dent clin n am 50 (2006) 607–623

8/14/2019 Dent Clin N Am 50 (2006) 607–623

http://slidepdf.com/reader/full/dent-clin-n-am-50-2006-607623 1/17

Management of Dental Patientswith Seizure Disorders

Robert B. Bryan, DDS *, Steven M. Sullivan, DDSDepartment of Oral and Maxillofacial Surgery,

University of Oklahoma Health Sciences Center, College of Dentistry,1201 N. Stonewall, Oklahoma City, OK 73117, USA

Seizures are one of the most commonly encountered neurological disor-ders. Seizures can manifest as an isolated incident with unknown etiology,or as a symptom of a condition that requires long-term treatment. Whenpatients experience recurring seizures, the disorder is termed epilepsy. Dur-ing a seizure, a fundamental brain abnormality results in synchronous,excessive, abnormal electrical discharges of the neurons in the central ner-

vous system [1]. The manifestation of these discharges is termed a seizure.This manifestation can take the form of motion disturbances, altered feel-ings, or changes in the patient’s level of consciousness. The treatment of sei-zures should be multifaceted because the patient can experience not onlyphysical disability, but also psychological and social issues.

Generally speaking, patients with epilepsy tend to have less than idealoral health and receive less dental treatment than the general population[2]. In treating patients with epilepsy, the dental practitioner should havean understanding of the basic nature of the condition as well as various

medications and surgical interventions used for its treatment. All dentalpractitioners should be familiar with epilepsy so that they can both preventand effectively treat many of the dental problems associated with epilepsy.In addition, dentists must be able to manage seizures acutely, as they mayoccur during office visits.

Epidemiology

An estimated 5% to 10% of the population in general will experience atleast one seizure over the course of a lifetime [1,3,4] . Approximately 0.5% to

* Corresponding author.E-mail address: [email protected] (R.B. Bryan).

0011-8532/06/$ - see front matter Ó 2006 Elsevier Inc. All rights reserved.doi:10.1016/j.cden.2006.06.004 dental.theclinics.com

Dent Clin N Am 50 (2006) 607–623

mailto:[email protected]

mailto:[email protected]

8/14/2019 Dent Clin N Am 50 (2006) 607–623


1% of people will be diagnosed with epilepsy [4]. It is important to distin-guish between those that have experienced a single seizure from those

who have had recurrent seizures (ie, epilepsy). Epilepsy is a disease with on-set at the extremes of life [1,5]. According to Annergers and colleagues [5],the periods of highest incidence of epilepsy occur in patients younger than1 year of age and older than 75.

Classication

The International League Against Epilepsy has classied seizures. Thisclassication system is based on the clinical manifestation of the seizure.The two main categories of seizure classication are (1) partial and (2)generalized.

If the seizure is the result of hyperactivity in a specic portion of the ce-rebral cortex, it is termed partial. If the activity involves the entire cerebralcortex, it is a generalized seizure. Seizures can evolve from one type to an-other as the electrical discharges spread from one area of the brain to otherparts. Therefore, a simple partial seizure can evolve into a complex partialseizure [6].

Partial seizures

A partial seizure occurs when the electrical discharge occurs in a localizedarea of the cortex. This classication of seizures can be further divided intothree categories:

Simple partial seizure (patient remains conscious)Complex partial seizure (impaired consciousness)Partial seizures evolving to secondarily generalized seizures

Simple partial seizuresSimple partial seizures can have motor signs (ie, clonic or tonic move-

ments of any body part), sensory signs (ie, paresthesias, visual changes, gus-tatory changes), psychic signs (ie, de ́ja ` vu), or autonomic symptoms (ie,tachycardia, dizziness) [3,5,6] . Close observation of the patient in both thepreictal and postictal phases can be helpful in determining the correct diag-nosis of the seizure disorder. Again, patients typically do not become uncon-scious during a simple partial seizure.

Complex partial seizuresComplex partial seizures are the most common type of seizures. They

cause an altered state of consciousness and may actually begin with a simplepartial seizure [3,5,6] . The electrical event typically originates at one or bothof the temporal lobes. In fact, approximately 70% to 80% of complex

608 BRYAN & SULLIVAN

8/14/2019 Dent Clin N Am 50 (2006) 607–623


partial seizures arise from the temporal lobe. These seizures usually presentwith an experiential or viscero-sensory aura, followed by impairment of con-

sciousness. The frontal lobe is the second most common area of origin of complex partial seizures [5,6]. Complex partial seizures have also been re-ported to have bruxism as a symptom, although this is quite rare [7]. Mesialtemporal lobe sclerosis, particularly affecting the hippocampus, is a commonradiological nding on MRI in this disorder [8]. The ‘‘syndrome’’ in whichpatients have recurrent complex seizures of temporal lobe origin is termedtemporal lobe epilepsy (TLE). Many patients with TLE do not achievegood seizure control with antiepileptic medications. More recently, surgicaltherapy is being considered superior to long-term drug therapy in these re-

fractory cases [9]. Seventy percent to 90% of patients who undergo surgicaltreatment for TLE become seizure-free.

Partial seizures evolving to secondarily generalized seizuresPartial seizures evolving to secondarily generalized seizures can begin as

a simple partial seizure or a complex partial seizure. Upon spreading toa generalized seizure, asymmetric tonic or clonic movements are observed.This is in contrast to the primary generalized seizure, which typically in-volves symmetrical tonic–clonic movements.

