Epilepsy

Developmental Disabilities: Epilepsy, Cerebral Palsy, and Autism

Stanley R. Surabian, DDS, JD

Copyright 2001 Journal of the California Dental Association.

This article provides the dentist with a review of the three developmental disabilities that do not have mental retardation as a diagnostic component: epilepsy, cerebral palsy, and autism. Discussion focuses on diagnostic criteria and other dental and medical considerations. A greater understanding of developmental disabilities allows the dentist to offer care in the dental office when feasible or to understand and develop referral relationships with colleagues who utilize the hospital operating room to provide comprehensive care.

"I asked my dentist if I could bring my child in for a dental checkup. Although I did not see any dental problems, and I brush and floss her teeth regularly, I felt it was time to start a routine of regular dental visits to prevent future problems. The dentist, at first, agreed to see my youngest child because my other children see the same dentist. I made the appointment and brought my daughter to the office; the dentist refused to see her upon realizing she has cerebral palsy."

Is this your practice? Probably not, however, the dentist who treats patients with developmental disabilities occasionally hears similar statements. Sometimes care may be more difficult because the normal routine needs to be modified, but most people with developmental disabilities bring something special to the office. The office staff may find the most fulfilling part of practice occurs when a certain individual comes to the office for an appointment and then hugs everyone on the staff on the way to the operatory, relates the experience of viewing a favorite television show or movie, or excitedly tells the office staff a joke or brief story. When this person’s name appears on the schedule, everyone’s day is made better. Some offices never enjoy such an experience because they turn away very special people requiring their professional skills. Oral Health in America: A Report of the Surgeon General addressed the magnitude of the problem:

"The oral health problems of individuals with disabilities are complex. These problems may be due to underlying congenital anomalies as well as to inability to receive the personal and professional health care needed to maintain oral health. There are more than 54 million individuals defined as disabled under the Americans With Disabilities Act, including almost a million children under age 6 and 4.5 million children between 6 and 16 years of age."¹

The purpose of this article is to provide the dentist with a review of the three developmental disabilities that do not have mental retardation as a diagnostic component: epilepsy, cerebral palsy, and autism. Discussion focuses on diagnostic criteria and other dental and medical considerations. A greater understanding of developmental disabilities allows the dentist to offer care in the dental office when feasible or to understand and develop referral relationships with colleagues who utilize the hospital operating room to provide comprehensive care. The discussion begins with epilepsy, the most prevalent major developmental disability that does not have mental retardation as a diagnostic component.

Epilepsy

A seizure is a transient episode of disturbed central nervous system dysfunction. Epilepsy is the tendency to have seizures.

Mechanism

Normal brain function is made possible by electrical charges passing between nerve cells in the brain to all parts of the body. In a seizure, intermittent bursts of intense electrical energy can disturb normal function.

Causes

In most cases, a cause cannot be determined. Estimations are that 70 percent of people with seizure disorders cannot be diagnosed with a specific cause of the disorder.² The remaining 30 percent are the result of permanent, nonprogressive cerebral changes. Head trauma, meningitis, tumors, lead poisoning, infections, and maternal injury affecting fetal brain development during pregnancy are most frequently identified as specific causes of seizure disorders.

Incidence

New cases of seizures and epilepsy occur each year at a significant rate, primarily in children and young adults. Of the 181,000 new cases, 45,500 are in children younger than 15; 74,000 are in people 15 to 64; and 60,000 are in people older than 65. Within two years, 75 percent will successfully control their seizures with treatment.³

Prevalence

The number of cases at any one time in the United States is 2.3 million.⁴ Thirty percent of cases occur in the developmental period up to age 18. Estimates of the number of people in the world with epilepsy are as high as 40 to 50 million; however, 75 percent of those do not receive treatment.²

Classification

A better understanding of epilepsy is made easier by a classification of the types of seizures and therapeutic measures used to control seizure activity (Table 1).

Generalized Seizures

Major Motor Seizures -- Grand Mal

The major motor seizure is called a grand mal seizure. This is the most common type of seizure. It is characterized by tonic movements where the muscles become board-like and by clonic movements where the extremities have rapid, jerking movements. There is a loss of consciousness; and the patient becomes akinetic, falling down. The major motor seizure has three distinct parts:

* Aura -- recognition of smells, tastes or visions that precede the seizure activity;

* Ictus -- the seizure period of tonic-clonic activity; and

* Post ictus -- a period of sleep immediately following the ictus period.

