SECTION SEVEN
Neurology
PRINCIPLES
Background
Stroke is the fifth leading cause of death in the United States and
a leading cause of long-term disability.1 It affects about 795,000
people per year. On average, someone has a stroke every 40
seconds, and someone dies of a stroke every 4 minutes.2 Stroke
patients have an in-hospital mortality rate of 5% to 10% for isch-
emic stroke and 40% to 60% for intracerebral hemorrhage (ICH).3
Only 10% of stroke survivors will recover completely, making
stroke a leading cause of adult disability.
Stroke can be defined as any vascular injury that reduces cere-
bral blood flow (CBF) to a specific region of the brain, retina, or
spinal cord, causing neurologic impairment. The onset of symp-
toms may be sudden or stuttering, often with transient or perma-
nent loss of neurologic function. Approximately 87% of all strokes
are ischemic in origin, caused by the occlusion of a cerebral vessel.
Approximately 13% are hemorrhagic strokes caused by the
rupture of a blood vessel into the parenchyma of the brain (ICH)
or into the subarachnoid space (subarachnoid hemorrhage
[SAH]). Only ischemic stroke involving the brain and ICH are
discussed in this chapter. SAH is discussed in Chapter 93.
Prior to the reperfusion era, treatment for stroke was not
focused on reversal of damage and consisted of stabilization,
observation, and rehabilitation. Current acute interventional
treatment regimens are designed to reverse or minimize brain
damage.4 Strategies include blood pressure (BP) management,
anticoagulation, thrombolytic therapy, catheter-based interven-
tions, and surgery.
Epidemiology
Ischemic Stroke
An estimated 610,000 “first-ever” ischemic strokes occur each year
in the United States. These may result from either in situ throm-
bosis or embolic obstruction from a more proximal source,
usually the heart. In more than one-third of these first-ever
strokes, no clear cause is identified. Strokes of all subtypes are
more common in African American and Hispanics versus non-
Hispanic whites.
Approximately one-third of all ischemic strokes are throm-
botic in nature. These can be caused by either large- or small-
vessel occlusions. Common areas for large-vessel occlusions are
cerebral vessel branch points, especially in the distribution of
the internal carotid artery. Thrombosis usually results from clot
formation in the area of an ulcerated atherosclerotic plaque
that forms in the area of turbulent blood flow, such as a vessel
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C H A P T E R 91 
Stroke
Todd J. Crocco | William J. Meurer
bifurcation. A marked reduction in flow results when the stenosis
occludes more than 90% of the blood vessel diameter. With
further ulceration and thrombosis, platelets adhere to the region.
A clot then either embolizes or occludes the artery.
Lacunae, or small-vessel strokes, involve small terminal sec-
tions of the vasculature and more commonly occur in patients
with diabetes and hypertension. A history of hypertension is
present in 80% to 90% of patients who experience lacunar strokes.
The subcortical areas of the cerebrum and brainstem often are
involved. The infarcts range in size from a few millimeters to 2 cm
and are seen most commonly in the basal ganglia, thalamus, pons,
and internal capsule. They may be caused by small emboli or by
a process termed lipohyalinosis, which occurs in patients with
hypertensive cerebral vasculopathy.
One-fourth of all ischemic strokes are cardioembolic in nature.
Embolization of a mural thrombus in patients with atrial fibrilla-
tion is the most common mechanism, and patients with atrial
fibrillation have an approximate fivefold increased risk for devel-
opment of a stroke. Noncardiac sources of emboli may include
diseased portions of extracranial arteries, resulting in an artery-
to-artery embolus. One common example is amaurosis fugax, in
which emboli from a proximal carotid artery plaque embolizes to
the ophthalmic artery, causing transient monocular blindness.
Although stroke risk increases with age, approximately 3% to
4% of all strokes occur in patients 15 to 45 years old, and there
have been trends observed showing the average age of first stroke
is becoming younger.5 Although atherosclerosis is the most
common cause in elders, causative disorders and conditions in
younger patients often are uncommon and may be reversible.
Pregnancy, the use of oral contraceptives, antiphospholipid
antibodies (such as, lupus anticoagulant and anticardiolipin anti-
bodies), protein S and C deficiencies, sickle cell anemia, and poly-
cythemia all predispose patients to sludging or thrombosis,
thereby increasing the risk of stroke. Fibromuscular dysplasia of
the cerebral vasculature also may lead to stroke, and in rare
instances prolonged vasoconstriction from a migraine syndrome
causes stroke. Recreational drugs such as cocaine, phenylpropa-
nolamine, and amphetamines are potent vasoconstrictors that
have been associated with both ischemic and hemorrhagic stroke.
Infectious processes, particularly varicella and recently fungal
meningitis, can induce vasculopathies that lead to stroke as well
or can induce longer-term inflammatory processes that ultimately
cause a clinical stroke.
Carotid and vertebral dissections often are associated with
trauma but may follow mild events such as sneezing. Dissections
are the leading determined cause of stroke in the young and are
slightly less common than idiopathic strokes. Carotid and verte-
bral dissections also are seen more frequently in people with
underlying pathology of the vessel wall, such as in fibromuscular
1241
1242 PART III  Medicine and Surgery  |  SECTION Seven  Neurology
dysplasia and connective tissue disorders. Alteration in the vessel
intima can lead to vessel stenosis, occlusion, or embolism. The
patient may report a minor preceding event, such as spinal manip-
ulation, yoga, working overhead, coughing, or vomiting. Present-
ing manifestations may include headache, facial pain, visual
changes, cranial nerve (CN) palsies, pain over the affected vessel,
Horner’s syndrome, amaurosis fugax, SAH, or an ischemic stroke.
The headache frequently is unilateral and may occur days before
onset of the other neurologic symptoms. Dissections are typically
diagnosed by noninvasive modalities, such as ultrasonography,
magnetic resonance angiography (MRA), and computed tomog-
raphy angiography (CTA). Medical therapy options include early
anticoagulation if SAH/intracranial dissection is not suspected.
The existing data comparing antiplatelet treatment to anticoagu-
lation is generally limited and antiplatelet treatment is generally
simpler and safer.6 The use of tissue plasminogen activator (tPA)
is considered as a safe and effective in extracranial carotid or
vertebral dissection patients as in any other eligible patient.7
Transient Ischemic Attack
A transient ischemic attack (TIA) was historically defined as a
neurologic deficit with complete resolution within 24 hours;
however, a portion of TIA cases have evidence of permanent brain
ischemia on neuroimaging. Therefore, the American Heart Asso-
ciation (AHA) has adopted a tissue-based definition: A transient
episode of neurologic dysfunction caused by focal brain, spinal
cord, or retinal ischemia, without acute infarction.
About 240,000 TIAs per year occur in the United States, with
an incidence rate of 8 per 1000 person years. TIAs constitute an
important warning sign for the future development of cerebral
infarction. Approximately 10% of the patients who experience a
TIA will experience a stroke within 3 months of the sentinel event,
and one-half of these occur within the first 2 days.
Hemorrhagic Stroke
Spontaneous ICH causes 10% to 15% of all acute strokes, affecting
approximately 65,000 patients per year. It carries a 30-day mortal-
ity rate of up to 50% with one-half of patients dying in the first
2 days. Among survivors, only one in five are living independently
at 6 months.
The two major underlying causes of ICH are hypertensive
vasculopathy (caused by long-standing hypertension) and cere-
bral amyloid angiopathy (usually found in elders, which is the
result of amyloid deposition in cerebral vessel walls). Hypertensive
hemorrhage results from degenerative changes in the small pen-
etrating arteries and arterioles, leading to lipohyalinosis of small,
deep penetrating arteries. Such hemorrhages generally occur in
the deep regions, including basal ganglia and thalamus. The most
common sites for hypertensive hemorrhage are listed in Box 91.1.
ICH caused by amyloid angiopathy tends to be lobar in nature
and to occur more commonly in older adults.
Other factors leading to ICH include underlying vascular mal-
formations (ie, arteriovenous malformations (AVMs) and aneu-
rysms), drug intoxication (particularly sympathomimetics, such
as cocaine), malignant hypertension, saccular aneurysms, blood
dyscrasias, venous sinus thrombosis, hemorrhagic transformation
of an ischemic stroke, moyamoya disease, and tumors). High-risk
features for such secondary forms of ICH include lobar location,
presence of intraventricular blood, and younger age.
Pathophysiology
The cerebral vasculature supplies the brain with a rich flow of
blood that contains the critical supply of oxygen and glucose
necessary for normal brain function. When a stroke occurs, there
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BOX 91.1 
Most Common Sites for Hypertensive
Intracranial Hemorrhage
AFFECTED AREA (FREQUENCY)
Putamen (44%)
Thalamus (13%)
Cerebellum (9%)
Pons (9%)
Other cortical areas (25%)
COMMON CLINICAL PRESENTATION
Contralateral motor/sensory loss
Limb pain, speech difficulty
Uncoordinated movements of trunk and limbs
Numbness, weakness, ataxia, dizziness
Numbness, weakness, language disturbances
are immediate alterations in CBF and extensive changes in cellular
homeostasis. The normal CBF is approximately 40 to 60 mL/100 g
of brain per minute. When CBF drops below 15 to 18 mL/100 g
of brain per minute, several physiologic changes occur. The brain
loses electrical activity, becoming electrically “silent,” although
neuronal membrane integrity and function remain intact. Clini-
cally, the areas of the brain maintaining electrical silence manifest
a neurologic deficit, even though the brain cells are viable. When
CBF is below 10 mL/100 g of brain per minute, membrane failure
occurs, with a subsequent increase in the extracellular potassium
and intracellular calcium and eventual cell death.
The ischemic penumbra is the area of the brain surrounding
the primary injury, which is preserved by a tenuous supply of
blood from collateral vessels. This border zone of neuronal tissue
is the area of greatest interest to investigators for possible salvage
in both ischemic and hemorrhagic stroke. In ischemic stroke, the
duration of occlusion plays a critical role in neuronal survival.
In ICH, acute vessel rupture is most often caused by underly-
ing small vessel disease and causes injury by several mechanisms.
First, there is mass effect from the hematoma itself, followed
by activation of the coagulation cascade, release of inflamma-
tory cytokines, and blood-brain barrier (BBB) disruption. This
leads to perihematomal edema formation and secondary brain
injury. Finally, continued bleeding, or hematoma expansion,
occurs in many patients—either continued bleeding from the
primary source, or secondary bleeding at the periphery of the
hemorrhage.
Anatomy and Physiology
Blood is supplied to the brain by the anterior and posterior cir-
culations. The anterior circulation originates from the carotid
system and perfuses 80% of the brain, including the optic nerve,
retina, and frontoparietal and anterior-temporal lobes. The first
branch off the internal carotid artery is the ophthalmic artery,
which supplies the optic nerve and retina. As a result, the sudden
onset of painless monocular blindness (amaurosis fugax) identi-
fies the stroke as involving the anterior circulation (specifically the
ipsilateral carotid artery) at or below the level of the ophthalmic
artery. The internal carotid arteries terminate by branching into
the anterior and middle cerebral arteries at the circle of Willis.
The anterior cerebral artery supplies the basal and medial
aspects of the cerebral hemispheres and extends to the anterior
two-thirds of the parietal lobe. The middle cerebral artery feeds