Generalized seizures

Generalized seizures are diffuse events that involve both hemispheres of the brain. Therefore, the motor manifestations and electroencephalogramsignals are bilateral. Generalized seizures are classied into six majorcategories:

Absence seizuresTonic seizuresClonic seizuresMyoclonic seizuresPrimary generalized tonic–clonic seizuresAtonic seizures

Absence seizuresAbsence seizures are brief periods of altered or impaired consciousness,

unresponsiveness, and cessation of activity. The prevalence of typical ab-

sences among children with epilepsies is about 10%. An electroencephalo-gram can conrm the diagnosis of absence seizures in 90% of children[10]. The duration is typically in the range of 3 to 20 seconds. These episodescan be so brief that they may go unnoticed. The event is more likely to berecognized if the patient is performing a continuous task in the companyof others. Absence seizures are typically not accompanied by an aura andthere is no postictal confusion. Usually, there is no recollection by the

609SEIZURE DISORDERS

8/14/2019 Dent Clin N Am 50 (2006) 607–623


patient that a seizure has occurred. Small clonic jerks of the arms and handsare seen at times [11,12] . Eye opening and minor orofacial automatisms are

frequently seen [13]. The course of this condition is usually benign and re-solves by the time the child reaches adulthood. In cases where the absenceseizures continue into adulthood, therapy with antiepileptic drugs hasbeen shown to be promising. If the patient has absence seizures accompa-nied by generalized tonic–clonic seizures, treatment becomes more difficult[14]. Ethosuximide and sodium valproate are two common medicationsused as monotherapy for absences.

Tonic seizures

Tonic seizures are manifest by sudden-onset tonic extension or exion of the head, trunk, or extremities. According to Engel [15], the characteristicsof a tonic seizure include a diffuse increase in muscle tone, impaired con-sciousness, and no clear clonic manifestations. This presentation lasts sev-eral seconds. If standing, the patient will fall to the ground. In addition,there are various autonomic changes that occur, such as bladder inconti-nence, tachypnea, tachy- or bradycardia, facial ushing, and pupil dilation[16]. Tonic seizures are often accompanied by other seizure types. For exam-ple, a study by Werhahn and colleagues [17] found that tonic seizures are

typically either preceded or followed by other seizure types. In this study,72% of tonic seizures were followed by either a clonic, a generalizedtonic–clonic, or other seizure type. The other 28% of events ended in tonicseizure, including those patients who experienced only a tonic seizure [17].These seizures typically resist treatment with antiepileptic drugs as well assurgery [15]. Tonic seizures are commonly part of an epileptic syndrome,most notably Lennox–Gastaut syndrome (LGS). This syndrome is charac-terized by a triad of multiple types of epileptic seizures, slow wave activityon electroencephalogram, and slow mental development. This disease affects

3% to 10% of all children with epilepsy. Treatment of LGS is often unsat-isfactory, resulting in poor quality of life because of the need for high dosesof antiepileptic drugs [18,19] .

Clonic seizuresClonic seizures are rhythmic, jerking movements with impaired conscious-

ness. These seizures occur frequently in people who have focal epilepsy. Thereis some suggestion in the literature that most focal clonic seizures are actuallyfocal tonic–clonic seizures with a tonic phase of variable expression [20].

Myoclonic seizuresMyoclonic seizures involve involuntary and excessive movement of the

body or the limbs. The onset of these seizures is quite sudden and the dura-tion short. These seizures can be focal or generalized with respect to bodymovement. A distinct feature of myoclonus is synchrony, although asyn-chronous jerking is sometimes seen [21]. The difficulty in classifying this


8/14/2019 Dent Clin N Am 50 (2006) 607–623


8/14/2019 Dent Clin N Am 50 (2006) 607–623


Pulse oximetry, electrocardiography, and the monitoring of blood pressureare indicated. In addition, peripheral venous access should be obtained to

administer uid resuscitation and medical therapy. Laboratory studiesshould be obtained, including those for electrolytes, glucose, liver function,complete blood count, creatine kinase, toxicology, and antiepileptic druglevels.

Intravenous lorazepam or midazolam will terminate status epilepticus in60% to 90% of patients. Lorazepam should be given at a dose of 4mg at2 mg/min. Diazepam can also be used and will terminate status epilepticusin 60% to 80% of patients. Diazepam should be administered at a dose of 10 to 20 mg at 2 mg/min. For office patients, emergency services should be

contacted immediately for transfer to the nearest emergency department fordenitive care. This condition may require admission to an ICU, neurologyconsultation, and intravenous infusion of anticonvulsants. These includebarbiturates, benzodiazepines, and propofol [25–30] .

Sudden unexpected death in epilepsy

Sudden unexpected death in epilepsy (SUDEP) has an incidence reportedto range from 1:100 to 1:1000. These deaths are nontraumatic, nondrowningevents in which postmortem exam does not reveal toxicological or anatom-ical cause for death. The most common nding among these deaths is thatthey are typically unwitnessed. Risk factors include presence of a seizure dis-order, poorly controlled seizures, refractory epilepsy, male sex, subtherapeu-tic doses of antiepileptic medications, and alcohol use. One study found thatthe greater the number of AEDs ever taken was linked to a higher risk of SUDEP [31]. This increased number of antiepileptic medications may be in-dicative of ‘‘uncontrolled epilepsy.’’ Postmortem studies in these cases typ-ically reveal pulmonary edema as a common nding. In some witnessedcases of SUDEP, according to reports, patients appeared to be having dif-culty breathing. Many now think SUDEP may be related to obstructiveor central apnea and pulmonary edema. It is theorized that assistance inpositioning and maintaining airways in seizure victims may help preventSUDEP [32–34] .