Dentists must be aware of the patient’s epilepsy. The patient’s medical history and follow-up oral dialogue will reveal the type of seizure and the course of seizure activity. This is very important because the trust between the patient and the dentist can help prevent injury in the dental office. The patient is able to recognize the aura and can relate this to the dentist when a seizure is impending. This allows enough time to protect the patient by rendering supportive care to prevent self-injury. The mouth must be left alone. No foreign objects such as tongue blades should be inserted into the mouth during the ictus phase of the seizure or injury may occur to the patient, the dentist, or the dental auxiliary staff.⁵ The staff should move the dental unit modules or instrument arms away from the patient while preventing the patient’s head from slipping off the headrest and the arms and legs from hitting surrounding equipment and furniture. The course of a grand mal seizure leads to the post ictus stage of sleep. When the patient recovers from this period, the dentist should remind the patient that he or she is in the dental office and has had a seizure. The patient will often be embarrassed and agitated, so a calming, understanding approach is best.

When the patient’s ictus phase lasts more than five minutes or a series of new seizures begins before the first episode is complete, the patient is in status epilepticus.⁶ This condition is rarely seen. It requires immediate treatment including administration of a parenteral benzodiazepine such as diazepam (Valium) or midazolam (Versed). Because the benzodiazepines are sedatives, the post ictus stage of sleep may be enhanced. A 911 call will allow paramedic management of the patient and transportation to a hospital emergency department.

Minor Motor Seizures -- Absence (Petit Mal)

The absence seizure makes up only 2 percent to 3 percent of all seizures. There is no aura, and the duration of the ictus period is a few seconds, rarely up to a minute in duration. Staring into space and rapid eye blinking creates the period of absence or the appearance of daydreaming.⁶ Some patients can trigger a petit mal seizure by hyperventilating. Onset is in early childhood and lasts into puberty with virtually no seizures after age 20.

Myoclonic Seizures

Myoclonic seizures are very rare and can occur in all ages as a result of permanent neurological damage from hypoxia or drug poisoning. The ictus period consists of short episodes of muscle contractions and spasms.⁶ There is no period of continuous seizure activity. The short episodes may reoccur after a period of time.

Febrile Seizures

During episodes of high fever, children up to 6 years of age can develop febrile seizures if body temperature is not well-controlled.⁶ Two percent to 3 percent of the population will experience a febrile seizure. Within one week, the child will have normal electroencephalogram and lab values, while 40 percent will have another seizure with another febrile episode.⁷

Partial Seizures

Simple Partial Seizures

The partial seizure occurs when the abnormal electrical activity is concentrated in a localized area of the brain. A simple partial seizure does not involve a loss of consciousness. The localized activity involves a certain muscle group, extremity, or various motor or sensory activities. Involuntary movements occur such as fumbling, lip smacking, senseless behavior, staring, visual sensations, and vocalizations.⁶

Complex Partial Seizures

The complex partial seizure involves loss of consciousness and can have secondary generalizations spreading to both cerebral hemispheres.⁶

Prognosis

Seizure disorders are diagnosed frequently in the pediatric population. A majority of patients with childhood epilepsy are free of seizures by adulthood.⁸ An increased understanding of epilepsy, concerns about antiepileptic drugs, and possible adverse effects in pediatric populations, result in no drug therapy at the time of diagnosis in 20 percent of the children in a community-based program; after one year, 10 percent continued with an antiepileptic drug.⁹ At one time, epilepsy was thought to be a chronic, progressive disease. It was believed historically that when a person had one seizure, a second seizure would ultimately occur and as the progression continued, seizure activity created more seizure activity "by increasing instability of the nerve elements."¹⁰ Drug interventions to prevent seizures early in the course of the disorder do not create a remission of the problem. The underlying condition of epilepsy, not the seizure itself, is responsible for the deterioration.¹¹

The ketogenic diet may be a benefit in children to control seizures when other forms of therapy do not succeed. Physician management is essential for this prescribed high-fat, low-carbohydrate, reduced-calorie diet.²

Traditional Antiepileptic Drugs

Antiepileptic drug therapy is based on three considerations. First, it blocks the initiation of electrical activity when a particular area of the brain is involved. Second, drug therapy prevents the spread of the electrical activity to other areas of the brain. Third, different drugs are available to treat different forms of epilepsy. Several drugs are currently prescribed (Table 2):

