Vol. 102 No.

August 2006

ORAL MEDICINE

Editor: Martin S. Greenberg

Stroke: epidemiology, classication, 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 decits 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, classication, 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 attack refers to an acute onset of neurologic decit 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 computes 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 expected 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 signicance 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.

Assistant Professor, Division of Oral Medicine. 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

PATHOGENESIS AND CLASSIFICATION The underlying pathogenic mechanism for cerebrovascular accidents is the interruption of blood ow 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 ow to 25 mL/100 g/min leads to neuronal ischemia, energy failure, and neurologic symptoms, followed by irreversible tissue damage within minutes should ischemia continue.11,14,15 Four neurologic phenomena have been dened for stroke based on their duration: transient ischemic attacks (TIAs), reversible ischemic neurologic defect (RIND), stroke in evolution, and completed stroke. A TIA is a sudden, short-lasting, focal neurologic decit or mini stroke caused by transient and localized brain ischemia.11 These neurologic decits 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 dened as strokeassociated symptoms that progressively worsen over time.11,16 In contrast, neurologic signs and symptoms that have been stable for more than 24 hours dene a completed stroke.11 Strokes are subclassied into ischemic and hemorrhagic types, based on the underlying pathogenesis.11 Eighty-ve percent of strokes are ischemic in nature and involve the occlusion of a cerebral vessel with subsequent brain ischemia and infarction distal to the site of

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obstruction, which may be caused by either athersclerotic thrombi or distant emboli.11,14,17 Embolic strokes are classied into arterial, cardioembolic, and cryptogenic subtypes, depending on the site of embolic origin.11 Common sources of cerebral embolism include atherothrombi in the carotid bifurcation or aortic arch, cardiac disease, and spontaneous thrombosis in hypercoagulable conditions.11,17 Multiple septic cerebral emboli may also arise from valvular vegetations in bacterial endocarditis.11,17 Diagnosing the exact source of embolism may be challenging, but this information 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, multifocal, and maximal neurologic decits 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 factors for lacunar strokes include aging and uncontrolled hypertension.11 In contrast, large-vessel stroke is characterized by extensive cerebral infarction and results from thrombotic occlusion of a major intracranial vessel.14 Frequently, high-level brain functions are affected and prognosis is poor.14 Brainstem stroke, the third ischemic stroke syndrome, may result from the occlusion of either small or large cerebral vessels and has a variable 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 twothirds 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 rst in the post-stroke cascade of events.1 The site, size, and duration of occlusion or hemorrhage, presence or absence

of collateral circulation, blood pressure (BP), and body temperature are factors that affect the nal 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, altered 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 decits typical of ischemia are less frequent, with hemorrhagic strokes.9,11 DIAGNOSIS AND LABORATORY TESTING Application of effective preventive and therapeutic interventions requires a precise knowledge of underlying stroke mechanism.14 Many other conditions can resemble the features of stroke and confound the diagnostic process. Focal neurologic decits 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 extensive 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 suggestive of stroke. Factors critical to the diagnostic process include patient age, medical history, clinical presentation, the temporal prole of the event, location of the infarct, stroke subtype, and specic etiology.9 Clinical examination should be thorough and focused on the heart, retinas, and peripheral vascular system.11 Vascular testing such as cerebral angiography or Doppler ultrasonography will often shed light on the nature, location, and severity of vascular lesions in signicant 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, erythrocyte sedimentation rate, screening for hypercoagulability, serologic tests for syphilis, blood sugar, cholesterol, and lipid levels.4,11 Lumbar puncture may assist in the exclusion of subarachnoid hemorrhage or meningitis as

