Stroke
CASE
A 67-year-old man with diabetes, long-standing hypertension, and a pack-a-day smoking habit presents to the emergency room 45 minutes after suddenly dropping his fork from his right hand at lunch. In the emergency room, he shows signs of a global aphasia, right hemiparesis affecting the arm and face more than the leg, and moderate hypertension. A CT scan is negative. He is considered for thrombolytic therapy.
Diagnosis
Cerebral infarction in left hemisphere, caused by embolus or thrombosis in the middle cerebral artery territory.
Stroke is one of the most common neurologic problems. It is the third leading cause of death in the United States. This chapter presents a basic approach to the patient with stroke, and outlines generally accepted therapy. Therapy of stroke is evolving with the introduction of newer medications and interventions.
STROKE TYPES
Stroke is a general term for the sudden onset of a focal neurologic deficit caused by vascular disease. There are subcategories of stroke, each with a specific cause, course, and treatment (Table 15.1). Infarction refers to stroke in which there is a loss of blood supply to part of the brain, so that ischemic injury occurs in one part of the brain. Infarction may be thrombotic (i.e., caused by blood clot formation within a vessel) or embolic (caused by material formed proximally, such as at a heart valve or carotid plaque, and then dislodged to occlude a distal vessel). Thrombotic stroke is often characterized as large vessel (e.g., carotid, vertebral, or basilar arteries) or small vessel (e.g., the lenticulostriate branches of the middle cerebral artery). Cerebral hemorrhage refers to abnormal bleeding within the skull. This may be intracerebral (in the brain parenchyma) or surrounding the brain (subarachnoid, subdural, or epidural).
TABLE 15.1. Stroke Types | ||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||||||||||||||||||||
WHERE IS THE STROKE? WHAT IS THE ANATOMY?
Intracerebral hemorrhage is usually deep in the brain, and may affect the putamen, thalamus, cerebellum, or pons. Lobar hemorrhages also occur.
Emboli tend to produce superficial wedge-shaped infarcts as a result of the distal migration of emboli, giving cortical deficits or deficits at the top of the basilar artery territory.
Thrombosis produces a variety of syndromes with the diagnosis based on history, anatomy of the lesion, mechanism of the thrombosis, and exclusion of embolic or hemorrhagic strokes. Any part of the brain or brainstem may be involved in thrombotic stroke.
Lacunar strokes usually involve the deep white matter, basal ganglia, or brainstem. The small, well-circumscribed lesions of lacunar disease cause characteristic clinical symptoms and signs that strongly suggest the diagnosis of lacunar disease (see Chapter 16).
Subarachnoid hemorrhage causes sudden and severe headache and stiff neck, and may also cause symptoms at the hemorrhage site (e.g., anterior communicating artery: mutism and paraparesis). Often there is no focal neurologic deficit.
HOW DID THE STROKE DEVELOP?
Intracranial hemorrhage occurs during waking hours, usually in a known hypertensive patient, or in a patient with a bleeding tendency (e.g., a patient receiving anticoagulant medication).
The full deficit is seldom present at onset but develops gradually over minutes to hours. There is usually no warning prior to the acute bleed. Headache, nausea, and vomiting are usually, but not invariably, present.
Emboli usually give a maximal deficit at onset, and often occur during waking hours. The deficit may improve in hours. There may be headache or focal seizures.
Thrombosis often occurs during sleep or is present on awakening. Symptoms and signs usually progress in a stepwise fashion; it may take hours or days for the full deficit to develop. A warning is common in thrombotic strokes. The patient may have a headache and frequently has a history of prior transient ischemic attacks (TIAs), which are brief episodes of neurologic symptoms resulting from vascular disease (see Chapter 17).
Lacunar or small-vessel thrombotic strokes occur either abruptly or in a stuttering course over hours or days. There may be warning TIAs, but headache is uncommon. There are usually risk factors such as hypertension, hyperlipidemia, smoking, and diabetes.
Subarachnoid hemorrhage occurs abruptly with a severe, “worst headache of my life” as the cardinal feature. Onset may be during exertion, with an associated stiff neck and photophobia. A “sentinel” headache may occur days or weeks prior to a major subarachnoid hemorrhage.
WHAT ARE HISTORICAL CLUES AND PHYSICAL FINDINGS?
One of the most common causes of TIA or stroke is atherosclerotic disease affecting the internal carotid artery at its origin, with stroke occurring as a result of thrombosis of the vessel or embolism to distal branches of the internal carotid.
Clinical signs may include a carotid bruit (most significant if high pitched, and at the angle of the jaw), contralateral ocular bruit, or a decreased pulsation of the carotid in the neck. Horner syndrome may be seen ipsilateral to a carotid occlusion or dissection.
The presence of a carotid bruit does not reliably predict severe carotid stenosis, and the absence of a carotid bruit does not rule out severe carotid stenosis (poor test sensitivity and specificity). Imaging studies need to be done that reliably measure the carotid (e.g., carotid ultrasound, angiogram).
Occasionally, atheromatous emboli (Hollenhorst plaques) to the retinal arteries may be seen on funduscopic examination on the same side as a carotid stenosis.
Noninvasive testing including duplex carotid ultrasound, and transcranial Doppler (TCD) help identify and characterize carotid lesions. Each of these tests assesses different aspects of cerebrovascular flow and anatomy, and may be used to determine the degree of stenosis and abnormalities of carotid flow (Table 15.2). Magnetic resonance angiography (MRA) may also be useful in assessing carotid stenosis. A combination of noninvasive vascular testing and imaging is supplanting conventional angiography in preoperative assessment for carotid endarterectomy. CT angiography (CTa) is another technique that is useful in showing stenosis in extracranial and intracranial vessels, but carries a large radiation load and moderate IV dye load.
TABLE 15.2. Major Cerebrovascular Disorders that Cause Stroke | ||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||||||||||||||||||
LARGE-VESSEL OR SMALL-VESSEL DISEASE?
Warning symptoms tend to be stereotyped in small-vessel disease and occur over hours to days. In large-vessel disease, the symptoms frequently vary depending on which territory of the vessel is involved during the warning; symptoms usually precede the stroke by days or weeks, but may occur over a period of months. See Table 15.2 for cerebrovascular diseases that cause stroke.
IS THERE AN EMBOLIC FOCUS?
The heart is the most common source of emboli, although emboli may arise from a plaque in a diseased carotid artery or aorta. Cardiogenic emboli account for 15% to 20% of all ischemic strokes. Cardiac factors predisposing to emboli include:
Mural thrombi, especially with anterior wall myocardial infarction (MI) and left-ventricular wall abnormality (emboli usually occur within 10 days but sometimes months after the MI and may be the presenting feature of an MI).
Mitral valve disease.
Atrial fibrillation.
Transesophageal echocardiography is valuable in more clearly imaging cardiac abnormalities that serve as potential sources of stroke. These include:
Mural thrombus.
Atrial septal defects.
Atrial septal aneurysms.
Patent foramen ovale.
Atherosclerotic plaques in the ascending aorta.Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
