Vol. 102 No.

2 August 2006

ORAL MEDICINE Editor: Martin S. Greenberg

Stroke: epidemiology, classification, risk factors, complications, diagnosis,

prevention, and medical and dental management
Mahnaz Fatahzadeh, DMD,a and Michael Glick, DMD,b Newark, NJ
DEPARTMENT OF DIAGNOSTIC SCIENCES, UNIVERSITY OF MEDICINE AND DENTISTRY OF NEW JERSEY

Cerebrovascular accident, or stroke, refers to an acute onset of neurologic deficits lasting more than 24 hours or
culminating in death caused by a sudden impairment of cerebral circulation. Stroke is the third leading cause of death and
a major cause of long-term disability in the United States. This article provides the dental community with an up-to-date
understanding of the epidemiology, classification, risk factors, complications, diagnosis, prevention, and medical and dental
management issues pertaining to stroke. (Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;102:180-91)

Cerebrovascular accident (CVA), stroke, or brain PATHOGENESIS AND CLASSIFICATION

attack refers to an acute onset of neurologic deficit
lasting more than 24 hours or culminating in death
caused by a sudden impairment of cerebral circulation.1
Stroke is the third leading cause of death in the United
States, Europe, and most countries in the world.1-4 In
2005, nearly 700,000 strokes and 160,000 stroke-related
deaths will occur in the United States,5,6 which com-
putes to 1 stroke every minute.7 In addition, magnetic
resonance imaging (MRI) studies reveal that nearly
22 million asymptomatic strokes occur every year.8
Stroke is also a major cause of prolonged neurologic
disability in adults,2,3,5,7,9 with an annual economic
burden of nearly $45 billion in the United States.10,11
Incidences of stroke-related deaths and disability are ex-
pected to rise even higher as the population ages.1,3,4,11-13
In fact, extrapolation of the current data predicts that
the mortality rate from stroke will double by 2020,1
which highlights the significance of stroke-prevention
measures.3 The preceding discussion reviews relevant
topics with regard to the stroke focusing on the medical
and dental management issues of concern to dental
practitioners.
a
Assistant Professor, Division of Oral Medicine.
b
Professor and Chairman.
Received for publication Dec 8, 2004; returned for revision Jul 15,
2005; accepted for publication Jul 29, 2005.
1079-2104/$ - see front matter
2006 Mosby, Inc. All rights reserved.
doi:10.1016/j.tripleo.2005.07.031
The underlying pathogenic mechanism for cerebro-
vascular accidents is the interruption of blood flow
and delivery of essential oxygen and glucose to the brain
tissue. The brain does not store glycogen and requires
60-70 mL of perfusion per 100 g of tissue per minute
for normal function.14 A drop in the blood flow to
25 mL/100 g/min leads to neuronal ischemia, energy
failure, and neurologic symptoms, followed by irrever-
sible tissue damage within minutes should ischemia
continue.11,14,15
Four neurologic phenomena have been defined for
stroke based on their duration: transient ischemic at-
tacks (TIAs), reversible ischemic neurologic defect
(RIND), stroke in evolution, and completed stroke. A
TIA is a sudden, short-lasting, focal neurologic deficit
or mini stroke caused by transient and localized brain
ischemia.11 These neurologic deficits are reversible
within 24 hours11 but often signal an impending stroke
within days.7,16 RIND refers to a neurologic impairment
that is reversible but recovery from which will exceed
24 hours.16 A stroke in evolution is defined as stroke-
associated symptoms that progressively worsen over
time.11,16 In contrast, neurologic signs and symptoms
that have been stable for more than 24 hours define a
completed stroke.11
Strokes are subclassified into ischemic and hemor-
rhagic types, based on the underlying pathogenesis.11
Eighty-five percent of strokes are ischemic in nature
and involve the occlusion of a cerebral vessel with sub-
sequent brain ischemia and infarction distal to the site of

180
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Volume 102, Number 2
obstruction, which may be caused by either atherscler-
otic thrombi or distant emboli.11,14,17
Embolic strokes are classified into arterial, cardioem-
bolic, and cryptogenic subtypes, depending on the site
of embolic origin.11 Common sources of cerebral embo-
lism include atherothrombi in the carotid bifurcation or
aortic arch, cardiac disease, and spontaneous thrombo-
sis in hypercoagulable conditions.11,17 Multiple septic
cerebral emboli may also arise from valvular vegeta-
tions in bacterial endocarditis.11,17 Diagnosing the exact
source of embolism may be challenging, but this in-
formation is critical for reduction of stroke-related
deaths.11 Cryptogenic strokes refer to cerebrovascular
events in which the source of occlusive emboli remains
unknown.11
Differentiation of ischemic stroke subtypes is not
clinically possible, although certain features may help
in diagnosis.14 In general, the neurologic symptoms of
thrombotic stroke develop slowly, whereas sudden, mul-
tifocal, and maximal neurologic deficits at the onset
often indicate an embolic stroke.11,17 In addition, early
seizures and hemorrhagic transformation are more
frequent with embolic events.11,17
Three main types of ischemic stroke syndromes
have been described. A lacunar stroke results from the
obstruction of the small penetrating arterioles that
feed the white matter structures and the thalamus.11,14
Symptoms of small-vessel stroke are often transient,
sparing high-level brain functions.14 Predisposing fac-
tors for lacunar strokes include aging and uncontrolled