Evaluation and diagnosis

Proper workup for diagnosing epilepsy involves multiple approaches.

Given the vast array of clinical presentations, more standardized techniquesneed to be employed to diagnose epilepsy and rule out other conditions.Such techniques include electroencephalography, MRI, routine blood tests,lumbar puncture, and electrocardiography.

The electroencephalogram is an important diagnostic study that hasmany limitations. Electroencephalogram ndings are critical for properlydiagnosing, classifying, and treating various forms of epilepsy and epileptic


8/14/2019 Dent Clin N Am 50 (2006) 607–623


syndromes. The electroencephalogram is a summation of excitatory and in-hibitory activity recorded by electrodes placed on the scalp or surface of the

brain. During the interictal period, neurologists look for interictal epilepti-form discharges (IEDs). The problem with electroencephalograms is thatnot all epileptic patients exhibit IEDs, while some nonepileptic patientsdo. Therefore, various techniques are employed to increase the likelihoodof IEDs when attempting to diagnose epilepsy. These techniques includesleep, sleep deprivation, hyperventilation, and photic stimulation [35–38] .These modalities may on rare occasions precipitate an epileptic seizure.The use of additional electrodes above the number typically used can alsoincrease the likelihood of capturing IEDs [39]. Intuitively, the more focal

IEDs suggest localized epilepsy, whereas generalized IEDs suggest general-ized epilepsy. The location of the IED can sometimes, but not always, pointto the origin of the seizure. Usually, a diagnosis can be rendered froma good history in collaboration with an interictal electroencephalogram.However, if the patient does not respond well to antiepileptic medications,then an ictal electroencephalogram may be necessary. This is often a videoelectroencephalogram, which will be discussed later.

MRI is used to visualize structural abnormalities in patients with epi-lepsy. MRI can provide extremely detailed images of the anatomy of the

brain and can be used to identify various anomalies in the brain that maybe causing seizures. Mesial temporal lobe sclerosis is a common conditionrelated to seizures of temporal lobe origin. MRI can be used to performquantitative analysis of the hippocampus. This can allow for the detectionof hippocampal neuronal loss (ie, hippocampal atrophy), which is typicallyindicative of mesial temporal lobe sclerosis and seizures of temporal lobe or-igin [40–42] . Neoplastic lesions can also be readily detected using MRI. Gli-omas, neuroepitheliomas, and gangliogliomas are common brain tumorsassociated with epilepsy [41]. Vascular malformations, such as arteriovenous

malformations, cavernous hemangiomas, venous angiomas, and telangiecta-ses are often seen in patients with partial seizures [43]. Neuronal migrationaldisorders, such as pachygyria and polymicrogyria, can also be detected.Some of these are linked to such conditions as Sturge–Weber syndrome.These images can help physicians decide to proceed with surgery much ear-lier now than in the past. If the patient has a condition that has historicallyresponded poorly to antiepileptic medications and favorably to surgery, thedecision to pursue surgery can be made much more easily for both the pa-tient and the physician [44]. These images help not only in the diagnosis, but

also in the actual surgical treatment.For some patients, an MRI will show no abnormalities. For such cases,a video electroencephalogram is used as part of diagnostic algorithms toclarify or rule out a particular diagnosis. This study is literally an electroen-cephalogram performed while being recorded on video. The neurologist willthen view the electroencephalogram and the video simultaneously on splitscreens. This allows for a very precise examination of how the patient acts


8/14/2019 Dent Clin N Am 50 (2006) 607–623


during the seizure in comparison to ndings on the electroencephalogram[45]. Any candidate being considered for surgical intervention or vagal nerve

stimulation should have a video electroencephalogram [46].

Management

Management of epilepsy includes medication, surgery, or vagal nervestimulation. In discussing management of epilepsy, proper diagnosis is espe-cially important. The practitioner must obtain the appropriate studies andcompare these to a thorough history so that a diagnosis can be reached be-fore initiating any treatment. Certainly one would want to be sure of the

diagnosis before suggesting surgical intervention. Conversely, surgical orother nonpharmacological treatment options should not be delayed if the di-agnosis has a history of poor response to antiepileptic medications.

Antiepileptic medications are effective in treating seizures when used in theright patients. Even so, many patients continue to experience seizures despitemedical treatment. Typically, a mainstay of six antiepileptic medications isused. These medications are phenobarbital, phenytoin, benzodiazepines, car-bamazepine, ethosuximide, and valproic acid. However, the number of newdrugs available has been increasing steadily over the past several years. The

goal of pharmacological therapy is obviously to control seizure activity whileminimizing the adverse effects of antiepileptic medications. This goal can beachieved in approximately 70% to 75% of patients with epilepsy. Most pa-tients are effectively controlled with a single antiepileptic medication. A smallpercentage of patients will require a second antiepileptic medication added tothe regimen. Initially, antiepileptic medications may cause drowsiness, dizzi-ness, or cognitive impairment. These symptoms are typically temporary, butmay result in noncompliance [47–50].

Long-term use of antiepileptic drugs has potentially serious adverse ef-

fects. Bone mineral density has been shown to be reduced in some patientswho take enzyme-inducing antiepileptic medications. These antiepilepticmedications include phenytoin, phenobarbital, and carbamazepine. This ef-fect has been shown to be independent of age. This decrease in bone mineraldensity coupled with the high fall rate of seizure patients results in an in-creased risk of osteoporotic fractures in this population [51,52] . The litera-ture includes some mention of the use of bisphosphonates in these patients.This would obviously have potential effects on dental therapy for these pa-tients, depending on the type of bisphosphonate used [51].

