C h a p t e r 3 7
Disorders of Brain Function
935
hemorrhage or ischemia, identify the stroke or TIA mech-
anism (i.e., large-vessel or small-vessel, atherothrombotic,
cardioembolic, hemorrhagic, cryptogenic, or other), char-
acterize the severity of clinical deficits, and unmask the
presence of risk factors.
31–34
A careful history, including
documentation of previous TIAs, the time of onset and
pattern and rapidity of system progression, the specific
focal symptoms (to determine the likely vascular terri-
tory), and any coexisting diseases, can help to determine
the type of stroke that is involved.
Computed tomographic scans and magnetic resonance
imaging have become essential brain imaging tools in
diagnosing stroke, differentiating cerebral hemorrhage
from ischemia, and excluding intracranial lesions that
mimic stroke clinically. CT scans are a necessary screening
tool in the acute setting for rapid identification of hemor-
rhage, but are insensitive to ischemia within 24 hours and
to any brain stem or small infarcts. MRI is superior for
imaging ischemic lesions in all territories and differentiat-
ing other nonstroke pathologic processes (e.g., tumors,
contusion, infection). Newer MRI techniques such as per-
fusion- and diffusion-weighted imaging (DWI) can reveal
cerebral ischemia immediately after onset and identify
areas of potentially reversible damage (i.e., penumbra).
Vascular imaging is accomplished with CT angiog-
raphy (CTA), magnetic resonance angiography (MRA),
catheter-based “conventional” arteriography, and ultra-
sonography. All except ultrasonography can demonstrate
the site of vascular abnormality (intracranial and extracra-
nial) and afford visualization of most intracranial vascu-
lar areas. MRA is noninvasive and most widely available,
but less sensitive and specific than CTA or catheter
angiography. CT angiography is exquisitely detailed for
a noninvasive technique, but is limited in availability
and requires iodinated contrast, which is nephrotoxic.
Catheter angiography remains the gold standard in sen-
sitivity and allows visualization of dynamic patterns of
collateral flow, but is invasive and requires significant
contrast doses. CT angiography and magnetic reso-
nance angiography have largely replaced angiography as
a screening tool for vascular lesions. Ultrasonographic
techniques allow quick bedside assessment of the carotid
bifurcation (duplex ultrasonography) or of flow velocities
in the cerebral circulation (transcranial Doppler).
Treatment.
Treatment of acute ischemic stroke has
changed markedly since the early 1990s, with an empha-
sis on salvaging brain tissue, preventing secondary
stroke, and minimizing long-term disability. The care of
patients with stroke has shifted away from the “near-
est hospital” to stroke centers that have been certified
by some external agency, most commonly the state or
Joint Commission.
33
Certification establishes that a hos-
pital can manage stroke patients with appropriate care
throughout the continuum—from emergency treat-
ments, through the inpatient stay, and into the rehabili-
tation phase. With this advancement, the medical and
lay communities acknowledge that care of the patient
with stroke requires specialized personnel and resources
to minimize stroke’s devastating effects, as stroke is the
leading cause of adult disability in the United States.
Stroke care begins with emergency treatments aimed
at reversing the evolving ischemic brain injury. The real-
ization that there is a window of opportunity during
TABLE 37-5
Signs and Symptoms of Stroke by Involved Cerebral Artery
Cerebral Artery
Brain Area Involved
Signs and Symptoms*
Anterior cerebral
Infarction of the medial aspect of
one frontal lobe if lesion is distal to
communicating artery; bilateral frontal
infarction if flow in other anterior
cerebral artery is inadequate
Paralysis of contralateral foot or leg; impaired gait;
paresis of contralateral arm; contralateral sensory loss
over toes, foot, and leg; problems making decisions or
performing acts voluntarily; lack of spontaneity, easily
distracted; slowness of thought; aphasia depends
on the hemisphere involved; urinary incontinence;
cognitive and affective disorders
Middle cerebral
Massive infarction of most of lateral
hemisphere and deeper structures
of the frontal, parietal, and temporal
lobes; internal capsule; basal ganglia
Contralateral hemiplegia (face and arm); contralateral
sensory impairment; aphasia; homonymous
hemianopia; altered consciousness (confusion to
coma); inability to turn eyes toward paralyzed side;
denial of paralyzed side or limb (hemiattention);
possible acalculia, alexia, finger agnosia, and left–right
confusion; vasomotor paresis and instability
Posterior cerebral
Occipital lobe; anterior and medial
portion of temporal lobe
Homonymous hemianopia and other visual defects such
as color blindness, loss of central vision, and visual
hallucinations; memory deficits, perseveration (repeated
performance of same verbal or motor response)
Thalamus involvement
Loss of all sensory modalities; spontaneous pain;
intentional tremor; mild hemiparesis; aphasia
Basilar and vertebral
Cerebral peduncle involvement
Oculomotor nerve palsy with contralateral hemiplegia
Cerebellum and brain stem
Visual disturbance such as diplopia, dystaxia, vertigo,
dysphagia, dysphonia
*Depend on hemisphere involved and adequacy of collaterals.
