Cerebral occlusions result in well-described, sudden, focal neurologic deficits, usually without vomiting, headache, or obtundation unless a large portion of the cerebrum is involved. Deficits caused by cerebral arterial thrombosis usually develop over minutes to hours and may often develop overnight. Patients at risk for thrombotic cerebral infarction may also have generalized atherosclerotic disease or hypercoagulable states caused by malignancy, thrombocytosis, and hyperosmolar states.

Cerebral embolic infarction occurs suddenly without warning and may occur at any time of the day or night. The neurologic deficit develops within seconds. Common sources of emboli include atrial thrombi in patients with chronic or paroxysmal atrial fibrillation, valvular vegetations, and myocardial infarction with mural thrombi and in patients with extracranial vascular disease who have ulcerated plaques in the carotid system. The acute phase of embolic stroke may present with focal or diffuse seizures corresponding to the area of the infarcted brain; loss of consciousness is unusual except in complete carotid occlusions with cerebral edema. Patients who have had a cerebral embolism caused by a cardiac source should be rapidly anticoagulated with heparin after cerebral imaging has ruled out acute hemorrhage.

TIAs present as focal neurologic deficits lasting less than 24 hours; in most cases, resolution is seen within 15 to 60 minutes. The causes of TIAs include fibrin/platelet emboli, vasospasm, arterial hypertension, hypercoagulable disorders, and polycythemia. Management is controversial, and is discussed in “Transient Ischemic Attacks” under “Evaluation and Management of Specific Stroke Syndromes.”

A series of TIAs occurring over days or weeks before ED presentation (crescendo TIAs) requires urgent evaluation and probably anticoagulation with heparin after normal cerebral imaging.

Transient focal neurological deficits may also be caused by seizures (Todd paralysis), complex migraine headaches, and closed head injuries; however, history and physical examination of the patient should aid in the differentiation of these conditions from TIAs.

Hemorrhagic stroke, SAH, and intracranial hemorrhage (ICH) may occur during stress or exertion. Precipitating events may include sexual intercourse, labor and delivery, and Valsalva maneuver. Alcohol appears to contribute to an increase in ICH and SAH. Focal deficits rapidly evolve and may be associated with confusion, coma, or immediate mortality.

Severe headache of sudden onset (the “worst ever”) is a cardinal symptom of a subarachnoid hemorrhage and may be accompanied by nuchal rigidity. Arteriovenous malformations (AVMs) may bleed into the subarachnoid space with lateralizing findings if cerebral parenchyma is involved. Spontaneous SAH is usually caused by rupture of a saccular aneurysm. Apart from focal seizures, lateralizing deficits are usually absent with SAH.

ICH will present with well-demarcated focal deficits because of intraparenchymal damage. Intracranial hemorrhage is often a complication of long-standing hypertension, amyloid angiopathy, or anticoagulation therapy. Common sites include the thalamus, putamen, cerebellum, and brainstem (in decreasing order of incidence).
Cerebellar hemorrhage is a critical diagnosis to make, because it may be amenable to neurosurgical intervention. Onset usually occurs during activity. Hemorrhagic infarction should be considered in patients who are anticoagulated, who have an unexplained headache history, or who have sustained craniocerebral trauma.

Carotid artery disease may present with a carotid bruit in asymptomatic individuals. Patients with symptomatic carotid disease may present with TIA, which is characteristically short-lived. Clinical symptoms of internal carotid (ICA) occlusion vary with extent of collateral blood flow but generally reflect ischemia in the middle cerebral artery (MCA) territory with contralateral hemiparesis and aphasia (if the dominant hemisphere is involved).

Watershed infarcts involve the extreme reaches of collateral circulation supplied by the larger intracranial arteries. These are vulnerable areas of circulation, especially during periods of relative hypotension. These infarcts present with hemiparesis, hemisensory loss, or even aphasia if the dominant hemisphere is involved.

The MCA supplies most of the convex surface of the brain and a significant portion of “deep” brain tissue, including the basal ganglia, putamen, caudate nucleus, and portions of the internal capsule. Occlusion of the MCA is responsible for most
stroke syndromes, with embolism from the ICA or heart to the MCA being the most common cause. Occlusion of the upper MCA produces a large infarct characterized by contralateral hemiplegia, deviation of the eyes toward the side of the infarct, global aphasia (in the dominant hemisphere), hemianopia, hemianesthesia, and hemineglect. The hemiparesis affects the upper body more than the lower body and leg. Loss of consciousness may occur after MCA infarct, often at 36 hours or more after the insult, and is caused by peri-infarct edema, elevated intracranial pressure, or cerebral herniation.

Hand dominance of the patient allows the clinician to infer hemispheric dominance. Infarcts of the dominant hemisphere will cause damage to areas of the brain responsible for speech. Broca aphasia (motor aphasia) is caused by infarction to the insular cortex from MCA occlusion and results in hesitant and broken speech caused by dyspraxia between the oropharyngeal muscles and respiratory elements responsible for smooth phonation. Wernicke aphasia (sensory aphasia) occurs after infarction to the posterior temporal and lateral temporo-occipital regions caused by lower MCA occlusion. The language disturbance is seen in the acute infarct phase and is recognized by speech containing few recognizable words.

The posterior cerebral artery (PCA) generally originates from the vertebrobasilar (VB) system and supplies clinically significant areas in the occipital lobe and thalamus. Occipital lesions manifest as a homonymous visual field defect with macular sparing; oculomotor palsies or intranuclear ophthalmoplegias may also be seen. Thalamic infarcts may result in sensory losses of pain, temperature, and touch on the affected side of the body.

The vascular anatomy of the VB system is complex and leads to a variety of clinical syndromes. Brief occlusion of a VB artery by a fibrin-platelet embolus (TIA), vasospasm, hypotension, or a fixed stenotic lesion may result in some or all of the following neurologic symptoms: perioral numbness, dizziness or vertigo, diplopia, dysarthria, hemiparesis, ataxia, vomiting, or impaired hearing. VB infarction is generally caused by occlusion of the basilar artery, which supplies the pons, midbrain, and a portion of the cerebellum. Clinical manifestations include coma, abnormal breathing patterns, quadriplegia with decerebrate posturing, and bilateral sensory loss. Occlusion of a vertebral artery results in lateral medullary infarction (Wallenberg syndrome), which is clinically manifested as vertigo, headache, facial pain, disequilibrium, nausea, vomiting, and an ipsilateral Horner syndrome.

Whereas large-vessel occlusions typically have predictable symptomatology, lesions of small penetrating branch arterioles have a separate set of symptoms. Lacunar (“island”) infarcts are common and involve the deep central regions of the brain, particularly the basal ganglia, thalamus, and pons. Lesions are characterized by a lack of visual disturbance, aphasia, or impaired consciousness. Pure motor hemiparesis or pure sensory loss of the face, arm, or leg is a common result of lacunar infarction. Other lacunar syndromes include ataxia/leg hemiparesis or a dysarthria/clumsy hand clinical presentation. Lacunar infarctions have a good prognosis, with a lower overall mortality than MCA infarctions. Predisposing causes to lacunar infarction include atherosclerotic disease, amyloid angiopathy, and nonneurologic causes such as pneumonia and coronary events.