In addition to bone density reduction, antiepileptic medications have alsobeen linked to obesity. Valproate, gabapentin, carbamazepine, and pregaba-lin have been linked to weight gain. This has numerous health consequences,such as increased risk of diabetes, cardiovascular disease, and polycysticovaries. Also, weight gain has obvious negative psychological effects[53,54] . Any of these negative effects could lead to noncompliance withantiepileptic therapy.


8/14/2019 Dent Clin N Am 50 (2006) 607–623


Weight loss has been shown to be associated with felbamate and topira-mate. The weight loss associated with felbamate typically occurs during the

rst 3 months of therapy. Some patients, however, experience severe weightloss, leading to noncompliance [55,56] .

Once a patient has been seizure-free for 2 years while on antiepileptic med-ications, the treating physician may consider withdrawing the patient fromdrug therapy. This has been shown to be a safe and viable option when consid-ering the long-term effects of antiepileptic drug therapy. Appropriate caseselection is key to the success of weaning a patient from antiepileptic medica-tions. Signicant predictors of excellent outcome in weaning include age of on-set younger than 6 years of age, idiopathic etiology, having only absence

seizures, lack of postictal signs, and normal electroencephalogram ndings.Age of onset at more advanced ages and severe forms of epilepsy syndromes,such as LGS, are poor indicators of successful seizure-free weaning. Childrenwho relapse after the rst attempt at weaning may be successfully weaned ata later time. According to some reports in the literature, weaning should notoccur over a period shorter than 6 months [57]. Other studies indicate thata shorter time period, such as 4 to 6 weeks, is safe [57–60] .

Brain surgery for epilepsy is a viable option for those suffering from re-fractory epilepsy. The type of surgery varies from removal of a small lesion

(lesionectomy), removal of a particular lobe (lobectomy), to removal of anentire hemisphere (hemispherectomy). Careful mapping occurs so that unto-ward effects of resection can be minimized. The advent of MRI has dramat-ically improved preoperative evaluation of patients. The idea of ‘‘surgicallyremediable epilepsies’’ was introduced by Engel and Shewmon in 1993. Thisrefers to epileptic disorders whose pathophysiology is well understood,whose natural history is known to be refractory or progressive once the ma- jor rst-line antiepileptic medications fail, and for which surgery offers anexcellent chance to eliminate disabling seizures completely. These syndromes

include mesial temporal lobe epilepsy, epilepsy with well-circumscribed le-sions and unilateral hemispheric disorders in infants and children. Althoughepilepsy surgery is considered a safe and viable option, it obviously is notwithout risks. Risks include memory loss, paralysis, visual disturbances,and failure. Given the devastating effect refractory epilepsy can have ona person’s life, evaluation for early surgical intervention after failure of an-tiepileptic medications should be considered. The negative effects of long-term antiepileptic medications should also be considered. The long-termoutcome of epilepsy surgery appears to be promising [61–64] .

Vagal nerve stimulation has been accepted as an effective adjunct in thetreatment of refractory epilepsy. This treatment is used after multiple med-ical treatments have failed. The exact mechanism that enables vagal nervestimulation to be effective is not fully understood. The device used for vagalnerve stimulation has helical-shaped leads that are placed around the leftvagus nerve. These leads receive impulses from a generator placed subcuta-neously in the chest. The impulse frequency, current, and on/off cycles can


8/14/2019 Dent Clin N Am 50 (2006) 607–623


be altered. There are varying opinions regarding the optimal settings for thedevice. Decrease in seizure frequency is not immediate. The most common

side effects of vagal nerve stimulation are frequent coughing, voice changes,diarrhea, and dyspnea. Much research is ongoing regarding the mechanismof vagal nerve stimulation as well as other uses for the device [65–68] .

Special populations

The category of special populations includes pregnant women and the el-derly. The literature indicates that women with epilepsy have an increased fre-

quency of seizures during pregnancy [69]. It is thought that noncompliancewith antiepileptic medications, sleep deprivation, and changes in pharmaco-dynamics are related to the increase in frequency of seizure activity [70,71] .

Most women with epilepsy bear normal, healthy children, although thereis a higher risk for adverse pregnancy outcomes [70].

Cerebrovascular disease is the most common cause of epilepsy in theelderly [72]. Other causes include hypoglycemia, metabolic disorders, braintumors, and head trauma. Antiepileptic medications are the rst line of treatment for elderly patients with epilepsy. These are usually effective.

Most elderly patients will remain on antiepileptic medications for the re-mainder of their lives. Implementation of antiepileptic drug therapy is bythe ‘‘start low and go slow’’ method. Lower doses are slowly titrated untilcontrol is achieved while balancing the negative effects [73].

Medical and dental considerations

Patients with epilepsy have been shown to demonstrate a signicantly

worse dental condition when compared with an age-matched group of thegeneral population [2]. This is particularly true in patients who sufferfrom poorly controlled generalized tonic–clonic seizures. There are manypossible explanations for this nding. In general, patients with poorly con-trolled epilepsy tend to have a low socioeconomic status. This is most likelydue to the prejudice and difficulty many poorly controlled epilepsy patientsface when seeking employment. Low socioeconomic status and poor oralhealth frequently go hand in hand.

Dentists should be as familiar with seizure disorders as possible. This will

reduce or eliminate any potential anxiety the dentist may have when treatingpatients with these disorders. Not only should dentists be able to managethese patients for routine dental care on a long-term basis, but also in anacute situation such as an in-office seizure.

During the rst appointment with an epileptic patient, the practitionermust obtain a very thorough medical history. The questions listed in Box 1are important when taking a history for seizures.


