27: Neurologic Disorders

Chapter 27

Neurologic Disorders

Neurologic diseases are common in the general population and therefore are commonly encountered in dental patients. Several diseases affecting the nervous system are of clinical significance in dental practice. Such diseases may vary in severity and consequences. The focus of this chapter is on five of the more important neurologic diseases—epilepsy, stroke, Parkinson’s disease, Alzheimer’s disease, and multiple sclerosis (MS). Also discussed are cerebrospinal fluid shunts, because of the assumed risk of bacterial seeding after an invasive dental procedure in patients with such shunts.



The term epilepsy includes disorders or syndromes with widely variable pathophysiologic findings, clinical manifestations, treatments, and outcomes.< ?xml:namespace prefix = "mbp" />1 Epilepsy is not a specific diagnosis but rather a term that refers to a group of disorders characterized by chronic and recurrent, paroxysmal changes in neurologic function (seizures), altered consciousness, or involuntary movements caused by abnormal and spontaneous electrical activity in the brain. Seizures may be convulsive (i.e., accompanied by motor manifestations) or may occur with other changes in neurologic function (i.e., sensory, cognitive, and emotional).2

Seizures are characterized by discrete episodes, which tend to be recurrent and often are unprovoked, in which movement, sensation, behavior, perception, and consciousness are disturbed. Symptoms are produced by excessive temporary neuronal discharging, which may result from intracranial or extracranial causes.3

Although seizures are required for the diagnosis of epilepsy, not all seizures imply presence of epilepsy. Seizures may occur during many medical or neurologic illnesses, including stress, sleep deprivation, fever, alcohol or drug withdrawal, and syncope.3 A list of epilepsy syndromes and the currently accepted classification of seizure types are presented in Box 27-1. This seizure classification, based on clinical behaviors and electroencephalographic changes, consists of two major groups: partial and generalized. Partial seizures are limited in scope (to a part of the cerebral hemisphere) and clinical manifestations and involve motor, sensory, autonomic, or psychic abnormalities.3 Partial seizures are subdivided into simple, in which consciousness is preserved, and complex, in which consciousness is impaired. Generalized seizures are more global in scope and manifestations. They begin diffusely, involve both cerebral hemispheres, are associated with alteration in consciousness, and frequently produce abnormal motor activity.3 Discussion in this section is limited to generalized tonic-clonic seizures (idiopathic grand mal), because these represent the most severe expression of epilepsy that the dentist is likely to encounter.


Box 27-1

Classification of Epileptic Syndromes and Seizure Types*

Epileptic Syndromes


       Benign epilepsy with centrotemporal spikes
       Autosomal dominant nocturnal frontal lobe epilepsy
       Juvenile myoclonic epilepsy
       Juvenile absence epilepsy
       Severe myoclonic epilepsy of infancy
       Progressive myoclonic epilepsies
       Generalized epilepsy with febrile seizures


       Mesial temporal lobe epilepsy
       Neoplasm (primary, metastatic)
       Infection (abscess, encephalitis, meningitis, syphilis, cysticercosis, Lyme disease, tuberculosis, fungal disease, herpes)
       Vascular (stroke, transient ischemic attack, migraine, hemorrhage)
       Developmental (migrational)
       Degenerative (e.g., Alzheimer’s disease)
       Immunologic (e.g., multiple sclerosis)
       West’s syndrome
       Lennox-Gastaut syndrome
       Tuberous sclerosis
       Sturge-Weber syndrome

Seizure Types*

I Partial (Focal, Local)

    Simple partial seizures
    Complex partial seizures
    Partial seizures evolving to secondarily generalized seizures

II Generalized (Convulsive or Nonconvulsive)

    Absence seizures (petit mal)
    Myoclonic seizures
    Tonic-clonic seizures (grand mal)
    Tonic seizures
    Atonic seizures

III Unclassified Epileptic Seizures

Data from Commission on Classification and Terminology of the International League Against Epilepsy. Proposal for revised clinical and electroencephalographic classification of epileptic seizures, Epilepsia 22:489-501, 1981.

* International classification of epileptic syndromes (condensed).