hypertension.11 In contrast, large-vessel stroke is char-
acterized by extensive cerebral infarction and results
from thrombotic occlusion of a major intracranial ves-
sel.14 Frequently, high-level brain functions are affected
and prognosis is poor.14 Brainstem stroke, the third is-
chemic stroke syndrome, may result from the occlusion
of either small or large cerebral vessels and has a varia-
ble clinical presentation.14
Fifteen percent of all strokes are hemorrhagic in
nature.11,14 Hemorrhagic brain infarction may result
either from displacement of cerebral tissues or from
toxic effects of extravasated blood.11,18 Whereas two-
thirds of hemorrhagic strokes are caused by intracerebral
bleeding, the remaining one-third may be attributed to
aneurysmal rupture and subarachnoid hemorrhage.14
Predisposing risk factors for intracranial hemorrhage
include hypertensive encephalopathy, advanced age,
hematologic disorders, head injury, strenuous exercise,
and abuse of alcohol or illicit drugs.11
CLINICAL MANIFESTATIONS
Irrespective of the etiology, brain edema is the first in
the post-stroke cascade of events.1 The site, size, and du-
ration of occlusion or hemorrhage, presence or absence
Fatahzadeh and Glick 181
of collateral circulation, blood pressure (BP), and body
temperature are factors that affect the final dimension of
brain infarct.11,18 Clinical manifestations of stroke vary,
depending on the site and size of the brain lesion.9,11
Signs and symptoms of stroke are numerous and may
include variable sensorimotor dysfunctions, such as
hemiplegia, hemiparesis, hypoesthesia, compromised
eye movements, visual defects, deafness, and language
problems, as well as memory disturbance, headache, al-
tered mental status, dizziness, nausea, and vomiting.9,11
Of these, progressive neurologic impairment, early
changes in mental status, abrupt headaches, seizures,
and vomiting are more common, and focal neurologic
deficits typical of ischemia are less frequent, with hem-
orrhagic strokes.9,11
DIAGNOSIS AND LABORATORY TESTING
Application of effective preventive and therapeutic
interventions requires a precise knowledge of underly-
ing stroke mechanism.14 Many other conditions can
resemble the features of stroke and confound the
diagnostic process. Focal neurologic deficits are not
unique to stroke and may also occur in the context of
an epileptic seizure attack or an acute hypoglycemic
episode.9 In addition, brain neoplasms, acute sepsis,
infectious encephalitis, multiple sclerosis, prolonged
migraneous aura, and severe metabolic imbalances
may occasionally mimic the signs and symptoms of
stroke.9 The precise etiology of an ischemic stroke
may remain unknown in many cases, even after ex-
tensive diagnostic work ups.9 The incidence rate for
ischemic strokes of unknown etiology has been reported
to be in the range of 18% to 40%.19,20
A number of diagnostic modalities can be used to
exclude conditions with signs and symptoms sugges-
tive of stroke. Factors critical to the diagnostic process
include patient age, medical history, clinical presentation,
the temporal profile of the event, location of the infarct,
stroke subtype, and specific etiology.9 Clinical examina-
tion should be thorough and focused on the heart, ret-
inas, and peripheral vascular system.11 Vascular testing
such as cerebral angiography or Doppler ultrasonogra-
phy will often shed light on the nature, location, and
severity of vascular lesions in significant vessels of the
head and neck.4 Cardiac auscultation, echocardiography
and electrocardiography can be used to disclose valvular
or rhythm abnormalities, conduction problems, and a
recent myocardial infarction (MI).11,17
Indicated laboratory tests include complete blood
count, chemistry, serum electrolytes, urinalysis, erythro-
cyte sedimentation rate, screening for hypercoagulability,
serologic tests for syphilis, blood sugar, cholesterol, and
lipid levels.4,11 Lumbar puncture may assist in the ex-
clusion of subarachnoid hemorrhage or meningitis as

182 Fatahzadeh and Glick
the underlying cause.11 Blood cultures and echocardiog-
raphy are indicated if septic emboli secondary to infec-
tive endocarditis is suspected.17
History and clinical examination cannot reliably
rule out hemorrhagic stroke, a distinction necessary be-
fore emergency management can begin.9,11 Diagnostic
imaging with computerized tomography (CT) or MRI
is always indicated to identify the presence, nature,
and extent of brain injury, particularly if thrombolytic
intervention is being considered.4,11 A noncontrast
head CT is the traditional diagnostic imaging technique
when clinical signs and symptoms are suggestive of
acute stroke,1,21 although advanced MRI techniques
are fast becoming the imaging modality of choice in
these situations.22,23 Recent work indicate that T2-
weighed MRI is more reliable than CT in the diagnosis
of intracerebral and subarachnoid hemorrhages.24-26 In
addition, diffusion-weighted MRI allows for distinction
of ischemic from hemorrhagic infarcts faster and better
than CT.27,28 Therefore, CT is no longer necessary for
diagnosis of acute stroke if modern MRI is accessible.24
Irrespective of the imaging technique selected,
knowing the date and time of stroke onset is critical to
proper interpretation of the imaging.1 The gold standard
for visualization of cerebrovascular anatomy is cerebral
angiography,21 which is nondiagnostic in many cases of
cardiogenic stroke but may identify the sites of vascular
stenosis where emboli are potentially trapped.29 Para-
doxically, cerebral angiography may precipitate an