8/14/2019 Dent Clin N Am 50 (2006) 607–623


Although the list of questions in Box 1 may seem tedious, the answers willensure that the dentist is well informed as to the nature of this illness. Thiswill allow the dentist to be better prepared for any acute episodes that occurin the office. A medical consultation is in order for patients with epilepsy. If the patient suffers from poorly controlled, frequent, severe seizures, a hospi-tal setting is more appropriate.

As with any other patient, anxiety control measures should be taken. Ad-mittedly, this is a vague recommendation because the term ‘‘anxiety control’’is not well dened. Such things should be common sense for most practi-tioners. By asking the patient what makes them most anxious can help guidepractitioners in the right direction. Maybe the patient would like to be con-stantly informed of what is going on during treatment, or maybe not. Reassur-ing the patient that things are going well often helps ease anxiety. Avoidingsudden, unexpected movements is typically a good idea. The use of nitrous ox-ideisnotcontraindicatedin epilepsypatients and shouldbeconsidereda viable

option. Intravenous sedation should be considered for those practitionerstrained to do so. Having a well-trained staff that understands epilepsy is crit-ical. In addition to knowing about epilepsy in general, it is a good idea for thestaff to know about each particular patient’s type of seizure so they can be onthe lookout for potential seizure activity.

Even in ‘‘well-controlled’’ patients, seizures can occur in the office for var-ious reasons, including fatigue, stress, alcohol use, medication noncompliance,

Box 1. Questions for an epileptic patient when taking

a history of seizuresWhen was the condition diagnosed?What were the presenting symptoms?Are there identiable precipitating circumstances?Do you experience an aura? If so, describe the aura.How long is a typical seizure? (Eyewitnesses are helpful whendiscussing this.)Do you become unconscious during the seizure?Is there a postictal phase? If so, describe it.How frequent are your seizures? When was the last event?What medications do you take? Do you get the plasma levelchecked?Have you had an electroencephalogram and MRI? If so, whatwere the results?Has surgery been considered? Do you have a vagal nervestimulator?Is there a history of head trauma, brain tumor, or othermalformation?


8/14/2019 Dent Clin N Am 50 (2006) 607–623


dental lights, local anesthetic, or other ‘‘idiopathic’’ causes. In preparing forthe possibility of a seizure in the office, the dentist and the entire staff must,

at the very least, be trained in basic life support. This training should includea plan of action that is specic to each member of the team. That plan of action should designate who is to contact emergency medical services. Ide-ally, each member of the team will have been assigned a task before anyemergency so that implementation of emergency treatment can occur calmlyand efficiently. At the onset of the seizure, the procedure should be stoppedimmediately. All instruments should be removed from the oral cavity. Thechair should be placed in the supine position and low to the ground. Thepatient should be stabilized to prevent injury to himself or herself during

the seizure. Basic life support should begin immediately. This should includeplacement of vital-sign monitors, such as electrocardiogram, pulse oximeter,and blood pressure cuff.

For most seizures, basic life support is adequate. However, if the seizurelasts longer than 5 minutes, more advanced techniques should be employedif the doctor and the staff have the proper training and equipment to do so.In this scenario, basic life support should be continued while venupunctureis performed. Once intravenous access has been gained, administration of an-ticonvulsant medication is highly effective in terminating seizures. Benzodiaz-

epines are the drugsof choice for emergency treatment of seizures. Lorazepam,diazepam, and midazolam are acceptable choices for administration.The doctor should not rule out the possibility that other medical emer-

gencies can mimic a seizure. Syncope, cerebrovascular accident, myocardialinfarction, cardiac arrest, and hypoglycemia should be considered. Place-ment of monitors as stated above will aid in ruling out these other possibil-ities. In addition, obtaining a nger-stick glucose level is important.

For general restorative purposes, missing teeth should be replaced withxed devices rather than removable devices. It is thought that a removable

device could be easily dislodged during a seizure, leading to intraoral traumaor aspiration. However, a xed prosthesis can also be dislodged during a sei-zure. The dental practitioner should perform a thorough oral exam aftera seizure to check for trauma or dislodgement of any appliance or naturalteeth. Metal occlusal surfaces are preferred over ceramic so as to withstandclenching forces [74,75] . Xerostomia may be a problem for patients takingantiepileptic medications. If xerostomia is present, uoride treatment shouldbe considered for caries reduction [3].

Antiepileptic medications have several negative side effects that should be

considered when rendering treatment. For example, phenytoin is related tothe barbiturates in chemical structure and may cause drowsiness, slurredspeech, and other depressant-type manifestations. Thrombocytopenia isalso possible with phenytoin. Many medications can either increase or de-crease plasma levels of phenytoin. For this reason, it is recommended thatthe practitioner always check the newest drug reference before prescribingmedications to epileptic patients. It is also important to know if the patient


8/14/2019 Dent Clin N Am 50 (2006) 607–623


obtains serum antiepileptic-drug levels from their neurologist or primarycare physician. If so, it is advised that the dentist consult the physician to

nd out if the patient is subtherapeutic, therapeutic, or above therapeuticserum levels. This is of particular importance if intravenous sedation or gen-eral anesthesia techniques are going to be employed.