Epilepsy, which is the most common chronic neurologic condition, affects people of all ages, with a peak incidence in childhood and old age. In the United States, the incidence of all types of epilepsy is 35 to 52 cases per 100,000 population, varying by age: 60 to 70 per 100,000 per year in young children (younger than 5 years of age), 45 per 100,000 in adolescents, as low as 30 per 100,000 in the early adult years, but rising through the sixth and seventh decades back to 60 to 70 per 100,000 and reaching as high as 150 to 200 per 100,000 in persons older than 75 years. The incidence in males is higher at every age. Estimates of the prevalence of epilepsy range from 4.7 to 6.9 per 1000, but its prevalence is much higher in less developed countries for all age groups.3

Approximately 10% of the population will have at least one epileptic seizure in a lifetime, and 2% to 4% will experience recurrent seizures at some point.2,3 The overall incidence of seizures is 0.5%.2,3 Seizures are most common during childhood, with as many as 4% of children experiencing at least one seizure during the first 15 years of life. Most children outgrow the disorder. About 4 in 1000 children do not outgrow the disorder and will require medical care. Seizures also are common in old age, with an estimated annual incidence of 134 per 100,000. In a typical dental practice of 2000 patients, 3 or 4 can be expected to have a seizure disorder. Cerebrovascular disease is the most common factor underlying seizures occurring in elderly persons.2,3


Epileptic seizures are idiopathic in more than half of all affected patients.2,3 Vascular (cerebrovascular disease) and developmental abnormalities (cavernous malformation), intracranial neoplasms (gliomas), and head trauma are causative in about 35% of adult cases. Other common causes include hypoglycemia, drug withdrawal, infection, and febrile illness (e.g., meningitis, encephalitis). Seizures occur with genetic conditions such as Down syndrome, tuberous sclerosis, and neurofibromatosis and are associated with several genetic abnormalities that result in neuronal channel dysfunction.2,3

Seizures sometimes can be evoked by specific stimuli. Approximately 1 of 15 patients reports that seizures occurred after exposure to flickering lights, monotonous sounds, music, or a loud noise.2,4 Syncope and diminished oxygen supply to the brain also are known to trigger seizures. It is valuable for the dentist to know what factors have the potential to exacerbate a seizure in a particular patient, so that certain stimuli can be avoided.2

Pathophysiology and Complications

The basic event underlying an epileptic seizure is an excessive focal neuronal discharge that spreads to thalamic and brain stem nuclei. The cause of this abnormal electrical activity is not precisely known, although a number of theories have been put forth.2,3 These include altered sodium channel function, altered neuronal membrane potentials, altered synaptic transmission, diminution of inhibitory neurons, increased neuronal excitability, and decreased electrical threshold for epileptic activity. During the seizure, blood becomes hypoxic, with consequent development of lactic acidosis.2,3

Approximately 60% to 80% of patients with epilepsy achieve complete control over their seizures within 5 years; the remainder achieve only partial or poor control.2,3,5 A significant problem in the medical management of epileptic patients is one of compliance (i.e., adherence to prescribed treatment regimens including medication). This problem is common to many chronic disorders, such as hypertension, because patients may have to take medication for the rest of their lives, even though they remain asymptomatic. Evidence suggests that patients who have epilepsy from an early age have a higher incidence of future complications and die at an earlier age. Noncompliance may be a clinically important consideration in dental patients because it is associated with a higher risk of later complications that may lead to death.4 Complications of seizures include trauma (as a result of falls) to the head, neck, and mouth and aspiration pneumonia. Also, frequent and severe seizures are associated with altered mental function, dullness, confusion, argumentativeness, and increased risk of sudden death (about 1 in 75 persons in this group die annually).2,3

Status Epilepticus

A serious acute complication of epilepsy (especially the tonic-clonic type) is the occurrence of repeated seizures over a short time without a recovery period, called status epilepticus. This condition most frequently is caused by abrupt withdrawal of anticonvulsant medication or an abused substance but may be triggered by infection, neoplasm, or trauma. Status epilepticus constitutes a medical emergency.2,3 Patients may become seriously hypoxic and acidotic during this event and suffer permanent brain damage or death. Patients with epilepsy also are at increased risk for sudden death and death due to accident.2,3