Phenytoin (Dilantin)

Phenytoin is a widely used drug to suppress major motor and partial seizures. It was introduced in 1938.¹² Its reduces the spread of electrical activity to other areas of the brain. In dentistry, phenytoin-induced gingival hyperplasia will occur in approximately 40 percent of patients using the medication in a routine regimen.¹³

While no correlation has been shown between the blood levels of phenytoin and the amount of gingival enlargement, a prophylactic program of oral hygiene control can prevent the development of pseudopockets. Nevertheless, the phenytoin-induced enlargement could not be prevented.¹⁴ This does not negate the value of initiating in-service education of care providers for clients of community-care programs.¹⁵ Correlation of phenytoin-induced gingival hyperplasia severity and calculus formation, inflammation, plaque score, and probing depth was evident without correlation with daily drug dose and duration of drug intake.¹⁶

Gingival overgrowth is noticed first in the interdental papillae with lobulations occurring coronally, and it decreases as it approaches the mucogingival junction.¹⁷ Slow overgrowth can lead to orthodontic-like forces that can displace teeth in the area. Phenytoin gingival overgrowth usually develops in the anterior areas during the first six months of phenytoin therapy with no enlargement after nine months.¹⁸

Surgical Treatment of Phenytoin-Induced Gingival Hyperplasia

When gingival overgrowth overcomes function by overgrowing the surfaces of the teeth, excision is necessary. Many people with epilepsy and phenytoin-induced gingival hyperplasia can be treated in a dental office. Surgery becomes necessary when function is compromised. Traditional periodontal surgery techniques may be used; however, many patients with epilepsy have other developmental disabilities. These concomitant disabilities may lead to a situation of patient uncooperation and resistance to routine oral hygiene measures. When a patient is compromised sufficiently by hyperplasia, overgrowth can limit mouth closure and biting, resulting in trauma to the overlying gingival tissues. Surgery may be required under controlled circumstances in a hospital operating room under general anesthesia. Periodontal surgery by traditional methods may become technically difficult and time-consuming, and considerable bleeding is probable.¹³ During the post-treatment period, the patient will continue to be uncooperative for definitive follow-up control including dressing or suture removal. Electrosurgery offers the best solution. The excision must be in attached gingiva, and care is given to avoid contacting periosteum or bone with the electrode tip. Remaining in one area with the electrode tip results in overheating the tissues, which leads to increased pain and possible necrosis. Following probing and pocket-marking, a large diamond-shaped electrode tip is used to excise the tissue to the proper gingival height. The same instrument is used to scallop gingival contour in the interdental papilla areas. Properly angled gingivectomy-gingivoplasty excisions complete tissue contouring. Other tips such as various loops are then used to finalize the removal of tissue tags and areas not accessible with larger tips. The unit is used in the cut setting. For persistent bleeding spots, a small ball tip may be used on cut-coagulation or coagulation settings to create hemostasis. The tissues should be frequently irrigated with sterile saline to prevent dehydration and to cool the tissues. Final debridement of root surfaces takes place when the teeth are made accessible by the surgery. Ultrasonic and hand instrumentation is used to debride calculus and smooth the root surfaces.

Phenobarbital (Luminal)

Phenobarbital, a long-acting barbiturate, is a widely used antiepileptic drug to suppress simple and, to a lesser extent, complex partial seizures and febrile seizures; and it is often used as an adjunctive medication with phenytoin for tonic-clonic seizures.⁶ Phenobarbital has been in use since 1912. It reduces the spread of electrical activity to other areas of the brain and elevates the seizure threshold. Phenobarbital is given in low dosages and is easily absorbed when administered orally. As with all barbiturates, depression of the central nervous system may occur.

Carbamazepine (Tegretol)

Carbamazepine is pharmacologically similar to tricyclic antidepressants. Introduced in 1974, carbamazepine is often used in the treatment of trigeminal neuralgia. Seizure control is achieved by reducing the spread of electrical activity to other areas of the brain and by blocking sodium channels, which inhibits generation of repeated bursts of electrical activity. As an effective agent to control simple and complex partial seizures and tonic-clonic seizures, it may be used to replace phenytoin and eliminate the possibility of gingival hyperplasia. In some patients, phenytoin may be the most effective antiepileptic drug; therefore, replacement is evaluated carefully by the treating physician. Part of the evaluation requires monitoring hepatic function because carbamazepine use may cause liver toxicity.⁶

Ethosuximide (Zarontin)

Succinimides are used for the effective management of absence seizures. Although well-absorbed orally, ethosuximide is a gastric irritant, making nausea and vomiting the most common side effects.⁶

Valproic Acid (Depakote)

Valproic acid is used to treat myoclonic seizures; secondarily, it is used to reduce the incidence of absence and tonic-clonic seizures. Its reduces the propagation of seizure-causing abnormal electrical activity in the brain. Monitoring hepatic function is essential to prevent hepatic toxicity.