It is well known that gingival enlargement is commonly seen with phenyt-oin use. In addition, valproic acid, carbamazepine, and vigabatrin havedemonstrated gingival enlargement. Gingival enlargement in patients takingthese medications is strongly correlated with poor plaque control, andplaque is an important cofactor in drug-associated gingival enlargement[76,77] . Gingival enlargement in this patient population may be reduced,

but not eliminated. The key is being fastidious about oral hygiene and pla-que removal. Patients taking medications related to gingival enlargementshould be placed on 3-month recall [78]. This appointment should includecomplete periodontal cleaning, both supra- and subgingival, as well as oralhygiene instruction. The advent of many new antiepileptic drugs opensthe possibility of converting to a different antiepileptic medication, therebypotentially eliminating the gingival enlargement. This change in medicationwould certainly be at the discretion of the treating neurologist or primarycare physician. Surgical intervention in the form of beveled gingivectomy

has been recommended. Recurrence is possible after surgery [79].Many dental practitioners have hospital privileges and routinely treat pa-tients in this setting. It is generally accepted that most anesthesia departmentswould like to evaluate patients with any neurological disorder before the dayof surgery. The anesthesiologist may want to obtain levels of phenytoin orphenobarbital before the procedure. Any additional studies, such as EKGand chest radiograph, will depend on other illnesses the patient may have.

The dentist should be sure to ask the patient if they have a vagus nervestimulator. There is a denitive contraindication to the use of diathermy de-

vices in patients with vagus nerve stimulators. There is a report in the liter-ature regarding a 70-year-old patient who received removal of his maxillaryteeth secondary to periodontal disease. The case was uneventful. The patientreturned to the office the following day for diathermy treatment. After thetreatment, the patient was not arousable. It was determined that he had suf-fered severe brain injury as a result of the diathermy treatment [80]. It can-not be assumed that all routine dental equipment is safe to use in treatingpatients with vagus nerve stimulators [81].

Summary

Treating patients with epilepsy and other medical problems is somethingthat all dental practitioners face frequently. It is critical to take a thorough his-tory for epileptic patients. This includes a complete description of the seizure,the type of treatmentcurrently being rendered, andhowwell controlled the pa-tient is at the time of treatment. The office staff should be fully prepared to


8/14/2019 Dent Clin N Am 50 (2006) 607–623


handle a seizure. The team should be organized ahead of time so the emer-gency treatment can be rendered efficiently. Delay in contacting emergency

medical services can cause increased morbidity and mortality in patientswho suffer from in-office medical emergencies. If the patient has severe, poorlycontrolled epilepsy, a hospital setting is recommended for treatment. Other-wise, a well-controlled patient should easily be treated in the office.

The practice of dentistry offers many challenges. These most often in-clude various dilemmas regarding restorative treatment options, prognosisfor teeth, and appropriate choices for implant design, among many other is-sues. Dentists must never forget that they have been given the charge of treating the patient as a whole. This brings with it the awesome responsibil-

ity of knowing as much about each patient as possible. As much as it is a re-sponsibility, it is also a privilege.

References

[1] Brodie MJ, French JA. Management of epilepsy in adolescents and adults. Lancet 2000;356(9226):323–9.

[2] Karolyhazy K, Kovacs E, Kivovics P, et al. Dental status and oral health of patients withepilepsy: an epidemiologic study. Epilepsia 2003;44(8):1103–8.

[3] Stoopler ET, Sollecito TP, Greenberg MS. Seizure disorders: update of medical and dentalconsiderations. Gen Dent 2003;51(4):361–6.[4] Sander JW, Shorvon SD. Epidemiology of the epilepsies. J Neurol Neurosurg Psychiatry

1996;61(5):433–43.[5] Wyllie E. The treatment of epilepsy principles and practice. 2nd edition. Baltimore (MD):

Williams &Wilkins; 1997.[6] Sirven JI. Classifying seizures and epilepsy: a synopsis. Semin Neurol 2002;22(3):237–46.[7] Meletti S, Cantalupo G, Volpi L, et al. Rhythmic teeth grinding induced by temporal lobe

seizures. Neurology 2004;62(12):2306–9.[8] Quarato PP, Di Gennaro G, Mascia A, et al. Temporal lobe epilepsy surgery: different sur-

gical strategies after a non-invasive diagnostic protocol. J Neurol Neurosurg Psychiatry

2005;76(6):815–24.[9] Jutila L, Immonen A, Mervaala E, et al. Long term outcome of temporal lobe epilepsy

surgery: analyses of 140 consecutive patients. J Neurol Neurosurg Psychiatry 2002;73(5):486–94.

[10] Panayiotopoulos CP. Typical absence seizures and their treatment. Arch Dis Child 1999;81(4):351–5.

[11] Duncan JS. Idiopathic generalized epilepsies with typical absences. J Neurol 1997;244(7):403–11.

[12] Andreoli TE, Cecil RL. Cecil essentials of medicine. 5th edition. Philadelphia: W.B. Saun-ders; 2001.

[13] Agathonikou A, Panayiotopoulos CP, Giannakodimos S, et al. Typical absence status in

adults: diagnostic and syndromic considerations. Epilepsia 1998;39(12):1265–76.[14] Wolf P, Inoue Y. Therapeutic response of absence seizures in patients of an epilepsy clinic for

adolescents and adults. J Neurol 1984;231(4):225–9.[15] Engel J, Pedley TA, Aicardi J. Epilepsy d a comprehensive textbook. Philadelphia: Lippin-

cott-Raven; 1997.[16] Chatrian GE, Lettich E, Wilkus RJ, et al. Polygraphic and clinical observations on tonic-

autonomic seizures. Electroencephalogr Clin Neurophysiol Suppl 1982;35:101–24.


8/14/2019 Dent Clin N Am 50 (2006) 607–623


[17] Werhahn KJ, Noachtar S, Arnold S, et al. Tonic seizures: their signicance for lateralizationand frequency in different focal epileptic syndromes. Epilepsia 2000;41(9):1153–61.