embolic event.14 Localization of vascular narrowing and
detection of cerebral emboli can also be accomplished
with transcranial doppler ultrosonography.17,21 In addi-
tion, brain and vascular imaging may be efficiently
obtained by magnetic resonance angiography and
perfusion CT.24,30 Moreover, transthoracic or transeso-
phageal echocardiography can be used to identify poten-
tial cardiac sources of embolism.31
RISK FACTORS AND PREVENTION
Management of the stroke patient starts with pre-
vention. Strategies to reduce stroke-related death and
disability significantly impact public health.7,11 Epide-
miologic studies have identified many predisposing fac-
tors associated with stroke, and primary prevention
focuses on the modification of those risk factors in the
general population.7 Nonmodifiable risk factors include
advanced age, male gender, nonwhite race, and hereditary
predisposition.3,32 Incidence of stroke increases with
age.11 Specifically, 75% of all strokes in white people
and the majority of ischemic strokes occur in people
over the age of 65.12,33,34 Other risk factors for stroke
include inherited or acquired hypercoagulable conditions,
oral contraceptive use, stress, and previous cerebrovascu-
lar events.4,7,11 Initiating life-style modifications such
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August 2006
as a healthier diet, greater physical activity, smoking
cessation, moderating intake of alcohol, and stress re-
duction are the core requirements for primary stroke
prevention.7,32 Screening for comorbidities such as
hypertension (HTN), MI, atrial fibrillation (AF), con-
gestive heart failure (CHF), diabetes mellitus, carotid
artery stenosis (CAS), and hypercholesterolemia is
also an effective primary prevention strategy.3,7,35
In contrast to the primary prevention of MI, the role of
antiplatelet drugs, including aspirin, in the prevention of
a first stroke is controversial.3,32 Nevertheless, adminis-
tration of antiplatelet or anticoagulation agents are po-
tential strategies for the prevention of cardioembolic
stroke in those with AF.3,11,17,18,32,36 Prophylactic anti-
coagulation is also indicated for patients with MI,
mechanical heart valves, and CHF who are at risk for
thromboembolism.17,37 Routine anticoagulation, how-
ever, is not warranted for patients with bioprosthetic
valves in the absence of previous thromboemolism.17
The annual incidence of intracranial hemorrhage, the
main adverse effect of anticoagulant therapy, is about
1%.17,38 A history of ischemic stroke, intensive antico-
agulation, HTN, and older age increase the risk of this
complication, highlighting the importance of patient
selection.17
Carotid endarterectomy is a well established preven-
tive strategy against cerebrovascular disease.11 Asymp-
tomatic CAS refers to the absence of clinical signs or
symptoms of stroke or TIA ipsilateral to the carotid
obstruction.11 Conversely, CAS on the same side as
vascular distribution of a stroke or TIA is defined as
symptomatic.11 The preventive approach for patients
with asymptomatic carotid disease remains controver-
sial.3,11,32 In general, aspirin therapy and risk-factor
modification are the recommended approaches for
patients with asymptomatic carotid disease.11
Stroke recurrence is a significant concern with regard
to an increase in mortality, disability, length of hospital
stay, and contribution to vascular dementia.39,40 Rates of
recurrence vary depending on the stroke subtypes, with
lacunar and thrombotic strokes having the lowest and
highest recurrence rates, respectively.39 A history of
TIAs or minor strokes predisposes patients to subse-
quent stroke and up to a third of recurrences occur
within 1 month of the initial event.11,41 Understanding
the underlying mechanism for the first stroke and iden-
tifying modifiable risk factors in the target population
are critical to secondary stroke prevention.9 Risk-factor
modification has a more direct effect on the prevention
of the first stroke than on recurrent strokes.3 Neverthe-
less, risk-factor modification should be part of a compre-
hensive stroke-prevention program.3,11 Reduction of BP
is a highly effective strategy in the prevention of both
ischemic and hemorrhagic strokes.42,43
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Volume 102, Number 2
Oral anticoagulation therapy with warfarin is a well
established strategy in the prevention of recurrent ische-
mic stroke in patients with AF and offers a definite
advantage over aspirin therapy.32,44-47 Warfarin therapy
also benefits patients with other potential cardiac sour-
ces of embolism, such as mechanical valve or left ven-
tricular aneurysm.48 In patients with extensive brain
lesions, oral anticoagulants are typically withheld dur-
ing the period immediately following an ischemic stroke
to reduce the risk of hemorrhagic transformation.48,49 In
general, however, the benefits of oral anticoagulation
with warfarin in secondary stroke prevention outweigh
the risk of hemorrhagic adverse effects.11
Single or combination antiplatelet agents, such as
aspirin, clopidogrel, ticlopidine, or dipyridamole, in a
variety of doses, constitute the primary strategy for the
prevention of recurrent ischemic stroke in patients with-
out a cardiogenic source.3,11,32,48 A potential drawback
associated with antiplatelet therapy is breakthrough
CVA or stroke recurrence while on antiplatelet ther-
apy.1 Individuals taking antiplatelet medications dem-
onstrate a wide variability in the inhibitory effect of
these agents on platelet aggregation as well as alteration
of response with chronic therapy.50 Therefore, failure of