Primidone (Mysoline)

Primidone is used to treat partial and tonic-clonic seizures. It is used primarily with carbamazepine and phenytoin as part of an antiepileptic drug regimen. There are two active metabolites, the first being phenobarbital for simple partial seizure control. The second active metabolite is phenylethylmalonamide for complex partial seizure control.

Clonazepam (Klonopin)

Clonazepam is a benzodiazepine drug used to treat absence and myoclonic seizures. Benzodiazepines primarily act on the brain’s limbic system; therefore, sedation may occur. Chronic use requires a level of medication that avoids sedation and minimizes the development of drug tolerance.

Mesphenytoin (Mesantoin)

Mesphenytoin was introduced in the 1940s. Physicians were advised in 2000 by Novartis Pharmaceuticals that Mesantoin has been discontinued. New, more effective antiseizure medications are now available.²

New Antiepileptic Drugs

No major FDA antiseizure drug approvals occurred between 1978 and 1993. Since 1993, several promising new drugs have been introduced (Table 3).² The dentist should monitor health questionnaires for patient use of these agents:

* Gabapentin (Neurontin) -- to control partial and tonic-clonic seizures;

* Lamotrigine (Lamictal) -- to control partial and tonic-clonic seizures;

* Zonisamide (Zonegran) -- to control partial seizures in people age 16 and older;

* Levetiracetam (Keppra) -- to control partial seizures in adults;

* Oxcarbazepine (Trileptal) -- to control partial seizures in adults and as add-on in children and adults; and

* Topiramate (Topramax) -- to control partial seizures in adults and as add-on in children.

Cerebral Palsy

Cerebral palsy is a nonprogressive chronic condition caused from damage to areas of the brain. Cerebral damage can occur during various stages of development: prenatal, during the birth process, or infancy. The resultant brain damage leads to limited motor function decreasing body movement, coordination, and muscle control (palsy). There are three main types of cerebral palsy or a combination of various types (Table 4):^{19, 20}

* Spasticity -- the most common type; movement is difficult because of stiffness and rigidity of the extremities;

* Athetoid -- movement is involuntary, purposeless, slow, and uncontrolled; and

* Ataxia -- balance and depth perception is disturbed and is uncoordinated, particularly when attempting voluntary movement.

Classification of Areas of Involvement

Cerebral palsy is classified by location and the number of involved extremities (Table 5):

* Monoplegia -- one extremity;

* Paraplegia -- two lower extremities;

* Hemiplegia -- two extremities on one side of the body; and

* Quadriplegia -- all four extremities.

Factors Affecting the Developing Brain

Any number of factors can affect the developing brain, but the following are the most common:¹⁹

* Insufficient oxygen reaching the brain,

+ Premature placenta separation from the uterus wall,

+ Awkward birth position in the uterus,

+ Labor period that is too long or too abrupt,

+ Disturbed circulation in the umbilical cord;

* Premature birth;

* Low birth weight;

* Rh or A-B-O blood-type problems;

* Infection of the mother early in pregnancy by a viral disease such as German measles; and

* Acquired in infancy -- head injuries, falls, child abuse.

Intelligence

Individuals with cerebral palsy may have normal or advanced intelligence. One person may have several developmental disabilities including mental retardation. Only when an individual has cerebral palsy and mental retardation does subaverage intellectual functioning become a factor in measuring intelligence. Cerebral palsy, by itself, does not have mental retardation as a component.

Treatment

Cerebral palsy is not a disease, and it is not curable or communicable as in a disease process. It is a developmental condition and requires intervention to enhance the individual’s ability to manage the condition. Several factors help the child achieve maximum, enhanced development:¹⁹

* Identifying the developmental disorder at the earliest age;

* Interdisciplinary attention to hearing, learning, movement and speech;

* Enhancing emotional, personal, and social development;

* Improving coordination;

* Preventing dysfunction; and

* Helping the child become as independent as possible.

