Examination of the Patient With a Probable Stroke

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.

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).

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.

Use the patient’s past medical history to assess for risk factors
for intrinsic vascular disease or thrombosis (e.g., diabetes, hypertension,
coronary artery disease, peripheral vascular disease, hypercoagulable states)
or risk factors for cardioembolism (e.g., atrial fibrillation, cardiomyopathy,
valvular disease). The presence of a risk factor for a particular stroke
etiology should not supersede the other elements of the patient’s history in
determining the likely stroke mechanism, however. For example, even in a
patient with atrial fibrillation, a stroke that was preceded by multiple TIAs
in the same distribution of the stroke is more likely to be due to intrinsic
vascular disease than cardioembolism.

In the emergency evaluation of a patient with a probable acute
ischemic stroke, it’s also important to determine the time of onset of the
stroke, although this does not provide information regarding the
pathophysiologic

stroke mechanism. The timing is especially
important when intervention with intravenous tissue plasminogen activator is a
consideration, because this medication needs to be given within 3 hours of
ischemic stroke onset. The time of stroke symptom onset is defined as the last
time the patient was known to be without the stroke symptoms. If a patient
awakens with a stroke, the time of onset must be considered the time the
patient went to sleep.

Listen for carotid bruits. Although the finding of a carotid
bruit is useful evidence for the presence of carotid artery disease, the
absence of a bruit does not exclude it. To listen for a bruit:

In neurologic diagnosis, there is no clinical role to palpating
the carotid arteries; this is potentially hazardous and provides no useful
diagnostic information.

When a disorder of language is suspected or when right-sided
weakness is present, examine the patient for aphasia (see Chapter 6, Language Testing); the finding of aphasia is strong
evidence of left hemispheric cortical involvement.

In patients with left-sided weakness or in any patient with a
suspicion for right hemisphere dysfunction, look for evidence of cortical
involvement by testing for left-sided neglect. Neglect can be tested by asking
the patient to draw a clock (see Chapter 8, Testing
Orientation, Concentration, Knowledge, and Constructional Ability); patients
with right parietal cortical dysfunction may neglect to fill in the numbers on
the left side. You can also test for asomatognosia (neglect of the left side
of the body) by holding the patient’s left arm in front of his or her eyes and
asking, “Whose arm is this?” Patients with asomatognosia may say the arm they
see is the examiner’s (“It’s your arm”) and not their own.

Test visual fields to confrontation (see Chapter
13, Visual Field Examination). When a possible right hemispheric lesion
is suspected, look for evidence

of left-sided extinction on double
simultaneous visual stimulation (see Chapter 31,
Examination of Cortical Sensation), especially when a visual field deficit is
not evident.

Look for evidence of facial weakness (see Chapter
16, Examination of Facial Strength). Upper motor neuron facial weakness
is seen in many patients with hemispheric strokes on the same side as the weak
extremities. Lower motor neuron facial weakness can occur due to some pontine
infarcts, often opposite to the side of extremity weakness as a crossed sign
of brainstem dysfunction.

Look at the optic fundi for the rare finding of Hollenhorst
plaques (see Fig. 49-1); the finding of these
cholesterol emboli supports the possibility of carotid disease, but the
absence of this finding does not exclude it.

In patients without obvious severe weakness, look for drift of
one of the outstretched arms as a subtle sign of weakness. When testing muscle
strength in any patient with a possible stroke, concentrate on assessing for
side-to-side asymmetries.

Patients with weakness in the face and arm with relative
preservation of leg strength most likely have infarction within the
contralateral middle cerebral artery territory. Severe leg weakness due to
stroke suggests involvement within the contralateral anterior cerebral artery
territory.

Patients with severe weakness involving the face, arm, and leg on
one side of the body but no sensory or cortical symptoms or signs have a
syndrome called pure motor hemiparesis. This finding
is typical of a deep lesion, usually a lacunar infarct, affecting the motor
fibers of the corticospinal tract, as they are concentrated together in the
internal capsule or pons and segregated from other pathways; such extensive
weakness would be difficult to attribute to a hemispheric cortical lesion
without causing other nonmotor symptoms.

Concentrate on assessing for significant side-to-side differences
in sensation, such as to pin or gross touch.

In patients with possible right hemisphere lesions, especially
when no obvious sensory loss is seen, look for signs of right hemispheric
cortical dysfunction by testing for left-sided extinction on double
simultaneous stimulation, or other cortical sensory tests such as
graphesthesia and stereognosis (see Chapter 31,
Examination of Cortical Sensation).

Patients with severe isolated hemisensory loss involving the
face, arm, and leg on one side of the body are likely to have a thalamic
stroke; these symptoms sometimes evolve to severe painful dysesthesias (called
the thalamic syndrome).

Dysmetria (see Chapter 33, Approach to the
Cerebellar Examination) of the extremities on one side of the body, especially
in the absence of weakness, suggests a cerebellar hemisphere stroke
ipsilateral to the clumsy extremities. Some cerebellar strokes, however,
particularly those involving the midline, may only have ataxia of gait with
little if any dysmetria. Cerebellar strokes (infarction or hemorrhage) are
important to recognize because they can become neurosurgical emergencies due
to mass effect in the small space of the posterior fossa. Consider the
possibility of

cerebellar stroke in any patient with
nausea, vomiting, or headache in the presence of difficulty with gait,
regardless of whether there is dysmetria of the extremities.

Prominent dysmetria of the extremities on one side of the body in
the presence of mild weakness (or other corticospinal tract signs) on the same
side is consistent with an ataxic-hemiparesis syndrome; this is usually due to
a small infarct (usually a lacunar stroke) involving cerebellar pathway fibers
and motor fibers within the contralateral internal capsule or pons (see Chapter 33, Approach to the Cerebellar
Examination).

Patients with hemispheric (deep or cortical) strokes or
unilateral brainstem strokes can have a side-to-side reflex asymmetry, brisker
on the weak side; however, such reflex changes might not be present acutely. A
Babinski sign may be present on the weak side of any patient with a stroke
causing motor weakness, even acutely.

Patients with hemiparesis from a stroke usually have a
characteristic hemiparetic gait, described in Chapter
39, Examination of Gait). Patients with cerebellar infarcts (or an
ataxic-hemiparesis syndrome) often have an ataxic gait, falling to the side of
the diseased cerebellar hemisphere, or may be unable to walk at all without
falling.