the lenticulostriate branches that supply the putamen, part of the
anterior limb of the internal capsule, the lentiform nucleus, and
the external capsule. Main cortical branches of the middle cerebral
artery supply the lateral surfaces of the cerebral cortex from the
anterior portion of the frontal lobe to the posterolateral occipital
lobe.
Although the posterior circulation is smaller and usually sup-
plies only 20% of the brain, it supplies the brainstem (which is
critical for normal consciousness, movement, and sensation), cer-
ebellum, thalamus, auditory and vestibular centers of the ear,
medial temporal lobe, and visual occipital cortex. The posterior
circulation is derived from the two vertebral arteries that ascend
through the transverse processes of the cervical vertebrae. The
vertebral arteries enter the cranium through the foramen magnum
and supply the cerebellum by the posterior inferior cerebellar
arteries. They join to form the basilar artery, which branches to
form the posterior cerebral arteries. Some variants exist, impor-
tantly, the fetal origin posterior cerebral artery, which is where
the posterior cerebral artery is actually fed by the anterior
circulation.
The extent of injury in either an anterior or a posterior stroke
depends on both the vessel involved and the presence of collateral
blood flow distal to the vessel occlusion. A patient with excellent
collateral blood flow from the contralateral hemisphere may have
minimal clinical deficits despite a complete carotid occlusion. By
contrast, a patient with poor collateral flow may have hemiplegia
with the same lesion.
CLINICAL FEATURES
Ischemic Stroke
The signs and symptoms of an ischemic stroke may appear sud-
denly and without warning or may have a stuttering, insidious
onset. Disruption of the flow to one of the major vascular limbs
of the cerebral circulation will result in physiologic disruption to
the anatomic area of the brain supplied by that blood vessel.
Ischemic strokes can be classified as anterior or posterior circula-
tion strokes, depending on the vasculature involved. The presence
of neurologic deficits is highly dependent on collateral flow. In
addition to the vascular supply involved, ischemic strokes can be
further described by the temporal presentation of their neurologic
deficits.
A “stroke in evolution” is one in which focal neurologic deficits
worsen over the course of minutes or hours. Approximately
20% of anterior circulation strokes and 40% of posterior circula-
tion strokes will show evidence of progression. Anterior circula-
tion strokes may progress within the first 24 hours, whereas
posterior strokes may progress for up to 3 days. Propagation of
thrombus is postulated as a likely mechanism for progression.
With anterior circulation strokes (involving variously and primar-
ily the carotid, anterior, and middle cerebral arteries), the clinical
presentation rarely includes complete loss of consciousness unless
the lesion occurs in the previously unaffected hemisphere of a
patient who has experienced a previous contralateral stroke.
Occlusions in the anterior cerebral artery mainly affect frontal
lobe function. The patient has altered mentation coupled with
impaired judgment and insight, as well as the presence of primi-
tive grasp and suck reflexes on physical examination. Bowel and
bladder incontinence may be features of anterior cerebral artery
stroke. Paralysis and hypesthesia of the lower limb opposite the
side of the lesion are characteristic. Leg weakness is more pro-
nounced than arm weakness in anterior cerebral distribution
stroke. Apraxia or clumsiness in the patient’s gait also may be
noted.
Marked motor and sensory disturbances are the hallmarks of
occlusion of the middle cerebral artery. They occur on the side of
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CH APTER 91  Stroke 1243
the body contralateral to the side of the lesion and usually are
worse in the arm and face than the leg. Such disturbances may
involve only part of an extremity or the face but almost always are
accompanied by numbness in the same region as that of the motor
loss. Hemianopsia, or blindness in one-half of the visual field,
occurs ipsilateral to the lesion. Agnosia, or the inability to recog-
nize previously known subjects, is common, and aphasia may be
present if the lesion occurs in the dominant hemisphere. Patients
often have a gaze preference toward the affected hemisphere
because of disruption of the cortical lateral gaze centers.
Aphasia, a disorder of language in which the patient articulates
clearly but uses language inappropriately or understands it poorly,
also is common in dominant-hemisphere stroke. Aphasia may be
expressive, receptive, or a combination of both. Wernicke’s aphasia
occurs when the patient is unable to process sensory input, such
as speech, and thus fails to understand verbal communication
(receptive aphasia). Broca’s aphasia refers to the inability to com-
municate verbally in an effective way, even though understanding
may be intact (expressive aphasia). Aphasia should be distin-
guished from dysarthria, which is a motor deficit of the mouth
and speech muscles; the dysarthric patient articulates poorly but
understands words and word choices. Aphasia is important to
recognize because it usually localizes a lesion to the dominant
(usually left) cerebral cortex in the middle cerebral artery distri-
bution. Aphasia and dysphasia are terms that are used interchange-
ably but must be distinguished from dysphagia, which is difficulty
in swallowing.
Pathology in the vertebrobasilar system (ie, posterior circula-
tion strokes) can cause the widest variety of symptoms and as a
result may be the most difficult to diagnose. The symptoms reflect
CN deficits, cerebellar involvement, and involvement of neurosen-
sory tracts. The brainstem also contains the reticular activating
system, which is responsible for mediating consciousness, and the
emesis centers. Unlike those with anterior circulation strokes,
patients with posterior circulation stroke can have loss of con-
sciousness and frequently have nausea and vomiting. The poste-
rior cerebral artery supplies portions of the parietal and occipital
lobes, so vision and thought processing are impaired. Visual
agnosia, the inability to recognize seen objects, may be a feature,
as may alexia, the inability to understand the written word. A third
nerve palsy may occur, and the patient may experience homony-
mous hemianopsia. One of the more curious facets of this syn-
drome is that the patient may be unaware of any visual problem
(visual neglect). Vertigo, syncope, diplopia, visual field defects,
weakness, paralysis, dysarthria, dysphagia, spasticity, ataxia, or
nystagmus may be associated with vertebrobasilar artery insuffi-
ciency. Posterior circulation strokes also demonstrate crossed defi-
cits, such as motor deficits on one side of the body and sensory
loss on the other. In anterior circulation strokes, by contrast,
abnormalities are always limited to one side of the body.
A focused neurologic examination should assess level of con-
sciousness, speech, CN function, motor and sensory function, and
cerebellar function. Level of consciousness and fluency of speech
can be rapidly assessed in a dialogue with the patient to determine
the presence of dysarthria or aphasia. The head should be
evaluated for signs of trauma. Pupillary size and reactivity and
extraocular movements provide important information about
brainstem function, particularly CN III through CN VI; an abnor-
mal third nerve function may be the first sign of tentorial hernia-
tion. Gaze preference suggests brainstem or cortical involvement.
Central facial nerve weakness from a stroke should be distin-
guished from the peripheral causes of CN VII weakness. With a
peripheral lesion, the patient is unable to wrinkle the forehead.
Assessment of facial sensation, eyebrow elevation and squinting,
smiling symmetry, gross auditory acuity, gag reflex, shoulder
elevation, sternocleidomastoid strength, and tongue protrusion
complete the CN evaluation.
1244 PART III  Medicine and Surgery  |  SECTION Seven  Neurology
Motor and sensory testing is performed next. Muscle tone can
be assessed by moving a relaxed limb. Proximal and distal muscle
group strength is assessed against resistance. Pronator drift of the
arm is a sensitive sign of motor weakness and can be tested simul-
taneously by having the patient sit with eyes closed and arms
outstretched, with palms toward the ceiling, for 10 seconds. Asym-
metrical sensation to pain and light touch may be subtle and
difficult to detect. Double simultaneous extinction evaluation
tests for sensory neglect and can be easily performed by simulta-
neously touching the right and left limbs. The patient may feel
both the right and left sides being touched individually but may
not discern touch on one side when both are touched simultane-
ously. Similarly, the ability to discern a number gently scratched
on a forearm, graphesthesia, is another easily tested cortical pari-
etal lobe function. These tests can help differentiate a pure motor
deficit of a lacunar stroke from a sensorimotor middle cerebral
artery deficit.
Cerebellar testing and the assessment of reflexes and gait com-
plete the examination. Finger-to-nose and heel-to-shin evalua-
tions are important tests of cerebellar functions. Asymmetry of
the deep tendon reflexes or unilateral Babinski’s sign may be an
early finding of corticospinal tract dysfunction. Gait testing is
commonly omitted yet is an informative part of the neurologic
examination when it can be safely performed. Observing routine
ambulation and heel-to-toe walking can assess for subtle ataxia,
weakness, or focal cerebellar lesions.
Several prehospital stroke scales have been created to assist
emergency medical service (EMS) personnel with the rapid assess-
ment of potential stroke patients. Many of these prehospital stroke
scales have been prospectively validated for their accuracy in
stroke detection. Two of the more commonly used scales include
the Cincinnati Prehospital Stroke Scale (Fig. 91.1) and Los Angeles
Prehospital Stroke Screen (Fig. 91.2).
The National Institutes of Health Stroke Scale (NIHSS) is a
useful and rapid tool for quantifying neurologic deficit in patients
with stroke and can be used in determining treatment options
(Table 91.1). NIHSS scores have been shown to be reproducible
and valid and to correlate well with the amount of infarcted tissue
on computed tomography (CT) scan. The baseline NIHSS score
can identify patients who are appropriate candidates for fibrino-
lytic therapy, as well as those at increased risk for hemorrhage,
although it is possible for patients to have disabling strokes with
an NIHSS of zero (severe truncal ataxia). In addition, it has been
used as a prognostic tool to predict outcome and is currently
being used by some stroke centers to stratify patients for entry
into treatment trials.
Cincinnati Prehospital Stroke Scale
Facial Droop
Normal: Both sides of face move equally
Abnormal: One side of face does not move at all
Arm Drift
Normal: Both arms move equally or not at all
Abnormal: One arm drifts compared to the other
Speech
Normal: Patient uses correct words with no slurring
Abnormal: Slurred or inappropriate words or mute
Fig. 91.1.  Cincinnati Prehospital Stroke Scale. (Adapted from Kothari
RU, Pancioli A, Liu T, et al: Cincinnati Prehospital Stroke Scale: reproduc-
ibility and validity. Ann Emerg Med 33[4]:373-378, 1999.)
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Hemorrhagic Stroke
The classic presentation of ICH is the sudden onset of headache,
vomiting, severely elevated BP, and focal neurologic deficits that
progress over minutes. Similar to ischemic stroke, ICH is often
associated with a motor and sensory deficit contralateral to the
brain lesion. Almost 40% of patients will demonstrate significant
growth in hemorrhage volume within the first few hours.
Although headache, vomiting, and coma are common, many
patients do not have these findings, and the clinical presentation
can be identical to that of patients with ischemic stroke; the two
cannot be reliably differentiated in the absence of neuroimaging.
Ongoing assessment of airway and mental status is of para-
mount importance in patients with ICH because precipitous dete-
rioration is always a possibility. Emergency airway management
requires careful judgment: On the one hand, airway control can
prevent aspiration, hypoxia, and hypercarbia; on the other, seda-
tion and paralysis can make it difficult to follow the neurologic
examination, which can help monitor for hemorrhage expansion,
elevated intracranial pressure (ICP), seizure activity, and brain-
stem herniation.
As with ischemic stroke, a careful neurologic examination is
important in localizing the region and extent of injury. Baseline
NIHSS and Glasgow Coma Scale scores can be used to assess
stroke severity, although the Glasgow Coma Score (GCS) may be
more practical to follow for neurologic deterioration (Table 91.2).
In addition, serial examinations can detect early changes that may
suggest ongoing bleeding during the acute phase. The ICH score
can predict mortality (Table 91.3).
Poor prognostic indicators for patients with ICH include a
decreased level of consciousness on arrival, intraventricular hem-
orrhage, and large ICH volume, all of which can be assessed in
the emergency department (ED) (Fig. 91.3).
DIFFERENTIAL DIAGNOSIS
Ischemic Stroke
Extra-axial collections of blood secondary to trauma can mimic
stroke. An epidural or subdural hematoma can cause an altered
mental status, focal neurologic signs, and rapid progression to
coma. Elders, who represent the age group at highest risk for
stroke, can be victims of recurrent falls that lead to chronic sub-
dural hematomas. Carotid dissection may occur after neck trauma
or sudden hyperextension and may be associated with focal neu-
rologic signs and symptoms, as with an aortic dissection that
extends into the carotid arteries.
Other structural lesions that may cause focal neurologic signs
include brain tumors and abscesses. Air embolism should be sus-
pected in the setting of marked atmospheric pressure changes,
such as in scuba diving or during medical procedures or injuries
that may allow air into the vascular system. Seizures, altered
mental status, and focal neurologic findings also may be manifes-
tations of air embolism.
Metabolic abnormalities also can mimic stroke syndromes.
Hypoglycemia often is responsible for an altered mental status and
is a well-known cause of sustained focal neurologic symptoms
that can persist for several days. Wernicke’s encephalopathy causes
ophthalmoplegia, ataxia, and confusion that can be mistaken for
signs of cerebellar infarction.
Migraine may present with focal neurologic findings, with or
without headache. A seizure followed by Todd’s postictal paralysis
may mimic stroke. Bell’s palsy, labyrinthitis, vestibular neuronitis,
peripheral nerve palsy, and demyelinating diseases may all mimic
stroke. Ménière’s disease may be difficult to distinguish from a
posterior circulation stroke or TIA. Dizziness, vertigo, hearing
loss, and tinnitus in Ménière’s disease are common, whereas
 CH APTER 91  Stroke 1245

