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364
Human immunodeficiency virus/acquired immunodeficiency
syndrome (HIV/AIDS) is now recognized as increasing the risk
of stroke. This is partially because patients with HIV/AIDS are living longer, and some are having strokes as a result of accelerated
development of typical stroke risk factors. It is also clear that modern drug therapy for AIDS can increase the risk of stroke (particu-
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larly ischemic stroke).
30
Systemic cancer is a commonly overlooked cause of strokes.
28,29
Sometimes the stroke diagnosis precedes diagnosis of the underlying cancer. Mechanisms for strokes related to cancer include a
hypercoagulable state and nonbacterial thrombotic endocarditis.
Oftentimes these strokes are multiple, variable in size, and in different vascular territories.
30,31
Such patients may also have deep
venous thrombosis (DVT). Liver failure appears to increase risk of
ischemic and hemorrhagic stroke.
Intracerebral Hemorrhage
In broad terms, ICH can be divided into traumatic and nontraumatic etiologies. This chapter will focus on nontraumatic
ICH, since ICH related to trauma is not routinely considered a
stroke. Intracerebral hemorrhage is typically caused by rupture
of a blood vessel within the brain parenchyma. Patients typically develop a focal neurological deficit suddenly, but symptoms
often evolve over 10 to 30 minutes as the hematoma gradually
expands. Headache is commonly present, and the vast majority of
patients have markedly elevated blood pressure (often in excess
of 200 mmHg systolic) even without a prior history of hypertension. Nausea and vomiting can also occur, particularly with ICH
that involves the brainstem and/or cerebellum.
Chronic or acute hypertension is the most common etiology
for nontraumatic ICH, and this type of bleed typically occurs in
specific brain locations (
location of the ICH is highly correlated with the type of symptoms produced. Recent studies using serial brain scans have
shown that 30% to 40% of ICHs will expand over the first 24 hours
after admission; such expansion is almost always associated with
clinical worsening.
for ICH expansion, although this association has not been mechanistically proven.
Another increasingly common etiology for ICH is cerebral amyloid angiopathy (CAA), which typically affects patients older than
70 years of age. Cerebral amyloid angiopathy is caused by deposition of one or more amyloid proteins within the wall of cerebral small arterioles. A typical CAA bleed occurs in a lobar region
(junction of gray matter and white matter), most commonly in the
parietal, temporal, and occipital lobes. Intracerebral hemorrhages
due to CAA can be multiple and recurrent.
Table 30-4). As with ischemic stroke,
6,32
High blood pressure may be a risk factor
33–35
There is a clear asso-
TABLE 30-4
ICH LOCATION
Basal ganglia Hypertension
Lobar Hypertension, CAA Cortical syndromes, weakness,
Thalamus Hypertension Altered mentation, sensory
Pons Hypertension Coma, gaze and pupil
Cerebellum Hypertension, AVM Ipsilateral ataxia, dizziness,
Hemispheric
cortex
AVM, arteriovenous malformation; CAA, cerebral amyloid angiopathy; ICH, intracerebral hemorrhage.
Location and Symptoms for Common Types
of Intracerebral Hemorrhage
LIKELY
ETIOLOGY
AVM, extreme
hypertension,
mycotic aneurysm
COMMON SYMPTOMS
Contralateral hemiparesis, speech
changes, gaze deviation,
altered mentation if large
visual field lesions, altered
mentation if large
changes, gaze abnormalities
abnormalities, quadriparesis
vertigo, nausea/vomiting
Headaches, seizures, cortical
syndromes
ciation between CAA, ICH, and Alzhemier's disease. Sometimes
an ischemic stroke can undergo hemorrhagic transformation and
become an ICH. This occurs in up to 15% of cases of ischemic
stroke and is associated with large strokes, cardioembolic strokes,
and the use of anticoagulants and thrombolytic agents.
A variety of vascular malformations can cause an ICH, particularly
arteriovenous malformations (AVMs) and cavernous malformations (less commonly, capillary telangiectasias and developmental
venous anomalies). Arteriovenous malformations are the most
common and serious type of vascular malformation that cause an
ICH, and recurrent ICHs, as well as producing seizures and local
neurological deficits.
36
The characteristics and hemorrhagic risk of
each of these lesions is shown in Table 30-5.
Intracerebral hemorrhage can occur as a consequence of anticoagulation use, administration of thrombolytic therapy (either
for a stroke or another systemic condition), other coagulopathies,
hematological disorders, endocarditis, infections (fungal, bacterial,
viral), drug abuse (cocaine, heroin, amphetamines), brain tumors
(typically metastases), and venous thrombosis.
6
Iatrogenic causes
of ICH deserve special mention, since there is now extensive use
of powerful antiplatelet agents and anticoagulants for a variety of
c onditions. The use of tissue plasminogen activator (tPA) as well as
endovascular therapies (thrombectomy, stenting) as therapies for
acute ischemic stroke can lead to ICH (and less commonly SAH).