Clinical Presentation

Signs and Symptoms

The clinical manifestations of generalized tonic-clonic convulsions (grand mal seizures) are classic. An aura (a momentary sensory alteration that produces an unusual smell or visual disturbance) precedes the convulsion in one third of patients. Irritability is another premonitory signal. After the aura warning, the patient emits a sudden “epileptic cry” (caused by spasm of the diaphragmatic muscles) and immediately loses consciousness. The tonic phase consists of generalized muscle rigidity, pupil dilation, rolling of the eyes upward or to the side, and loss of consciousness. Breathing may stop because of spasm of respiratory muscles.2,3 This phase is followed by clonic activity consisting of uncoordinated beating movements of the limbs and head, forcible jaw closing, and up and down head rocking.2,3 Urinary incontinence is common, but fecal incontinence is rare. The seizure (ictus) usually does not last longer than 90 seconds; thereafter, movement ceases and muscles relax, with a gradual return to consciousness, accompanied by stupor, headache, confusion, and mental dulling. Several hours of rest or sleep may be needed for the patient to regain full cognitive and physical abilities.2,3

Laboratory Findings

The diagnosis of epilepsy generally is based on the history of seizures and presence of abnormalities on the electroencephalogram (EEG).2,3 Seizures produce characteristic spike and sharp wave patterns on the EEG tracing. Serial recordings during sleep deprivation, which can induce seizures, may help to establish the diagnosis. Other diagnostic procedures that are useful for ruling out other causes of seizures include computed tomography (CT), magnetic resonance imaging (MRI), single-photon emission computed tomography (SPECT), lumbar puncture, serum chemistry profiles, and toxicology screening.2,3

Medical Management

The medical management of epilepsy usually is based on long-term drug therapy. Phenytoin (Dilantin), carbamazepine (Tegretol), and valproic acid are considered first-line agents for treatment of this disease. Several other drugs are available for control of generalized tonic-clonic seizures5,6 (Table 27-1). These drugs reduce the frequency of seizures by elevating the seizure threshold of motor cortex neurons, depressing abnormal cerebral electrical discharge, and limiting the spread of excitation from abnormal foci. Phenytoin and carbamazepine are efficient at blocking sodium or calcium channels of motor neurons.57 Many of the other antiepileptic drugs augment γ-aminobutyric acid (GABA), which inhibits glutamate activity—the major determinant of brain excitability. Adverse effects of phenytoin include anemia, ataxia, gingival overgrowth, cosmetic changes (coarsening of facial features, hirsutism, facial acne), lethargy, skin rash, and gastrointestinal disturbances. Phenobarbital, which is considered a second-line drug, can induce hepatic microsomal enzymes that promote the metabolism of concurrently used drugs.8 Several antiseizure medications (see Table 27-1) may cause drowsiness, sedation, ataxia, weight gain, cognitive impairment, and hypersensitivity reactions.57 Adverse effects are more common at the start of therapy, when drugs are administered rapidly or at high dose. For these reasons, and to facilitate compliance, single-drug therapy and a slow increase in dose are recommended. Unfortunately, the use of combination therapy frequently is necessary for seizure control.57 Drug therapy usually is continued in children until a 1- to 2-year seizure-free period is attained, or until around age 16 years. Attempts to taper the antiepileptic drug regimen are made thereafter.

TABLE 27-1 Anticonvulsants Used in the Management of Generalized Tonic-Clonic (Grand Mal) Seizures


Vagus nerve stimulation (VNS) is reserved for patients who have been unable to achieve satisfactory seizure control with several medications, and it is an option for some before brain surgery. The mechanism of VNS is similar to that of an implantable cardiac pacemaker, in which a subcutaneous pulse generator is implanted in the left chest wall and delivers electrical signals to the left vagus nerve through a bipolar lead. The stimulated vagus nerve provides direct projection to regions in the brain potentially responsible for the seizure. The VNS device generally is used in combination with antiepileptic medications.57

Dental Management

Medical Considerations

The first step in the management of an epileptic dental patient is identification of the patient as having the disorder (Box 27-2). This is best accomplished by the medical history and by discussion with the patient or family members. Once a patient with epilepsy has been identified, the dental practitioner must learn as much as possible about the seizure history, including the type of seizures, age at onset, cause (if known), current and regular use of medications, frequency of physician visits, quality of seizure control, frequency of seizures, date of last seizure, and any known precipitating factors. In addition, a history of previous injuries associated with seizures and their treatment may be helpful.