Los Angeles Patient name:

Prehospital Rater name:
Stroke Scale (LAPSS) Date:

Screening criteria Yes No

4. Age over 45 years

5. No prior history of seizure disorder

6. New onset of neurologic symptoms in last 24 hours

7. Patient was ambulatory at baseline (prior to event)

8. Blood glucose between 60 and 400

9. Exam: Look for obvious asymmetry

Normal Right Left

Facial smile / grimace: Droop Droop

Grip: Weak grip Weak grip

No grip No grip

Arm weakness: Drifts down Drifts down

Falls rapidly Falls rapidly

Based on exam, patient has only unilateral (and not bilateral) weakness: Yes No

10. If yes (or unknown) to all items above LAPSS screening criteria met: Yes No

11. If LAPSS criteria for stroke met, call receiving hospital with “CODE STROKE,” if not
then return to the appropriate treatment protocol. (Note: The patient may still be
experiencing a stroke if even if LAPSS criteria are not met.)

Provided by the internet stroke center — www.strokecenter.org

Fig. 91.2.  Los Angeles Prehospital Stroke Screen. (Adapted from Kidwell CS, Starkman S, Eckstein M,
et al: Identifying stroke in the field: prospective validation of the Los Angeles Prehospital Stroke Screen
[LAPSS]. Stroke 31:71-76, 2000.)

difficulties with vision or speech or other focal symptoms are
uncommon.
Like stroke, giant cell arteritis is a disease of older adults. It may
cause severe headache, visual disturbances, and, rarely, aphasia
and hemiparesis. Other symptoms include intermittent fever,
malaise, jaw claudication, morning stiffness, and myalgias. The
diagnosis should be suspected in patients with a very high eryth-
rocyte sedimentation rate (ESR) and is confirmed by temporal
artery biopsy. Collagen vascular diseases such as polyarteritis
nodosa, lupus, and other types of vasculitis may cause stroke
syndromes.
Cerebral venous sinus thrombosis (CVST) is another cause of
focal neurologic symptoms that most commonly affects the supe-
rior sagittal sinus and lateral sinuses (see Chapter 93).8 The diag-
nosis of CVST can be difficult because of the nonspecific nature
of symptoms, as well as the variable time frame of symptom onset
(from hours to a few weeks). Patients may have generalized head-
aches, nausea, vomiting, paresis, visual disturbances, depressed

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1246 PART III  Medicine and Surgery  |  SECTION Seven  Neurology

TABLE 91.1 

National Institutes of Health Stroke Scale Scoring Form

ITEM
1a. Level of consciousness (LOC)
1b. LOC-related questions: Ask patient’s age
and month. Must be exact.
1c. Commands: Open and close eyes, grip and
release nonparetic hand. (Other one-step
commands or mimic also acceptable.)
2. Best gaze: Horizontal EOM by voluntary or
doll’s eye maneuver.
3. Visual field: Use visual threat if necessary.
If monocular, score field of good eye.
4. Facial palsy: If patient is stuporous, check
symmetry of grimace to pain.
5. Motor arm: Arms outstretched 90 degrees
(sitting) or 45 degrees (supine) for 10
seconds. Encourage best effort. Indicate
paretic limb in score box.
6. Motor leg: Raise leg to 30 degrees (from
supine) for 5 seconds. Indicate paretic limb
in score box.
7. Limb ataxia: Check finger-nose-finger,
heel-shin position sense; and score only if
out of proportion to paralysis.
8. Sensory: Use safety pin. Check grimace or
withdrawal if patient is stuporous. Score
only stroke-related losses.
9. Best language: Describe cookie jar picture,
name objects, read sentences. May use
repeating, writing, stereognosis.
10. Dysarthria: Read list of words.
11. Extinction or neglect: Simultaneously check
bilateral visual fields and auditory
sensation, touch in both hands and
recognition of body parts looking for
extinction or neglect.
Android Free App: https://play.google.com/store/apps/details?id=com.myprograms.nihss
Apple Free App: https://itunes.apple.com/us/app/nih-stroke-scale-from-statcoder/id408788598?mt=8
Online NIHSS Calculator: www.mdcalc.com/nih-stroke-scale-score-nihss/
EOM, Extraocular movement; L, left; LOC, level of consciousness; NLF, nasolabial fold; R, right; UMN, upper motor neuron.
Modified from Massachusetts General Hospital Stroke Service. NIH stroke scale materials. Scoring form. Available at www2.massgeneral.org/stopstroke/pdfs/scoring
_form.pdf.
SCORING DEFINITIONS SCORE
0 = Alert and responsive
1 = Arousable to minor stimulation
2 = Arousable only to painful stimulation
3 = Reflex responses or unarousable
0 = Both correct
1 = One correct (or dysarthria, intubated, foreign language)
2 = Neither correct
0 = Both correct (acceptable if impaired by weakness)
1 = One correct
2 = Neither correct
0 = Normal
1 = Partial gaze palsy; abnormal gaze in one or both eyes
2 = Forced eye deviation or total paresis that cannot be overcome by doll’s eye maneuver
0 = No visual loss
1 = Partial hemianopsia, quadrantanopia, extinction
2 = Complete hemianopsia
3 = Bilateral hemianopsia or blindness
0 = Normal
1 = Minor paralysis, flat NLF, asymmetrical smile
2 = Partial paralysis (lower face = UMN lesion)
3 = Complete paralysis (upper and lower face)
0 = No drift for 10 seconds L or R
1 = Drift but does not hit bed
2 = Some antigravity effort, but cannot sustain
3 = No antigravity effort, but even minimal movement counts
4 = No movement at all
X = Unable to assess owing to amputation, fusion, fracture, and so on
0 = No drift for 5 seconds L or R
1 = Drift but does not hit bed
2 = Some antigravity effort, but cannot sustain
3 = No antigravity effort, but even minimal movement counts
4 = No movement at all
X = Unable to assess owing to amputation, fusion, fracture, and so on
0 = No ataxia (or aphasic, hemiplegic) L or R
1 = Ataxia in upper or lower extremity
2 = Ataxia in upper and lower extremity
X = Unable to assess owing to amputation, fusion, fracture, and so on
0 = Normal
1 = Mild-moderate unilateral loss but patient aware of touch (or aphasic, confused)
2 = Total loss, patient unaware of touch; coma, bilateral loss
0 = Normal
1 = Mild-moderate aphasia (speech difficult to understand but partly comprehensible)
2 = Severe aphasia (almost no information exchanged)
3 = Mute, global aphasia, coma; no one-step commands
0 = Normal
1 = Mild-moderate; slurred but intelligible
2 = Severe; unintelligible or mute
X = Intubation or mechanical barrier
0 = Normal, none detected (visual loss alone)
1 = Neglects or extinguishes to double simultaneous stimulation in any modality (visual,
auditory, sensation, spatial, body parts)
2 = Profound neglect in more than one modality

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 CH APTER 91  Stroke 1247

TABLE 91.2  TABLE 91.3 

Glasgow Coma Scale Score* Intracerebral Hemorrhage Score Predicting Mortality

EYE OPENING VERBAL RESPONSE MOTOR RESPONSE After Acute Intracerebral Hemorrhage
(E) (V) (M) FEATURE POINTS
4 = Spontaneous 5 = Normal conversation 6 = Normal GLASGOW COMA SCALE SCORE
3 = To voice 4 = Disoriented 5 = Localizes to pain
2 = To pain conversation 4 = Withdraws to pain 3 to 4 2
1 = None 3 = Words, but not 3 = Decorticate posture 5 to 12 1
coherent 2 = Decerebrate posture
2 = No words; only 1 = None 13 to 15 0
sounds INTRACEREBRAL HEMORRHAGE VOLUME
1 = None
>30 mL 1
*Total score = E + V + M
Shoestring Graphics: Glasgow coma score. ≤30 mL 0
Available at www.ssgfx.com/CP2020/medtech/glossary/glasgow.htm. INTRAVENTRICULAR HEMORRHAGE
(INTRAVENTRICULAR BLOOD)
Present 1
Absent 0
INTRACEREBRAL HEMORRHAGE LOCATION
Infratentorial 1
Supratentorial 0
AGE
≥80 years 1
A
<80 years 0
B 30-DAY MORTALITIES FOR TOTAL INTRACEREBRAL
HEMORRHAGE SCORES
0 = 0%
1 = 13%
2 = 26%
3 = 72%
4 = 97%
5 = 100%

