Managing Older Patients Who Have Neurologic Disease: Alzheimer Disease and Cerebrovascular Accident

Neurologic diseases represent some of the most common disabling and costly conditions in older age. Alzheimer disease and cerebrovascular accidents (strokes) are two of the most common neurologic conditions, and represent the leading causes of nursing home placement. Dental professionals will be caring for older patients who have age-associated neurologic diseases, including Alzheimer disease and stroke because of the increased longevity of the United States population coupled with improved survivorship of these conditions as a result of advanced medical diagnosis and treatment. Understanding the clinical manifestations of these two common, but distinctly different, neurologic conditions will enable dental professionals to provide safe and rational dental care.

Neurologic diseases/conditions in older age can be classified into three primary categories. The first, degenerative disorders, implies some type of degeneration in the central nervous system or an accelerated aging process. Alzheimer disease (AD) is the most prevalent example of this type of disorder. The second category encompasses structural abnormalities in the brain or central nervous system, such as brain tumors, which may lead to seizures and may occur at any age. However, tumors that occur in the elderly have different implications, manifestations, treatment, and prognosis. The third category is cerebrovascular disorders. These disorders occur with greater frequency in older age and are associated with risk factors such as hypertension and atherosclerosis. Cerebrovascular accidents (CVA), or strokes, would represent this type of neurologic condition.

In contrast to these three categories, several neurologic conditions are not characteristic in the elderly. Conditions including epilepsy, the muscular dystrophies, demyelinating conditions such as multiple sclerosis, and migraine generally occur at young or middle ages. These patients live into older age with “acquired” disabilities. More and more elderly patients who have primary or acquired neurologic conditions are being seen today in dental offices because effective interventions and therapies for treating these diseases/conditions are adding years to life. This article reviews the two most common neurologic diseases affecting the elderly, AD and stroke, focusing on oral and dental concerns and providing suggestions for dental personnel to manage patients who have these conditions.

Alzheimer disease

Definition and Cause of Alzheimer Disease

AD is the most common form of dementia, which is the loss of intellectual and social abilities severe enough to interfere with daily functioning. AD is a progressive, degenerative disease that attacks the brain and results in impaired memory, thinking, and behavior It typically occurs after age 65 with prevalence increasing with advanced age. From age 70, prevalence doubles every 5 years. By age 85, more than 40% of individuals will have developed AD. Although an estimated 5.2 million people in the United States have AD, the prevalence is predicted to triple by the year 2050. An average dental practice of 2000 adult patients is predicted to include about 46 patients who have AD.

The cause of AD is unknown, although the following have been shown to be associated risk factors: advanced age (85+), having trisomy 21 (Down’s syndrome), a history of severe head trauma, or having a first-degree relative who has the disorder. Recent findings suggest that unidentified factors trigger the deposition of beta-amyloid plaques, initiating an inflammatory response that results in neurofibrillary tangles and the loss of cortical neurons. This process begins in the hippocampus and entorhinal cortex and spreads to the areas in the brain responsible for memory and learning (the temporal, parietal, and frontal lobes). Eventually, continued destruction of neurons leads to atrophy of the cerebral cortex and enlargement of the ventricles. However, motor, visual, and somatosensory portions of the cerebral cortex generally remain intact.

Genetic predisposition, known as familial Alzheimer disease, contributes less than 20% of all cases. Numerous environmental factors, such as aluminum, mercury, and viruses have been proposed as causes of AD but none have been proved as causative factors. Risk factors for AD are seen in Box 1 .

Box 1

  • Advanced age (the older the person, the greater the risk)

  • Genes: families with history of AD

    • Distributed according to autosomal-dominant gene

    • Early-onset familial AD involves mutation in at least three genes on chromosomes 14, 1, 21 (20%)

    • Strong relationship between gene for apolipoprotein E (APOE) on chromosome 19 and sporadic and familial late-onset Alzheimer disease

    • Persons homozygous for APOE 4 allele have 10 times the risk for AD

    • Persons heterozygous for APOE 4 allele have 4 times the risk for AD

  • Trisomy 21 (Down syndrome) family history (increases risk for AD 2–3 times)

    • Down syndrome gene and AD gene are associated with chromosome 21

  • Head injury or trauma

  • Limited education or limited linguistic ability early in life

  • Gender predilection (controversial): greater prevalence of AD in women may be attributed to increase in survivorship of women into older age

Data from Refs.