[18] Markand ON. Lennox–Gastaut syndrome (childhood epileptic encephalopathy). J ClinNeurophysiol 2003;20(6):426–41.

[19] Blume WT. Pathogenesis of Lennox–Gastaut syndrome:considerations and hypotheses.Ep-ileptic Disord 2001;3(4):183–96.

[20] Hamer HM, Luders HO, Knake S, et al. Electrophysiology of focal clonic seizures inhumans: a study using subdural and depth electrodes. Brain 2003;126(3):547–55.

[21] Fahn S, Marsden CD, Van Woert MH. Denition and classication of myoclonus. AdvNeurol 1986;43:1–5.

[22] Genton P, Roger J, Guerrini R, et al. History and classication of ‘‘myoclonic’’ epilepsies:from seizures to syndromes to diseases. Adv Neurol 2005;95:1–14.

[23] Malamed SF, Robbins KS. Handbook of medical emergencies in the dental office. 3rd edi-tion. St. Louis (MO): Mosby; 1987.

[24] Ikeno T, Shigematsu H, Miyakoshi M, et al. An analytic study of epileptic falls. Epilepsia1985;26(6):612–21.

[25] Bleck TP. Refractory status epilepticus. Curr Opin Crit Care 2005;11(2):117–20.[26] Claassen J, Hirsch LJ, Emerson RG, et al. Treatment of refractory status epilepticus with

pentobarbital, propofol, or midazolam: a systematic review. Epilepsia 2002;43(2):146–53.[27] Tasker RC. Emergency treatment of acute seizures and status epilepticus. Arch Dis Child

1998;79(1):78–83.[28] Manno EM. New management strategies in the treatment of status epilepticus. Mayo Clin

Proc 2003;78(4):508–18.[29] Willmore LJ. Epilepsy emergencies: the rst seizure and status epilepticus. Neurology 1998;

51(5, Suppl 4):S34–8.[30] Walker M. Status epilepticus: an evidence based guide. BMJ 2005;331(7518):673–7.[31] Langan Y, Nashef L, Sander JW. Case-control study of SUDEP. Neurology 2005;64(7):

1131–3.[32] Langan Y, Nashef L, Sander JW. Sudden unexpected death in epilepsy: a series of witnessed

deaths. J Neurol Neurosurg Psychiatry 2000;68(2):211–3.[33] Nashef L, Garner S, Sander JW, et al. Circumstances of death in sudden death in epilepsy:

interviews of bereaved relatives. J Neurol Neurosurg Psychiatry 1998;64(3):349–52.[34] Kloster R, Engelskjon T. Sudden unexpected death in epilepsy (SUDEP): a clinical perspec-

tive and a search for risk factors. J Neurol Neurosurg Psychiatry 1999;67(4):439–44.[35] Goodin DS, Aminoff MJ, Laxer KD. Detection of epileptiform activity by different nonin-

vasive EEG methods in complex partial epilepsy. Ann Neurol 1990;27(3):330–4.[36] Goodin DS, Aminoff MJ. Does the interictal EEG have a role in the diagnosis of epilepsy?

Lancet 1984;1(8381):837–9.[37] Ellingson RJ, Wilken K, Bennett DR. Efficacy of sleep deprivation as an activation proce-

dure in epilepsy patients. J Clin Neurophysiol 1984;1(1):83–101.[38] Proceedings of symposium on epilepsy, sleep and sleep deprivation. Bad Kreuznach, Ger-

many, September 24–25, 1982. Epilepsy Res Suppl 1991;2:1–285.[39] Homan RW, Jones MC, Rawat S. Anterior temporal electrodes in complex partial seizures.

Electroencephalogr Clin Neurophysiol 1988;70(2):105–9.[40] Sisodiya SM, Moran N, Free SL, et al. Correlation of widespread preoperative magnetic

resonance imaging changes with unsuccessful surgery forhippocampal sclerosis. Ann Neurol

1997;41(4):490–6.[41] Bergen D, Bleck T, Ramsey R, et al. Magnetic resonance imaging as a sensitive and specic

predictor of neoplasms removed for intractable epilepsy. Epilepsia 1989;30(3):318–21.[42] Kuzniecky R, de la Sayette V, Ethier R, et al. Magnetic resonance imaging in temporal lobe

epilepsy: pathological correlations. Ann Neurol 1987;22(3):341–7.[43] DodickDW,Cascino GD,Meyer FB. Vascular malformations and intractable epilepsy:out-

come after surgical treatment. Mayo Clin Proc 1994;69(8):741–5.


8/14/2019 Dent Clin N Am 50 (2006) 607–623


[44] Urbach H, Hattingen J, von Oertzen J, et al. MR imaging in the presurgical workup of pa-tients with drug-resistant epilepsy. AJNR Am J Neuroradiol 2004;25(6):919–26.

[45] Benbadis SR, O’Neill E, Tatum WO, et al. Outcome of prolonged video-EEG monitoring ata typical referral epilepsy center. Epilepsia 2004;45(9):1150–3.

[46] Benbadis SR, Tatum WO, Vale FL. When drugs don’t work: an algorithmic approach tomedically intractable epilepsy. Neurology 2000;55(12):1780–4.

