lower facial droop. There is total paralysis of the right upper extremity and, to a lesser degree, weakness of the right lower extremity. The left side displays full antigravity power without drift for 5 seconds. An electrocardiogram reveals atrial fibrillation.

▶ What is the most likely diagnosis and what part of the brain is likely affected?

▶ What is the best next diagnostic step?

▶ What is the best next step in therapy?

ANSWERS TO CASE 11:

Acute Cerebral Infarct                                        

Summary: A 68-year-old woman presents with 30 minutes of right hemiparesis and aphasia, with vascular risk factors of hypertension and coronary artery disease and physical findings of atrial fibrillation.

• Most likely diagnosis: Acute cerebral ischemia in the left middle cerebral artery
• Next diagnostic step: Noncontrast computed tomography (CT) scan of the head
• Next step in therapy: Thrombolytic therapy if eligible by criteria, and consideration of endovascular treatment with embolectomy if appropriate

ANALYSIS

Objectives

1. Recognize the clinical presentation of an acute stroke.
2. Be familiar with the evaluation and treatment of stroke.
3. Describe the risk factors and pathophysiology of stroke.

Considerations

When a patient presents with the abrupt onset of focal neurologic deficits, the most likely diagnosis is an acute cerebrovascular event. This patient’s neurologic deficits, right hemiparesis of the upper more than lower extremity, aphasia, and gaze deviation point to a perfusion defect in the left middle cerebral artery territory. Focal neurologic deficits can include hemiparesis, hemisensory loss, speech disturbance, hemineglect, homonymous hemianopia, or hemiataxia. Other diagnostic considerations include hypoglycemia, a seizure with postictal Todd paralysis, or complicated migraine. If the acuity of onset is less certain, a brain tumor, subdural hematoma, multiple sclerosis, herpes encephalitis, or a brain abscess can mimic a subacute stroke. The distinction between a stroke and a transient ischemic attack (TIA) rests on the duration of symptoms. The symptoms of a TIA resolve within 24 hours, usually lasting from several minutes to 1 to 2 hours. While the definition of TIA varies in some references, imaging criteria are now the preferred means for determining if an event is a TIA or an infarct. Magnetic resonance imaging (MRI) using a diffusion-weighted sequence can reliably determine the presence of an infarct, even if the clinical symptoms have resolved. Furthermore, distinguishing between an ischemic stroke and an intracerebral hemorrhage requires a brain imaging study, either CT or MRI. The etiologies and treatment of ischemic stroke and intracerebral hemorrhage are quite different. Because intervention can improve the outcome, the patient should be rapidly assessed for possible thrombolytic therapy (a hemorrhage on CT is a contraindication for thrombolytics). Recent studies have also pointed to a potential benefit of endovascular treatment with embolectomy or intra-arterial tissue plasminogen activator (tPA) for patients with a large proximal occlusion and a salvageable ischemic penumbra or area surrounding the stroke. The treatment of hemorrhagic stroke is primarily supportive and involves controlling hypertension and careful intracranial pressure (ICP) monitoring. If there is any evidence of elevated ICP, treatment strategies include hyperventilation, osmotic therapy, and, occasionally, surgical decompression with hemicraniectomy and durotomy.

APPROACH TO:

Acute Cerebral Infarct                                        

DEFINITIONS

ISCHEMIC STROKE: Cerebral infarction associated with acute neurologic symptoms.

TRANSIENT ISCHEMIC ATTACK (TIA): A cerebral ischemic event associated with focal neurologic deficits lasting less than 24 hours with no evidence of cerebral infarction on brain imaging, preferably MRI.

INTRACEREBRAL (OR INTRAPARENCHYMAL) HEMORRHAGE: A cerebrovascular event characterized by arterial rupture and parenchymal hemorrhage.

HOMONYMOUS HEMIANOPIA: The loss of one-half of the field of view on the same side in both eyes.

TODD PARALYSIS: A brief period of temporary paralysis following a seizure.

CLINICAL APPROACH

Stroke, or cerebrovascular accident (CVA), is a neurologic deficit of sudden onset attributable to the loss of perfusion of a portion of the brain from vascular occlusion or hemorrhage. Ischemic stroke is caused by vascular insufficiency, whereas hemorrhagic stroke is associated with mass effect or cytotoxicity related to a parenchymal hematoma. Understanding the vascular supply to the brain can help in correlating the neurologic finding to the affected artery. The carotid arteries are the vascular supply for the frontal and parietal lobes and most of the temporal lobes and basal ganglia. The main branches of the carotid artery are the middle cerebral and the anterior cerebral arteries. The vertebrobasilar territory encompasses the brainstem, cerebellum, occipital lobes, and thalami. The posterior inferior cerebellar artery is the only large artery that arises directly from the vertebral artery. The posterior cerebral, superior cerebellar, and anterior inferior cerebellar arteries are branches of the basilar artery.