Box 27-2 Dental Management

Considerations in Patients with Seizure Disorders


Patient Evaluation/Risk Assessment (see Box 1-1)

Evaluate to determine the nature, severity, control, and stability of disease.

Potential Issues/Factors of Concern

Well-controlled seizure disorders pose no specific management problems.

Analgesics Clinicians should provide good pain control to avoid stress, which may precipitate a seizure.
Antibiotics There is no need for antibiotic prophylaxis.
Anesthesia It is very important to obtain adequate anesthesia to reduce stress as possible precipitant for a seizure. Epinephrine (1 : 100,000 and no more than two carpules) in local anesthetics generally is well tolerated.
Anxiety Paatients with untreated or poorly controlled seizure-associated disorders may appear very anxious and stressed, increasing the risk for a seizure. Use of special anxiety and stress reduction techniques may be indicated.
Allergy Allergic skin changes (rash, erythema multiforme) may signify a reaction to antiepileptic medications.
Bleeding The possibility of a bleeding tendency has been noted in patients taking valproic acid (Depakene) or carbamazepine (Tegretol) as the result of platelet interference.
Blood pressure Monitor blood pressure, because it may significantly increase or decrease with onset of a seizure.
Chair position This usually is not a problem if the patient is under good medical management; with symptoms of impending syncope associated with cardiac stress or pulmonary congestion, however, a supine position may not be tolerated. In patients at risk for seizure, the chair back should be in supported supine position.
Consultation Once the patient is under good medical management, the dental treatment plan is unaffected. However, consultation with the patient’s physician to establish the level of control is recommended as part of the management program.
Devices No issues.
Drugs These patients typically are on anticonvulsant drugs, which may have adverse effects including drowsiness, slow mentation, dizziness, others.
Equipment No issues.
Emergencies Be prepared for occurrence of a grand mal seizure:

Placement of a ligated mouth prop at the beginning of the procedure may be considered.

The dental chair should be in supported supine position.

During a seizure:

Clear the area.

Turn the patient to the side (to avoid aspiration).

Do not attempt to use a padded tongue blade.

Passively restrain.

After a seizure:

Examine for traumatic injuries.

Discontinue treatment; arrange for patient transport.

Most commonly seizures are self-limited, but rarely a seizure may progress to cardiac arrest, necessitating emergency medical treatment; call 911. A patient who is ambulatory and stable should seek urgent medical care. Ongoing vital signs must be monitored and cardiopulmonary resuscitation initiated if necessary; transport patient to emergency medical facilities.

Follow-up Follow-up with the patient (and physician) is indicated. after any seizure event in the dental office. In patients who have undergone surgery, a follow-up phone call within the next day or two is advised.


Fortunately, most epileptic patients are able to attain good control of their seizures with anticonvulsant drugs and are therefore able to receive normal routine dental care. In some instances, however, the history may reveal a degree of seizure activity that suggests noncompliance or a severe seizure disorder that does not respond to anticonvulsants. For these patients, a consultation with the physician is advised before dental treatment is rendered. A patient with poorly controlled disease may require additional anticonvulsant or sedative medication, as directed by the physician.