Dental Management

The most important consideration for a patient with cerebral palsy is to ask what his or her preferences are in receiving dental care, particularly the most comfortable position in the dental chair. Often patients have an exaggerated gag reflex. A rubber dam and sometimes a mouth prop are useful. The patient’s head is kept in the midline. Turning the head results in asymmetric/symmetric neck reflexes. The head should be cradled with the forearms and hands while dental procedures are performed. Soft ties can help the patient feel more stable. Soft ties are restraints, and therefore they require specific informed consent from the patient or consent giver. With paraplegic involvement, the patient may not be capable of keeping the legs positioned on the dental chair. Especially for female patients, a soft tie to help keep the legs in position addresses concerns about patient dignity, which should never be compromised. Preventive programs are essential to allow the individual to realize the full potential in personal oral hygiene practices, attitudes, and motivation toward oral health.²⁰

Caries

Early studies in the United States and Europe could not correlate the caries rate with the degree of mental and motor disability.²¹ Only small variations are shown among children in various diagnostic categories of cerebral palsy. A more recent finding shows the lowest caries rate in the most seriously motor and mentally challenged patients at ages 14 and 15 years. There is a suggestion that a patient with greater disabilities has less access to sugar-containing foods, and possibly a delay in eruption of permanent teeth. Differences in oral hygiene care, which is generally poorer in the cerebral palsy group, cannot explain a reduced rate of caries in children with cerebral palsy.²² While the caries rate did not differ greatly between children with cerebral palsy and controls, the ability to receive restorative care is less likely to occur and more likely to have a greater number of extractions.²³

Children with cerebral palsy may drool because of the inability to control saliva in the oral cavity. Medications and behavioral modifications sometimes work to control drooling. In extreme cases, a surgery procedure called sialodochoplasty is sometimes suggested. Salivary ducts are either rerouted or ligated, thereby reducing saliva flow and drooling.²⁴ Long-term effects on the dentition have a potential downside. Increased caries particularly in the mandibular incisors and canines suggest IgA antibodies to Streptococcus mutans are similarly reduced in saliva increasing bacteria prevalence and caries activity.²⁵

Barriers

A respondent total of 57 adults with cerebral palsy were surveyed about barriers to dental care. A majority of respondents could move about unaided, make themselves understood in conversation, did not require general anesthesia, and maintained regular dental appointments.²⁶ Patients with greater needs are those who have barriers to care. Patients requiring dentistry performed in a hospital operating room under general anesthesia may find more barriers in locating dentists in the community who are prepared to provide this level of care.²⁷

Autism

Kanner was the first to ascribe the following characteristics to autism:

* Relating to others in an ordinary interaction was not possible; the individual is isolated;

* Sameness with no spontaneous activity; and

* Language was not for communication.²⁸

Modernly, for diagnostic purposes, autism or autistic disorder is the qualitative impairment in social interaction and communication and restricted, repetitive, and stereotyped patterns of behavior, interests, and activities with delays or abnormal functioning in at least one of the following: social interaction, language as used in social communication, or symbolic or imaginative play. Onset occurs prior to 3 years of age.²⁹

Diagnostic Criteria

Social Interaction

At least two characteristics out of four must manifest to show a qualitative impairment of social interaction:

* Marked impairment in the use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body postures, and gestures to regulate social interaction;

* Failures to develop peer relationships appropriate to developmental level;

* Lack of spontaneous seeking to share enjoyments, interests, or achievements with other people; and

* Lack of social or emotional reciprocity.²⁹

Language Used in Social Communication or Play

At least one characteristic out of four must manifest to show a qualitative impairment of communication:

* Delay or lack of the development of spoken language not accompanied by attempts to compensate through gesture or mime;

* Those individuals with adequate speech have a marked impairment to initiate or sustain a conversation with others;

* Stereotyped or repetitive use of language or idiosyncratic language; and

* Lack of varied, spontaneous make-believe play or social initiative play appropriate to developmental level.²⁹

Restricted Repetitive and Stereotyped Patterns of Behavior, Interests and Activities

At least one characteristic must manifest to meet this criterion:

* Preoccupation of interest abnormal either in intensity or focus;

* Inflexible routines or rituals;

* Stereotyped or repetitive motor mannerisms; and

* Preoccupation with parts of objects.