Risk factors for Alzheimer disease

Mild cognitive impairment is the decline in memory function that may occur in normal aging, or be a precursor to AD. The focus of studies on mild cognitive impairment is to discover factors that may decrease the risk for AD. Current findings are listed in Box 2 . Further research is needed to determine the importance of each in controlling/preventing AD.

Box 2

  • Genes: presence of ApoE2/ApoE2 genotype

  • Attainment of higher educational levels

  • Moderate (no more than two glasses/day) red wine consumption

  • Regular exercise

  • Good control of high blood pressure

  • Medications (under investigation):

    • Use of statins (for cholesterol)

    • Use of anti-inflammatory medications (nonsteroidal anti-inflammatory agents)

    • Use of histamine (H2) blockers

    • Use of antioxidants (vitamin E and selegiline) (may actually decrease the progression of AD if given in high doses)

    • Ginkgo (extract believed to have antioxidant properties): remains unclear

    • Estrogen

Data from Refs.

Factors that decrease the risk for Alzheimer disease

Dementia and Alzheimer Disease

Dementia is the loss of intellectual functions (such as thinking, remembering, and reasoning) to such an extent that it interferes with a person’s daily life and activities. Dementia is not a disease in itself, but a group of symptoms that often accompanies a disease or condition. More than 70 different diseases or conditions can cause dementia, some of which are treatable, whereas others are less responsive or not possible to treat. Table 1 lists causes of dementias, including those that are less responsive to treatment or are incurable.

Table 1
Meta-analysis of dementia causes: 1987–2002
Alzheimer disease 56.3%
Vascular dementias (multi-infarct dementia/strokes) 20.3%
Mixed 6.2%
Infectious 0.3%
Metabolic 1.1%
Tumor 0.9%
Normal pressure hydrocephaly 1.0%
Subdural hematoma 0.3%
Depression 0.9%
Medications 0.1%
Trauma 0.2%
Anoxic 0.2%
Huntington’s 0.1%
Parkinson’s 1.6%
Alcohol 0.6%
Miscellaneous 7.6%

Data from Clarfied A. The degreasing prevalence of reversible dementia: an updated meta-analysis. Arch Intern Med 2003;163:2219.

AD is the most prevalent form of dementia and is considered progressive and incurable. The cost of caring for a person who has AD either at home or in a skilled nursing facility was estimated to be $47,000 per year in 1996 and is estimated to have risen to $75,000 per year in 2002. The total cost to society at present is estimated at $100 billion, ranking behind heart disease ($183 billion) and cancer ($109) as the third costliest disease in the United States.

The human costs of caring for patients who have AD (and dementias) are incalculable and include the burdens born by family members who act as the primary caregivers and health care personnel (nurses and nursing assistants/licensed practical nurses) who provide daily care such as cleaning the oral cavity and teeth. Emotional burdens are often overwhelming for family members who struggle with symptoms of a loved one (patient) for a disease that has no cure and becomes progressively worse. The Alzheimer Association ( www.alz.org ) estimates that for every person who has AD, at least two to three family members see their lives significantly affected by caring for that individual.

Clinical Signs and Symptoms

The clinical course of AD can be divided into three stages. The early stage usually begins subtly, with the first sign generally being recent memory loss. To many older adults, this occurrence is frightening, because they may feel they are experiencing symptoms of AD. However, normal aging changes can also lead to recent memory loss (benign senescence) and may not be a sign of AD. In AD, however, memory problems increase, ultimately interfering with a person’s ability to keep up with daily activities such as balancing a checkbook or finances, finding his/her way around, or remembering where he/she put things. Other signs of AD in the early stage include a gradual and steady deterioration in the ability to remember names, recent events, and conversations; misplacing items; missing appointments; and repeating questions or answers during conversations. In this stage, the person prefers familiarity and can be easily upset when confronted with new situations. Family members, relatives, or coworkers may report strange behaviors (eg, getting lost on the way home or to work), which may be accompanied by the onset of emotional outbursts when confronted. Some patients remain unaware of these problems, and others are aware of them and become frustrated and anxious.