Fig. 91.3.  The computed tomography (CT) slice with the largest area of
hemorrhage is identified. The largest diameter of the hemorrhage on this
slice is measured in centimeters (line A). The largest diameter 90 degrees
to A on the same slice is measured (line B). C is the approximate number
of 10-mm slices on which the intracerebral hemorrhage (ICH) was seen.
(Many centers use 5-mm slices, in which case an adjustment can be made
by dividing by 2.) The volume of the hemorrhage = A × B × C ÷ 2 (ABC/2).
level of consciousness, seizures, or even symptoms generally
ascribed to psychiatric disorders (such as, depression). Depending
on the location of the thrombus, physical examination of the
patient may reveal papilledema, proptosis, or palsies of CNs III,
IV, and VI, as well as other focal neurologic signs and symptoms.
Risk factors for CVST include trauma, infectious processes, hyper-
coagulable states, low-flow states, compression of the venous
sinus, dehydration, various drugs (such as, androgens, “ecstasy,”
and oral contraceptives), and pregnancy or the postpartum state.
Hemorrhagic Stroke
The differential diagnosis for ICH is similar to that for ischemic
stroke; considerations include migraine, seizure, tumor, abscess,
hypertensive encephalopathy, and trauma. Hypertensive encepha-
lopathy and migraine also can manifest with headache, nausea,
6 = Estimated to be 100%; no patients in the study fell into this
category
Adapted from Hemphill JC, et al: The ICH Score. Stroke 32:891-897, 2001.
and vomiting, although focal neurologic signs are less common
in these entities. With hypertensive encephalopathy, patients
usually exhibit marked elevation in BP and other evidence of
end-organ injury, such as proteinuria, cardiomegaly, papilledema,
and malignant hypertensive retinopathy. These patients usually
improve significantly with treatment of their hypertension. The
posterior reversible encephalopathy syndrome is an important
subset of hypertensive encephalopathy presentations and has
characteristic CT or magnetic resonance imaging (MRI) changes.
Once ICH is appreciated on neuroimaging, it can be difficult
to determine the underlying cause. Primary ICH typically mani-
fests as a parenchymal hematoma with new onset neurologic
symptoms. Patients with hemorrhagic transformation of an isch-
emic stroke may have recurrence or worsening of previously
established deficits. Patients with known underlying cancer, or
perihematomal edema out of proportion to the hemorrhage,
should be considered for hemorrhage into a metastasis or primary
tumor. Finally, patients with known underlying venous thrombo-
embolic risk factors may have underlying CVST.

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1248 PART III  Medicine and Surgery  |  SECTION Seven  Neurology

DIAGNOSTIC TESTING

Ischemic Stroke
Although clinical data can help establish the diagnosis, cause, and
location of the stroke, confirmatory diagnostic tests are often
required to establish the final cause or to eliminate other causes
for the deficits. The immediate evaluation includes cranial
imaging, an electrocardiogram (ECG) and hematologic testing,
particularly blood glucose determination.
An emergent noncontrast cranial CT is the standard initial
imaging technique for evaluating a patient with a potential stroke.
It can quickly differentiate an ischemic stroke from ICH and other
mass lesions. This information is crucial to the subsequent thera-
peutic decisions that will be rapidly made. A CT scan can identify
almost all parenchymal hemorrhages larger than 1 cm in diameter
and it has a high sensitivity for the detection of SAH.9 In a major-
ity of ischemic strokes, gross signs of infarction will not appear
on routine CT scans for at least 6 to 12 hours, depending on the
size of the infarct. However, subtle, early ischemic changes have A
been noted in up to 67% of noncontrast CT scans within the first
3 hours. These early ischemic changes include the hyperdense
artery sign (acute thrombus in a vessel), sulcal effacement, loss of
the insular ribbon, loss of gray-white interface, mass effect, and
acute hypodensity (Fig. 91.4). In addition, CTA can be used to
identify the presence of intravascular thrombosis, vasculature dis-
section, or stenosis. In cases in which arterial dissection is sus-
pected, imaging with MRA or CTA is indicated.10
The clinical importance of early ischemic CT findings with
regard to fibrinolytic therapy within 3 hours of symptom onset is
questionable, because the ability of treating physicians to repro-
ducibly identify these findings is poor and their clinical signifi-
cance is questionable. Only acute hypodensity and mass effect
have been shown to be associated with an increased risk of
ICH after fibrinolysis (over that in treated patients without
these findings). However, these findings do not exclude patients
from fibrinolytic therapy, which is associated with an improved
neurologic outcome. Patients with a hyperdense artery sign and
acute hypodensity of one-third of the middle cerebral artery
distribution tend to have a poorer prognosis; however, their
outcomes are still better with tPA treatment than without such B
treatment.
MRI can visualize ischemic infarcts earlier and identify acute Fig. 91.4.  A, Computed tomography (CT) scan taken 2 hours and 50
posterior circulation strokes more accurately than CT, and it may minutes after a large right middle cerebral artery occlusion. There are
be as effective as CT in identifying ICH.10 However, availability, subtle, ultra-early ischemic changes, including loss of the gray-white
interface (arrows) and subtle evidence of sulcal effacement. B, CT scan
difficulty in accessing critically ill patients, and scan time limit the
of same patient approximately 8 hours after symptom onset shows acute
use of MRI in acute stroke. Advances in MRA technology have hypodensity (arrows) and more prominent sulcal effacement.
allowed a noninvasive method of demonstrating large-vessel
occlusions of the anterior and posterior circulation, although
small intracranial vascular occlusions may not be readily appar-
ent. With the improvements in MRI and MRA speed and resolu-
tion, some stroke centers are replacing CT protocols with limited
“stroke protocol” MRI or MRA as the initial imaging modality of brain. In addition, CTA and perfusion CT can differentiate revers-
choice. The choice of initial cranial imaging modality is highly ible from irreversible ischemic insults.
dependent on the speed with which these scans can be performed An ECG is indicated in all patients with acute ischemic stroke,
and interpreted at each individual center. because atrial fibrillation and acute myocardial infarction are
Diffusion-weighted imaging (DWI) and perfusion-weighted associated with up to 60% of all cardioembolic strokes. The hema-
imaging (PWI) are MRI techniques that take minutes to perform tologic evaluation includes a complete blood count with platelet
and may allow differentiation between reversible and irreversible count, prothrombin time (including international normalized
neuronal injury. Other potential imaging modalities include CTA ratio [INR]), partial thromboplastin time, cardiac enzymes, and
and perfusion scans. In CTA, a CT scan is enhanced by an intra- serum glucose measurement. Elevated blood viscosity, even when
venous (IV) contrast agent to better define the vasculature of the hematocrit levels are not frankly polycythemic, can affect blood
brain. Areas of vascular stenosis and occlusion can be visualized flow and prognosis. A platelet count can identify thrombocytosis
with this technique. This information can then be used by inter- or thrombocytopenia, which may precipitate a thrombosis or
ventionalists to determine whether a lesion is amenable to endo- hemorrhage. Coagulation studies are especially helpful to guide
vascular thrombectomy. Also requiring IV contrast, perfusion CT management for patients in whom anticoagulation is being con-
scans can reveal perfusion deficits within different regions of the sidered or for patients with a hemorrhagic stroke.