Patients who take anticonvulsants may suffer from the toxic effects of these drugs, and the dentist should be aware of these manifestations. In addition to the more common adverse effects (see Table 27-1), allergy may be seen occasionally as a rash, erythema multiforme, or worse (e.g., Stevens-Johnson syndrome). Phenytoin, carbamazepine, and valproic acid can cause bone marrow suppression, leukopenia, and thrombocytopenia, resulting in an increased incidence of microbial infection, delayed healing, and gingival and postoperative bleeding. Valproic acid can decrease platelet aggregation, leading to spontaneous hemorrhage and petechiae.8

Propoxyphene and erythromycin should not be administered to patients who are taking carbamazepine because of interference with metabolism of carbamazepine, which could lead to toxic levels of the anticonvulsant drug.57 Aspirin and other nonsteroidal antiinflammatory drugs (NSAIDs) (see Table 27-1) should not be administered to patients who are taking valproic acid, because these agents can further decrease platelet aggregation, leading to hemorrhagic episodes. No contraindication has been identified to the use of local anesthetics in proper amounts in these patients. Patients who have a VNS device implanted in the chest do not need antibiotic prophylaxis before undergoing invasive dental procedures.57

Seizure Management

Despite consistent use of appropriate preventive measures by both dentist and patient, the possibility always exists that an epileptic patient may experience a generalized tonic-clonic convulsion in the dental office. The dentist and office staff members should anticipate and be prepared for such events. Preventive measures include knowing the patient’s history, scheduling the patient at a time within a few hours of taking the anticonvulsant medication, using a mouth prop, removing dentures, and discussing with the patient the urgency of mentioning an aura as soon as it is sensed. The clinician also should be aware that irritability often is a symptom of impending seizure. With a premonitory stage of sufficient duration, 0.5 to 2 mg of lorazepam can be given sublingually, or diazepam 2 to 10 mg can be given intravenously.9

If the patient has a seizure while in the dental chair, the primary task of management is to protect the patient and try to prevent injury. No attempt should be made to move the patient to the floor. Instead, the instruments and instrument tray should be cleared from the area, and the chair should be placed in a supported supine position (Figure 27-1). The patient’s airway should be maintained patent. No attempt should be made to restrain or hold the patient down. Passive restraint should be used only to prevent injury that may result when the patient hits nearby objects or falls out of the chair.10,11


FIGURE 27-1 Dental chair in the supine position with the back supported by the operator’s or assistant’s stool.

If a mouth prop (e.g., a padded tongue blade between the teeth to prevent tongue biting) is used, it should be inserted at the beginning of the dental procedure (see Box 27-2). Trying to insert a mouth prop is not advised during the seizure, because doing so may damage the patient’s teeth or oral soft tissue and may be nearly impossible. An exception is the case in which the patient senses an impending seizure and can cooperate.10,11

A grand mal seizure generally does not last longer than a few minutes. Afterward, the patient may fall into a deep sleep from which he or she cannot be aroused. Oxygen (100%), maintenance of a patent airway, and mouth suction should be provided during this phase. Alternatively, the patient can be turned to the side to control the airway and to minimize aspiration of secretions. Within a few minutes, the patient gradually regains consciousness but may be confused, disoriented, and embarrassed. Headache is a prominent feature during this period. If the patient does not respond within a few minutes, the seizure may be associated with low serum glucose, and delivery of glucose may be needed.10,11

No further dental treatment should be attempted after a generalized tonic-clonic seizure, although examination for sustained injuries (e.g., lacerations, fractures) should be performed. In the event of avulsed or fractured teeth (Figure 27-2) or a fractured appliance, an attempt should be made to locate the tooth or fragments to rule out aspiration. A chest radiograph may be required to locate a missing fragment or tooth.10,11


FIGURE 27-2 Fracture of teeth and laceration of lower lip sustained during a grand mal seizure.

(Courtesy Gerald A. Ferretti, DDS, Lexington, Kentucky.)

In the event that a seizure becomes prolonged (status epilepticus) or is repeated, intravenous lorazepam (0.05 to 0.1 mg/kg) 4 to 8 mg, or 10 mg diazepam, generally is effective in controlling it. Lorazepam is preferred by many experts because it is more efficacious and lasts longer than diazepam.2,3 Oxygen and respiratory support should be provided, because respiratory function may become depressed. If the seizure lasts longer than 15 minutes, the following protocol should be implemented: secure intravenous access, repeat lorazepam dosing, administer fosphenytoin, and activate the emergency medical services (EMS) system.10,11

Treatment Planning Considerations

Because gingival overgrowth is associated with phenytoin administration, every effort should be made to maintain a patient at an optimal level of oral hygiene. This may require frequent visits for monitoring of progress. If gingival overgrowth is significant, surgical reduction will be necessary. This correction must be accompanied by an increased awareness of oral hygiene needs and a positive commitment by the patient to maintain oral cleanliness.