The middle, or moderate, stage may occur within a few months or years. In this stage, the person is unable to work, becomes easily lost and confused, and has lost the ability to care for him/herself. Patients become agitated easily and have disturbances in language use, learning skills, judgment, and decision making. Although they remain ambulatory, they are at significant risk for falls or accidents secondary to confusion. Behavioral problems include agitation, hostility, uncooperativeness, or physical aggressiveness. During this stage, the patient has lost all sense of time and place and begins to have perceptual problems (may not recognize his/her own face in a mirror).

The late, or severe, stage finds the patient profoundly apathetic, disoriented, incontinent, and totally dependent. Recent and remote memory are completely lost. Aggressiveness and anxious behavior are common, and a typical behavioral complication is for patients to reach and grasp objects that are close by. Patients in this stage are at risk for pneumonia, malnutrition, aspiration, and pressure necrosis of the skin. The progression of the disease is gradual, with some patient’s symptoms seeming to plateau for a time. The end stage is coma and death.

Diagnosing Alzheimer disease

Definitive diagnosis of AD is determined by autopsy confirmation of changes in the brain. Microscopic features include cerebral cortical atrophy and ventricular enlargement, and microscopic features include cerebral cortical atrophy and ventricular enlargement of the microscopic features, inluding neurofibrillary tangles and neuritic plaques containing beta-amyloid in abnormally high proportions for a normal aging brain. However, clinical diagnosis of AD can be made with more than 90% accuracy based on patient history and clinical findings alone. The patient and family must be questioned, with a thorough history to establish if the patient demonstrates any sign or symptom of dementia. A thorough history can identify other causes of dementia that are not AD and may be treatable, including infections, injuries, anoxia, cardiovascular problems, alcohol abuse, illegal drugs, or prescription medications. Diagnosis of probable AD is given based on meeting six criteria:

  • Dementia established by clinical examination and documented with testing

  • Deficits in two or more areas of cognition

  • Progressive worsening of memory and other cognitive functions

  • No disturbance of consciousness

  • Onset between ages 40 and 90

  • Absence of systemic disorders or other brain diseases that could account for the progressive memory and cognitive changes

Essentially, the clinical diagnosis of AD is one by exclusion following a complete assessment, including a health history and physical examination, neurologic and mental status assessments (such as the Mini-Mental State Examination), and other diagnostic tests including blood studies, urinalysis, ECG, chest radiographs, CT scan, electroencephalograms, medication removal, and sometimes spinal tap. If all tests are considered normal, and the six criteria for probable AD are met, then the clinical diagnosis of AD is given.

Diagnosing Alzheimer disease

Definitive diagnosis of AD is determined by autopsy confirmation of changes in the brain. Microscopic features include cerebral cortical atrophy and ventricular enlargement, and microscopic features include cerebral cortical atrophy and ventricular enlargement of the microscopic features, inluding neurofibrillary tangles and neuritic plaques containing beta-amyloid in abnormally high proportions for a normal aging brain. However, clinical diagnosis of AD can be made with more than 90% accuracy based on patient history and clinical findings alone. The patient and family must be questioned, with a thorough history to establish if the patient demonstrates any sign or symptom of dementia. A thorough history can identify other causes of dementia that are not AD and may be treatable, including infections, injuries, anoxia, cardiovascular problems, alcohol abuse, illegal drugs, or prescription medications. Diagnosis of probable AD is given based on meeting six criteria:

  • Dementia established by clinical examination and documented with testing

  • Deficits in two or more areas of cognition

  • Progressive worsening of memory and other cognitive functions

  • No disturbance of consciousness

  • Onset between ages 40 and 90

  • Absence of systemic disorders or other brain diseases that could account for the progressive memory and cognitive changes

Essentially, the clinical diagnosis of AD is one by exclusion following a complete assessment, including a health history and physical examination, neurologic and mental status assessments (such as the Mini-Mental State Examination), and other diagnostic tests including blood studies, urinalysis, ECG, chest radiographs, CT scan, electroencephalograms, medication removal, and sometimes spinal tap. If all tests are considered normal, and the six criteria for probable AD are met, then the clinical diagnosis of AD is given.