37
TABLE 30-5 Common Types of Central Nervous System Vascular Lesions That Lead to Cerebral Hemorrhage
LESION TYPE TYPICAL LOCATION
Aneurysm Arterial bifurcations
AVM Anywhere in CNS Arteries draining directly into
Cavernous
angioma
Telangiectasia
(capillary)
Venous angioma Hemisphere,
AVM, arteriovenous malformation; CNS, central nervous system; ICH, intracerebral hemorrhage; SAH, subarachnoid hemorrhage.
around circle of Willis
Anywhere is CNS Collection of enlarged capillar-
Anywhere; brainstem
and white matter
most common
cerebellum
Degeneration of parts of vessel
wall leads to outpouching of
vessel
veins; abnormal intervening
brain tissue
ies; no intervening brain tissue
Dilated capillaries with normal
intervening brain
Collection of small veins; radial
pattern; draining vein; normal
brain tissue
ANATOMY
PRESSURE
CHARACTERISTICS
High SAH Depends on size; about
High ICH and/or SAH High; may also cause
Low ICH most common Low in most cases; may
Low Pontine ICH Low
Low Deep white matter,
TYPICAL
HEMORRHAGE TYPE
cerebellum
RISK OF BLEEDING/
OTHER EVENTS
1% or less in general
population
seizures
cause seizures
Very low
Subarachnoid Hemorrhage
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As noted earlier, most cases of nontraumatic SAH are due to
rupture of a saccular aneurysm that typically occurs at the bifurcation of blood vessels around the circle of Willis at the base of
the brain. However, using modern imaging techniques, we can now
image aneurysms that occur more distally in the arterial tree. Such
lesions are often due to an underlying infection (most commonly
endocarditis), although they can be seen as a complication of
vasculitis or inherited conditions (polycystic kidney disease,
Marfan's syndrome).
Subarachnoid hemorrhage typically produces a severe and sudden headache along with nausea/vomiting, nuchal rigidity, and elevated blood pressure. Depending on the location of the ruptured
aneurysm, some patients may have additional focal neurological
findings. For example, an aneurysm involving the posterior communicating artery can produce an ipsilateral third nerve palsy that
involves the pupil. Rupture of an aneurysm of the anterior communicating artery can produce speech and behavioral changes.
Aneurysmal rupture that leads to extensive bleeding around the
brain and into the ventricles can lead to altered mental status, coma,
and sometimes early or sudden death due to dramatic increases in
intracranial pressure. A listing of common aneurysm locations and
symptoms can be found in
Following an aneurysmal SAH, patients are at high risk for a
number of complications including rebleeding (if the aneurysm
TABLE 30-6
LOCATION CLINICAL SYMPTOMS
Anterior communicating artery Leg weakness, speech disturbance,
Posterior communicating artery/
internal carotid artery (ICA) junction
Bifurcation of middle cerebral
artery (MCA)
Basilar artery tip Altered mentation, pupil and gaze
38
Table 30-6.
Common Locations for Saccular Aneurysms
and Related Symptoms in Subarachnoid
Hemorrhage
personality changes, seizures,
memory loss
Ipsilateral 3rd nerve palsy
Contralateral weakness, sensory
changes, speech changes
abnormalities
is not secured by surgery or coiling), vasospasm causing ischemic
stroke, seizures, hydrocephalus, SIADH (syndrome of inappropriate antidiuretic hormone secretion), and central fever, among
others.
An ICH or SAH that causes extensive hemorrhage into the ventricular system can produce an acute or subacute hydrocephalus syndrome with worsening headaches, nausea/vomiting, and
altered mental status leading to coma in some cases. All strokes,
but particularly ICH or SAH, can produce seizures, particularly if
the blood involves parts of the cortex or epileptogenic deep structures such as the hippocampus. In the long term, such patients may
develop dementia and personality changes.
Stroke Mimics
It is incumbent upon the clinician to ensure that a patient with
a presumed stroke is having a real cerebrovascular event. Many
medical conditions can present with stroke-like symptoms and
even physical findings, but with a different etiology. This has
obvious implications in terms of acute therapy, ongoing care,
and secondary prevention.
Table 30-7 lists some common stroke
mimics and diagnostic tests that may be helpful for making the
diagnosis.
Clinical Assessment Tools
History and Physical
Any assessment of a patient with suspected stroke or TIA begins
with a focused history and physical. Factors of key concern
include prior medical history with assessment of stroke risk factors
(hypertension, diabetes, heart disease, etc.), as well as the presenting symptoms, their mode of onset, precipitating factors, and time
course (stable, improving, getting worse). We are particularly concerned about symptoms such as disturbances of speech, language,
and mentation; evidence of cranial nerve dysfunction ( diplopia,
vision loss in one eye or sector, dysarthria, dysphagia, facial weakness); focal motor weakness or coordination problems; gait
abnormalities; and sensory symptoms. A particular challenge for
stroke patients is that often their ability to sense or report these
various symptoms may be affected by the very stroke causing
the symptoms. This makes obtaining historical details from family,
friends, or caregivers very important.
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CliniCAl PREsEnTATion And diAgnosis of CEREbRovAsCulAR disEAsE
TABLE 30-7 Common Stroke Mimics: Diagnosis and Treatment
STROKE MIMIC DIAGNOSTIC CLUES CONFIRMATORY TESTS TREATMENT
Hypoglycemia/
hyperglycemia
Electrolyte disturbance Predisposing condition, taking medications Electrolyte monitoring Correct underlying condition
Migraine Gradual Sx onset; prior Hx of headaches;
Seizures Aura at beginning; preexisting illness;
Conversion reaction Nonphysiological neurological
Demyelinating
disease (MS)
CNS tumor Lesion in nonvascular territory; risk factors
Subdural hematoma Head trauma; bleeding risk factors Head CT or MRI Correct coagulopathy; surgical drainage
Medication side effects Sx associated with medication ingestion Rule out other conditions Change/discontinue medications
Infection Fever, high white count Brain imaging, LP, blood cultures Antibiotics, antiviral medications
CT, computed tomography; EEG, electroencephalogram; Hx, history; LP, lumbar puncture; MRI, magnetic resonance imaging; MS, multiple sclerosis; Sx, symptom(s).