182 Fatahzadeh and Glick the underlying cause.11 Blood cultures and echocardiography are indicated if septic emboli secondary to infective endocarditis is suspected.17 History and clinical examination cannot reliably rule out hemorrhagic stroke, a distinction necessary before 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 T2weighed 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 Paradoxically, 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 addition, brain and vascular imaging may be efciently obtained by magnetic resonance angiography and perfusion CT.24,30 Moreover, transthoracic or transesophageal echocardiography can be used to identify potential cardiac sources of embolism.31 RISK FACTORS AND PREVENTION Management of the stroke patient starts with prevention. Strategies to reduce stroke-related death and disability signicantly impact public health.7,11 Epidemiologic studies have identied many predisposing factors associated with stroke, and primary prevention focuses on the modication of those risk factors in the general population.7 Nonmodiable risk factors include advanced age, male gender, nonwhite race, and hereditary predisposition.3,32 Incidence of stroke increases with age.11 Specically, 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 cerebrovascular events.4,7,11 Initiating life-style modications such

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as a healthier diet, greater physical activity, smoking cessation, moderating intake of alcohol, and stress reduction are the core requirements for primary stroke prevention.7,32 Screening for comorbidities such as hypertension (HTN), MI, atrial brillation (AF), congestive 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 rst stroke is controversial.3,32 Nevertheless, administration of antiplatelet or anticoagulation agents are potential strategies for the prevention of cardioembolic stroke in those with AF.3,11,17,18,32,36 Prophylactic anticoagulation is also indicated for patients with MI, mechanical heart valves, and CHF who are at risk for thromboembolism.17,37 Routine anticoagulation, however, 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 anticoagulation, HTN, and older age increase the risk of this complication, highlighting the importance of patient selection.17 Carotid endarterectomy is a well established preventive strategy against cerebrovascular disease.11 Asymptomatic 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 dened as symptomatic.11 The preventive approach for patients with asymptomatic carotid disease remains controversial.3,11,32 In general, aspirin therapy and risk-factor modication are the recommended approaches for patients with asymptomatic carotid disease.11 Stroke recurrence is a signicant 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 subsequent stroke and up to a third of recurrences occur within 1 month of the initial event.11,41 Understanding the underlying mechanism for the rst stroke and identifying modiable risk factors in the target population are critical to secondary stroke prevention.9 Risk-factor modication has a more direct effect on the prevention of the rst stroke than on recurrent strokes.3 Nevertheless, risk-factor modication should be part of a comprehensive 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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Oral anticoagulation therapy with warfarin is a well established strategy in the prevention of recurrent ischemic stroke in patients with AF and offers a denite advantage over aspirin therapy.32,44-47 Warfarin therapy also benets patients with other potential cardiac sources of embolism, such as mechanical valve or left ventricular aneurysm.48 In patients with extensive brain lesions, oral anticoagulants are typically withheld during the period immediately following an ischemic stroke to reduce the risk of hemorrhagic transformation.48,49 In general, however, the benets 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 without a cardiogenic source.3,11,32,48 A potential drawback associated with antiplatelet therapy is breakthrough CVA or stroke recurrence while on antiplatelet therapy.1 Individuals taking antiplatelet medications demonstrate 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 gastrointestinal bleeding or ticlopidine-induced agranulocytosis 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 asymptomatic patients.52,53 Signicant reduction in the risk of recurrent stroke has been reported with surgical intervention 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 should be educated about the symptoms of stroke, potential complications, prevention measures, and the absolute 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 benets of medical and rehabilitative options, individualize therapy, prevent potential

complications, and attempt to minimize stroke recurrence.56 In general, stroke victims are most effectively managed in stroke centers equipped with advanced technology 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 hospital wards.56-58 Immediate poststroke interventions focus 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 elevated intracranial pressure (ICP).11,48,58 Stroke victims are also closely monitored for signs and symptoms of neurologic deterioration indicative of intracerebral hemorrhage.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 hemorrhage, 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 established, 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 ischemic stroke are often larger, harder, older, more variable in their composition, and, consequently, less responsive to thrombolytic interventions.59 Also, vessels involved in the stroke are more tortuous, often transversing through bony cranial foramina, which can make catheterization mechanically difcult 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 intravenous (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 The time of stroke onset is critical to an optimal outcome for thrombolysis. Stroke onset is dened 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 thrombolytic intervention with IV t-PA is benecial and cost

