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Examination of the Patient with Cerebrovascular Disease

Examination of the Patient with Cerebrovascular Disease
Course

Clinical Exposure in Mental Health (OT2316L)

6 Documents
Students shared 6 documents in this course
Academic year: 2022/2023
Listed bookSynopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry
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EXAMINATION OF THE PATIENT WITH CEREBROVASCULAR DISEASE

The goal of the examination of a patient suspected of having a stroke is to gain immediate information about the probable size, location, and etiology of the stroke. Successful treatment depends on starting within a few hours after the onset. Brain imaging has advanced to allow detection of ischemia within minutes to hours after symptoms begin; imaging is necessary to identify hemorrhage before treatment is considered. Nevertheless, the examining physician has the responsibility to identify the symptoms and signs that guide subsequent therapy. For patients who arrive too late, beyond the time window for acute treatment, the neurologic examination is the first step in the diagnostic workup to establish stroke etiology and to start proper treatment aimed at preventing recurrence of stroke.

GENERAL EXAMINATION

Evaluation of the patient with a suspected stroke of large size must first address the level of consciousness and cardiopulmonary status. Irregular or labored breathing and a decreased level of consciousness, particularly if accompanied by gaze deviation, hemiparesis, or unequal pupils, may indicate the need for immediate intubation to treat impending herniation from massive infarction. Reduced alertness is a sign of either extensive hemispheral injury or involvement of the brainstem reticular activating system, which could result from brainstem infarction or from compression on the brainstem by the herniating uncus of the temporal lobe. The terms <lethargic= and <stuporous= are often used to describe levels of decreasing consciousness, but it is most useful to describe alertness in terms of the minimal stimulus required for a given response (e., <opens eyes to voice= or <semipurposeful withdrawal to moderate noxious stimulus=).

Subtler impairment of attention and concentration is tested by asking the patient to count backward from 20 to 1 or say the months of the year backward. The level of alertness may fluctuate after injury to the thalamus, often a hemorrhage. Coexisting metabolic derangement such as drug toxicity or hyperglycemia must be ruled out with appropriate laboratory tests. Papilledema is an additional sign of increased intracranial pressure. Cheyne-Stokes respirations with normal level of consciousness may be associated with a smaller territory infarction that involves the insula. Cardiac conduction defects, arrhythmias, subendothelial myocardial infarction, and neurogenic pulmonary edema may occur as a consequence of subarachnoid hemorrhage or large territory infarction, presumably from centrally mediated increase in sympathetic neurotransmitter release. The blood pressure rises acutely in 70% to 80% of stroke patients as a consequence of the infarction or hemorrhage and then returns to baseline spontaneously over the course of a few days. Except for malignant hypertension with encephalopathy or hypertensive cerebral hematoma identified on brain computed tomography, blood pressure is not treated acutely. Nuchal rigidity is often present in subarachnoid hemorrhage. Fever may rarely be caused by brainstem infarction or subarachnoid hemorrhage.

A systemic etiology must be sought and treated, however, because fever can exacerbate ischemic brain injury. Beyond the examination required for emergency management of acute stroke, the general examination should focus on the cardiovascular system to seek a likely stroke etiology. Examination of the neck includes auscultation for carotid bruits, which result from turbulent flow in an artery narrowed by an atherosclerotic plaque. Auscultation of bruits may be misleading if the sound arises from stenosis of the unimportant external carotid artery or if the degree of stenosis in the internal carotid artery is great enough to dampen flow velocity below that which produces an audible bruit. Doppler ultrasound or magnetic resonance angiogram of the neck is needed if carotid stenosis is suspected.

The presence of murmurs or arrhythmia on cardiac examination suggests valvular disease or atrial fibrillation, both independent risk factors and indications for anticoagulation therapy to prevent recurrence of stroke. The presence of fever with a cardiac murmur requires blood culture to rule out bacterial endocarditis. Auscultation of the lungs is important as a means of identifying signs of aspiration pneumonia or pulmonary oedema caused by congestive heart failure.

NEUROLOGIC EVALUATION

The neurologic examination can provide valuable clues to the size, location, and etiology of the stroke. A few syndromes are predictive of specific stroke etiologies. For example, Wernicke aphasia, homonymous hemianopia, and the <top-of-the-basilar= syndrome of cortical blindness, agitation, and amnesia are nearly always caused by embolism from a proximal arterial or cardiac source. The Wallenberg syndrome, due to infarction of the dorsolateral medulla, is typically caused by thrombosis of the vertebral artery.