Hx of diabetes, taking glycemic
medications
family Hx of migraine
postictal lethargy
examination; prior psychiatric events;
secondary gain
Young age; gradual Sx onset MRI findings; LP results Treat MS with immunotherapy
for cancer
Blood glucose; serial testing Correct underlying disease
Rule out other conditions; identify
precipitating factors
EEG; may require serial monitoring Antiepileptic medications
Rule out other conditions; repeated
examinations with inconsistent findings
MRI findings; serial scans evaluate for
systemic neoplasm
Avoid triggers; prophylactic medications
if frequent migraines, discontinue
hormone therapies
Psychiatric evaluation
Treat tumor
366
Another key aspect is time of onset of stroke symptoms, since
this will determine whether the patient is a candidate for acute
intervention (this is of particular importance for ischemic stroke).
Time of stroke onset is often (and incorrectly) assumed to be
when the patient is found with evidence of a stroke. The correct
definition of time of onset is when stroke symptoms first began. If
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a patient has been under constant observation, the time of onset
30
will be when the patient was first noticed to have stroke symptoms.
But if a patient has been home alone and discovered with stroke
symptoms by a family member, the time of onset has to be when
the patient was last known to be normal (assuming the patient
cannot determine the time of onset). Therefore, in the case of a
patient who awakens in the morning unable to speak at 7 am, time
of onset is assumed to be when the patient went to bed normal the
night before, unless there is clear documentation otherwise. This
strict definition essentially rules out many patients with so-called
wakeup strokes from receiving acute
Physical examination will provide valuable information about
the likely location of the stroke and suggest the vascular territory and blood vessel or vessels most likely to be involved. As
already noted, this is a key step in determining stroke mechanism and etiology. Besides vital signs and a thorough neurological examination, there are particular aspects of the general
medical examination that provide important diagnostic information to the clinician. These include an assessment for cervical
bruits, a complete cardiac examination, checking blood pressure
and pulses in both arms, a skin examination, and evidence of
trauma to the head and neck.
neurological assessment for patients with known or suspected
cerebrovascular disease.
Clinicians often use a variety of scales or scoring systems to
assess severity of various types of stroke. These scoring systems
can provide guidance about treatment options as well as overall
prognosis. The National Institutes of Health Stroke Scale (NIHSS)
is often used to assess patients with an ischemic stroke. The NIHSS
is a formalized neurological examination, and scores can range
form 0 to 42 (0 being normal, higher score being more severe).
The Glasgow Coma Scale (GCS) is often used in patients with ICH
and SAH. It measures a patient's responses to a variety of stimuli.
The GCS can range from 0 to 15, with 15 being normal. The Hunt
and Hess Scale is used to assess severity of SAH, with 1 being an
asymptomatic headache and 5 being deep coma. The Fisher Grade
is used to measure the amount of subarachnoid blood seen on the
head CT. Scores range from 1 (no blood seen) to 4 (intraventricular or parenchymal blood).
therapies such as tPA.
Table 30-8 offers an outline of a
Brain Imaging
Our ability to rapidly and accurately image the brain and cerebral
vasculature has been an important step and driver in our capability to determine the type of stroke, its locations, and likely mecha-
40
nism.
Almost every hospital in the United States is able to perform
a head CT scan on patients in the emergency department. On-site
personnel or remote radiology reading technologies and services
can provide a reading within 30 to 60 minutes. The ability to rapidly
perform and interpret brain imaging is a key component of a
primary stroke center.
A head CT scan can easily, rapidly, and safely be used to diagnose
an acute stroke, especially if it is a hemorrhagic stroke. In some cases
when a patient with an ischemic stroke is imaged very soon after
symptom onset, the head CT may be negative or show only subtle
changes. In such cases, a repeat head CT in 12 to 24 hours will almost
39
certainly show changes indicative of a large or medium-sized ischemic stroke (
Fig. 30-1). However, a head CT can miss small and acute
strokes, particularly if they are in the brainstem or posterior fossa.
Head CT is very sensitive for imaging hemorrhagic strokes, particularly ICH. Intracerebral hemorrhages appear as white lesions
in the brain parenchyma that represent the actual hematoma
(
Fig. 30-2A). Often there is early evidence of edema around the
ICH, which can worsen over several hours and days. In 30% to 40%
of ICH cases, the actual hematoma will expand and lead to clinical worsening. In patients with a large SAH, the head CT will show
bright signal (blood) at the base of the brain and within some
cortical sulci (
may be missed by CT and even MRI. Hence a lumbar puncture is
needed to definitively rule out a small SAH.
Numerous studies as well as recent guidelines have supported
use of brain MRI for assessment of patients with known or
suspected strokes.42 Magnetic resonance imaging using DWI
techniques is extremely sensitive and accurate for diagnosing
essentially all types of ischemic strokes (and some types of hemorrhagic stroke). Magnetic resonance imaging is particularly useful
for imaging small strokes, acute strokes, and those in the posterior
41
Fig. 30-2B). However, a small SAH or sentinel bleed
TABLE 30-8
TESTING DOMAIN SPECIFIC FUNCTIONS TESTED
Mentation and
cognition
Cranial nerves Testing of nerves II-XII typically performed, including
Motor function Tone, bulk, abnormal movements; strength, fine
Cerebellar function Coordination, rapid movements, balance
Gait Ability to walk, balance, tandem gait
Sensory Pain/pin prick, light touch, vibration/proprioception
Reflexes Deep tendon reflexes, plantar response (Babinski);
Vascular system Auscultation of neck and heart; blood pressure
Typical Components of a Neurological
Examination Pertinent to Stroke
Level of alertness, orientation, speech, naming/
repetition, memory, personality, apraxia, agnosia,
neglect syndromes
visual acuity and funduscopic examination
movements
cutaneous reflexes, primitive reflexes (snout, suck,
grasp, palmomental)
measurements in both arms; check pulses in hands
and feet; consider ankle-brachial index (ABI)
FIGURE 301 Head computed tomography (CT) scan without contrast.