One characteristic helps pinpoint the demeanor of the people with autism; that characteristic is unresponsiveness to others such as parents, teachers, or care providers. The inability to be responsive signals a warning to others that diverting attention to a task such as cooperating with the dentist may be nearly futile, yet possible, depending on how encompassing the disorder manifests in each individual.²⁹

Causation

The specific etiology of autism is undetermined.³⁰ Links to genetics are in dispute. Some studies show no genetic cause of autism.^31,32 Others have focused research on chromosome 7.^33,34 Hoxa 1, a small gene on chromosome 7, plays a role in brain stem development.³⁴ Miller linked autism to thalidomide embryopathy, suggesting that brain stem damage probably occurs early in embryogenesis at 3 to 4 weeks of age in utero. Ocular anomalies during the same period link the timing of damage to the early embryological period.^35-37 The comorbid occurrence of autism and Down syndrome is at least 7 percent.³⁸ These studies suggest autism occurs in early embryology; and, while a genetic link is a strong possibility, specific factors are unknown.

Problems in Dental Care

The person with autism generally presents a challenge to the dentist. How effective is teaching? Children with autism tend to remember the last things said and use different organizational strategies to retrieve items from memory.³⁹ Adults with autism demonstrate increased independence by developing skills through a structured teaching model.⁴⁰

Visual teaching can be used to introduce children with autism to dentistry.⁴¹ They require patience to "show, tell, do." The "show, tell" may not be understood, leading the child to resist "do." Simple rehearsals at home by parents can help condition the child for the office experience. Props such as mouth mirrors, film packets, prophylaxis cups, and pastes can be used at home by parents when adequately instructed by the dentist.⁴² While behavior modification techniques have value in changing self-injurious behaviors, use of the reward system fails when the promised reward is no longer possible.⁴³

A combined modality of desensitization, symbolic remodeling, and reinforcement treatment suggest children can be trained to undergo a dental exam.⁴⁴ Successful initial oral exams and radiographs were achieved 50 percent of the time. Successful management includes reinforcing positive behavior. If unsuccessful, negative reinforcement is recommended ("You don’t get to go home unless you let me finish the procedure").⁴⁵ Children with autism resist eye contact, so the dentist must be firm and yet provide frequent verbal approval for appropriate responses.⁴⁶ Comprehensive dental treatment under general anesthesia may be required 30 percent of the time.⁴⁷ In a 10-year follow-up, patients resisted efforts to establish personal contact with the dental staff. Furthermore, sedative techniques were ineffective because of atypical response patterns. Use of general anesthesia was the only solution to provide necessary dental care.⁴⁸ A combination of factors might change considerations for care in the individual patient. When dental needs are great and attempts at behavior modification are unsuccessful, general anesthesia in the operating room creates a controlled environment where care is delivered efficiently and effectively.

Conclusion

Dentists offer their best services when they understand their patients. Each new generation of professionals will have greater knowledge and will use that knowledge to benefit society. Progress is slow, yet it has never been so rapid. Patients with special needs include those with developmental disabilities such as epilepsy, cerebral palsy, and autism. For the purpose of this article, categories were developed for discussion; however, each patient is an individual who requires unique attention. Understanding how developmental disabilities may affect the individual patient and the provision of dental care puts into motion the value of prevention and treatment for all patients seeking care. The ability of the dentist to manage care for patients with developmental disabilities as a routine part of practice is an achievable goal. Patients who are unable to cooperate for care in a dental office require treatment by dentists with hospital privileges. These practitioners are a resource for dentists when they consider options of care for their patients. The importance of identifying these dentists in the community cannot be overemphasized. The dental profession’s ability to provide an expansive spectrum of care helps meet the future oral health care expectations of all individuals.

Author

Stanley R. Surabian, DDS, JD, is chief of dental services and program director, general practice residency, Community Medical Centers, in Fresno, Calif.

References

1. U.S. Department of Health and Human Services, Oral Health in America: A Report of the Surgeon General. U. S. Department of Health and Human Services, National Institute of dental and Craniofacial Research, National Institutes of Health, Rockville, MD, 2000.

2. Epilepsy Foundation, Epilepsy facts and figures. http://www.efa.org/education/facts

3. Begley CE, Famulari M, et al, The cost of epilepsy in the United States: an estimate from population-based clinical and survey data. Epilepsia 41(3):342-51, 2000.