Medical management of patients who have Alzheimer disease

No definitive treatment of AD exists, although drugs have been developed recently that can reduce or delay certain symptoms of AD. Cholinesterase inhibitors (donepezil/Aricept, tacrine/Cognex, rivastigmine/Exelon, galantamine/Reminyl) are drugs that inhibit the enzyme acetyl cholinesterase from degrading acetylcholine (a key neurotransmitter between neurons). Using these agents has resulted in short-term (1–5 years) cognitive improvement (especially in memory and attention) and improvement in daily function and behavior in some patients who have mild-to-moderate AD. Unfortunately, fewer than 50% of patients who have AD who are prescribed these drugs appear to benefit from their use. Side effects are dose related and may include nausea, vomiting, diarrhea, anorexia, weight loss, muscle cramps, bradycardia, heart block, syncope, and fatigue. The first drug developed in this class (Tacrine/Cognex) is infrequently prescribed today because it requires frequent dosing and can be hepatoxic.

Only one medication, memantine (Axura) has been approved by the Food and Drug Administration to manage symptoms of people who have moderate-to-severe AD. Memantine (an N-Methyl-D-Aspartate receptor antagonist) prevents elevated concentrations of glutamate, the principal excitatory neurotransmitter in the central nervous system, from destroying cholinergic neurons. Studies suggest that memantine may preserve or improve memory and learning. When given with cholinesterase inhibitors, memantine appears not only to improve cognitive function but also to reduce the person’s decline in activities of daily living (dressing, bathing, and so forth) and reduce the frequency of new behavioral symptoms. Adverse effects of memantine include dizziness, headaches, hypertension, and confusion. No information suggests that any special precautions are required when using local anesthetics with a vasoconstrictor for any of the cholinesterase inhibitors or memantine.

Vitamin E is often added as another AD-specific treatment for its antioxidant effect and role in neuroprotection. One study suggested that vitamin E delayed the development of severe dementia, placement in a nursing home, and death.

Symptom-specific medications are used when behavioral approaches such as providing a predictable routine, modifying the environment, and simplifying tasks, fail. For anxiety, depression, irritability, and sleep disturbances, medications such as short-acting benzodiazepines (eg, lorazepam/Ativan), antidepressants (eg, tricyclics/Elavil), and antipsychotics (eg, haloperidol/Haldol) are prescribed with unpredictable degrees of success. AD is the number one cause of nursing home placement in the United States, because of caregiver’s inability to manage a loved one at home in the severe stage of the disease.

Dental management of patients who have Alzheimer disease

Patients who have AD in the moderate-to-severe stages will generally require assistance in daily oral hygiene from a caregiver (spouse, child, nursing assistant, nurse) because of a progressive neglect and lack of interest in caring for themselves. Assistance may range from gently reminding the person to brush, to stand-by assistance, to ultimately providing hands-on daily care. Beginning in the moderate stage, the unique combination of impaired cognition, apathy, and apraxia (difficulty in ordered movement) results in not only a disinterest in oral care but also an inability to perform oral hygiene techniques. Compromised daily oral hygiene leads to destruction of the dentition by coronal and root caries and periodontal disease. For patients who wear dentures or partials, AD changes may result in patients forgetting to remove the appliances for days at a time. Dentures are often not removed from the mouth unless directed by others. Dentures are frequently broken or lost. Medications that are commonly used to control symptoms often cause hyposalivation, resulting in dry mouth, furthering oral deterioration. Caregivers report that oral hygiene becomes too difficult when the patient becomes resistant or combative. Finally, caregivers stop taking patients who have AD to the dental office because of the overwhelming and increasing problems required from them to manage day-to-day living. As a result, when the patient who has AD is seen by a dentist, extensive oral disease is present.

General Suggestions for Patients who have Alzheimer Disease

Most patients who have AD will have been clinically diagnosed before their dental visit. If not, dentists should be able to recognize the signs and symptoms of dementia, such as a decline in recent memory, inability to follow directions, or obvious personality changes, and refer them for medical evaluation and treatment.

The patient who has AD should always be treated with respect and approached in an empathetic way. A humane way to view the patient who has AD is as someone who has a progressive terminal disease, not as a child who has no autonomy or abilities.