184 Fatahzadeh and Glick effective for all subtypes of ischemic stroke, because patients often return home earlier and have less residual 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 effective 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 initiating 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 brinolytic agent derived from the venom of the Malaysian pit viper, 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-benet analysis and careful patient selection.59,73 If thrombolytic therapy is selected, BP should be closely monitored and the use of heparin or aspirin should be avoided during the rst 24 hours.9,74 Exclusion criteria for thrombolysis have been specied in the literature.9,59,74 They include late thrombolytic intervention beyond three hours window period, current oral anticoagulation or heparinization within 48 hours with respectively high PTT and INR, thrombocytopenia 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 intracerebral bleeding, recent major surgical procedure, onset 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 thrombolytic intervention and patient arrival beyond the 3-hour window period.62,76 Initiating intra-arterial thrombolysis 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 rst 48 hours of an ischemic stroke

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has been efcacious 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 benet from both IV and intra-arterial thrombolysis initiated more than 3 hours after the onset of stroke symptoms.68,81 The role of anticoagulation in the emergency management of AIS is uncertain.9,11 Emergent full-dose anticoagulation 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 benet 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 thirdgeneration 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 autoregulation 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 hypotension may exacerbate the infarction and should be prevented.9,11,14 Cerebral nutritive perfusion and neuronal salvage may be improved by the restoration of blood ow through thrombolysis and increasing collateral circulation to the ischemic regions.14 In addition, supplemental oxygen and hyperventilation may be indicated for hypoxic patients.9 Cerebral perfusion is also inuenced by gravity, which is demonstrated by the exacerbation 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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respectively.9 Hyperglycemia-induced lactic acidosis may exacerbate cerebral infarction, which emphasizes the importance of poststroke normoglycemia.92 Fever negatively impacts stroke outcome, whereas hypothermia improves neuronal salvage.93-94 Neuroprotection refers to therapeutic modalities that improve cerebral tissue tolerance to oxygen deprivation while denitive 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 ischemia.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 cytokine inhibitors.9,11,71

COMPLICATIONS The prevention and management of poststroke complications 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, aspiration 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 pupils, 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 include raising the head of the bed, administering osmotic diuretics, restricting uids, hyperventilation, hypothermia, and decompression surgery to preserve and increase cerebral perfusion.9,11,48 Ten percent of stroke victims may experience seizures, 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 subcutaneous heparin or heparinoid compounds, external compression stockings, and early ambulation are effective 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 swallowing.9 Moreover, the possibility of silent aspiration

pneumonia should be acknowledged and early patient mobilization encouraged.14 Poststroke sleep-disordered breathing and hypersomnia are serious complications of stroke.98 Hypersomnia often interferes with neurologic recovery and the rehabilitation process, exacerbates memory and cognitive impairment, and reduces the stroke patients overall quality of life.98-100 Chronic episodic hypoxia and hypercapnia 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 sedative medications and administration of continuous positive 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 deconditioning,98 which refers to harmful physiologic changes such as reduced cardiac performance and diminished postural reexes that can predispose stroke victims to cardiac events and orthostasis. Neurovascular deconditioning 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 elevation, motion exercises, corticosteroid injections, or taking analgesics may help relieve hemiplegic shoulder pain, a frequent complication of stroke.98 Poststroke spasticity may also be reduced by medications, stretching exercises, and positioning devices.98 Urinary tract infections and constipation are frequent poststroke complaints, often manageable by discontinuing indwelling catheters and encouraging ambulation to assist with intestinal motility.9,14 Nearly 20% of stroke victims with left-sided brain injury have difculty 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 Unexpected physical disability, communication impairment, and poor self-perception may foster denial, hopelessness, 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 mortality.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 communication decit.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 decits have been reported with extensive left-sided brain infarcts.107 Vascular dementia or the cumulative 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 difculties secondary to left hemispheric 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 difculties in an attempt to overcome 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 signicant 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 disability at discharge.111 The pathologic type of stroke, as well as the subtype of ischemic stroke, inuence strokerelated mortality.1,16 The reported mortality rates for strokes caused by intracerebral hemorrhage, subarachnoid hemorrhage, and thrombotic vascular blockage are 80%, 50%, and 30%, respectively.16 In addition, the poorest survival rate is reported for the cardioembolic subtype of ischemic stroke.33 More than half of stroke survivors are aficted with signicant temporary or permanent neurologic impairment.1,112 Although stroke-related decits may improve over time, recovery depends on the nature and extent of the initial decit and is not always predictable.113 A signicant long-range goal in medical management involves physical, occupational, 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 orofacial structures.11,101,114 Impaired movement of oral structures may manifest as inability to manage oral secretions, maintain a protective gag reex, articulate speech, expectorate, or reproduce a jaw posture necessary for a functional occlusion.101,102,115 More than 50% of stroke patients suffer from dysphagia, often having more difculties 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 t of oral appliances101,117,118 Oral sensorimotor impairment may

