Examination of the Patient With a Probable Stroke


Ovid: Field Guide to the Neurologic Examination





Authors: Lewis,
Steven L.

Title: Field
Guide to the Neurologic Examination, 1st Edition


> Table of Contents > Section 3 –
Neurologic Examination in Common Clinical Scenarios >Chapter 52 –
Examination of the Patient With a Probable Stroke




Chapter 52

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, thisChapter focuses
on the clinical role of the history and examination in ischemic stroke
diagnosis.


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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

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    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

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    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.








TABLE 52-1 Historical Clues to
Ischemic Stroke Mechanism Based on Temporal Course of Symptoms or the
Presence of Preceding Symptoms



























Symptoms


Most Likely Stroke
Mechanism


Least Likely Stroke
Mechanism


Gradual progression


Intrinsic vascular disease


Cardioembolism


Sudden onset


Cardioembolism or intrinsic vascular disease


Stroke of any mechanism can be sudden in onset


Recent transient ischemic attacks in same vascular territory as
the stroke


Intrinsic vascular disease


Cardioembolism


Recent amaurosis fugax in eye on same side as current brain
dysfunction


Intrinsic vascular disease involving carotid artery


Cardioembolism, medium or small vessel disease


Previous transient ischemic attacks in multiple vascular
territories


Cardioembolism


Intrinsic vascular
disease



EXAMINING THE PATIENT WITH A STROKE

After completing the history, use the examination to help confirm,
refute, or refine your hypothesis regarding your patient’s stroke localization
and mechanism. In addition to the routine general and neurologic examinations
(see Chapter 40, Performing a Complete Neurologic
Examination), the specific elements listed below may be of particular value in
the evaluation of patients with possible stroke.


Carotid Examination



  • 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:



    • Place your stethoscope on one side of the patient’s
      neck.


    • Ask the patient to hold his or her breath or to breathe quietly
      while you listen.


    • If you hear a bruit, try to confirm that the sound you’re
      hearing doesn’t represent a transmitted cardiac murmur. To do this, listen
      to the heart, the aortic area, and then the neck again. A sound heard
      primarily over the carotid area but not over the other regions is most
      suggestive that the bruit is of carotid origin.


    • Repeat the same on the other side of the
      neck.


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


Mental Status Testing of the Patient with
Stroke



  • 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.


Cranial Nerve Examination of the Patient with
Stroke



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

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    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.


Motor Examination of the Patient with
Stroke



  • 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.


Sensory Examination of the Patient with
Stroke



  • 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).


Cerebellar Examination of the Patient with
Stroke



  • 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

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    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).


Reflex and Gait Examination of the Patient with
Stroke



  • 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.


ADDITIONAL COMMENTS

There are a few specific stroke syndromes not described above that
deserve mentioning here:



  • Patients with Wallenberg’s syndrome have symptoms of vertigo,
    dysarthria, dysphagia, and unsteadiness. The examination shows diminished pin
    sensation on one side of the face and on the opposite side of the body, with
    findings of cerebellar ataxia, Horner’s syndrome, and weakness of one side of
    the palate (see Fig. 19-1), all on the same side as the
    facial numbness. This classic, and not uncommon, syndrome results from an
    infarct of the lateral medulla.


  • Gerstmann’s syndrome consists of difficulty with writing
    (agraphia), calculations (acalculia), and finger naming (finger agnosia), with
    right/left confusion. This classic, but uncommon, stroke syndrome results from
    lesions involving the angular gyrus of the dominant posterior parietal
    lobe.