A missing tooth or teeth should be replaced if possible to prevent the tongue from being caught in the edentulous space during a seizure (as commonly happens). Generally, a fixed prosthesis or implant is preferable to a removable one. (The removable prosthesis becomes dislodged more easily.) For fixed prostheses, all-metal units should be considered when possible, to minimize the chance of fracture. When placing anterior castings, the dentist may wish to consider using three-quarter crowns or retentive nonporcelain facings.

Removable prostheses are, nevertheless sometimes constructed for epileptic patients. Metallic palates and bases are preferable to all-acrylic ones. If acrylic is used, it should be reinforced with wire mesh.

Oral Complications and Manifestations

The most significant oral complication seen in epileptic patients is gingival overgrowth, which is associated with phenytoin (Figure 27-3) and rarely with valproic acid and vigabatrin.7,10 The incidence of phenytoin-induced gingival overgrowth in epileptic patients ranges from 0% to 100%, with an average rate of approximately 42%. A greater tendency to develop gingival overgrowth occurs in youngsters than in adults. The anterior labial surfaces of the maxillary and mandibular gingivae are most commonly and severely affected.7,10


FIGURE 27-3 Phenytoin-induced gingival overgrowth.

(Courtesy H. Abrams, Lexington, Kentucky.)

Meticulous oral hygiene is important for preventing overgrowth and significantly decreasing its severity. Good home care must always be combined with the removal of irritants, such as overhanging restorations and calculus. Frequently, enlarged tissues interfere with function or appearance, and surgical reduction may become necessary.

Traumatic injuries such as broken teeth, tongue lacerations, and lip scars also are common in patients who experience generalized tonic-clonic seizures. Stomatitis, erythema multiforme, and Stevens-Johnson syndrome are rare adverse effects associated with the use of phenytoin, valproic acid, lamotrigine, phenobarbital, and carbamazepine. These complications are more common during the first 8 weeks of treatment.7,10

Stroke (Cerebrovascular Accident)


Stroke is a generic term that is used to refer to a cerebrovascular accident (CVA)—a serious and often fatal neurologic event caused by sudden interruption of oxygenated blood to the brain. The associated ischemic injury results in focal necrosis of brain tissue, which may be fatal if the damage is catastrophic. Even if a stroke is not fatal, the survivor often is to some degree debilitated in motor function, speech, or cognition. The scope and gravity of stroke are reflected in the fact that stroke is the leading cause of serious, long-term disability in the United States; 5% of the population older than 65 years of age has had one stroke.2,3


Incidence and Prevalence

Stroke is one of the most significant health problems in the United States. Stroke is the third leading cause of death (behind heart disease and cancer) in the United States, with 275,000 Americans dying of stroke annually.12 Each year in the United States, about 700,000 people experience new or recurrent stroke. This figure translates to the occurrence of one stroke about every minute, and 75% of persons survive their stroke.12,13

Hypertension is the most important risk factor for ischemic and hemorrhagic stroke.12,13 The incidence of stroke increases directly in relation to the degree of elevation of systolic and diastolic arterial blood pressure above threshold values. More important, conclusive evidence accrued since 1980 indicates that control of hypertension prevents strokes. Metaanalyses of randomized controlled trials confirm an approximate 30% to 40% reduction in stroke risk with lowering of blood pressure.12,13

Approximately 7% to 10% of men and 5% to 7% of women older than 65 years have asymptomatic carotid stenosis of greater than 50%. Epidemiologic studies suggest that the rate of unheralded stroke evolving ipsilateral to a stenosis is about 1% to 2% annually.12,13

Nonvalvar atrial fibrillation carries a 3% to 5% annual risk for stroke, with the risk becoming even higher in the presence of advanced age, previous transient ischemic attack (TIA) or stroke, hypertension, impaired left ventricular function, and diabetes mellitus.12,13

In epidemiologic studies, the risk for stroke in smokers is almost double that in nonsmokers, but the risk becomes essentially identical to that in nonsmokers by 2 to 5 years after quitting. The relative risk for stroke is two to six times greater for patients with insulin-dependent (type 1) diabetes.12,13 An association with race has been recognized: Compared with whites, African Americans are at 38% greater risk for a first stroke. Also, 40,000 more women than men have a stroke each year. Risk of stroke increases with age; however, on average, 28% of people who have a stroke are younger than 65 years.1214 A total of 4.7 million stroke survivors live in the United States, and an average dental practice of 2000 adult patients will include about 31 patients who have had or will experience a stroke.