Regardless of the stage of dementia, the dentist should begin with a careful medical and dental history, including a review of medications. Communication should always take place in the presence of a family caregiver (spouse, child, or responsible adult). If the patient is able to understand and respond to questions, the dentist should address the patient directly. Verbal directions should be presented in short, simple phrases, giving only one direction at a time. It may be appropriate to address the patient by his/her first name or nickname, because they may forget their own last name at times. One should be prepared to repeat comments or questions frequently, and to repeat the words exactly in a calm, slow, and clear voice, at a low pitch. Rephrasing questions leads to confusion. One should only ask/respond to one question/comment at a time and wait for a response. Nonverbal communication is even more important in these patients and includes a relaxed, calm, and confident manner, using direct eye contact. Firm but gentle touching on the patient’s hand, arm, or shoulder can be used as a sign of encouragement. Demonstrating procedures before performing them is a good management strategy.

The presence of a caregiver (likely a family member) will often alleviate a dementia patient’s anxiety. Because dementia interferes with the patient’s ability to communicate, it is important to have the caregiver’s input to verify reported symptoms such as dental pain. Often, caregivers will be able to interpret the meaning behind a sudden worsening of behavior, moaning, or increased restlessness as an indicator of dental pain. Facial expressions appear to be helpful in assessing dental pain in dementia patients.

Informed Consent

The dentist and staff should always determine whether the patient is legally able to make informed decisions. The elements of informed consent include the capability of the patient to make decisions by the demonstration of (1) understanding relevant information, (2) understanding the situation and consequences, (3) manipulating the information rationally, and (4) communicating a choice. If the patient who has AD is verbally aggressive (cursing), resistant (moving away, refusing to open), or combative (striking out), the important questions to ask are, “Does the patient really not want dental care?” and if so, “Is the informed consent process in place?” If the patient is legally competent and capable of making decisions, he/she should sign his/her own consent. If unable to sign his/her own consent, the legal guardian or health care proxy has the authority to give permission. If no proxy is identified, state law takes precedence and usually the person in the closest, loving relationship can give consent.

If patients wander or curse, or are restless, resistant, or combative, nonpharmacologic and pharmacologic approaches of management should be considered. Nonpharmacologic approaches include having the caregiver hold the patients hand or hands, keeping the caregiver in the operatory for familiarity and helping with management, reducing background noise, reducing excess activity, using an extraoral mouth prop (eg, Molt prop), cradling the head to reduce movements, having the patient hold onto a soft textured object (stuffed animal), and moving with the patient. If a soft (cloth) restraint is used to hold a patient in the chair to keep him/her from wandering/getting up during treatment, it is important to follow the guidelines for restraint use. It is important to document clearly why the restraint was used, where it was placed and for how long a period of time, and whether a separate consent was given for its use.

Dental Treatment by Stage

Table 2 provides some suggestions for dental management of the patient who has AD at different stages. In a patient who has mild dementia, good oral health should be attained aggressively, with restorative work completed and early lesions restored (no “watches”). Restorations should be long lasting and easily maintained. Crowns would be preferable to large restorative buildups, in most cases. Materials selected should be based on the ability to manage the patient and to maintain a dry operating field (eg, can you use a rubber dam?). Glass ionomers are good materials for root surfaces because of their ability to release fluoride and prevent recurrent decay.

Table 2
Managing Alzheimer disease in the dental office
Early Moderate Severe
Aggressive prevention including caregiver involvement: daily oral hygiene, topical fluorides, caregiver education are all critical beginning in the early stage and continuing through severe
Minimal changes needed
  • Shorter visits

  • More frequent recalls

  • Possible oral or intravenous sedation

Treatment plan anticipating decline Treatment plan with minimal changes in mind Treatment plan to maintain dentition if possible
Restore ASAP!
  • Simpler interventions:

    • Extract versus complex restore

    • Reline/repair versus new denture

    • Partials versus fixed crown and bridge

  • Palliative care:

    • Maintain comfort, dignity

    • Treat infection

    • Treat symptomatic problems

Data from Refs. ; and Shuman S, personal communication; and continuous education lecture October 2007.