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Other ancillary diagnostic tests to consider include an echo-
cardiogram, carotid duplex scan, and angiogram. Some centers
are performing these studies as part of a TIA observation unit
protocol to exclude a patent foramen ovale or valvular vegetation
in those patients in whom a cardioembolic stroke is suspected. An
echocardiogram should also be performed in patients with no
obvious cause for their stroke.11 Finally, conventional angiography
can demonstrate stenosis or occlusion of both large and small
blood vessels of the head and neck. It can detect subtle abnormali-
ties, such as with dissection, that may not be demonstrated with
noninvasive imaging techniques.
Transient Ischemic Attack
Patients with new-onset TIAs should receive an expedited evalu-
ation and treatment owing to the substantial short-term risk of
stroke and other adverse events.12 Emergency neuroimaging, vas-
cular imaging (such as, with a carotid Doppler study, MRA, or
CTA), electrocardiography, and basic blood tests should be per-
formed. A medically or surgically treatable cause for TIAs (eg,
high-grade carotid stenosis, mural thrombus) should be sought,
which would require in-hospital treatment such as anticoagula-
tion, stenting, or carotid endarterectomy.
Hemorrhagic Stroke
The hematologic evaluation for the patient with hemorrhagic
stroke should be performed in the same manner as for the patient
with ischemic stroke. Particular attention should be directed to
uncovering the presence of a coagulopathy. A drug screen should
be obtained to evaluate for use of sympathomimetics if substance
abuse is suspected. Increased sympathetic outflow secondary to
the hemorrhage may lead to an increase in dysrhythmias. Dys-
rhythmias also may signal impending brainstem compression
from an expanding hemorrhage.
As in ischemic stroke, the cranial CT scan is the diagnostic test
of choice to evaluate for an ICH. The noncontrast CT scan will
reliably diagnose patients with clinically relevant acute ICH.
Hemorrhages that are several days old may not be as apparent as
acute hemorrhages and appear as isodense regions.
Also, as with ischemic stroke, advanced neuroimaging modali-
ties are gaining favor in ICH. CTA produces high-quality images
of the larger arterial vessels and can help exclude secondary causes,
such as aneurysm, AVM, or fistula. Some patients with primary
ICH show contrast extravasation on CTA, and such patients are
at particularly high risk of ongoing bleeding and hematoma
expansion. A venous phase can be added to this study (computed
tomography venography [CTV]) to evaluate for CVST. A MRI can
help detect underlying lesions (such as, tumor) and may offer
better resolution for evaluating perihematomal edema. When
available, MRA and magnetic resonance venography (MRV) can
be used in place of CTA and CTV.
MANAGEMENT
Ischemic Stroke
With a focus on rapid recognition, evaluation, and treatment of
stroke, many hospitals have streamlined care to meet recom-
mended time goals (Table 91.4). This has led to the development
of stroke protocols, critical pathways, and acute interventional
stroke teams that may even be deployed in the field before the
patient arrives at the ED.
In the prehospital setting, the focus should be on ensuring
central nervous system (CNS) oxygenation and perfusion, rapid
identification, early hospital notification, and rapid transport.
Although it is unusual for patients with ischemic stroke to be
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CH APTER 91  Stroke 1249
TABLE 91.4 
National Institute of Neurological Disorders and
Stroke Recommended Stroke Evaluation Targets for
Potential Thrombolytic Candidates
MANAGEMENT COMPONENT TARGET TIME FRAME
Door to doctor 10 minutes
Door to CT completion 25 minutes
Door to CT scan reading 45 minutes
Door to treatment 60 minutes
Access to neurologic expertise* 15 minutes
Access to neurosurgical expertise* 2 hours
*By phone or in person.
CT, computed tomography.
unresponsive on presentation, their ability to communicate may
be altered by dysphasia. After an ischemic stroke, patients usually
can maintain their airway unless the brainstem is affected or sig-
nificant cerebral edema is compressing the opposite hemisphere.
Patients with intact protective airway reflexes should receive
oxygen if they are hypoxic (oxygen saturation less than 95%), and
a monitor and IV line should be established. Routine oxygen
supplementation of normoxic stroke patients should be avoided.13
Overhydration should be avoided to prevent cerebral edema.
By contrast, dehydration may lead to decreased cerebral perfusion,
and saline infusion should be given if dehydration is suspected.
Dextrose-containing solutions should be avoided in normoglyce-
mic patients suspected of having had a stroke because elevated
blood glucose levels may worsen an ischemic deficit. Out-of-
hospital personnel should attempt to rapidly ascertain the patient’s
blood sugar; if this is not possible, glucose should be given when
hypoglycemia is strongly suspected with an understanding that
hyperglycemia may be neurotoxic. Electrocardiographic monitor-
ing is recommended to identify life-threatening arrhythmias and
atrial fibrillation.
The circumstances surrounding the stroke as well as concomi-
tant medical conditions should be ascertained. A key part of the
initial information on stroke patients is the prehospital providers’
documentation of the exact time the patient was last seen to be
neurologically normal and the level of neurologic functioning.
This is especially important because reversible defects may com-
pletely resolve by the time the patient has arrived at the hospital.
The level of consciousness, gross focal motor deficits, difficulty
with speech, clumsiness, facial asymmetry, and any other focal
deficits should be noted. Prehospital stroke scales assist in identi-
fying patients who have had a stroke and who are potential can-
didates for fibrinolytic therapy. Early recognition, notification,
and transport by EMS are associated with delivery of fibrinolytic
treatment and improved patient outcomes.14
In the ED setting, the vital signs should be reassessed on an
ongoing basis because patients may rapidly deteriorate even with
subacute stroke. Some stroke patients are found at home 1 or 2
days after the event has occurred and may have concomitant ill-
nesses, such as aspiration pneumonia, dehydration, hypothermia,
rhabdomyolysis, or myocardial ischemia. Fever necessitates an
evaluation to identify sources of infection, followed by prompt
institution of treatment. Even minor degrees of hyperthermia
have been associated with increased neurologic injury. Oral medi-
cations (and food) should be withheld until some form of swal-
lowing assessment has been performed, given the risk of aspiration
in patients with an acute stroke.
1250 PART III  Medicine and Surgery  |  SECTION Seven  Neurology
Blood Pressure Management
The management of BP in patients with acute ischemic stroke and
TIA is controversial because of limited data. Current guidelines
for the management of hypertension in patients with acute isch-
emic stroke recommend that antihypertensive treatment be
reserved for those with markedly elevated BPs, unless fibrinolytic
therapy is planned or specific medical indications are present.
These medical indications include acute myocardial infarction,
aortic dissection, hypertensive encephalopathy, and severe left
ventricular heart failure.
Oral or parenteral agents are withheld unless the patient’s sys-
tolic pressure is greater than 220 mm Hg, diastolic pressure is
greater than 120 mm Hg, or mean arterial pressure (MAP) is
greater than 130 mm Hg (Box 91.2). If parenteral agents are used,
labetalol 10 to 20 mg IV push, or a calcium channel blocker (eg,
nicardipine starting at 5 mg/hour IV), is favored because of ease
of titration and limited effect on cerebral blood vessels. Sublingual
BOX 91.2  bral perfusion.
Emergency Antihypertensive Therapy for Acute
Ischemic Stroke
INDICATION THAT PATIENT IS ELIGIBLE FOR TREATMENT
WITH INTRAVENOUS RECOMBINANT TISSUE PLASMINOGEN
ACTIVATOR OR OTHER ACUTE REPERFUSION INTERVENTION
Blood Pressure Level
Systolic >185 mm Hg or diastolic >110 mm Hg
Labetalol 10 to 20 mg IV over 1 to 2 minutes; may repeat 1 time
or
Nicardipine infusion, 5 mg/hr; titrate up by 2.5 mg/hr at 5- to
15-minute intervals, maximum dose 15 mg/hr; when desired BP
attained, reduce to 3 mg/hr
Other agents (hydralazine, enalaprilat, and so on) may be considered
when appropriate.
If BP does not decline and remains >185/110 mm Hg, do not
administer rtPA.
MANAGEMENT OF BLOOD PRESSURE DURING AND AFTER
TREATMENT WITH RECOMBINANT TISSUE PLASMINOGEN
ACTIVATOR OR OTHER ACUTE REPERFUSION INTERVENTION
Monitor BP every 15 minutes during treatment and then for another 2
hours, then every 30 minutes for 6 hours, and then every hour for 16
hours.
Blood Pressure Level
Systolic 180 to 230 mm Hg or diastolic 105 to 120 mm Hg
Labetalol 10 mg IV over 1 to 2 minutes; may repeat every 10 to 20
minutes; maximum dose of 300 mg
or
Labetalol 10 mg IV followed by an infusion at 2 to 8 mg/min
Systolic >230 mm Hg or diastolic 121 to 140 mm Hg
Labetalol 10 mg IV over 1 to 2 minutes; may repeat every 10 to 20
minutes; maximum dose of 300 mg
or
Labetalol 10 mg IV followed by an infusion at 2 to 8 mg/min
or
Nicardipine infusion, 5 mg/hr; titrate up to desired effect by
increasing 2.5 mg/hr every 5 minutes to maximum of 15 mg/hr
If BP not controlled, consider sodium nitroprusside.
BP, Blood pressure; IV, intravenous; rtPA, recombinant tissue plasminogen activator.
Adapted from Jauch EC, Saver JL, Adams HP Jr, et al: Guidelines for the early manage-
ment of adults with ischemic stroke: a guideline for healthcare professionals from the
American Heart Association/American Stroke Association. Stroke 44(3):870-947,
2013.
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nifedipine or sublingual nitroglycerin are not recommended,
because either agent can produce a precipitous drop in BP.
If fibrinolytic therapy is planned, stringent control of BP is
indicated to reduce the potential for intracranial hemorrhage after
the thrombolytic is administered (see Box 91.2).
Thrombolytic therapy is not recommended for patients whose
systolic pressure is consistently higher than 185 mm Hg or whose
diastolic pressure is 110 mm Hg at the time of treatment. Simple
measures can be used to try lowering BP below this level. Recom-
mended approaches include the use of IV labetalol 10 to 20 mg
or continuous nicardipine. Once thrombolytic therapy has been
initiated, BP must be monitored closely and hypertension treated
aggressively.
Just as problematic as high BP can be, low BP can be quite
detrimental to patients with ischemic stroke. Normally normo-
tensive stroke patients with low BP or normally hypertensive
stroke patients with low or even low-normal BP are given a fluid
bolus to try to increase cerebral perfusion. This is especially
important in patients in a dehydrated state. If initial fluid chal-
lenge is ineffective, the patient may require vasopressor therapy
(eg, with dopamine) to gradually increase MAP and improve cere-
Thrombolytic Therapy
To date, the only IV thrombolytic agent approved by the U.S. Food
and Drug Administration (FDA) for treatment of patients with
acute ischemic stroke is the recombinant tissue plasminogen acti-
vator (rtPA), alteplase (Activase). Approval was initially based on
the results of the National Institute of Neurological Disorders and
Stroke (NINDS) trial, although subsequent analysis of other
studies has supported its use.15,16 There was initial concern regard-
ing the safety of alteplase when used in community practice;
however, a meta-analysis of non–trial-related use in community
practice has demonstrated efficacy and safety similar to that
reported in the NINDS trial; this was also replicated within a
cluster randomized controlled trial performed in Michigan.17 The
recommended dose for rtPA is 0.9 mg/kg IV to a maximum of
90 mg (10% of the dose given as a bolus followed by an infusion
lasting 60 minutes). Although the initial recommended time
window for IV rtPA administration was 3 hours because the
patient was last known to be at their neurologic baseline, a sub-
sequent study has demonstrated the usefulness of IV rtPA at 3 to
4.5 hours in a carefully selected subgroup of acute ischemic stroke
patients (Table 91.5 and Box 91.3). A larger open-label random-
ized trial focusing on patients presenting with “reasonable uncer-
tainty” regarding the expected benefit of rtPA found reduced
death and dependency at 6 months; a large proportion of patients
in this study were quite old, or had old stroke (>4.5 hours), or
both.18 These results should not influence clinical practice, because
the bulk of the population included in this large trial was mark-
edly different from the population of stroke patients who receive
thrombolysis within the context of current guidelines.
The American Stroke Association recommends that rtPA be
given within 60 minutes of arrival to appropriately selected isch-
emic stroke patients. Recent guidelines from the American College
of Emergency Physicians concur but also emphasize that proper
systems of care must also be in place to ensure safety and to maxi-
mize good outcomes.19
Studies suggests that patients with mild or rapidly resolving
symptoms may still benefit from the use of IV rtPA, and a clinical
trial is ongoing in this area. A promising early phase trial
of tenecteplase was recently completed for patients with mild
stroke and high-grade large-vessel stenosis. However, this strategy
cannot be recommended yet. If feasible clinicians should consider
urgent transfer of patients with mild symptoms and high grade
stenosis for potential reperfusion strategies, including mechanical

TABLE 91.5 
Comparison of AHA/ASA Acute Stroke Management Guidelines and Previous and New FDA Prescribing
Information for Alteplase (Activase) Treatment in Acute Ischemic Stroke
Inclusion criteria for fibrinolytic therapy
• Diagnosis of ischemic stroke causing measurable neurological deficit
• Onset of symptoms less than 3 hours before beginning treatment
AHA/ASA ACUTE STROKE
CRITERION MANAGEMENT GUIDELINE 2013a
Prior stroke Exclusion: prior stroke within 3 mo
Seizure at onset Relative exclusion: seizure at onset
with postictal neurological
impairments
Bleeding diathesis/ Exclusion:
OACs Platelet count <100 000/mm3
Heparin received within 48 h,
resulting in abnormally
elevated aPTT
Current use of anticoagulant with
INR >1.7 or PT >15 s
Current use of direct thrombin
inhibitors or direct factor Xa
inhibitors with elevated
sensitive laboratory tests
ICH Exclusion: history of previous ICH
BP Exclusion: Elevated BP (systolic
>85 mm Hg or diastolic
>10 mm Hg)
Blood glucose Exclusion: blood glucose <50 mg/dL
Severe stroke Not listed
Mild stroke Relative exclusion: only minor or
rapidly improving stroke symptoms
(clearing spontaneously)
Neuroimaging Exclusion: CT demonstrates multilobar
findings infarction (hypodensity >1/3
cerebral hemisphere)
SAH Exclusion: symptoms suggest SAH
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CH APTER 91  Stroke 1251
OLD ALTEPLASE (ACTIVASE) PI NEW ALTEPLASE (ACTIVASE)
(UPDATED 2009) PI (FEBRUARY 2015)
Contraindication: recent (within 3 mo) previous Removed entirely
stroke
Contraindication: seizure at the onset of stroke Removed entirely
Contraindication: known bleeding diathesis Bleeding diathesis remains a
including but not limited to: contraindication, but all
Current use of OACs (eg, warfarin sodium), laboratory values and specific
an INR >I.7, or a PT >15 s examples removed
Administration of heparin within 48 h
preceding the onset of stroke with an
elevated aPTT at presentation
Platelet count <100 000/mm3
Warning for all indications: patients currently
taking OACs
Contraindication: history of ICH Contraindication removed
Warning added for recent ICH
Contraindication: uncontrolled hypertension at Contraindication: current severe
the time of treatment (eg, >185 mm Hg uncontrolled hypertension
systolic or >110 mm Hg diastolic) remains, specific BP values
removed
Warning for BP >175/110 mm Hg
remains for all alteplase
(Activase) indications
Warning: because of the increased risk for Removed entirely
misdiagnosis of acute ischemic stroke, special
diligence is required in making this diagnosis
in patients whose blood glucose values are
≈50 or >400 mg/dL
Warning: patients with severe neurological deficit Removed entirely
(NIHSS score >22) at presentation; there is
an increased risk of ICH in these patients
Warning: safety and efficacy in patients with Removed entirely
minor neurological deficit or with rapidly
improving symptoms have not been
evaluated; therefore, treatment of patients
with minor neurological deficit or with rapidly
improving symptoms is not recommended
Warning: Major early infarct sign (substantial Removed entirely
edema, mass effect, or midline shift on CT)
Contraindication: Suspicion of SAH on Contraindication: subarachnoid
pretreatment evaluation hemorrhage
Continued
1252 PART III  Medicine and Surgery  |  SECTION Seven  Neurology