antiplatelet therapy in the prevention of recurrence may
be caused by patients incomplete response to therapy or
development of resistance with prolonged therapy.50,51
In addition, adverse effects such as aspirin-induced gas-
trointestinal bleeding or ticlopidine-induced agranulo-
cytosis are examples where the therapy is not tolerated
by patients.13
Patients with greater than 70% CAS and a history of
stroke or TIAs are 6 times more at risk of a recurrent
stroke on the side of the stenosis compared to asymp-
tomatic patients.52,53 Significant reduction in the risk
of recurrent stroke has been reported with surgical inter-
vention in patients with greater than 70% CAS, provided
the surgical risk is less than 7%.1,11,54,55
MEDICAL MANAGEMENT
Timely recognition and management of stroke is
critical for reduction of stroke-related morbidity
and mortality.9 The phrase time is brain implies that
immediate intervention improves neuronal salvage and
functional recovery.1,4,9,14 Caregivers have a critical
role in the overall management of stroke victims.
Caregivers are important members of the team and The time of stroke onset is critical to an optimal out-
should be educated about the symptoms of stroke, poten-
tial complications, prevention measures, and the abso-
lute necessity for emergent care if the need arises.9
In the overall management of stroke patients, physicians
address the acute and long-term effects of stroke,
consider risks and benefits of medical and rehabilita-
tive options, individualize therapy, prevent potential
Fatahzadeh and Glick 183
complications, and attempt to minimize stroke
recurrence.56
In general, stroke victims are most effectively man-
aged in stroke centers equipped with advanced technol-
ogy and experienced multidisciplinary personnel.4,14
Studies have shown a dramatic reduction in mortality,
disability, and long-term care needs of patients who
were managed in stroke centers compared to regular hos-
pital wards.56-58 Immediate poststroke interventions fo-
cus on life support through respiratory and cardiac care,
control of BP, monitoring oxygen saturation and blood
glucose level, prevention of metabolic disturbances,
maintenance of organ function, and management of ele-
vated intracranial pressure (ICP).11,48,58 Stroke victims
are also closely monitored for signs and symptoms of
neurologic deterioration indicative of intracerebral hem-
orrhage.59 Tight control of BP, adequate hydration, and
close follow-up is especially important for patients
with hemorrhagic stroke.11 Neurosurgical evaluation
may also be necessary for those with cerebellar hemor-
rhage, ischemic cerebellar lesions, and depressed mental
status.9,11 In addition, the head of the bed should be kept
elevated until high ICP is excluded.11
Optimal therapeutic outcome in stroke management
depends on having a clear understanding of underlying
mechanisms.14 After the type of stroke has been estab-
lished, efforts center on preserving ischemic brain
tissue, maximizing neuronal survival, and preventing
further thrombosis or hemorrhage.14,48 In contrast to
myocardial salvage of ischemic heart, recanalization
is more challenging in the context of acute ischemic
stroke (AIS), perhaps because thromboemboli in the is-
chemic stroke are often larger, harder, older, more var-
iable in their composition, and, consequently, less
responsive to thrombolytic interventions.59 Also, ves-
sels involved in the stroke are more tortuous, often
transversing through bony cranial foramina, which
can make catheterization mechanically difficult and
time consuming.59 In addition, intracranial hemorrhage
is a more common side effect of thrombolytic therapy in
the very old, who are particularly prone to ischemic
strokes.60
Dissolution of clots can be attempted with the in-
travenous (IV) tissue plasminogen activator (t-PA) in
appropriately selected patients who have symptoms of
ischemic stroke less than 3 hours in duration.9,14,61-63
come for thrombolysis. Stroke onset is defined as the
time the patients symptoms started or the time the
patient was last seen in the normal state of health.9,11
Even within the 3-hour window period, the earlier that
t-PA is administered the greater is the likelihood of a
successful outcome.64 Studies demonstrate that throm-
bolytic intervention with IV t-PA is beneficial and cost

184 Fatahzadeh and Glick
effective for all subtypes of ischemic stroke, because
patients often return home earlier and have less re-
sidual disability.62,65 Recent evidence suggests that
effectiveness of thrombolytic therapy with IV t-PA
may also depend on the genotype of the patient.66
Thrombolytic intervention with IV t-PA appears to
have a low rate of early recanalization.59 Intra-arterial
administration of t-PA, urokinase, and prourokinase
have been attempted to achieve faster and more effec-
tive thrombolysis and neurologic recovery.59,67-68 This
approach appears to shorten the time from onset of
symptoms to arterial recanalization and to achieve a
higher rate of recanalization, posing the same level
of risk for intracerebral hemorrhage reported for IV
t-PA.59 Studies have shown a correlation between initi-
ating intra-arterial thrombolysis within 3 to 4 hours of
symptom onset and higher rates of early recanalization
and more favorable therapeutic outcomes.69-70
Intravenous streptokinase and viprinex, a fibrinolytic
agent derived from the venom of the Malaysian pit vi-
per, have been tested in a number of thrombolytic trials
but with little success.59,71-72 Of the agents described,
only IV t-PA is approved for thrombolytic therapy in
the United States.14,59,71 A frequent and serious adverse