[47] Devinsky O. Patients with refractory seizures. N Engl J Med 1999;340(20):1565–70.[48] Sander JW. The useof antiepileptic drugs d principles and practice. Epilepsia 2004;45(Suppl 6):

28–34.[49] Kwan P, Brodie MJ. Early identication of refractory epilepsy. N Engl J Med 2000;342(5):

314–9.[50] Morrell MJ. Antiepileptic medications for the treatment of epilepsy. Semin Neurol 2002;

22(3):247–58.[51] Verrotti A, Greco R, Latini G, et al. Increased bone turnover in prepubertal, pubertal, and

postpubertal patients receiving carbamazepine. Epilepsia 2002;43(12):1488–92.[52] Sheth RD. Metabolic concerns associated with antiepileptic medications. Neurology 2004;

63(10, Suppl 4):S24–9.[53] Luef G, Abraham I, Haslinger M, et al. Polycystic ovaries, obesity and insulin resistance in

women with epilepsy. A comparative study of carbamazepine and valproic acid in 105women. J Neurol 2002;249(7):835–41.

[54] Isojarvi JI, Laatikainen TJ, Knip M, et al. Obesity and endocrine disorders in women takingvalproate for epilepsy. Ann Neurol 1996;39(5):579–84.

[55] Canger R, Vignoli A, Bonardi R, et al. Felbamate in refractory partial epilepsy. Epilepsy Res1999;34(1):43–8.

[56] Carmant L, Holmes GL, Sawyer S, et al. Efficacy of felbamate in therapy for partial epilepsyin children. J Pediatr 1994;125(3):481–6.[57] Mastropaolo C, Tondi M, Carboni F, et al. Prognosis after therapy discontinuation in

children with epilepsy. Eur Neurol 1992;32(3):141–5.[58] Geerts AT, Niermeijer JM, Peters AC, et al. Four-year outcome after early withdrawal of

antiepileptic drugs in childhood epilepsy. Neurology 2005;64(12):2136–8.[59] Dooley J, Gordon K, Cameld P, et al. Discontinuation of anticonvulsant therapy in

children free of seizures for 1 year: a prospective study. Neurology 1996;46(4):969–74.[60] Bouma PA, Peters AC, Brouwer OF. Long term course of childhood epilepsy following

relapse after antiepileptic drug withdrawal. J Neurol Neurosurg Psychiatry 2002;72(4):507–10.

[61] Wiebe S. Early epilepsy surgery. Curr Neurol Neurosci Rep 2004;4(4):315–20.[62] Tellez-Zenteno JF, Dhar R, Wiebe S. Long-term seizure outcomes following epilepsy sur-

gery: a systematic review and meta-analysis. Brain 2005;128(Pt 5):1188–98.[63] Holmes G. Epilepsy surgery in children: when, why, and how. Neurology 2002;58

(12, Suppl 7):S13–20.[64] Wiebe S. Brain surgery for epilepsy. Lancet 2003;362(Suppl):S48–9.[65] Charous SJ, Kempster G, Manders E, et al. The effect of vagal nerve stimulation on voice.

Laryngoscope 2001;111(11 Pt 1):2028–31.[66] DeGiorgio C, Heck C, Bunch S, et al. Vagus nerve stimulation for epilepsy: randomized

comparison of three stimulation paradigms. Neurology 2005;65(2):317–9.[67] Murphy JV, Torkelson R, Dowler I, et al. Vagal nerve stimulation in refractory epilepsy: the

rst 100patients receivingvagal nerve stimulation at a pediatricepilepsy center. Arch PediatrAdolesc Med 2003;157(6):560–4.

[68] Sanossian N, Haut S. Chronic diarrhea associated with vagal nerve stimulation. Neurology2002;58(2):330.

[69] Knight AH, Rhind EG. Epilepsy and pregnancy: a study of 153 pregnancies in 59 patients.Epilepsia 1975;16(1):99–110.


8/14/2019 Dent Clin N Am 50 (2006) 607–623


[70] Yerby MS. Special considerations for women with epilepsy. Pharmacotherapy 2000;20(8 Pt 2):159S–70S.

[71] Pschirrer ER. Seizure disorders in pregnancy. Obstet Gynecol Clin North Am 2004;31(2):373–84 [vii.].

[72] Pohlmann-Eden B. Issues when treating epilepsy in the elderly. Acta Neurologica Scandi-navica 2005;112(S181):40–6.

[73] Brodie MJ, Kwan P. Epilepsy in elderly people. BMJ 2005;331(7528):1317–22.[74] Sanders BJ, Weddell JA, Dodge NN. Managing patients who have seizure disorders: dental

and medical issues. J Am Dent Assoc 1995;126(12):1641–7.[75] Hupp WS. Seizure disorders. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001;

92(6):593–6.[76] Casetta I, Granieri E, Desidera M, et al. Phenytoin-induced gingival overgrowth: a commu-

nity-based cross-sectional study in Ferrara, Italy. Neuroepidemiology 1997;16(6):296–303.[77] Dongari-Bagtzoglou A. Drug-associated gingival enlargement. J Periodontol 2004;75(10):

1424–31.[78] Hall EE. Prevention and treatment considerations in patients with drug-induced gingival

enlargement. Curr Opin Periodontol 1997;4:59–63.[79] Ilgenli T, Atilla G, Baylas H. Effectiveness of periodontal therapy in patients with drug-

induced gingival overgrowth. Long-term results. J Periodontol 1999;70(9):967–72.[80] Nutt JG, Anderson VC, Peacock JH, et al. DBS and diathermy interaction induces severe

CNS damage. Neurology 2001;56(10):1384–6.[81] Roberts HW. The effect of electrical dental equipment on a vagus nerve stimulator’s

function. J Am Dent Assoc 2002;133(12):1657–64.


dent clin n am 50 (2006) 607–623

Documents