Examination of the Patient With a Probable Stroke
GOAL
The main goal of the examination of the patient with a probable stroke is to try to determine the most likely location in the brain (and, therefore, the most likely vascular distribution) where the stroke occurred, as well as the most likely pathogenesis of the stroke, paving the way for the most appropriate investigation and management.
PATHOPHYSIOLOGY OF STROKE
A stroke is acute destruction of brain tissue occurring from infarction or hemorrhage.
Cerebral Infarction
Infarction can occur due to stenosis or occlusion of a blood vessel from disease or thrombosis within the vessel itself (referred to here as intrinsic cerebrovascular disease) or embolism from a proximal source, such as the heart (cardioembolism). Embolism from an artery to an artery can also occur (such as distal embolism from a carotid plaque), but it is helpful to think of artery-to-artery embolism within the spectrum of intrinsic cerebrovascular disease.
Intrinsic cerebrovascular disease can involve large (e.g., carotid, vertebral, or basilar) arteries, medium (e.g., middle and anterior cerebral) arteries, or small (e.g., lenticulostriate or other small end vessels) arteries of the anterior or posterior circulation.
Strokes due to intrinsic disease of large or medium-sized blood vessels or strokes due to cardioembolism may involve the cerebral cortex or deeper structures. Strokes due to disease of small blood vessels, such as lacunar strokes (seen in patients with small vessel disease from hypertension or diabetes), only involve deep brain structures and don’t involve the cortex. In other words, hemispheric infarcts that involve the cortex can’t be due to small vessel disease.
Cerebral Hemorrhage
Hemorrhage within the substance of the brain, called intraparenchymal or intracerebral hemorrhage, occurs due to rupture of a vessel within the brain. Intraparenchymal hemorrhages and ischemic infarcts are usually indistinguishable on clinical grounds alone, and any patient who presents with an acute stroke syndrome could potentially have a hemorrhagic or ischemic etiology of the event. Intracerebral hemorrhages are usually easily acutely visualized on imaging, such as computed tomography scanning, however. Because the presence and cause of acute ischemic strokes are not always immediately obvious, this chapter focuses on the clinical role of the history and examination in ischemic stroke diagnosis.
TAKING THE HISTORY OF A PATIENT WITH A STROKE
The history and examination are performed to attempt to determine the general vascular distribution in which the stroke occurred and the most likely pathophysiology of the stroke.
Using the History to Determine Stroke Localization
Use the history to try to generate a hypothesis as to the most likely gross anatomic localization of the stroke based on the symptoms of the deficit. Don’t be too fancy or try to overlocalize. Be happy if, after the history is obtained, you have a pretty good idea as to whether the stroke is in the left hemisphere (deep or cortical), right hemisphere (deep or cortical), brainstem, or cerebellum. The following are historical features helpful in stroke localization:
Don’t forget to ask if your patient is right- or left-handed, because symptoms of aphasia from left hemispheric cortical lesions or neglect from right hemispheric lesions are less likely to occur in left-handed patients.
Symptoms of weakness or numbness of the right side of the body (especially of the face and arm, with or without leg weakness) suggest a lesion of the left hemisphere, which could be deep or cortical. A cortical localization of a left hemisphere stroke is suggested by the presence of aphasia, which may be evident while the history is being taken.
Symptoms of weakness or numbness of the left side of the body (especially of the face and arm, with or without leg weakness) suggest a lesion of the right hemisphere, which could be deep or cortical. A cortical localization of a right hemispheric stroke is suggested during the history by the patient’s denial of the left-sided deficit (anosognosia) or left-sided neglect, such as the patient’s failure to dress the left side of the body (dressing apraxia).
Symptoms of a brainstem stroke can include double vision, nausea, vomiting, weakness (which can be unilateral or bilateral), numbness (which also can be unilateral or bilateral), clumsiness, unsteadiness, and vertigo. Crossed symptoms, such as weakness or numbness on one side of the face and the opposite side of the body, can also be seen due to some brainstem infarcts.
Symptoms of a cerebellar stroke include clumsiness, unsteadiness, vertigo, nausea, vomiting, and, sometimes, headache. Weakness and sensory loss are not accompaniments of an isolated cerebellar stroke.
Symptoms of visual field loss (hemianopsia) can occur with strokes in the anterior or the posterior circulation. Prominent isolated visual field symptoms, however, are more likely to occur due to strokes involving the posterior circulation involving the occipital cortex (posterior cerebral artery territory).
Using the History to Determine the Stroke Mechanism
The temporal course of symptom development, as well as the presence of any previous symptoms, such as transient ischemic attacks (TIAs), can provide useful information as to the most likely cause of an ischemic stroke (Table 52-1).
Intrinsic vascular disease is the most likely cause of ischemic stroke when symptoms are gradual or when there are preceding symptoms consistent with TIAs in the same vascular distribution. Patients who present with a history of multiple TIAs in the same distribution of the stroke are especially
unlikely to have a cardiogenic embolic cause, given the low probability of multiple emboli from the heart repeatedly entering a single vascular distribution.
Cardiogenic embolic strokes typically cause sudden symptoms; however, sudden symptoms can also occur due to strokes from intrinsic vascular disease (or from hemorrhage).
Symptoms of cortical dysfunction in a patient with a hemispheric infarct suggest that the stroke is due to intrinsic large or medium-sized vessel disease or due to cardiogenic embolism, and not due to small vessel disease. The absence of cortical involvement, however, doesn’t exclude a large vessel or cardiac cause.
Ask the patient specifically about any symptoms of monocular vision loss consistent with amaurosis fugax (see Chapter 49, Examination of the Patient with Visual Symptoms). Patients with such visual symptoms often don’t recognize their significance, and they are unlikely to volunteer the information because they often assume it is irrelevant to their presenting stroke symptoms. A history consistent with amaurosis fugax of the eye on the same side as the current brain dysfunction (i.e., opposite to the weak extremities) is highly suggestive of the possibility of an extracranial carotid stenosis.Related posts:
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