event associated with thrombolysis is intracerebral
hemorrhage, which necessitates a thorough risk-benefit
analysis and careful patient selection.59,73 If thrombo-
lytic therapy is selected, BP should be closely moni-
tored and the use of heparin or aspirin should be
avoided during the first 24 hours.9,74
Exclusion criteria for thrombolysis have been speci-
fied in the literature.9,59,74 They include late thrombo-
lytic intervention beyond three hours window period,
current oral anticoagulation or heparinization within
48 hours with respectively high PTT and INR, thrombo-
cytopenia with platelet count of less than 100,000/mm3,
consistently high pre-treatmet BP readings (systolic
[185 mm Hg or diastolic[110 mm Hg), previous intra-
cerebral bleeding, recent major surgical procedure, on-
set of seizures simultaneous with stroke symptoms,
rapid resolution of neurological impairment and other
contraindications.9,59,74
Currently, less than 5% of patients with AIS receive
thrombolytic therapy with IV t-PA.75-76 Failure to treat
is most often due to the stringent criteria for thrombo-
lytic intervention and patient arrival beyond the 3-hour
window period.62,76 Initiating intra-arterial thromboly-
sis within 6 hours of the ischemic stroke onset may be
attempted for patients who do not meet the criteria for
IV thrombolysisif skilled personnel and equipment
are available.14 Alternatively, these patients may receive
oral aspirin (160-325 mg) soon after the stroke in the
absence of contraindications.1,9,77-78 Administration of
aspirin within the first 48 hours of an ischemic stroke
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August 2006
has been efficacious in preventing recurrent stroke,
death, and disability.1,9,11,77-80
It should be emphasized that currently used inclusion
and exclusion criteria for thrombolytic therapy were
established by the National Institute of Neurological
Disorders and Stroke a decade ago when diagnostic
technology was much less sophisticated.26,75 Even
though guidelines emphasize a time frame of less than
3 hours duration for treatment, other studies have shown
potential benefit from both IV and intra-arterial throm-
bolysis initiated more than 3 hours after the onset of
stroke symptoms.68,81
The role of anticoagulation in the emergency man-
agement of AIS is uncertain.9,11 Emergent full-dose an-
ticoagulation therapy with heparin was commonly used
early after the onset of mild ischemic stroke to prevent
its progression.11,82-84 Heparin administration often
was continued for a few days before substitution with
long-term warfarin or antiplatelet drugs.11 However,
recent studies have revealed no benefit for using early,
full-dose, subcutaneous, low-molecular-weight heparin
over aspirin alone in patients with AF who had suffered
ischemic strokes.34,84 Potential indications for early
heparin administration after AIS may include transient
ischemic attacks in patients with severe CAS or AF
who are scheduled to receive surgical endarterectomy
or oral anticoagulation therapy, respectively.48
Multifaceted interventional strategies aimed at
improving recanalization include administration of
combined IV and intra-arterial t-PA, angioplasty, and
mechanical disruption of the clot using special catheters,
laser, or ultrasound energy.60,85-87 Intra-arterial third-
generation recombinant t-PA and abciximab, a GIIb/
IIIa receptor blocker, as well as their combination, are
examples of newer agents currently under investigation
for IV administration in patients with AIS.88-89
A potential sequela of stroke is loss of cerebral auto-
regulation and a subsequent drop in the perfusion
pressure.9,11,14 Although management of poststroke BP
depends on the stroke etiology,9,14 dehydration and hypo-
tension may exacerbate the infarction and should be pre-
vented.9,11,14 Cerebral nutritive perfusion and neuronal
salvage may be improved by the restoration of blood
flow through thrombolysis and increasing collateral cir-
culation to the ischemic regions.14 In addition, supple-
mental oxygen and hyperventilation may be indicated
for hypoxic patients.9 Cerebral perfusion is also influ-
enced by gravity, which is demonstrated by the exacerba-
tion of neurologic impairments upon standing and clinical
improvement when the stroke victim is supine.14,90 For
optimal outcome, victims of ischemic stroke should be
placed in a horizontal position if ICP is normal.91
Antibiotics, antipyretics, and insulin should be used in
the management of infection, fever, and hyperglycemia,
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Volume 102, Number 2
respectively.9 Hyperglycemia-induced lactic acidosis
may exacerbate cerebral infarction, which emphasizes
the importance of poststroke normoglycemia.92 Fever
negatively impacts stroke outcome, whereas hypother-
mia improves neuronal salvage.93-94
Neuroprotection refers to therapeutic modalities that
improve cerebral tissue tolerance to oxygen deprivation
while definitive measures are taken to curtail ischemic
insult.11 The most effective neuroprotective measure
is applied hypothermia within 2 hours of stroke onset
accompanied by other efforts to correct brain ische-
mia.11,48 Despite positive outcomes in animal studies,
no neuroprotective agents are currently approved for
clinical use.11,95 Other potential neuroprotective agents
currently under study include blockers of excitatory
amino acid pathways, free-radical scavengers, and cyto-
kine inhibitors.9,11,71
COMPLICATIONS
The prevention and management of poststroke com-
plications is critical to overall care of stroke patients.