Arrow indicates a subacute stroke (darker gray area) in right occipital lobe in a
patient with a new visual field deficit present for about 24 hours.
FIGURE 302 A, Head computed
AB
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tomography (CT) scan without contrast.
Arrows indicate a deep intracerebral
hemorrhage (ICH) with rupture into the
ventricular system (white area). B, Head
CT scan without contrast. Arrows indicate
a subarachnoid hemorrhage (SAH) (white
areas) at the base of the brain filling the
basal cisterns.
FIGURE 303 Magnetic resonance imaging (MRI) of brain with
diffusion-weighted sequence. White dots (arrows) show areas of acute
ischemic or infarction consistent with several acute strokes in a patient with
atrial fibrillation.
fossa (Fig. 30-3). In addition to DWI sequences, use of gradient
echo sequences allows detection of small amounts of blood. Using
this technique, studies have shown that up to 40% of ischemic strokes
may have microhemorrhages within the area of ischemia.
43
Magnetic resonance imaging results will often provide invaluable
information about stroke etiology, even if the patient's symptoms and
presentation suggest an alternative etiology. For example, a patient may
present with symptoms pointing to a small-vessel stroke deep in the
brain. In the proper setting, this type of stroke might be caused by typical vascular risk factors such as hypertension or diabetes. However, if
the MRI showed evidence of other small acute strokes in other vascular
territories, this would shift focus away from an isolated small-vessel
stroke to alternative mechanisms such as cardioembolic strokes due to
atrial fibrillation, a hypercoagulable state, or even a vasculitis.
Another advantage of MRI is that it can accurately distinguish
acute strokes from subacute strokes using lesion characteristics.
An acute ischemic stroke will be bright on DWI, dark on apparent diffusion coefficients (ADC) and not show enhancement with
gadolinium (Fig. 30-4A-B). A stroke that is 7 to 10 days old will be less
bright on DWI, less dark on ADC, and show enhancement with gadolinium (
Fig. 30-4C). A chronic stroke may be bright on DWI (due to
T2 shine through), bright on ADC, and show no enhancement.
Advanced MRI techniques are now available that can identify
potentially salvageable brain from infarcted brain based on comparing DWI lesions with magnetic resonance (MR) perfusion lesions
(
Fig. 30-5). Patients with an acute stroke who have a large area of
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30
CliniCAl PREsEnTATion And diAgnosis of CEREbRovAsCulAR disEAsE
FIGURE 304 A, Magnetic resonance
imaging (MRI) of the brain with
diffusion-weighted sequences shows
evidence of a large left hemispheric
stroke (white areas with arrows). B,
Apparent diffusion coefficient (ADC) of
same region; dark area is abnormal and
indicates ischemia/infarction consistent
with an acute stroke. C, Brain MRI
after infusion of gadolinium showing
enhancement of a right occipital stroke
consistent with a subacute infarction (at
least 5-7 days old).
AB C
368
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30
FIGURE 305 Magnetic resonance imaging (MRI) of brain with
superimposed perfusion and diffusion images showing areas of
“mismatch” indicating existence of an apparent ischemic penumbra.
Perfusion defect is blue; infarcted brain is pink/purple.
perfusion abnormality on an MR perfusion study but a smaller area
of ischemia (DWI lesion) may benefit from reperfusion therapy
using lytic or endovascular therapies even 6 to 8 hours after stroke
onset. Use of these advanced MRI techniques to select patients with
an apparent “ ischemic penumbra” is an area of active research.
Magnetic resonance imaging of an ICH is more complex, owing
to signal changes caused by metabolism of various blood constituents. About 48 to 72 hours after an ICH, the hemoglobin (Hb) in
the hematoma is metabolized into intracellular methemoglobin,
which appears bright on the MRI using T1 sequences and dark
on T2 sequences. After a week or more, methemoglobin becomes
extracellular and becomes bright on T1 and T2 sequences.
Hemosiderin is then formed in the hematoma and produces a
dark signal in gradient echo sequences
45
(Fig. 30-6).
42,44
A
B
Imaging Cerebral Vasculature
Of equal importance to imaging brain parenchyma is detailed
imaging of the cerebral vasculature, both extracranial (aorta,
carotid and vertebral arteries) and intracranial vessels.
in most cases we are focusing on the arterial vasculature, in certain
cases it is also important to image the cerebral veins (so-called
sinuses) to rule out a cerebral venous thrombosis.
There are several noninvasive modalities available for imaging the
cerebral vessels, including magnetic resonance angiography (MRA)
(see Chapter 13), computed tomographic angiography (CTA) (see
Chapter 14), duplex Doppler ultrasound (see Chapter 12), and
transcranial Doppler (TCD) (Figs. 30-7 and 30-8). Each method has
certain advantages as well as some limitations (
Table 30-9). We typi-
cally use either MRA or CTA because they are capable of imaging
the entire cerebral vasculature (from the great vessels in the chest to
ABC
40
Although
C
FIGURE 307 Magnetic resonance angiogram (MRA) with gadolinium,
showing normal extracranial common, internal, and external carotid
arteries (A) and intracranial vessels (B). C, Stenosis due to atherosclerosis
in proximal internal carotid artery (ICA) (arrow). D, MRA of vertebral-basilar
system showing irregularity of left vertebral artery due to either fibromuscular
dysplasia (FMD) or dissection (arrows).