When a patient presents with weakness, sensory loss, or speech difficulties, a brain imaging study such as a CT or MRI is necessary to distinguish between an ischemic stroke and an intracerebral hemorrhage and to help rule out a stroke mimic. In general, CT is preferred in the acute setting because it is readily available, accurate for the detection of blood, and rapid. MRI is more sensitive for detecting acute ischemia; however, it is rarely necessary in the first few hours of stroke evaluation and can be performed after a patient is stabilized and able to lie still. An electrocardiogram and laboratory studies including a complete blood count, glucose, prothrombin time (PT), and partial thromboplastin time (PTT) are also essential. With recent studies showing the potential benefit of endovascular embolectomy or thrombectomy, vascular imaging with CT angiogram or CT perfusion may be pertinent in determining an appropriate candidate for this added treatment.

A patient with an acute intraparenchymal hemorrhage should be admitted to the intensive care unit (ICU) in most circumstances for at least 24 hours of monitoring and blood pressure lowering. A patient with an ischemic stroke may not require ICU care but should be admitted to a specialized unit that provides neurologic and cardiac monitoring. Intravenous (IV) fluids to maintain euvolemia (normal volume status) should be considered, and dysphagia should be evaluated to avoid potential aspiration pneumonia. All patients with stroke, either hemorrhagic or ischemic, should have prophylaxis for deep venous thrombosis, albeit nonpharmacologic in the first days after a hemorrhagic stroke. Hypertension is often encountered in the stroke patient; in general, the blood pressure should be monitored and if necessary, it can be cautiously lowered in the first few days of an ischemic stroke. Abrupt lowering of the blood pressure is not recommended and may worsen collateral flow to the ischemic penumbra. Conversely, accelerated hypertension will place a patient at risk of hemorrhagic conversion. A judicious approach to blood pressure control, informed by the size of the infarct, the patient’s preexisting blood pressure, and the mechanism of the infarct, is more appropriate than following precise numerical goals.

In addition to a CT and MRI (if possible), the diagnostic evaluation for an ischemic stroke may include a carotid ultrasound, transcranial Doppler, echocardiogram, magnetic resonance angiogram of the head and neck, and/or a cerebral arteriogram. Cardiac telemetry monitoring for at least 24 hours while in the acute setting is recommended to rule out any arrhythmias that may change treatment for secondary stroke prevention. A fasting lipid panel and hemoglobin A1C are usually warranted. Other laboratory studies are low yield but may be considered if there is a valid clinical suspicion; these studies include serum B12, folate, homocysteine levels, erythrocyte sedimentation rate (ESR), rapid plasma reagent (RPR), human immunodeficiency virus (HIV), and toxicology screens.

Etiologies

The most common etiologies of ischemic stroke include cardiac embolism, large-vessel atherothrombosis, and small-vessel intracranial occlusive disease, although the comprehensive list of potential stroke etiologies is quite extensive (see also Case 13). As many as 30% of ischemic strokes remain cryptogenic (without discernible etiology) after a thorough diagnostic evaluation.

Acknowledged sources of cardiac embolism to the brain include atrial fibrillation, mechanical prosthetic heart valves, acute myocardial infarction, low left ventricular ejection fraction less than 30%, focal myocardial hypokinesis, patent foramen ovale, and endocarditis. Large-vessel atherosclerosis can affect the carotid bifurcation, the major intracranial vessels, or the extracranial vertebral artery. Small-vessel strokes, also known as lacunar strokes, are often characterized by classic clinical syndromes (pure motor stroke or pure sensory stroke, ataxic hemiparesis, dysarthria/clumsy hand) and are related to occlusive disease of penetrating arteries in the brain usually associated with hypertension and/or diabetes. Major risk factors for stroke are similar to those of coronary heart disease and include age, hypertension, smoking, diabetes, hyperlipidemia, heart disease, and family history.

CLINICAL PRESENTATION

Hemiparesis involving mostly the right arm, aphasia, and left gaze deviation point to an anatomic localization in the left middle cerebral artery territory (Figure 11–1). Cortical symptoms such as aphasia (impairment of the ability to use or comprehend words), hemineglect, agnosia (loss of ability to recognize objects, persons, sounds, shapes, or smells), and apraxia (loss of the ability to execute or carry out learned purposeful movements) indicate a lesion in the anterior (or carotid) circulation. Symptoms such as diplopia, vertigo, crossed facial and body findings, and homonymous hemianopia, however, suggest a posterior (or vertebrobasilar) circulation lesion. The symptoms of an intracerebral hemorrhage cannot be reliably distinguished from those of an ischemic stroke on clinical grounds alone. The presence of headache, depressed level of consciousness, or extreme elevations in blood pressure, however, can raise the suspicion of a hemorrhagic stroke.