Neurologic complications include intracranial bleeding,
edema, and poststroke seizures.48 Secondary infections,
deep vein thrombosis (DVT), pulmonary embolism, as-
piration pneumonia, and decubitus ulcers are potential
medical complications.48 Increased ICP secondary to
brain edema or hematoma is a serious stroke-related
sequela.9 Ischemic brain edema develops within the
initial 24 to 48 hours after stroke and may clinically
manifest with altered mental status, asymmetrical pu-
pils, cranial nerve paralysis, papilledema, and episodic
breathing.9,48 Elevated ICP is often fatal in young stroke
victims because of potential cerebral herniation.96
Management approaches for ischemic brain edema in-
clude raising the head of the bed, administering osmotic
diuretics, restricting fluids, hyperventilation, hypother-
mia, and decompression surgery to preserve and in-
crease cerebral perfusion.9,11,48
Ten percent of stroke victims may experience sei-
zures, most often in the context of hemorrhagic stroke
or extensive cortical lesions.9 Anticonvulsants can be
used to control poststroke seizures. Nonambulatory
stroke victims are at risk for DVT.97 Low-dose IVor sub-
cutaneous heparin or heparinoid compounds, external
compression stockings, and early ambulation are effec-
tive strategies for DVT prophylaxis.9,48,83,97 In addition,
bronchiolar atelectasis secondary to prolonged bed
rest, together with the patients inability to protect his
or her airway while feeding, frequently predispose
stroke victims to aspiration pneumonia.14 Oral feeding
should be withheld until the stroke victim has been
evaluated and deemed to be capable of normal swallow-
ing.9 Moreover, the possibility of silent aspiration
Fatahzadeh and Glick 185
pneumonia should be acknowledged and early patient
mobilization encouraged.14
Poststroke sleep-disordered breathing and hypersom-
nia are serious complications of stroke.98 Hypersomnia
often interferes with neurologic recovery and the reha-
bilitation process, exacerbates memory and cognitive
impairment, and reduces the stroke patients overall
quality of life.98-100 Chronic episodic hypoxia and hy-
percapnia secondary to sleep apnea could also lead to
serious sequelae such as pulmonary hypertension and
cor pulmonale.98 Stroke-related central and obstructive
sleep apnea may improve with discontinuation of seda-
tive medications and administration of continuous pos-
itive airway pressure.98 In addition, administration of
a central nervous system stimulant often improves
stroke patients attention to rehabilitative efforts.98
Prolonged bed rest can lead to neurovascular decondi-
tioning,98 which refers to harmful physiologic changes
such as reduced cardiac performance and diminished
postural reflexes that can predispose stroke victims to
cardiac events and orthostasis. Neurovascular decondi-
tioning may be improved by exercising in the supine
position, sitting in a chair several hours at a time, and
performing isometric exercises.98 Periodic arm eleva-
tion, motion exercises, corticosteroid injections, or tak-
ing analgesics may help relieve hemiplegic shoulder
pain, a frequent complication of stroke.98 Poststroke
spasticity may also be reduced by medications, stretch-
ing exercises, and positioning devices.98
Urinary tract infections and constipation are frequent
poststroke complaints, often manageable by discontinu-
ing indwelling catheters and encouraging ambulation to
assist with intestinal motility.9,14
Nearly 20% of stroke victims with left-sided brain
injury have difficulty with speech, comprehension,
reading, and writing.101,102 Temporary or permanent
debilitation in vision, communication, mentation, or
motor function greatly impacts the stroke survivors
independence and psychological well-being.4,103 Unex-
pected physical disability, communication impairment,
and poor self-perception may foster denial, hopeless-
ness, anxiety, and anger before a stroke patient learns
to accept the new limitations.101
Poststroke depression is reported in 50% of stroke
victims and appears to be linked with higher mortal-
ity.101,104 Manifestations of poststroke depression,
such as depressed mood, anxiety, irritability, poor sleep,
lack of drive, social withdrawal, and loss of appetite,
are frequently compounded by a stroke patients com-
munication deficit.98,101,105-106 Timely recognition and
treatment of poststroke depression positively impacts
survival, functional rehabilitation, quality of life, and
the overall cost of care.105 Cognitive functions are
frequently intact in poststroke victims; however,

186 Fatahzadeh and Glick
intellectual deficits have been reported with extensive
left-sided brain infarcts.107 Vascular dementia or the cu-
mulative effect of multiple cerebral infarctions on the
progressive impairment of intellectual capacity account
for 5%-20% of cases of cognitive impairment.40,108
Poststroke sexual difficulties secondary to left hemi-
spheric lesions, loss of drive, depression, concern about
relapse, or even embarrassment with intimacy have been
reported in the literature.109,110 An integral part of a
comprehensive rehabilitation protocol is the evaluation
of poststroke sexual difficulties in an attempt to over-
come any psychologic barriers and improve the stroke
patients quality of life.110
PROGNOSIS
The size and location of the brain lesion determine
stroke outcomes, such as death and disability. The
most significant sequela of stroke is death and nearly
one-third of stroke victims die within 1 year of the
event.1 Important predictors of stroke recurrence and
mortality within 3 years of the initial event include prior
history of TIAs, AF, coronary heart disease, and disabil-
ity at discharge.111 The pathologic type of stroke, as well
as the subtype of ischemic stroke, influence stroke-
related mortality.1,16 The reported mortality rates for
strokes caused by intracerebral hemorrhage, subarach-
noid hemorrhage, and thrombotic vascular blockage
are 80%, 50%, and 30%, respectively.16 In addition,
the poorest survival rate is reported for the cardioem-
bolic subtype of ischemic stroke.33 More than half of
stroke survivors are afflicted with significant temporary
or permanent neurologic impairment.1,112 Although
stroke-related deficits may improve over time, recovery
depends on the nature and extent of the initial deficit and
is not always predictable.113 A significant long-range
goal in medical management involves physical, occupa-
tional, and speech rehabilitation of the stroke victims.