D
FIGURE 306 A, Head computed
tomography (CT) showing right
thalamic intracerebral hemorrhage
(ICH) (white area with arrow). B,
Brain magnetic resonance imaging
(MRI) with gradient echo sequences
showing same stroke (arrow). Dark
area represents iron deposition
caused by the bleed. C, Subacute ICH
white area (arrow) is methemoglobin
formed from a recent cerebral
hemorrhage.
AB
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FIGURE 308 Computed tomographic angiogram (CT) of neck vessels.
A, Side oblique view shows severe calcification of distal common carotid artery
(CCA) and proximal internal carotid artery (ICA) (arrow). B, Axial images show a
normal right carotid artery (blue arrow) and calcified left ICA. Calcified region is
depicted with yellow area; soft plaque is shown by red arrow.
medium-sized intracranial vessels) at one time in only 5 to 10 minutes
for CTA, and 25 to 30 minutes for MRA. Computed tomographic angiography requires intravenous contrast agents, whereas Magnetic resonance angiography can be done either with intravenous gadolinium
or without (using a time-of-flight [TOF] protocol). Magnetic resonance
angiography with contrast (vs. no contrast) provides better images, permitting visualization of small lesions such as dissections or a vasculitis.
Computed tomographic angiography provides modestly more precise
anatomical detail in terms of its ability to detect small aneurysms and
small dissection flaps, and accurately determine the degree of arterial
stenoses. However, CTA does expose patients to ionizing radiation.
Carotid duplex ultrasound is a safe and noninvasive method
to image selected segments of the large vessels in the neck.
Transcranial Doppler is another safe and noninvasive technique
to image segments of the intracranial vasculature. Both techniques
can provide information about direction and velocity of blood
flow. Carotid ultrasound can be performed serially over the course
of months and years to assess changes in the degree of stenosis of
a neck artery, and it can determine plaque size and composition.
Transcranial Doppler is often performed daily after SAH to determine whether there is development of cerebral vasospasm that
may cause an ischemic stroke.
The gold-standard imaging modality for cerebral vessels remains
the digital subtraction angiogram (DSA). In cases where CTA and
MRA show different degrees of stenosis, we may do a DSA to determine the exact degree of stenosis (often before doing a carotid
endarterectomy or carotid artery stent). Besides offering precise
imaging of small, medium, and large vessels, a DSA also provides
invaluable information about cerebral hemodynamics. By injecting the various cerebral vessels, an angiogram can determine (in
cases of a vessel stenosis or occlusion) exactly where the blood
supply is coming from and going to. The angiogram can detect
collateral vessels (or lack thereof) that may be supplying a region
of brain thought to be poorly perfused due to occlusion of a proximal vessel. We have often seen patients with apparent lack of
flow through a severely diseased basilar artery, only to find that
abundant collaterals are supplying the brainstem with adequate
perfusion. A DSA is also very important when planning surgical
treatment for an AVM, aneurysm, and other vascular lesions.
Using computer reconstruction algorithms, images from all the
above techniques can be assembled into three-dimensional (3D)
pictures to provide a comprehensive view of the cerebral vessels.
These images can be rotated and flipped as needed to aid the clinician in determining the type, location, and severity of the lesion
(stenosis, aneurysm, etc.).
Laboratory Tests
All patients with a stroke (ischemic or hemorrhagic) require standard testing that should include a complete blood cell count (CBC),
chemistry panel, coagulation studies, chest x-ray, electrocardiogram
(ECG), urinalysis, and the brain imaging already detailed.
all patients should undergo toxicology screening for drug use, since
this is a common condition, and patients are often not forthcoming
about drug abuse. The Centers for Disease Control and Prevention
46
Again,
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CliniCAl PREsEnTATion And diAgnosis of CEREbRovAsCulAR disEAsE
TABLE 30-9 Vascular Imaging Techniques
TEST NAME
Carotid Doppler Ultrasound Extracranial carotid and
TCD Ultrasound Intracranial arteries Safe, noninvasive, no radiation,
MRA Magnetic
CTA X-ray Extracranial and intracranial
Digital cerebral
angiography
CTA, computed tomographic angiography; MRA, magnetic resonance angiography; TCD, transcranial Doppler.
Some data derived from Latchaw RE, Alberts MJ, Lev MH, et al: Recommendations for imaging of acute ischemic stroke: a scientific statement from the American Heart Association. Stroke 40:3646–
3678, 2009.