Treatment

Treatment of ischemic stroke begins with assessment of eligibility for thrombolysis. Treatment must be initiated urgently. IV tPA can significantly improve the odds of neurologic recovery but must be administered within 4.5 hours of onset of stroke symptoms. tPA is associated with a risk, albeit minimal if contraindications have been ruled out, of hemorrhagic conversion of an ischemic infarct. Thus, urgent imaging of the brain such as a CT scan is imperative to assess for hemorrhagic stroke. Contraindications to tPA include active bleeding, recent stroke, or a history of intracerebral hemorrhage. Recent studies have shown benefits of intra-arterial endovascular therapy for patients with proximal anterior circulation occlusions within 6 hours of symptom onset. Other studies have shown benefits of endovascular treatment up to 8 hours after onset of symptoms. In these cases, screening patients with moderate to severe strokes with vascular imaging, such as CT angiogram, may be useful since neurointervention may be indicated if a large-vessel occlusion is present. Other acute stroke treatments are currently under investigation and could in the near future include administration of IV tPA in the field via the Mobile Stroke Unit as well as neuroprotective therapies. Patients who are not candidates for thrombolytic or endovascular therapy should be acutely treated with aspirin unless contraindicated.

Figure 11–1. Noncontrast axial CT image of a subacute left major coronary artery infarction. (Reproduced, with permission, from Chen MY, Pope TL, Ott DJ. Basic Radiology. New York, NY:

McGraw-Hill; 2004:338.)

Secondary stroke prevention should be implemented. Antiplatelet drugs such as aspirin, clopidogrel, or the combination of aspirin and extended-release dipyridamole are the mainstays of stroke prevention treatment for most patients with ischemic stroke and TIA. Patients with high-risk cardioembolic conditions such as atrial fibrillation, however, warrant long-term anticoagulation with warfarin or another novel oral anticoagulant, which has been demonstrated to be superior to antiplatelet treatment for this indication. Newer oral anticoagulants, such as dabigatran, rivaroxaban, edoxaban, and apixaban, have had success to varying degrees in clinical trials, and for some patients they may be safer and more effective than warfarin.

Risk factor management is crucial to preventing recurrent stroke. Long-term control of hypertension is most important. Treatment should be initiated as soon as a patient is stable after an ischemic stroke. Statins for hyperlipidemia lower the odds of stroke recurrence, and current guidelines recommend a target low-density lipoprotein (LDL) of under 100 mg/dL. Ipsilateral carotid stenosis of greater than 50% in a patient with ischemic stroke or TIA is an indication for carotid endarterectomy or, in a patient who is at high surgical risk, carotid stenting. Rehabilitation is especially beneficial for patients who have gait difficulty or aphasia or who require assistance with activities of daily living. It can especially help with resuming gainful employment after a stroke.

The treatment of hemorrhagic stroke is primarily supportive and involves control of hypertension. ICP monitoring may be considered if the Glasgow coma scale is less than 8, and if the ICP is elevated, it can potentially be addressed with osmotic therapy. Surgical decompression remains an unproven strategy in hemorrhagic stroke but may be considered, especially in cases where hemicraniectomy may relieve cerebral edema. IV thrombolytic therapy is contraindicated.

CASE CORRELATION

• See also Case 13 (Stroke in a Young Patient)

COMPREHENSION QUESTIONS

11.1 An 81-year-old patient arrives in the emergency department with acute left hemiparesis and neglect. What finding is most important in determining eligibility for thrombolytic treatment?

A. Time of last known well less than 4.5 hours

B. History of any previous myocardial infarction

C. Patient taking any antihypertensive medication

D. Distant history of gastrointestinal (GI) bleeding

11.2 For this patient in Question 11.1, what study is most useful to rule out an intracerebral hemorrhage?

A. Electrocardiogram

B. Noncontrast head CT

C. Complete blood count

D. Cerebral arteriogram

11.3 After receiving stroke therapy, this patient is being discharged home on physical therapy. The usual treatment would include long-term medical management with antiplatelet or anticoagulation. If present, which of the following conditions would benefit most from anticoagulation instead of antiplatelet therapy?

A. Diabetes

B. Ischemic heart disease

C. Carotid stenosis

D. Atrial fibrillation

ANSWERS

11.1 A. A patient is potentially eligible for thrombolysis if they were last known well within 4.5 hours.

11.2 B. The noncontrast CT scan of the head is a rapid and reliable test to assess for cerebral hemorrhage.

11.3 D. When atrial fibrillation is present, anticoagulation is preferred over antiplatelet therapy.

    CLINICAL PEARLS    

▶ Sudden onset of focal neurologic deficits equals stroke until proven otherwise. ▶ Time is brain; treat ischemic stroke with thrombolytics within 4.5 hours to preserve brain tissue and assess for a potential benefit of endovascular/intra-arterial therapy if within 6 hours. ▶ Stroke risk factors are similar to those of ischemic heart disease, such as hypertension, hyperlipidemia, diabetes, and smoking. ▶ Cortical symptoms suggest a carotid territory stroke; brainstem or cerebellar findings suggest a vertebrobasilar territory stroke.

REFERENCES

Berkhemer OA, Fransen PS, Beumer D, et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015;372:11-20. 

Mohr JP, Wolf PA, Grotta J, et al. Stroke: Pathophysiology, Diagnosis, and Management. 5th ed. New York, NY: Elsevier; 2011. 

Ropper AH, Brown RH. Adams and Victor’s Principles of Neurology. 8th ed. New York, NY: McGraw-Hill; 2005.

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