For moderately demented patients, subsequent care should concentrate on preventing dental disease through aggressive home care and frequent recalls (every 3 months). Complex dental procedures should rarely be performed (if at all) before the disease has reached the advanced stage. If a patient loses a partial or denture, it is hard to predict whether or not new removable prostheses should be made. General guidelines include discussing this with the caregiver and making the decision based on the perceived risk/benefit. An understanding should be reached with the caregivers that the patient will not likely be able to wear prostheses in the future. If the caregiver is willing to assume the risk and cost, a new partial/denture can be fabricated, but the long-term prognosis is questionable at best.

Patients in the advanced stage often display behavior problems such as anxiety, hostility, wandering, and inability to sit still and open their mouths, and are generally uncooperative. These patients are difficult to treat but likely will require short appointments for simple procedures (like fluoride treatments or treatment planning) and sedation (oral or intravenous) for everything else. Nitrous oxide is not indicated because of the inability of the patient to understand and cooperate, but short-acting oral benzodiazepines (lorazepam/Ativan or triazolam/Halcion) work well for some procedures. Intravenous sedation works well for longer or complex procedures such as oral surgery and restorative care. However, Midazolam/Versed should be used with extreme caution in older patients who have AD because it has a profound effect at low doses. Rarely should more than 1 mg be given as an incremental dose, with a maximum total dose for a 1 hour procedure totaling to no more than 5 mg in most cases.

Several specially adapted preventive products are helpful for caregivers to use with patients who have AD. A foam mouth prop called the Open-Wide Plus (Specialized Care Com., Edison, New Jersey) is designed for caregivers to use to keep the mouth open during oral hygiene. A specialized toothbrush, the Collis Curve (Collis Curve, Inc., Brownsville, Texas) has three rows of bristles that, when placed correctly, can clean the lingual, facial, and occlusal surfaces of teeth at the same time. Approved by the American Dental Association for assisted brushing, the Collis Curve uses a simplified scrubbing motion, making it easier for caregivers to use than conventional or electric brushes.

Other conventional preventive products may be helpful for caregivers to maintain oral hygiene in patients who have AD. For cleaning between teeth, proxabrushes work well. Caregivers need to be reminded to keep their fingers from between the teeth of their patients because of the danger of biting. Finally, fluoride use is an essential preventive tool. Toothpaste, mouth rinses (if the patient is not late stage and at risk for aspiration), the use of gels at home or varnish in the office should all be considered as part of a daily plan to prevent new caries.

Definition and cause of stroke

The term “stroke” is used to refer to a CVA, which is defined as a serious and often fatal neurologic event occurring when a part of the brain is suddenly deprived of oxygenated blood. This event results in tissue necrosis in the part of the brain affected and can range from mild to severe disabilities, and even death. In recent years, the term “acute stroke” is rapidly being replaced by the term “brain attack,” to indicate that a stroke is similar to a heart attack: It is a medical emergency in which immediate intervention can prevent and even reverse the effects of early brain damage.

The two main causes of stroke are a blockage of an artery that supplies blood to a part of the brain (ischemic), or bleeding (hemorrhagic) into the brain because an artery has burst. If the blockage of the artery is temporary and blood flow is quickly restored, the brain may recover quickly. A transient ischemic attack (TIA) is defined as a stroke that lasts less than 24 hours and has no residual effect. Some people think of a TIA as a ministroke. Although most TIAs last less than 10 minutes, up to one third of patients will have noticeable changes on brain imaging studies that indicate injury to the brain. If the blockage of the artery is long lasting, the part of the brain supplied by that artery is permanently damaged and dies. The damaged area is said to be infarcted, so ischemic strokes are also called brain infarctions, or cerebral infarctions (similar to myocardial infarctions in the heart).

Ischemic strokes result from occlusion of a cerebral artery by a blood clot formed on the arterial wall obstructing blood flow (thrombus) or by having the clot break off (embolus) from the arterial wall and travel through the bloodstream until it becomes lodged. Obstruction of the blood flow distal to the embolus results in infarction. The primary factors associated with thromboembolic strokes are atherosclerosis and cardiac pathology, such as a previous myocardial infarction and atrial fibrillation. Approximately 10% of persons who have had a myocardial infarction will have a stroke within 6 years.

In hemorrhagic stroke, bleeding occurs into the brain (intracerebral) or into the space between the brain and the inner lining of the skull (subarachnoid). Hypertension is the most important risk factor for intracerebral hemorrhagic stroke. Preventing this type of stroke can largely be accomplished by effective blood pressure (BP) control. Four types of blood vessel abnormalities can lead to cerebral arteries rupturing: arteriovenous malformations, aneurysms, cavernomas or cavernous angiomas, and lobar hemorrhages.