IMAGING
TECHNIQUE
resonance
X-ray All arteries and veins, including
VASCULATURE IMAGED
vertebral arteries
Large and medium extracranial
and intracranial arteries and
veins; great vessels in chest
arteries and veins; great
vessels in chest; can detect
some small vessels
small vessels
ADVANTAGES
Safe, noninvasive, no radiation,
inexpensive; provides some
anatomical and physiological data
inexpensive; provides some
physiological data
Safe, noninvasive, no radiation; some
anatomical details; can image
most vessels; can evaluate cerebral
perfusion; some aneurysm detection
Significant anatomical detail; can
evaluate cerebral perfusion; can
image most vessels; accurate stenosis
and aneurysm measurements
Significant anatomical detail; can
evaluate cerebral perfusion and
collateral flow; accurate stenosis and
aneurysm measurement
DISADVANTAGES
Limited to extracranial vasculature
in the neck
Limited to mostly intracranial
vasculature; limited anatomical
detail
Cannot be used with a pacemaker
or metal; limited in severe
claustrophobia; contrast often
needed; expensive
Radiation exposure; requires
contrast; limited use with renal
dysfunction; expensive
Invasive procedure; radiation
exposure; requires contrast;
limited use with renal dysfunction;
expensive
370
TABLE 30-10 Suggested Laboratory Testing for Patients with Stroke
ROUTINE TESTS TESTS FOR SPECIAL CASES* COMMENTS FOR SPECIAL TESTS
CBC with differential Hb electrophoresis Useful if SCD or thalassemia suspected
Comprehensive chemistry profile Vasculitis screen (ANA, rheumatoid factor, etc.) Useful if arteries show beading
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APTT, PT, INR Hypercoagulable screen (lupus anticoagulant,
30
Sedimentation rate Fibrinogen, DIC screen Detects ongoing thrombosis
Fasting lipid profile CADASIL gene mutation Characteristic MRI and positive family history
Hb A
1C
Homocysteine Fabry's disease test Positive family history; skin changes; renal disease
Vitamins B12 and folate Blood cultures Suspected endocarditis; multiple strokes
Thyroid panel Assay of clotting factors Recurrent cerebral hemorrhages
HIV CT of chest/abdomen/pelvis Look for cancer in patient with recurrent stroke
Urine toxicology screen (drug abuse)
Platelet function tests
*Special cases refer to unusual or atypical presentations or stroke syndromes, including cryptogenic etiologies.
†
Benefits of platelet function testing for improving efficacy and safety of stroke therapy remain experimental; however, such testing may be important for detecting platelet dysfunction in
patients with hemorrhagic stroke.
ANA, antinuclear antibody; APTT, activated partial thromboplastin time; CAA, cerebral amyloid angiopathy; CADASIL, cerebral autosomal dominant arteriopathy with subcortical infarcts and
leukoencephalopathy; (CBC), complete blood cell count; DIC, disseminated intravascular coagulopathy; Hb, hemoglobin; HIV, human immunodeficiency virus; ICH, intracerebral hemorrhage;
INR, International Normalized Ratio; MRI, magnetic resonance imaging; PT, prothrombin time; SCD, sickle cell disease.
†
anticardiolipin antibodies, protein C and S activity; factor
V Leiden and prothrombin gene mutations; cryoglobulin
screen; antithrombin III level
Apolipoprotein E genotype CAA with recurrent ICH, dementia, MRI changes
Useful for ischemic strokes in young adults;
postpartum; cryptogenic strokes
(CDC) recommends HIV testing for most adults who are hospitalized,
and this would include patients with an acute stroke.
47
Table 30-10
lists routine laboratory testing for patients with ischemic stroke.
Special blood tests are warranted if a hypercoagulable state is
suspected based on the patient's age, lack of other risk factors,
or if another condition is suspected.
48
An elevated D-dimer may
indicate ongoing thrombosis. Blood cultures may be obtained in
patients with multiple embolic strokes to rule out endocarditis. In
patients with suspected vasculitis or a possible autoimmune disorder, tests for inflammatory conditions, such as a sedimentation
rate, antinuclear antibody (ANA) titers, and other serologies, may
be performed. Hemoglobin electrophoresis can rule out SCD or
trait, as well as thalassemia.
Since the heart can be the cause of up to 25% of all strokes, a
thorough cardiac assessment is needed in most cases. Beyond
the cardiac clinical examination and an electrocardiogram, all
patients with an ischemic stroke should receive at least 48 hours
of cardiac monitoring using computerized telemetry to detect
rhythm changes that could cause a stroke (e.g., atrial fibrillation)
as well as dysrhythmia that could indicate underlying coronary
artery disease (CAD) or cardiomyopathy (e.g., ventricular tachy-
46
cardia).
In some cases, more prolonged monitoring using the
Holter device is warranted to further assess for paroxysmal atrial
fibrillation. Cardiac imaging including a transthoracic echocardiogram (TTE) or a transesophageal echocardiogram (TEE) is often
performed to evaluate cardiac function and assess for presence of
a cardiac clot or other structural lesion. Typically we begin with a
TTE, and if negative then proceed to the TEE.
49
Monitoring a patient's respiratory status and oxygen saturation
is important in the acute setting, since changes may indicate an
increase in intracranial pressure or presence of obstructive sleep
apnea (OSA) (which is an underrecognized risk factor for stroke).
Duplex ultrasound examination of the lower and upper extremities is commonly performed to detect DVT when this is considered
a possible source of stroke (in patients with a patent foramen ovale)
or a complication of stroke (in patients who are obese, sedentary,
or were found down at home after many hours or days). Presence
of DVT can also be an indicator of an underlying hypercoagulable
state or cancer. A thorough evaluation for underlying malignancy
should be considered in patients with a stroke and DVT, as well as
patients with cryptogenic strokes.
A lumbar puncture is warranted in patients with suspected
vasculitis or if a small SAH is suspected but not proven based
on brain CT or MRI. Special genetic testing is performed in cases
of suspected disorders such as CADASIL or Marfan's syndrome.
Apolipoprotein E genotype analysis in patients with suspected
CAA may be appropriate, since the e2 and e4 alleles are strongly
associated with CAA-related ICH.
The utility of these tests is greatest in patients with strokes of
unusual type, size, and location, particularly if there are no risk factors for atherothrombotic and cerebrovascular disease. A typical
patient with one or more risk factors who has an uncomplicated
ischemic stroke of known mechanism does not require the special
testing listed (in most cases).
Conclusions
Stroke is a complex and heterogeneous disease that is the culmination of a variety of medical factors and cerebral vascular anatomy.
