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Nervous System
which ischemic but viable brain tissue can be salvaged
has led to the use of reperfusion techniques and neuro-
protective strategies in the early treatment of ischemic
stroke.
18,30–33
Although the results of emergent treatment
of hemorrhagic stroke have been less dramatic, contin-
ued efforts to reduce disability have been promising.
Reperfusion techniques include thrombolytic therapy
(administered either intravenously or intra-arterially),
catheter-directed mechanical clot disruption, and aug-
mentation of cerebral perfusion pressure during acute
stroke.
34
The first and only agent approved by the U.S.
Food and Drug Administration (FDA) for treatment
of acute ischemic stroke is tissue plasminogen activa-
tor (tPA). A subcommittee of the Stroke Council of the
American Heart Association has developed guidelines
for the use of tPA for acute stroke.
20
These guidelines
recommend that in persons with suspected stroke, the
diagnosis of hemorrhagic stroke be excluded through the
use of CT scanning before administration of I.V. throm-
bolytic therapy, which must be administered within
3 hours of onset of symptoms, or 4.5 hours in some
cases.
34
The major risk of treatment with thrombolytic
agents is intracranial hemorrhage of the infarcted brain.
A number of conditions, including therapeutic levels of
oral anticoagulant medications, a history of gastrointes-
tinal or urinary tract bleeding in the previous 21 days,
prior stroke or head injury within 3 months, major
surgery within the past 14 days, and a blood pressure
greater than 185/110 mm Hg, are considered contrain-
dications to intravenous thrombolytic therapy.
33
Emerging experimental treatments for ischemic stroke
are being increasingly used as alternative methods of
reperfusion beyond intravenous thrombolysis. New
catheter-based methods allow recanalization of a directly
visualized cerebral clot with intra-arterial techniques,
often beyond the 4.5-hour window. Patient candidates
for invasive reperfusion strategies are generally identified
using newer perfusion imaging techniques such as CT or
MR perfusion in order to detect a region of reversible
injury (ischemic penumbra) and to exclude completed
infarcts. Once a penumbra is found, the interventional
specialist might mechanically disrupt the clot, extract the
clot (thrombectomy), or deliver the thrombolytic drug
intra-arterially at the clot surface, or urgently stent intra-
cranial vessels to restore flow and rescue the penumbra.
Additional methods (drugs, ultrasound, hypothermia)
aimed at either extending that therapeutic window until
revascularization occurs or improving recanalization
rates are under active investigation.
36
These methods
require an experienced interventional angiography team,
neurocritical care services, and extensive institutional
infrastructure, and thus remain limited to tertiary care
centers.
Poststroke Management and Deficits
Poststroke treatment is aimed at preventing recurrent
stroke and medical complications while promoting the
fullest possible recovery of function.
37
The risk of stroke
recurrence is highest in the first week after a stroke or
TIA, so the early implementation of antiplatelet agents in
most cases, or warfarin (an anticoagulant) in cardioem-
bolic stroke, is imperative. Long-term stroke recurrence
is most effectively prevented with aggressive reduction
of risk factors, primarily hypertension, diabetes, smok-
ing, and hyperlipidemia. In cases of carotid territory
stroke with carotid stenosis, revascularization with sur-
gery or stenting should be considered. Early hospital
care also requires careful prevention of aspiration, deep
vein thrombosis, and falls. Recovery is maximized with
early and aggressive rehabilitation efforts that include all
members of the rehabilitation team—physician, nurse,
speech therapist, physical therapist, and occupational
therapist—and the family.
Poststroke Motor Deficits.
Poststroke motor deficits
are most common, followed by deficits of language,
sensation, and cognition. After a stroke affecting the
corticospinal tract such as the motor cortex, posterior
limb of the internal capsule, basis pontis, or medullary
pyramids, there is profound weakness on the contra-
lateral side (hemiparesis; see Chapter 36, Fig. 36-4).
Involvement at the level of the motor cortex is most
often in the territory of the middle cerebral artery, usu-
ally with a sparing of the leg, which is supplied by the
anterior cerebral artery. Subcortical lesions of the corti-
cospinal tracts cause equal weakness of the face, arm,
and leg. Within 6 to 8 weeks, the initial weakness and
flaccidity are replaced by hyperreflexia and spasticity.
Spasticity involves an increase in the tone of affected
muscles and usually an element of weakness. The flexor
muscles usually are more strongly affected in the upper
extremities and the extensor muscles more strongly
affected in the lower extremities. There is a tendency
toward foot drop; outward rotation and circumduction
of the leg with gait; flexion at the wrist, elbow, and fin-
gers; lower facial paresis; slurred speech; an upgoing toe
to plantar stimulation (Babinski sign); and dependent
edema in the affected extremities. A slight corticospinal
lesion may be indicated only by clumsiness in carrying
out fine coordinated movements rather than obvious
weakness. Passive range-of-motion exercises help to
maintain joint function and to prevent edema, shoulder
subluxation (i.e., incomplete dislocation), and muscle
atrophy, and may help to reestablish motor patterns.
If no voluntary movement or movement on command
appears within a few months, significant function usu-
ally will not return to that extremity.
Poststroke Dysarthria and Aphasia.
Two key aspects
of verbal communication are speech and language.
Speech involves the mechanical act of articulating verbal
sounds, the “motor act” of verbal expression, whereas
language involves the written or spoken use of symbolic
formulations, such as words or numbers.
7
Dysarthria
is a disorder of speech, which manifests as the imper-
fect articulation of speech sounds or changes in voice
pitch or quality. It results from a stroke affecting the
muscles of the pharynx, palate, tongue, lips, or mouth
and does not relate to the content of speech. A person
with dysarthria may demonstrate slurred speech while
still retaining language ability, or may have a concurrent