The most common cause of subarachnoid hemorrhage is rupture of a saccular aneurysm at the bifurcation of a major cerebral artery. Of all strokes, 87% are ischemic (either from thrombus or emboli), 10% are intracerebral hemorrhage, and 3% are subarachnoid hemorrhagic strokes.

Risk factors

TIAs confer a significant short-term risk for stroke, hospitalization for cardiovascular events, and death. In one study of 1707 TIA patients evaluated in the emergency room, 180 patients (10%) developed a stroke within 90 days. Ninety-one patients (5%) did so within 2 days. Cigarette smoking doubles the risk for ischemic stroke compared with that of nonsmokers after adjusting for other risk factors. Atrial fibrillation is an independent risk factor for stroke, increasing risk approximately fivefold. Older age increases the risk for stroke. For adults older than 55, the lifetime risk is greater than one in six. Women have a higher risk than men, perhaps because of women’s survival advantage. BP is a powerful determinant of stroke risk. Subjects who have BP of less than 120/80 mm Hg have approximately half the lifetime risk for stroke compared with subjects who have hypertension (higher than 120/80). Diabetes increases ischemic stroke incidence at all ages but this risk is most prominent before 55 years of age in blacks and before 65 years of age in whites. A study of more than 37,000 women older than 45 years of age participating in the Women’s Health Study suggests that a healthy lifestyle (abstinence from smoking, low body mass index, moderate alcohol consumption, regular exercise, and a healthy diet) was associated with a significantly reduced risk for ischemic stroke but not for hemorrhagic stroke. Box 3 presents risk factors on stroke according to the ability to change, influence, or modify risk factors.

Box 3

  • Stroke risk factors one can change

    • Smoking

    • Exercise

    • Illicit drug use

    • Obesity

    • Physical inactivity

    • Periodontal disease

  • Stroke risk factors one can influence (by seeking medical care)

    • History of diabetes mellitus a

    • History of high BP a

    • Congestive heart failure a

    • TIA or previous stroke a

    • History of high cholesterol

    • History of heart conditions (such as atrial fibrillation)

    • History of narrowing of the arteries (such a carotid stenosis)

  • Stroke risk factors one cannot change

    • Age older than 75 a

    • Race (Native Americans, Alaska Natives, multiracial persons, and blacks have higher risk)

    • Sex (men have greater risk if younger than 65 and women have greater risk if older than 65)

    • Family history of medical conditions related to stroke

a Risk for stroke increases by a factor of 1.5. Having multiple risk factors contributes to an incrementally increased risk for stroke.

Data from Stein J, Silver J, Frates E. Risk factors for having a stroke. In: Life after stroke. Baltimore (MD): Johns Hopkins Press; 2006. p. 3–13, 87–90.

Stroke risk factors

Medications can also be risk factors for strokes in several ways: by creating a tendency to form blood clots (hypercoagulable state ) within the body or by increasing BP. The mechanism by which some medications cause stroke remains unknown. Table 2 lists medications and their mechanism that may lead to stroke if taken improperly or in excess.

Periodontal disease has been described as a risk factor for ischemic stroke because of the effect of inflammatory products (C-reactive protein, interleukins, and so forth) on systemic vasculature. It has been suggested that periodontal disease produces three harmful systemic responses related to strokes: inflammation in arterial walls, contributing to the build-up of atherosclerotic plaques, and increasing the risk for atheroma rupture. Studies confirm the relationship between periodontal disease and ischemic strokes. Persons who have periodontal disease have been found to be three times as likely to have a stroke. A direct relationship has been demonstrated between the thickness of the carotid artery wall and the presence of periodontal bacteria. Live periodontal bacteria have been found in atherosclerotic plaques. The conclusion from this evidence is that periodontal disease has a significant association with atheroma formation. Therefore, prevention of periodontal disease should be considered an important modifiable risk factor.

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Oct 29, 2016 | Posted by in General Dentistry | Comments Off on Managing Older Patients Who Have Neurologic Disease: Alzheimer Disease and Cerebrovascular Accident
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