Based on results of the history, physical, blood, and imaging tests, the
clinician can make an accurate assessment as to the location, type,
mechanism and cause of the stroke. Based upon this formulation,
an approach for acute therapy can be planned, along with interventions to avoid secondary complications and prevent a recurrent
stroke. A better understanding of the basics of stroke in terms of type,
cause, presentation, and diagnosis will lead to improved therapies
and increase the chance that the patient will have a better outcome.
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371
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30
CliniCAl PREsEnTATion And diAgnosis of CEREbRovAsCulAR disEAsE
CHAPTER
31 Prevention and Treatment
of Stroke
Marc Fisher, Mehmet Zülküf Önal
Medical management of stroke encompasses a wide range of therapies that include interventions directed at reducing the extent
of acute injury, managing physiological parameters in the acute
phase, and preventing recurrent strokes. Ischemic stroke is the
most common form of cerebrovascular disease and will be the
focus of this chapter, which will overview acute treatments and prevention measures. Only a brief mention of primary intracerebral
hemorrhage (ICH) in regard to acute management and secondary
prevention will be included.
Acute ischemic stroke (AIS) occurs after occlusion of an intracranial or extracranial vessel by a thrombus that in most cases has
embolized from the heart or a more proximal vessel. Unlike acute
myocardial infarction (AMI), in situ thrombosis is uncommon. As
a consequence of acute vascular occlusion, a cascade of intracellular events (
lead to irreversible tissue injury such as infarction.
Fig. 31-1) is initiated; over varying periods of time, they
1
The temporal development of infarction within the ischemic brain region is
quite variable, and portions of the ischemic brain tissue may not be
irreversibly injured for many hours after the initial vascular occlu-
2
sion.
Ischemic brain tissue that remains viable and potentially
amenable to salvage with timely initiation of therapeutic interventions is called the ischemic penumbra, and this potentially salvageable tissue is the target of AIS therapies.
3,4
The basic concept
underlying AIS therapy is that reducing the extent of brain infarction should translate into improved clinical outcome, as measured
by commonly used outcome scales such as the modified Rankin
Scale (mRS) or Barthel Index.
5
The most important factor predisposing ischemic brain tissue
to infarction is the severity of cerebral blood flow (CBF) decline.
Regions with little or no residual CBF will evolve into infarction
rapidly and are not the target of AIS therapies because reperfusion cannot in most cases be performed rapidly enough to salvage
this ischemic core region. In the ischemic penumbra, CBF decline
is more modest, and this ischemic tissue progresses more slowly
toward infarction, providing a time window for intervention that can
salvage tissue to some extent. A variety of definitions for the ischemic
penumbra were suggested over time and are outlined in
Box 31-1.
Besides the severity of CBF decline, other factors that affect evolution of ischemic injury include temperature, glucose, blood pressure, and other metabolic factors.
7,8
The implication of these factors
that contribute to the evolution of ischemic injury is that individual
AIS patients have quite variable therapeutic time windows for successful therapeutic intervention, and that the earlier a therapy is initiated, the more likely it is to be beneficial. Acute ischemic stroke
therapy can be divided into two broad areas: (1) recanalization/
reperfusion approaches directed at improving altered CBF within
ischemic tissue and (2) neuroprotection designed to impede the
cellular consequences of ischemic injury. The focus of this chapter
will be on the former because no neuroprotection strategies have
been demonstrated to be of significant benefit. Recanalization/
reperfusion can be accomplished with intravenous (IV) or intraarterial (IA) thrombolytics as well as mechanical devices. These
approaches comprise the currently available AIS treatments.
Prehospital and Emergency Department
Management of Ischemic Stroke
Prehospital management and field treatment are critically important to increasing survival rates of stroke patients. This phase starts
with the emergency medical services (EMS) call and continues in
the hospital emergency department (ED;
Table 31-1). The majority
of ischemic stroke patients do not reach the hospital soon enough,
owing to lack of local services, facilities, and social reasons. When
first suspected to have a stroke, the patient should be rapidly transported to an appropriate facility for diagnostic evaluation and treatment initiation.
of symptom onset are eligible for IV thrombolysis.
9
Stroke patients who present within 3 to 4.5 hours
10–14
Emergency
medical services use is strongly associated with a decreased time
to initial physician examination, initial computed tomography (CT)
imaging, and neurological evaluation.
contact are superior to contacting the family physician or hospital
directly, and were confirmed with several studies.
be given a priority dispatch as for MI and trauma.
13,15–17
The benefits of EMS
18,19
Stroke should
20
Patients who
show signs and symptoms of hyperacute stroke must be treated as
time-sensitive emergency cases and transported without delay to
the closest institution that provides emergency stroke care.
To ease and facilitate this process, medical authorities and
media sources should encourage the recognition of stroke signs
by providing public education about this condition.
21
All members
of the public should be able to recognize and identify the signs
and symptoms of stroke, which include sudden localized weakness, difficulty speaking, loss of vision, headache, and dizziness.
Patient, family, and caregiver education is an integral part of stroke
care that should be addressed at all stages across the continuum
of stroke care for both adult and pediatric patients.
thrombolytic treatment with tissue plasminogen activator (tPA) is
the only approved treatment option for AIS. The National Institute
of Neurological Disorders and Stroke (NINDS) and Advanced
6
Cardiac Life Support Resources (ACLSR) recommend the possible
timing sequences shown in
Table 31-2 for the potential thromboly-
sis candidate.