TABLE 91.5 

Comparison of AHA/ASA Acute Stroke Management Guidelines and Previous and New FDA Prescribing
Information for Alteplase (Activase) Treatment in Acute Ischemic Stroke—cont’d
AHA/ASA ACUTE STROKE OLD ALTEPLASE (ACTIVASE) PI NEW ALTEPLASE (ACTIVASE)
CRITERION MANAGEMENT GUIDELINE 2013a (UPDATED 2009) PI (FEBRUARY 2015)
Use in specific
populations
 Pregnancy Relative exclusion Warning: pregnancy No change
Category C
  Nursing mothers Not listed Not mentioned Unknown risk
 Children Inclusion: ≥18 y of age Indicated for adults Pediatric use not established
 Elderly Not listed Warning for all indications: advanced age (eg, Warning added: age >77 y was 1
>75 y) may increase risks of several interrelated baseline
characteristics associated with
an increased risk of ICH;
efficacy results suggest a
reduced but still favorable
clinical outcome
Gastrointestinal or Warning: gastrointestinal or Warning: gastrointestinal or genitourinary Warning: gastrointestinal or
genitourinary genitourinary bleeding within the bleeding within the past 21 d genitourinary bleeding
bleeding past 21 d
a
From Jauch EC, Saver JL, Adams HP Jr, et al; on behalf of the American Heart Association Stroke Council; Council on Cardiovascular Nursing; Council on Peripheral Vascular
Disease; Council on Clinical Cardiology. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American
Heart Association/American Stroke Association. Stroke 44:870–947, 2013.
AHA/ASA, American Heart Association/American Stroke Association; aPTT, activated partial thromboplastin time; BP, blood pressure; CT, computed tomography; FDA, US Food
and Drug Administration; ICH, intracerebral hemorrhage; INR, international normalized ratio; NIHSS, National Institute of Health Stroke Scale; OAC, oral anticoagulant; PI,
prescribing information; PT, prothrombin time; SAH, subarachnoid hemorrhage.
From Demaerschalk BM, Kleindorfer DO, Adeoye OM, et al; American Heart Association Stroke Council and Council on Epidemiology and Prevention. Scientific Rationale for
the Inclusion and Exclusion Criteria for Intravenous Alteplase in Acute Ischemic Stroke: A Statement for Healthcare Professionals From the American Heart Association/American
Stroke Association. Stroke 47(2):581–641, 2016.

BOX 91.3  patient will have differing probabilities of benefits and risks.
Fibrinolytic Therapy for Acute Ischemic Stroke
in the 3- to 4.5-Hour Time Window Inclusion
and Exclusion Criteria
INCLUSION CRITERIA
Diagnosis of ischemic stroke causing measurable neurological deficit
Onset of symptoms within 3 to 4.5 hours before beginning treatment
RELATIVE EXCLUSION CRITERIA
Older than 80 years old
Severe stroke (NIHSS > 25)
Taking an oral anticoagulant regardless of INR
History of both diabetes and prior ischemic stroke
INR, International normalized ratio; IV, intravenous; NIHSS, National Institutes of
Health Stroke Scale; rtPA, recombinant tissue plasminogen activator.
thrombectomy.20 Less favorable outcomes without thrombolysis
have been demonstrated in this population of minor stroke
patients in particular. Because the risk of symptomatic intra-
cranial hemorrhage (SICH) is proportional to severity, we recom-
mend carefully discussing the benefits and risks with patients
when considering rtPA in patients with minor or improving (but
not cleared) deficits. These patients are at lower risk of complica-
tions relative to patients with moderate to severe stroke, yet many
who are not treated still have significant long-term disability.21
IV tPA is not recommended when the time of stroke onset
cannot be ascertained reliably, including strokes recognized on
awakening. Although the aggregate risk of symptomatic ICH is
about 6% in trials and observational studies, each individual
Optimal methods of communicating benefits and risks promptly
have not been developed or widely disseminated, because
all reviewed decision aids have methodological deficiencies.22
However, younger patients and milder strokes (NIHSS < 10)
clearly have a lower risk of SICH. It is reasonable to adjust outcome
expectations when discussing benefits and risks with older patients
with more severe strokes (including significant early CT changes).
The risk of severe disability and death is quite high in this popula-
tion with or without fibrinolysis. Prompt fibrinolysis of severe
strokes will shift the outcomes of a population of treated patients
toward less disability.23 Several recent trials suggest these out-
comes can be further improved with careful selection of patients
for endovascular rescue therapy.
Endovascular Rescue Therapy
The results of several concurrent trials investigating prompt endo-
vascular rescue therapy (usually following IV thrombolysis) versus
medical management were published in late 2014 and early
2015. These studies have conclusively demonstrated that patients
with severe strokes and evidence of proximal large vessel occlu-
sions have significantly better functional outcomes when treated
with the new generation devices.24-26 Each of these trials used dif-
ferent imaging and clinical selection criteria, although the pres-
ence of a proximal occlusion and prompt treatment, preferably
within 3 hours, were common to all of the protocols. These trials
emphasize the need for better regionalization of stroke care to
reduce the time to definitive reperfusion.27 Unlike acute ischemic
stroke, non-acute cases of intracranial occlusions are best treated
with medical therapy and not permanent intracranial stents.28
Intra-arterial thrombolysis currently does not have a defined role
in the treatment of acute ischemic stroke.