ORAL IMPLICATIONS
The oral manifestations of stroke include loss of
sensation of oral tissues and unilateral paralysis of oro-
facial structures.11,101,114 Impaired movement of oral
structures may manifest as inability to manage oral
secretions, maintain a protective gag reflex, articulate
speech, expectorate, or reproduce a jaw posture neces-
sary for a functional occlusion.101,102,115 More than 50%
of stroke patients suffer from dysphagia, often having
more difficulties managing liquids than solids.101,116
Poststroke swallowing impairment may manifest as
tongue hypermobility, coughing, and choking.101
Dysphagia-related changes in mastication and dietary
habits can potentially lead to poor nutrition, weight loss,
and subsequent problems such as poor fit of oral appli-
ances101,117,118 Oral sensorimotor impairment may
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August 2006
result in pocketing of food and neglect of oral hygiene
on the affected side, both of which predispose patients
to caries, periodontal disease, and halitosis.101,114 The
caries susceptibility is further exacerbated by the xero-
stomia-inducing medications used in the management
of stroke and its sequelae.101,118
Certain medications used in the management of
stroke interfere with hemostasis.114,118 In addition,
disability and neurologic deficits affecting hearing,
vision, speech, and memory frequently lead to difficulty
with communication and follow-up with dental instruc-
tions.101,114 Poststroke depression and lack of motiva-
tion often result in failure of patients to keep their
appointments, appreciate treatment objectives, or com-
ply with recommendations.101
Some studies suggest a possible association between
chronic inflammatory periodontal disease and the inci-
dence of cerebrovascular events119-121 Although the
precise mechanisms of this interaction are not fully un-
derstood, periodontal pathogens and systemic immu-
noinflammatory processes have been implicated in the
initiation or progression of atherosclerosis and ulti-
mately susceptibility to stroke.119-121 Though advocated
by some investigators, the contribution of prevention or
aggressive treatment of periodontal infections to reduc-
tion in the risk of stroke remains controversial.122
DENTAL MANAGEMENT
In general, a standard evidence-based protocol for
dental management of stroke patients is not available,
and current recommendations are based primarily on
intuitive extrapolations from the medical literature.
Major issues to be considered when treating patients
at risk for or after a stroke include screening for risk
factors, hemostasis, drug actions and interactions,
stress induced by the dental care, empathetic approach
by the dental staff, and individualized oral care
programs.
Dentists see their patients regularly and are in a key
position to contribute to stroke prevention through iden-
tification of susceptible patients and education aimed at
modification of risk factors, as well as medical referral
for further evaluation. Calcified atherosclerotic lesions
at the common carotid bifurcation are occasionally
detected on panoramic dental radiographs in neurologi-
cally asymptomatic patients.123,124 Some investigators
have suggested that these calcifications are markers of
advanced extracranial carotid disease and subsequent
risk for ischemic cerebrovascular events.123-127 Al-
though the significance of carotid calcified atheromas
visible on panoramic radiographs is controversial, den-
tal professionals should understand the epidemiology
and pathogenesis of carotid calcifications, differentiate
them from other potential anatomical and pathological
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Volume 102, Number 2
radiopacities in the region of the carotid artery, and refer
patients for follow-up as needed.123,124
Dental professionals should also be able to recognize
signs and symptoms of stroke and appropriately manage
an emergency in the dental office. In general, mainte-
nance of patient in the supine position, administration
of oxygen, monitoring of vital signs, activation of emer-
gency medical support, and prompt transportation to an
emergency facility are essential for timely and effective
medical interventions. In addition, dental professionals
should accurately describe the patients signs and symp-
toms and the precise time of onset to the emergency
personnel.