Data from the Thomas Lewis Latané (TLL) Temple Foundation
Stroke Project controlled trial showed the benefits of educational
interventions on stroke identification and management targeting
patients, EMS, hospitals, and community physicians. This approach
increased thrombolytic use in patients with ischemic stroke from
2.21% to 8.65% as compared with communities that did not have
such programs, which saw only a 0.06% increase. For patients with
ischemic stroke who were eligible for thrombolytic therapy, rates
of tPA usage increased from 14% to 52% in intervention communi-
23,24
ties.
Prehospital delays continue to contribute the largest pro-
portion of time to late initiation of therapy.
25
Emergency medical services arrival starts the diagnostic and management processes. The EMS crew should transfer the patient to a
medical center that can provide appropriate diagnostic and treatment modalities to stroke patients.
9
After the ambulance arrives on
the scene, EMS providers should obtain a brief history and patient
examination, stabilize vital signs, and rapidly transport the patient to
the closest, most appropriate facility (
Table 31-3). Prehospital evalua-
tion is helpful for ED physicians and the inpatient care team for planning treatment options. The Los Angeles Prehospital Stroke Screen
and Cincinnati Prehospital Stroke Scale are the most widely used
and preferred prehospital evaluation instruments and facilitate evaluation of potential stroke patients. Critical medical interventions in
the ED should focus on the need for intubation, blood pressure control, and determining risk/benefit for thrombolytic intervention.
General ED stroke care issues are outlined in
Table 31-4.
27,28
Acute stroke patients urgently need IV access and cardiac monitoring in the ED, preferably initiated in the transporting ambulance. These patients are at also risk for acute cardiac diseases
such as arrhythmias and myocardial infarction (MI). In addition,
22
Currently,
22
26
372
373
Glutamate release
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Cerebral ischemia
++
Ca
Ca++ ↑
Inflammatory
response
• Cytokine release
• Activation of
inflammatory
NO Caspases Free radicals
DNA+Protein damage
Membrane damage
blood cells
Necrotic+Apoptotic
cell death
• Neurogenesis
• Synaptogenesis
• Axogenesis
Regeneration
Box 31-1 Definitions of the Ischemic Penumbra
Over Time
■ A region of reduced CBF with absent electrical activity but preserved ion
homeostasis and transmembrane electrical potentials
■ A region with reduced CBF and preserved energy metabolism
■ A region with impaired protein synthesis but preserved ATP levels
■ A region that is potentially salvageable with timely intervention*
*This definition is the most clinically relevant one and relates directly to imaging
identification.
ATP, adenosine triphosphate; CBF, cerebral blood flow.
TABLE 31-1 Stroke Chain of Survival
DETECTION RECOGNITION OF STROKE SIGNS AND SYMPTOMS
Dispatch Call 911 (emergency phone number) and priority EMS
Delivery Prompt transport and prehospital notification to hospital
Door Immediate ED triage
Data ED evaluation, prompt laboratory studies, and CT
Decision Diagnosis and decision about appropriate therapy
Drug Administration of appropriate drugs or other
CT, computed tomography; ED, emergency department; EMS, emergency medical services.
Adapted from Adams HP Jr, del Zoppo G, Alberts MJ, et al: Guidelines for the early management
of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke
Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention
Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in
Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the
value of this guideline as an educational tool for neurologists. Stroke 38:1655–1711, 2007.
atrial fibrillation may be associated with acute stroke as either the
etiology (embolic disease) or as a result.
evaluation in the ED should include a detailed history, physical
examination, neurological examination, and stroke scale scores
(National Institutes of Health Stroke Scale [NIHSS] and appropriate diagnostic tests;
Patients presenting with compromised ventilation require emergent airway control via nasal oxygenation or rapid sequence intubation. Adequate tissue oxygenation is important in the acute
dispatch
imaging
interventions
Box 31-2).
9
29,30
Acute stroke patient
9
Protease
activation
Cell membrane
FIGURE 311 Depiction of the
Recovery
zone
major events that encompass
the ischemic cascade of cellular
injury. DNA, deoxyribonucleic acid;
NO, nitric oxide. (Courtesy Dr. WolfRudiger Schaebitz.)
TABLE 31-2
Stroke Evaluation Time Benchmarks for
Potential Thrombolysis Candidate
TIME INTERVAL TIME TARGET
Door to doctor
10 min
Access to neurological expertise 15 min
Door to CT scan completion 25 min
Door to CT scan interpretation 45 min
Door to treatment 60 min
Admission to monitored bed 3 h
CT, computed tomography.
Guidelines for Emergency Medical Services
TABLE 31-3
Management of Patients with Suspected
Stroke
RECOMMENDED NOT RECOMMENDED
Manage ABCs Dextrose-containing fluids in nonhypogly-
Cardiac monitoring Hypotension/excessive blood pressure
IV access Excessive IV fluids
Oxygen (as required for O
saturation <92%)
2
Assess for hypoglycemia
Nil per os (NPO)
Alert receiving emergency
department
Rapid transport to closest
appropriate facility capable
of treating acute stroke
ABCs, airway, breathing, circulation; IV, intravenous.
Adapted from Adams HP Jr, del Zoppo G, Alberts MJ, et al: Guidelines for the early management
of adults with ischemic stroke: a guideline from the American Heart Association/American Stroke
Association Stroke Council, Clinical Cardiology Council, Cardiovascular Radiology and Intervention
Council, and the Atherosclerotic Peripheral Vascular Disease and Quality of Care Outcomes in
Research Interdisciplinary Working Groups: the American Academy of Neurology affirms the
value of this guideline as an educational tool for neurologists. Stroke 38:1655–1711, 2007.
cemic patients
reduction
9
CH
31
PREVENTION AND TREATMENT OF STROKE
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