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The recent trials demonstrating clear benefit of endovascular
thrombectomy come after a decade of negative studies. The dif-
ference in results is due to a combination of improved devices,
emphasis on early intervention, and careful patient selection.29-31
Data from two large trials involving almost 40,000 patients indi-
cate that early use of aspirin in patients with acute ischemic stroke
who were not treated with a fibrinolytic agent was associated with
a small but significant reduction in rates of stroke recurrence and
mortality. These studies in combination suggest a number needed
to treat of 77 (ie, 77 stroke patients would need to be treated with
daily aspirin therapy to prevent a poor outcome, such as death,
dependency at discharge, or at 6 months after stroke, in one
patient). The more recent CHANCE trial found that dual-
antiplatelet therapy with aspirin and clopidogrel for 90 days sig-
nificantly reduced recurrent stroke (from 11.7% to 8.2%) in
patients initially presenting with high-risk TIA or mild stroke
(NIHSS below 4).32 Aspirin should not be given for the first 24
hours to patients who have received a fibrinolytic agent and not
until a swallowing study has been performed.
Anticoagulation
The use of therapeutic dosing of low–molecular-weight heparin
(LMWH) or unfractionated heparin is now generally abandoned
in the routine care of stroke patients; prophylactic dosing to
prevent venous thromboembolism however is a hospital level
quality measure and publically reported.33 It may be that any
reduction in risk of subsequent ischemic stroke is balanced by an
increased risk of hemorrhagic stroke. To date, no studies have
definitively established the efficacy of anticoagulants in the man-
agement of patients with acute ischemic stroke, and current AHA
guidelines recommend against the routine use of heparinoids in
this population.4 However, heparin is sometimes considered by
vascular neurologists in select patients at high risk for stroke pro-
gression, including patients with crescendo TIAs or TIA from a
cardioembolic source (eg, atrial fibrillation, patients with a high-
grade carotid artery stenosis, patients with posterior circulation
TIA, and patients with evolving strokes). Heparin or LMWH is
often instituted to treat carotid and vertebral artery dissection,
unless a contraindication such as intracranial extension is present.
If a dissection is diagnosed and the patient has no symptoms of
ischemia, treatment with antiplatelet therapy alone may be an
option. Heparin therapy should not be initiated in patients with
suspected endocarditis or in any patient until a CT scan has ruled
out intracranial bleeding.
Intracerebral Hemorrhage
No specific therapy has been demonstrated to substantially
improve the outcome of patients with ICH. One of the strongest
predictors of mortality when considering ICH patients with com-
parable severity is the implementation of early care limitations.
When health care providers initiate early do not resuscitate (DNR)
orders, patients with otherwise equivalent prognoses are more
likely to die. As a result, we believe that early prognostication in
the ED should be avoided. Current evidence supports the benefit
of aggressive medical care. Patients admitted to a specialized unit,
patients who are expedited to the intensive care unit (ICU), those
admitted on a weekday, and those treated more aggressively
appear to have better neurologic outcomes.61-63 Therefore, even in
the absence of therapies specifically proven in phase III trials,
multidisciplinary care by specially trained care teams appears to
provide benefit.
The patient with suspected ICH requires rapid assessment and
transport to a care center with rapid neuroimaging and intensive
care management facilities. Out-of-hospital management is
similar to that for ischemic stroke, including determination of
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CH APTER 91  Stroke 1253
time of onset, concomitant medications, and application of a
prehospital stroke scale.
Supportive care involving attention to airway management and
perfusion is of the highest priority. Patients with hemorrhagic
stroke are more likely to have an altered level of consciousness that
may rapidly progress to unresponsiveness requiring emergent
endotracheal intubation. After intubation, a short-acting medica-
tion for sedation should be considered so that a neurologic exami-
nation can be repeatedly performed and the findings evaluated.
Standard care includes establishing IV access and cardiac moni-
toring. Evaluation of blood glucose and appropriate dextrose and
naloxone administration are essential in any patient with altered
mental status.
Patients seen early after symptom onset are at high risk of
ongoing bleeding. Approximately 30% of such patients will have
significant hematoma expansion on presentation, leading to neu-
rologic deterioration and worse outcome. Major therapies aimed
at reducing this risk include BP reduction, anticoagulation rever-
sal, and hemostatic therapy.
BP control is commonly performed after ICH. This inter-
vention is controversial, because hypertension may potenti-
ate further bleeding, but lowering BP in a patient with chronic
hypertension may decrease CBF, worsening brain injury. One
randomized trial found that lowering systolic BP to below 140
reduced ongoing bleeding, but there was no change in neurologic
outcome, suggesting that this therapy may not provide clinical
benefit in unselected patients. A larger trial focused on func-
tional outcomes demonstrated that prompt reduction to a systolic
blood pressure (SBP) of 140 mm Hg may slightly reduce dis-
ability and was generally safe.34 The current consensus regard-
ing management of ICH is to provide antihypertensive treatment
with parenteral agents for systolic pressures higher than 160 to
180 mm Hg or MAP higher than 130 mm Hg. Recommended
agents include labetalol, esmolol, nicardipine, clevidipine, and
hydralazine.3
Many patients are coagulopathic at the time of their ICH; and
for patients on anticoagulants, emergency reversal will theoreti-
cally minimize the risk of further bleeding, although this is not
backed up by clinical trial evidence. For patients on warfarin,
reversal is achieved using IV vitamin K (10 mg IV or subcutane-
ously), supplemented with either fresh frozen plasma (FFP) (2 to
4 units) or prothrombin complex concentrate (PCC) (Kcentra 25
to 50 units/kg depending on INR—dosing varies for other PCCs
by formulation).3 Of the new generation oral anticoagulants, at
this time only dabigatran has a specific antidote (idarucizumab)
proven to reverse coagulant effects in human clinical trials.35 Four-
factor PCC is likely to be the most quickly available reversal agent
for apixaban and rivaroxaban; hemodialysis will rapidly eliminate
dabigatran from the circulation but is not generally practical for
patients with serious bleeding.36 Hemostatic therapy (treatment
with procoagulant agents; eg, recombinant activated factor VII in
patients without baseline coagulopathy) was initially promising;
however, a phase III trial showed no clinical benefit.
To consider other iatrogenic coagulopathies, post-thrombolytic
symptomatic intracranial hemorrhage is a serious complica-
tion. Although various protocols have been employed for post-
thrombolysis intracranial hemorrhage, a comparative observa-
tional study comparing reversal with FFP or cryoprecipitate versus
conservative management (no reversal) demonstrated poor out-
comes in both groups. Mortality was slightly higher in the reversal
group, although this study only included 48 patients.37 Based on
the limited evidence, at this point in time we would recommend
administering cryoprecipitate (6 to 8 units) for thrombolytic asso-
ciated ICH that occurs shortly (0 to 3 hours) after alteplase admin-
istration. Later ICH (3 hours to days) is unlikely to be associated
with a persistent coagulopathy, because the fibrinogen depletion
following alteplase administration is transient; therefore, reversal
1254 PART III  Medicine and Surgery  |  SECTION Seven  Neurology
agents appear to confer risk without a potential biological benefit
in this time window.
Finally, the data on treatment of patients with spontaneous
ICH who are on preexisting antiplatelet treatments, such as aspirin
or clopidogrel, is conflicting. A small subgroup of an observa-
tional trial (27 patients) suggested patients receiving a platelet
infusion within 12 hours of onset had an increased odds of a good
functional outcome.38 At this time, the data do not support plate-
let transfusions in patients with spontaneous ICH being treated
with antiplatelet agents, unless a new thrombocytopenia (platelet
count <30,000) has also developed.
For patients with clinical or radiographic evidence of elevated
ICP, therapies aimed at lowering ICP should be considered. First,
neurosurgical consultation is obtained to evaluate the benefits of
an external ventricular drain (EVD) placement or hematoma
evacuation. Pending consultation, a number of medical therapies
aimed at decreasing ICP are available; however, these interven-
tions should not be used prophylactically.3 Hyperventilation can
be a temporizing measure pending more definitive treatment.
Mannitol moves fluid from the intracranial compartment, thereby
reducing cerebral edema. Hypertonic saline (3% or 23.4%) can be
used as an alternative to mannitol or in combination. Other exper-
imental modalities include barbiturate coma and hypothermia.
Seizure activity can cause neuronal injury, elevations in ICP,
and destabilization of an already critically ill patient. However,
there is observational evidence that prophylactic administration
of antiepileptic drugs (AEDs) may be harmful; therefore, AEDs
should be reserved for patients with known or suspected seizure,
including nonconvulsive seizures.3
Surgical evacuation of the hematoma is not beneficial in most
cases of non-cerebellar ICH. Selected patients with a sizable lobar
hemorrhage that is proximal to the cortical surface and associated
with progressive neurologic deterioration may benefit from surgi-
cal drainage. Recent studies have also suggested that minimally
invasive surgery (eg, stereotactic insertion of a catheter) may
provide some benefit to selected patients. For patients with cere-
bellar hemorrhage, surgery can be lifesaving, because the infraten-
torial space is much more limited and high ICP can disrupt vital
brainstem functions. For this reason, many neurosurgeons will
consider emergent surgery for patients with cerebellar hemor-
rhage within 48 hours of onset.
In cases of severe intraventricular hemorrhage or hemorrhages
in the posterior fossae, the normal circulation of cerebrospinal
fluid (CSF) can become interrupted, leading to the development
of hydrocephalus. This condition is characterized by an abnormal
rise in CSF volume. In such cases, neurosurgeons will often place
a ventricular catheter. Some groups infuse thrombolytic agents
through the catheter to help break up the clot and minimize the
risk of hydrocephalus.
Finally, as with ischemic stroke, general supportive care should
be provided to minimize neuronal injury. This includes treating
hyperthermia (such as, with acetaminophen) and treating hyper-
glycemia with insulin.
DISPOSITION
Ischemic Stroke and Transient Ischemic Attacks
“Stroke center” definitions have been established, and there is a
national certification process for primary stroke centers (PSCs)
and comprehensive stroke centers (CSCs) in the United States. In
broad terms, institutional certification as a PSC requires the estab-
lishment of a stroke infrastructure (ie, a stroke team, stroke unit,
patient care protocols, and support services, including CT scan-
ning and laboratory testing availability), as well as institutional
administrative support and strong leadership.4,39 CSCs offer
advanced imaging modalities, perform surgical and endovascular
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interventions, and maintain a core infrastructure, such as a stroke
unit and stroke registry. The establishment of PSCs and CSCs is
intended to improve outcomes for stroke patients by ensuring a
high level of coordinated care.
The most recent level of stroke classification for hospitals is the
acute stroke-ready hospital (ASRH). These hospitals are typically
smaller facilities with lower stroke patient volumes. An ASRH is
capable of establishing the initial stroke diagnosis, as well as
providing acute stabilization and treatment. The use of tele-
technologies between the ASRH and PSC/CSC will likely serve a
pivotal role in support of clinical care. After initial stabilization
and treatment, stroke patients will frequently be transferred to
PSC or CSC institutions.40
It is recommended that patients with symptoms consistent
with an acute stroke be transported to emergency facilities capable
of initiating fibrinolytic therapy within 1 hour of hospital arrival.
At a minimum, this requires emergent CT capabilities, an institu-
tional “acute stroke protocol,” and availability of a physician
knowledgeable in the use of thrombolytic therapy. Intensive care
monitoring and neurosurgery capabilities should be available
within 2 hours of drug initiation, either at the treating hospital or
by helicopter or ground transport to an appropriate health care
facility.39
In most cases, once the diagnosis of an acute stroke or stroke
syndrome is established and the patient is stabilized, hospitaliza-
tion will be necessary for further evaluation and treatment.
Patients may deteriorate over the first 24 hours and require close
in-hospital monitoring. Most patients can be managed on a
general medical or telemetry unit, although there is evidence sug-
gesting a benefit from admission to a stroke-specific unit. Patients
with large acute hemispheric strokes (associated with increased
risk of herniation) or with significant posterior circulation-related
changes and those treated with a fibrinolytic agent should be
monitored in a step-down or ICU for at least 24 hours.
In many centers, patients require admission to receive a prompt
evaluation for TIA. However, some centers have developed ED
observation unit protocols or rapid outpatient TIA clinics to
ensure an expedited evaluation (see Chapter e6). One commonly
used tool available to help select which TIA patients are at highest
risk (and thus likely should be admitted) versus those at lowest
TABLE 91.6 
ABCD2 Score for Assessing Stroke Risk in Patients
With a Transient Ischemic Attack
RISK FACTOR POINTS
Age >60 years old 1
Initial BP >140/90 mm Hg 1
Unilateral weakness 2
SPEECH IMPAIRMENT
Without weakness 1
Symptoms 10 to 59 minutes 1
Symptoms ≥60 minutes 2
History of diabetes 1
RESULT
0 to 3 = Low risk (1% risk of stroke in 48 hours)
4 to 5 = Moderate risk (4.1% risk of stroke in 48 hours)
≥6 = High risk (8% risk of stroke in 48 hours)
BP, Blood pressure.
 CH APTER 91  Stroke 1255

risk (who might therefore be safe for expedited outpatient evalu- The majority of patients with an acute hemorrhagic stroke
ation) is the ABCD2 score (Table 91.6). In addition, most patients should be admitted to an ICU in which specialty consultation is
without a contraindication will be started on antithrombotic available. If this is unavailable at the evaluating institution, the
therapy in the ED after consultation with a neurologist. patient should be transported to an appropriate institution.

KEY CONCEPTS
• Anterior circulation strokes result in contralateral hemiparesis of the
face and body.
• Vertebrobasilar strokes result in ipsilateral CN deficits and
contralateral hemiparesis.
• Posterior cerebral artery stroke causes ipsilateral CN III palsy and
contralateral homonymous hemianopsia.
• Wallenberg’s syndrome (lateral medullary syndrome) causes vertigo,
Horner’s syndrome, ipsilateral facial numbness, loss of corneal reflex,
and contralateral loss of pain/temperature.
• Cervical artery dissection is a common cause of stroke in young
patients; TIAs preceding stroke in these patients are often missed.
• The goal for eligible patients is to receive thrombolytics within 90
minutes of symptoms onset; the dose of alteplase is 0.9 mg per kg
with 10% given as a bolus and the remaining 90% given over
1 hour.
• Acute ischemic stroke patients receiving alteplase are at risk of
developing a spontaneous intracranial hemorrhage; the risk is lowest
in patients with a low stroke score, no hypertension, no diabetes,
and age younger than 70.
• In acute ischemic stroke, the patient and or their families should be
informed of the risk and benefit of treatment with alteplase.
• Patients with a hemorrhagic stroke on coumadin should be promptly
reversed using vitamin K and either FFP or PCC.
• Prognosis is worse in acute stroke in the setting of fever,
hypotension, hypoxia, and hyperglycemia.
• Carotid Doppler, MRA, or CTA studies are recommended before
discharge of a patient with TIA from the ED.
• Overly aggressive BP management should be avoided in patients
with acute ischemic stroke.
• Accurate identification of the last time a patient was known to be at
his or her neurologic baseline should be documented in all patients
with stroke.
• IV alteplase followed by endovascular thrombectomy is
recommended in patients with large anterior circulation artery
occlusion.

The references for this chapter can be found online by accessing the accompanying Expert Consult website.