Stroke is caused by the interruption of blood supply and oxygen to the brain as a result of ischemia or hemorrhage. The most common type is ischemic stroke induced by thrombosis (in 60% to 80% of cases) of a cerebral vessel. Ischemic stroke also can result from occlusion of a cerebral blood vessel by distant emboli. Hemorrhage causes about 15% of all strokes and carries a 1-year mortality rate greater than 60%.12,13

Cerebrovascular disease is the primary factor associated with stroke. Atherosclerosis and cardiac pathosis (myocardial infarction, atrial fibrillation) increase the risk of thrombolic and embolic strokes, whereas hypertension is the most important risk factor for intracerebral hemorrhagic stroke.12,13 Approximately 10% of persons who have had a myocardial infarction will have a stroke within 6 years.12,13 Additional factors that increase the risk for stroke include the occurrence of transient ischemic attacks, a previous stroke, high dietary fat, obesity and elevated blood lipid levels, physical inactivity, uncontrolled hypertension, cardiac abnormalities, diabetes mellitus, elevated homocysteine levels, elevated hematocrit, elevated antiphospholipid antibodies, heavy tobacco smoking, increasing age (risk doubles each decade after the age of 65 years), and periodontal disease.12,13 Increased risk for hemorrhagic stroke also occurs with use of phenylpropanolamine, an α-adrenergic agonist.12,13

Pathophysiology and Complications

Pathologic changes associated with stroke result from infarction, intracerebral hemorrhage, or subarachnoid hemorrhage. Cerebral infarctions most commonly are caused by atherosclerotic thrombi or emboli of cardiac origin. The extent of an infarction is determined by a number of factors, including site of the occlusion, size of the occluded vessel, duration of the occlusion, and collateral circulation. The production and circulation of proinflammatory cytokines, the occurrence of clotting factors, and arterial inflammation contribute to platelet aggregation. Neurologic abnormalities result from excitotoxicity, free radical accumulation, inflammation, mitochondrial and DNA damage, and apoptosis of the region supplied by the damaged artery.12,13

The most common cause of intracerebral hemorrhage is hypertensive atherosclerosis, which results in microaneurysms of the arterioles (Figure 27-4). Vessels within the circle of Willis often are affected (Figure 27-5). Rupture of these microaneurysms within brain tissue leads to extravasation of blood, which displaces brain tissue, causing increase in intracranial volume until resultant tissue compression halts bleeding. Hemorrhagic strokes also may be caused by subarachnoid hemorrhage. The most common cause of subarachnoid hemorrhage is rupture of a saccular aneurysm at the bifurcation of a major cerebral artery.15,16


FIGURE 27-4 Cerebral infarction in a patient who had chronic hypertension.


FIGURE 27-5 Aneurysm of the middle cerebral artery.

The most serious outcome of stroke is death, which occurs in 8% of those who experience ischemic strokes and 38% to 47% of those with hemorrhagic strokes within a month of the event. Overall, about 23% of patients die within 1 year.1517 Mortality rates are directly related to type of stroke, with 80% of patients dying after an intracerebral hemorrhage, 50% after a subarachnoid hemorrhage, and 30% after occlusion of a major vessel by a thrombus. Death from stroke may not be immediate (sudden death) but rather may occur hours, days, or even weeks after the initial stroke episode.1517

If the victim survives, it is highly likely that a neurologic deficit or disability of varying degree and duration will remain. Of those who survive the stroke, 10% recover with no impairment, 50% have a mild residual disability, 15% to 30% are disabled and require special services, and 10% to 20% require institutionalization. Approximately 50% of those who survive the acute period (the first 6 months) are alive 7 years later.1517