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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 xerostomia-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 decits affecting hearing, vision, speech, and memory frequently lead to difculty with communication and follow-up with dental instructions.101,114 Poststroke depression and lack of motivation often result in failure of patients to keep their appointments, appreciate treatment objectives, or comply with recommendations.101 Some studies suggest a possible association between chronic inammatory periodontal disease and the incidence of cerebrovascular events119-121 Although the precise mechanisms of this interaction are not fully understood, periodontal pathogens and systemic immunoinammatory processes have been implicated in the initiation or progression of atherosclerosis and ultimately susceptibility to stroke.119-121 Though advocated by some investigators, the contribution of prevention or aggressive treatment of periodontal infections to reduction 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 identication of susceptible patients and education aimed at modication of risk factors, as well as medical referral for further evaluation. Calcied atherosclerotic lesions at the common carotid bifurcation are occasionally detected on panoramic dental radiographs in neurologically asymptomatic patients.123,124 Some investigators have suggested that these calcications are markers of advanced extracranial carotid disease and subsequent risk for ischemic cerebrovascular events.123-127 Although the signicance of carotid calcied atheromas visible on panoramic radiographs is controversial, dental professionals should understand the epidemiology and pathogenesis of carotid calcications, differentiate them from other potential anatomical and pathological

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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 ofce. In general, maintenance of patient in the supine position, administration of oxygen, monitoring of vital signs, activation of emergency 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 symptoms and the precise time of onset to the emergency personnel. The initial evaluation of the dental patient with a history of cerebrovascular disease should include determination of the specic 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 rst 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 rst 90 days,130 and up to 30% of ischemic recurrences are reported to occur within 1 month of the rst stroke.41,128,131 Extrapolating from this type of data, some authors recommend a cautious approach by deferring the elective dental care for the rst 6 months following a stroke and in patients experiencing TIAs or RINDs.114 Therapeutic administration of single/combination antiplatelet agents or subcutaneous low molecular weight heparin is usually not clinically signicant, necessitating little modication 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 thromboembolic event caused by the interruption of oral anticoagulants and subtherapeutic international normalized ratio (INR) frequently outweighs the benets of postoperative hemostasis in a patient undergoing uncomplicated oral surgery.134,135 Local measures such as atraumatic surgical techniques, pressure, gelfoam, suturing, electrocautery, and topical hemostatic agents are often sufcient for control of excess bleeding136 and usually negate the need for reduction in dose or interruption of anticoagulation when INR is \3.5. For complicated oral surgery, however, consultation with the physician is recommended if INR is [3.5 or if the patient is on intravenous heparin. Aspirin and other nonsteroidal antiinammatory agents may increase postoperative bleeding in patients taking oral anticoagulants.137,138 Acetaminophen-containing products, cyclooxygenase-2especic inhibitors,

opioids, and related analgesics may be considered as suitable substitutes.137,139,140 Potential interactions between prescribed dental medications and oral anticoagulants are also a concern. For instance, metronidazole and erythromycin as well as tetracycline may increase INR by inhibiting metabolism of coumadin as well as reducing 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 treatment may be accomplished by N2O-O2 inhalation sedation and/or premedication with oral anxiolytics as well as profound anesthesia and short dental appointments.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 perform effective oral care.114 Recommendations and treatment goals should be realistic and modiable, have clearly dened 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 uoride, daily rinses with chlorhexidine, and frequent recalls.101,114 Oral rehabilitation with xed 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, xed 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 community 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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