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CHAPTER 91: QUESTIONS & ANSWERS
91.1. Which of the following statements concerning ischemic
stroke is true?
A. Anterior circulation strokes are more likely than
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the time of presentation.
B. Anterior circulation strokes rarely present with
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C. Posterior cerebral artery strokes are associated with
incontinence, leg weakness greater than arm
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D. The presence of aphasia suggests an anterior cerebral
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E. The presence of diplopia suggests an anterior
circulation stroke.
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For personal use only. No other uses without permission. Copyright ©2020. Elsevier Inc. All rights reserved.
CH APTER 91  Stroke 1255.e1
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crit Care 16(1):82–87, 2012.
39. Alberts MJ, Latchaw RE, Jagoda A, et al: Revised and updated recommendations for
the establishment of primary stroke centers: a summary statement from the brain
attack coalition. Stroke 42(9):2651–2665, 2011.
40. Alberts MJ, Wechsler LR, Jensen ME, et al: Formation and function of acute stroke-
ready hospitals within a stroke system of care recommendations from the brain attack
coalition. Stroke 44(12):3382–3393, 2013.
has been a previous contralateral stroke. ACA strokes primarily
affect frontal lobe functions and may also present with primitive
grasp and such reflexes. In addition to contralateral motor and
sensory defects, MCA strokes may present with expressive aphasia,
agnosia, and ipsilateral hemianopsia.
91.2. Which of the following is not associated with posterior
circulation strokes?
A. Diplopia
B. Homonymous cranial nerve (CN) and extremity
motor deficits
C. Loss of consciousness
D. Loss of visual object recognition
E. Nausea, vomiting, and ataxia
Answer: B. Posterior circulation (vertebrobasilar) strokes involve
the vertebral, basilar, and posterior cerebral arteries. Because
this system supplies the reticular activating system, cerebellum,
brainstem, occipital lobe, and brainstem vomiting centers, loss of
1255.e2 PART III  Medicine and Surgery  |  SECTION Seven  Neurology

consciousness with vomiting, visual changes, and cerebral ataxia D. 5

may be seen. Ipsilateral CN deficits (because these nuclei largely E. 6
reside in the brainstem) occur with contralateral “body” deficits
Answer: E. Thus ischemic stroke trials, using fibrinolytic or anti-
resulting from motor/sensory fiber decussation.
platelet agents, have attempted to recanalize occluded arteries and
reperfuse ischemic areas of the brain within a 2- to 6-hour thera-
91.3. Headache, vomiting, and a decreased level of
peutic window.
consciousness are most commonly seen with which of
the following disorders?
91.7. Which of the following areas of the brain is perfused by
A. Ischemic stroke
the posterior circulation?
B. Intracranial hemorrhage
A. Internal capsule
C. Migraine headache
B. Posterior aspect of the temporal lobe
D. Subarachnoid hemorrhage (SAH)
C. Putamen
E. Tic douloureux
D. Speech areas of the temporal lobe
Answer: D. The incidence of headache is highest by far in patients E. Thalamus
with SAH. Vomiting and depressed loss of consciousness are also
Answer: E. The thalamus is perfused by the posterior circulation.
generally more common in this group. Pure migraine headache
The other areas are perfused by the anterior circulation.
rarely, if ever, causes a depressed loss of consciousness. Tic head-
aches do not cause loss of consciousness.
91.8. Which of the following statements regarding stroke
etiology is true?
91.4. What percentage of patients with hemorrhagic stroke
A. Lacunar strokes reliably cause a pure motor deficit.
experience clinical deterioration because of growth in
B. Less than 1% of strokes occur in the 15- to 45-year-
hemorrhage volume within the first hours?
old age group.
A. 10%
C. One-third of ischemic strokes are thrombotic.
B. 20%
D. Strokes resulting from atrial fibrillation likely involve
C. 30%
small vessels.
D. 50%
E. Two-thirds of ischemic strokes are cardioembolic.
E. 75%
Answer: C. One-third of ischemic strokes are thrombotic. Lacunar
Answer: C. Thirty percent of patients with intracerebral hemor-
strokes may cause a pure motor, pure sensory, or ataxic/hemiparesis
rhage (ICH) experience early hemorrhage expansion. Progression
stroke. Vessel occlusion resulting from atrial fibrillation–induced
of neurologic deficits and decreasing mental status suggest the
emboli more likely involves the large vessels. Three percent to 4%
diagnosis.
of ischemic strokes occur in the 15- to 45-year-old age group.
91.5. A 69-year-old male presents with headache, vomiting,
91.9. A 29-year-old female presents with a left-sided headache
aphasia, a right lower facial palsy, and right upper greater
after a moderate-speed motor vehicle collision (MVC).
than right lower extremity weakness. The symptoms
She suffered no loss of consciousness and has no other
began approximately 4 hours before arrival. Vital signs
complaints or obvious injuries. Physical examination is
are temperature 99° C, blood pressure (BP)
remarkable only for drooping of the left eyelid and slight
180/90 mm Hg, respiratory rate 18 breaths per minute,
miosis of the left pupil compared with the right. Which
heart rate 92 beats per minute, and oxygen saturation
of the following would be the diagnostic test of choice?
96% on room air. Emergent computed tomography (CT)
A. Brain magnetic resonance imaging (MRI) with
scan shows a left temporal intracerebral hemorrhage
gadolinium
(ICH). Soon after presentation, the patient experiences
B. Contrasted computed tomography (CT) scan of the
increased vomiting and a diminishing level of
brain
consciousness. What is the most likely explanation for
C. CT angiogram of the carotid arteries
this deterioration?
D. Uncontrasted CT scan of the brain
A. Accompanying subarachnoid hemorrhage (SAH)
E. Urine drug screen
B. Acute brainstem herniation
C. Hypoxia from neurogenic pulmonary edema Answer: C. Carotid or vertebral artery dissection can occur after
D. Increase in volume of the ICH trauma or mild events, such as yoga, twisting, or prolonged static
E. Myocardial infarction with cardiogenic shock positions looking upward. The hallmark is unilateral neck pain,
face pain, or headache, often with accompanying Horner’s syn-
Answer: D. Approximately one-third of patients with ICH experi-
drome. Acutely, cerebral ischemic changes would not be seen on
ence early hemorrhage volume expansion. Although brainstem
brain imaging. Carotid and vertebral dissection is not a contrain-
herniation is a possibility, this is typically a later sequelae with a
dication for thrombolytic therapy in the eligible patient.
more gradual presentation. Acute myocardial infarction may be
associated with intracranial emergencies but would not likely
91.10. What percentage of patients who experience a transient
cause an abrupt mental status change. Neurogenic pulmonary
ischemic attack (TIA) will develop a stroke within 3
edema may accompany any condition with elevated intracranial
months?
pressure (ICP) but, again, would not likely cause an abrupt mental
A. 5%
status change.
B. 10%
C. 15%
91.6. After complete occlusion of cerebral vessels, irreversible
D. 20%
neurologic deficits are expected to reliably occur within
E. 25%
how many hours?
A. 2 Answer: B. One-tenth of them will occur within 2 days of the
B. 3 sentinel event.
C. 4

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 CH APTER 91  Stroke 1255.e3

91.11. A 28-year-old G3P3 woman who is 2-weeks postpartum D. Seizure at the onset of the stroke
after an uncomplicated vaginal delivery presents with E. Symptoms rapidly improving
acute onset of mild headache, lethargy, and double
Answer: B. In the 3- to 4.5-hour window, patients cannot exceed
vision. Physical examination is remarkable for normal
80 years of age. Heparin administration within the 48 hours pre-
vital signs and a left eye lateral gaze palsy. The most
ceding stroke onset is a contraindication in both the 0- to 3-hour
appropriate intervention is likely to be which of the
window as well as the 3- to 4.5-hour window. Similarly, high clini-
following?
cal suspicion for SAH, seizure at the onset of the stroke symptoms,
A. Computed tomography (CT) scan of the brain with
and rapidly improving symptoms are contraindications to fibri-
possible lumbar puncture
nolysis in both time windows.
B. CT scan of the brain and intravenous (IV) heparin
C. Erythrocyte sedimentation rate (ESR) and IV
91.14. A 66-year-old female presents with a possible transient
corticosteroids
ischemic attack (TIA). Approximately 1 hour before her
D. IV magnesium
arrival, she had a 15-minute episode of strictly right arm
E. Lumbar puncture and IV antibiotics
and right leg weakness, and her symptoms have now
Answer: B. Cerebral venous thrombosis may present with head- resolved. Her blood pressure (BP) is 165/92 mm Hg. Her
ache, lethargy, cranial nerve (CN) deficits, seizures, or even psy- prior medical history is significant for hypertension, high
chiatric complaints. CT scan and/or magnetic resonance imaging cholesterol, and diabetes mellitus. What is her ABCD2
(MRI)/magnetic resonance angiography (MRA) are likely to score?
reveal the diagnosis. Treatment includes heparin. Neurosurgical A. 4
consultation is not useful. Subarachnoid hemorrhage (SAH) B. 5
would not be expected to cause a focal neurologic deficit. Eclamp- C. 6
sia and meningitis would be expected to give characteristic find- D. 7
ings on history and examination. E. 8
Answer: C. The patient’s ABCD2 score is 6 (age >60 years, BP
91.12. Which of the following statements is true regarding
>140/90 mm Hg, unilateral weakness, symptoms lasting 10 to 59
management of acute ischemic stroke?
minutes, and history of diabetes). No speech impairment is
A. Heparin is indicated for patients in whom
reported.
thrombolysis is not an option.
B. If the initial computed tomography (CT) scan shows
91.15. A 72-year-old male presents with an apparent stroke.
a large left middle cerebral artery (MCA) distribution
Computed tomography (CT) imaging of the brain
stroke but no hemorrhage, thrombolysis would be
demonstrates only a hyperdense middle cerebral artery
indicated.
(MCA) sign and no other ischemic changes. He was last
C. Initial blood pressure (BP) greater than
seen neurologically normal 4 hours earlier. Which of the
185/110 mm Hg would contraindicate thrombolytic
following is a contraindication to fibrinolytic therapy in
treatment.
this patient?
D. Mechanical thrombectomy may be indicated up to 6
A. His blood glucose is 372 mg/dL.
hours after stroke onset.
B. His National Institutes of Health (NIH) Stroke Scale
E. No clot retrieval devices have been U.S. Food and
score is 24.
Drug Administration (FDA) approved for acute
C. His platelet count is 110,000/mm3.
ischemic stroke management.
D. His systolic blood pressure (BP) is 180 mm Hg.
Answer: D. Intra-arterial thrombolysis may offer benefit up to 6 E. He takes warfarin daily.
hours past stroke onset. BPs higher than 185/110 mm Hg are not
Answer: E. Any oral anticoagulant treatment (regardless of the
an absolute contraindication to thrombolysis if they can be
patient’s international normalized ratio [INR]) is a contraindica-
lowered to this level with one or two doses of a parenteral agent,
tion to fibrinolysis in the 3- to 4.5-hour treatment window. Other
such as labetalol or enalapril. The Mechanical Embolus Removal
contraindications include an NIH stroke scale score greater than
in Cerebral Ischemia (MERCI) retrieval device was FDA approved
25, platelet count less than 100,000/mm3, blood glucose greater
in 2004, and several newer stent-retriever devices have been
than 400 mg/dL, and systolic BP greater than 185 mm Hg.
approved since then. In recent trials of thrombectomy, improved
outcomes were demonstrated at least to 6 hours; and outcomes
91.16. A 75-year-old man is brought to the emergency
were even better when patients received reperfusion within 4.5
department (ED) for altered mental status. After
hours of onset. Aspirin has a proven benefit in patients who do
computed tomography (CT) imaging of the brain is
not receive tissue plasminogen activator (tPA). There is no proven
performed, he is found to have a large intracerebral
benefit to heparin, although some practitioners use it in cases at
hemorrhage (ICH). Which of the following options is
high risk of stroke progression.
not an appropriate strategy for lowering intracranial
pressure (ICP)?
91.13. An 82-year-old male presents with an apparent stroke.
A. Barbiturate-induced coma
He is rapidly evaluated and determined to be within
B. Hyperthermia induction
the 3- to 4.5-hour window for fibrinolytic therapy.
C. Hypertonic saline administration
Which of the following exclusion criteria applies only
D. Hyperventilation
to the 3- to 4.5-hour criteria and not the 0- to 3-hour
E. Mannitol administration
criteria?
A. Administration of heparin within the 48 hours Answer: B. Hypothermia is an experimental modality for lower
preceding the stroke onset ICP. Hyperventilation can serve as a temporizing measure for
B. Age older than 80 years reducing ICP. Mannitol and/or hypertonic saline can also be
C. High clinical suspicion for subarachnoid hemorrhage administered. Inducing a barbiturate coma is also an experimental
(SAH) modality.

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