The initial evaluation of the dental patient with a his-
tory of cerebrovascular disease should include deter-
mination of the specific diagnosis, date of the event,
current status, medical management, and any residual
disability.101 The risk of recurrent stroke in a patient
with a history of stroke or TIAs is greater than the risk
of the first stroke in a person with no prior cerebrovascular
event.11,16,128 The risk of recurrence is highest soon after
the initial event, but it may remain elevated for several
years.129 The presence of TIAs before or after an acute
stroke predicts early recurrence within the first 90
days,130 and up to 30% of ischemic recurrences are re-
ported to occur within 1 month of the first stroke.41,128,131
Extrapolating from this type of data, some authors recom-
mend a cautious approach by deferring the elective dental
care for the first 6 months following a stroke and in pa-
tients experiencing TIAs or RINDs.114
Therapeutic administration of single/combination
antiplatelet agents or subcutaneous low molecular
weight heparin is usually not clinically significant, nec-
essitating little modification to the dental protocol.132,133
However, a preoperative assessment of hemostasis
prior to invasive oral procedures should be undertaken
in patients taking oral anticoagulants. The risk of a throm-
boembolic event caused by the interruption of oral antico-
agulants and subtherapeutic international normalized
ratio (INR) frequently outweighs the benefits of postoper-
ative hemostasis in a patient undergoing uncomplicated
oral surgery.134,135 Local measures such as atraumatic
surgical techniques, pressure, gelfoam, suturing, electro-
cautery, and topical hemostatic agents are often sufficient
for control of excess bleeding136 and usually negate the
need for reduction in dose or interruption of anticoagula-
tion when INR is \3.5. For complicated oral surgery,
however, consultation with the physician is recommen-
ded if INR is [3.5 or if the patient is on intravenous
heparin.
Aspirin and other nonsteroidal antiinflammatory
agents may increase postoperative bleeding in patients
taking oral anticoagulants.137,138 Acetaminophen-con-
taining products, cyclooxygenase-2especific inhibitors,
Fatahzadeh and Glick 187
opioids, and related analgesics may be considered as
suitable substitutes.137,139,140 Potential interactions be-
tween prescribed dental medications and oral anticoag-
ulants are also a concern. For instance, metronidazole
and erythromycin as well as tetracycline may increase
INR by inhibiting metabolism of coumadin as well as re-
ducing prothrombin activity, respectively.141-144 These
interactions require the clinician to avoid concurrent
administration of metronidazole or erythromycin with
oral anticoagulants and closely monitor INR when the
patient is taking both coumadin and tetracycline.141
Alleviation of stress before and during dental treat-
ment may be accomplished by N2O-O2 inhalation seda-
tion and/or premedication with oral anxiolytics as well
as profound anesthesia and short dental appoint-
ments.145 Pre- and intraoperative vital signs should
also be monitored and recorded. In addition, the use of
rubber dam, effective oral evacuation, and facilitative
head positioning alleviate patients fear of choking
and reduce the risk of aspiration.101 Though many
stroke victims are adequately managed in an outpatient
environment, some may require airway protection
through intubation in the operating room.
Dental staff should demonstrate an empathetic and
supportive approach in understanding the patients
physical and emotional limitations and allocate extra
time for communication and clinical procedures.102,114
Hemiplegic stroke victims may require assistance
while walking or transfering to and from the dental
chair.101,114 Oral hygiene aids and instructions should
be individualized based on the patients ability to per-
form effective oral care.114 Recommendations and treat-
ment goals should be realistic and modifiable, have
clearly defined steps, and involve the personal care
givers as necessary.101,114 Prevention of oral disease
caused by xerostomia, dietary changes, and ineffective
oral hygiene may be accomplished by reinforcing oral
care practices, topical application of fluoride, daily
rinses with chlorhexidine, and frequent recalls.101,114
Oral rehabilitation with fixed dental prostheses having
easily cleansed embrasures is generally preferable
owing to the inconvenience of daily placement and
removal of removable appliances for stroke patients.114
However, edentulous stroke patients with dentures
should be instructed to wear their removable prostheses
in order to preserve oral stereognosis.146 In addition, to
reduce attrition and wear of the opposing dentition in
patients with stroke-related oral parafunction, fixed or
removable prostheses with porcelain occlusion are to
be avoided.114
CONCLUSION
Cerebrovascular disease is the third leading cause of
death and a major cause of long-term disability in the

188 Fatahzadeh and Glick
United States. This article provides the dental commu-
nity with an up-to-date understanding of the relevant
issues pertaining to stroke. Dental management of
stroke patients is relatively straight forward. Major issues
of concern in dental management include screening
for risk factors, hemostasis, drug actions and interactions,
stress induced by the dental care, empathetic approach by
the dental staff, and individualized oral care programs.
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Reprint requests:
Dr Mahnaz Fatahzadeh, DMD
Division of Oral Medicine
Department of Diagnostic Sciences
New Jersey Dental School
University of Medicine & Dentistry of New Jersey
110 Bergen Street
Newark, NJ 07103
fatahza@umdnj.edu