The "lacunar syndromes" nearly always result from lipohyalinosis and fibrinoid necrosis of small penetrating arterioles arising from the middle cerebral artery stems, the basilar artery, or the first portion of the posterior cerebral arteries. The severity of the clinical syndrome at onset is highly correlated with the ultimate functional outcome. Level of alertness, ocular motility, motor power, and higher cerebral function are the keys to initial assessment. The most common sign of large stroke is the combination of gaze deviation, hemiparesis, and altered mentation. Hyperhydrosis, or excessive sweating, sometimes unilateral, may also occur in brainstem hemorrhage or large hemisphere stroke. In a comatose patient, asymmetry of tendon reflexes supports a diagnosis of unilateral brain injury when motor and sensory testing are not possible.

Hypotonia may occur early after stroke, whereas tone often increases only after several days. Even if fully alert, patients with gaze deviation and hemiparesis who are within the first several hours after stroke onset are at high risk for profound clinical worsening because of an edemarelated mass effect that may peak as late as 3 to 5 days after stroke. Gaze palsies often occur with infarction involving the dorsolateral frontal lobes, producing gaze deviation to the opposite side of the hemiparesis. Infarction of the lateral pons, on the other hand, produces

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Examination of the Patient with Cerebrovascular Disease

Course: Clinical Exposure in Mental Health (OT2316L)

6 Documents
Students shared 6 documents in this course

University: University of Perpetual Help System DALTA

Was this document helpful?
EXAMINATION OF THE PATIENT WITH CEREBROVASCULAR DISEASE
The goal of the examination of a patient suspected of having a stroke is to gain immediate
information about the probable size, location, and etiology of the stroke. Successful treatment
depends on starting within a few hours after the onset. Brain imaging has advanced to allow
detection of ischemia within minutes to hours after symptoms begin; imaging is necessary to
identify hemorrhage before treatment is considered. Nevertheless, the examining physician has
the responsibility to identify the symptoms and signs that guide subsequent therapy. For patients
who arrive too late, beyond the time window for acute treatment, the neurologic examination is
the first step in the diagnostic workup to establish stroke etiology and to start proper treatment
aimed at preventing recurrence of stroke.
GENERAL EXAMINATION
Evaluation of the patient with a suspected stroke of large size must first address the level of
consciousness and cardiopulmonary status. Irregular or labored breathing and a decreased level
of consciousness, particularly if accompanied by gaze deviation, hemiparesis, or unequal pupils,
may indicate the need for immediate intubation to treat impending herniation from massive
infarction. Reduced alertness is a sign of either extensive hemispheral injury or involvement of
the brainstem reticular activating system, which could result from brainstem infarction or from
compression on the brainstem by the herniating uncus of the temporal lobe. The terms
<lethargic= and <stuporous= are often used to describe levels of decreasing consciousness, but it
is most useful to describe alertness in terms of the minimal stimulus required for a given response
(e.g., <opens eyes to voice= or <semipurposeful withdrawal to moderate noxious stimulus=).
Subtler impairment of attention and concentration is tested by asking the patient to count
backward from 20 to 1 or say the months of the year backward. The level of alertness may
fluctuate after injury to the thalamus, often a hemorrhage. Coexisting metabolic derangement
such as drug toxicity or hyperglycemia must be ruled out with appropriate laboratory tests.
Papilledema is an additional sign of increased intracranial pressure. Cheyne-Stokes respirations
with normal level of consciousness may be associated with a smaller territory infarction that
involves the insula. Cardiac conduction defects, arrhythmias, subendothelial myocardial
infarction, and neurogenic pulmonary edema may occur as a consequence of subarachnoid
hemorrhage or large territory infarction, presumably from centrally mediated increase in
sympathetic neurotransmitter release. The blood pressure rises acutely in 70% to 80% of stroke
patients as a consequence of the infarction or hemorrhage and then returns to baseline
spontaneously over the course of a few days. Except for malignant hypertension with
encephalopathy or hypertensive cerebral hematoma identified on brain computed tomography,
blood pressure is not treated acutely. Nuchal rigidity is often present in subarachnoid
hemorrhage. Fever may rarely be caused by brainstem infarction or subarachnoid hemorrhage.

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