The type of residual deficit that results from a stroke is directly dependent on the size and location of the infarct or hemorrhage. Deficits include unilateral paralysis, numbness, sensory impairment, dysphasia, blindness, diplopia, dizziness, and dysarthria. Return of function is unpredictable and usually takes place slowly, over several months. Even with improvement, patients frequently are left with some permanent residual problem, such as difficulty in walking, using the hands, performing skilled acts, or speaking. Dementia also may be an outcome of stroke.1519

Clinical Presentation

Signs and Symptoms

Familiarity with the warning signs and symptoms and the phases of stroke can lead to appropriate action that may be lifesaving. Four events associated with stroke are (1) the transient ischemic attack (TIA), (2) reversible ischemic neurologic deficit (RIND), (3) stroke-in-evolution, and (4) the completed stroke. These events are defined principally by their duration.12,13

A TIA is a “mini” stroke that is caused by a temporary disturbance in blood supply to a localized area of the brain. A TIA often is associated with numbness of the face, arm, or leg on one side of the body (hemiplegia); weakness, tingling, numbness, or speech disturbances that usually last less than 10 minutes. Most commonly, a major stroke is preceded by one or two TIAs within several days of the first attack.1517

A RIND is a neurologic deficit that is similar to a TIA but does not clear within 24 hours. Eventual recovery is the rule, however.1517

Stroke-in-evolution is a neurologic condition that is caused by occlusion or hemorrhage of a cerebral artery in which the deficit has been present for several hours and continues to worsen during a period of observation. Signs of stroke include hemiplegia, temporary loss of speech or trouble in speaking or understanding speech, temporary dimness or loss of vision, particularly in one eye (may be confused with migraine), unexplained dizziness, unsteadiness, or a sudden fall.1517

Clinical manifestations that remain after a stroke vary in accordance with the site and size of residual brain deficits; these include language disorders, hemiplegia, and paresis, a form of paralysis that is associated with loss of sensory function and memory and weakened motor power. Box 27-3 presents the different behavioral manifestations of right-sided brain damage versus left-sided brain damage. Of note, in most patients with stroke, the intellect remains intact; however, massive left-sided stroke has been associated with cognitive decline.151820


Box 27-3 Manifestations of Right-Sided Versus Left-Sided Brain Damage

Right-Sided Brain Damage Left-Sided Brain Damage

Paralyzed left side

Spatial-perceptual deficits

Impaired thought process

Quick, impulsive behavior

Inability to use mirror

Difficulty performing tasks (toothbrushing)

Memory deficits—for events or people, generalized

Neglect of left side

Paralyzed right side

Language and speech problems

Decreased auditory memory (inability to remember long instructions)

Slow, cautious, disorganized behavior

Memory deficits—language-based



Laboratory Findings

Patients suspected of having had a stroke usually undergo a variety of laboratory tests and diagnostic imaging procedures to rule out conditions that can produce neurologic alterations, such as diabetes mellitus, uremia, abscess, tumor, acute alcoholism, drug poisoning, and extradural hemorrhage.12,13 Such investigations often include urinalysis, blood sugar level, complete blood count, erythrocyte sedimentation rate, serologic tests for syphilis, blood cholesterol and lipid levels, chest radiographs, and electrocardiogram (ECG). Various abnormalities may be disclosed by the test results, depending on the type and severity of stroke and its causative factors. A lumbar puncture also may be ordered by the physician to check for blood or protein in the cerebrospinal fluid (CSF) and for altered CSF pressure, which would be suggestive of subarachnoid hemorrhage.12,13 Doppler blood flow studies, EEG, cerebral angiography, CT (Figure 27-6), and MRI, including diffusion and perfusion studies of the brain, are important for determining the extent and location of arterial injury.121421


FIGURE 27-6 Computed tomography (CT) scan of the brain demonstrating a cerebrovascular accident (stroke) lesion that extended from the midbrain to the temporal lobe.

Medical Management


The first aspect of stroke management is preven/>

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Jan 4, 2015 | Posted by in General Dentistry | Comments Off on 27: Neurologic Disorders

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