4. Reid R, New employment program to begin at four sites nationwide. Epilepsy USA 33(2):1-22, 2000.

5. Braham RL, Casamassimo PS, et al, The dental implications of epilepsy. DHEW Pub. No. (HAS) 78-5217:1-18, 1977.

6. Sanders BJ, Weddell JA, Dodge NN, Managing patients who have seizure disorders: dental and medical issues. J Am Dent Assoc 126:1641-7, 1995.

7.Hirtz DG, Nelson KB, The natural history of febrile seizures. Ann Rev Med 34:453-71, 1983.

8. Sillanpaa M, Jalava M, et al, Long-term prognosis of seizures with onset in childhood. N Engl J Med 338(4):1715-22, 1998.

9. Berg AT, Levy SR, et al, Treatment of newly diagnosed pediatric epilepsy -- a community-based study. Arch Pediatr Adolesc Med 153:1267-71, 1999.

10. Gowers WR, Epilepsy and other chronic convulsive disorders: their causes, symptoms and treatment. J & A Churchill, London, 1981.

11. Berg AT, Shinnar S, Do seizures beget seizures? An assessment of the clinical evidence in humans. J Clin Neurophysiol 14(2):102-10, 1997.

12. Silverstein LH, Garnick JJ, et al, Medication-induced gingival enlargement: a clinical review. Gen Dent 45(4):371-6, 1997.

13. Walker CR, Tomich CE, Hutton CE, Treatment of phenytoin-induced gingival hyperplasia by electrosurgery. J Oral Surgery 38:306-11, 1980.

14. Dahllof G, Modeer T, The effect of a plaque control program on the development of phenytoin-induced gingival overgrowth. A 2-year longitudinal study. J Clin Periodontol 13:845-9, 1986.

15. Penarrocha-Diago M, Bagan-Sebastian JV, Vera-Sempere F, Diphenylhydantoin-induced gingival overgrowth in man: a clinico-pathological study. J Periodontol 61:571-4, 1990.

16. Tesini DA, Fenton SJ, Oral health needs of persons with physical or mental disabilities. Dent Clin North Am 38(3):483-98, 1994.

17. Dongari A, McDonnell HT, Langlais RP, Drug-induced gingival overgrowth. Oral Surg Oral Med Oral Path 76:543-8, 1993.

18. Pilstrom BL, Carlson JF, et al, Prevention of phenytoin-induced associated gingival enlargement -- a 15 month longitudinal study. J Periodontol 51(6):311-7, 1980.

19. United Cerebral Palsy, Cerebral palsy facts and figures. http://www.nettally.com/ucp/cerebral.htm.

20. Leary BA, Zucker SB, Teaching preventive dentistry to adolescents with cerebral palsy. Spec Care Dent 1(1):13-7, 1981.

21. Nielson LA, Caries among children with cerebral palsy: relation to CP-diagnosis, mental and motor handicap. J Dent Child 57(4):267-73. 1990.

22. Fishman SR, Young WO, et al, The status of oral health in cerebral palsy children and their siblings. J Dent Child 34:219-27, 1967.

23. Pope JE, Curzon ME, The dental status of cerebral palsied children. Pedriatr Dent 13(3):156-62, 1991.

24. Hallett KB, Lucas JO, et al, Dental health of children with cerebral palsy following sialodochoplasty. Spec Care Dent 15(6):234-8, 1995.

25. Rose PT, Cregory RL, et al, IgA antibodies to Streptococcus mutans in caries-resistant and -susceptible children. Pediatr Dent 16:272-5, 1994.

26. Russell GM, Kinirons MJ, A study of the barriers to dental care in a sample of patients with cerebral palsy. Comm Dent Health 10(1):57-64, 1993.

27. Glassman P, Miller CE, et al, A dental school’s role in developing a rural, community-based, dental care delivery system for individuals with developmental disabilities. Spec Care Dent 16(5):188-93, 1996.

28. Kanner L, Early infantile autism. J Pediat 25:211-7, 1944.

29. Waldman HB, Swerdloff M, and Perlman SP, Children with mental retardation: stigma and stereotype images are hard to change. J Dent Child 66(5):343-7, 1999.

30. Klein U, Nowak AJ, Characteristics of patients with autistic disorder presenting for dental treatment: a survey and chart review. Spec Care Dent 19(5):200-7, 1999.

31. Fisher E, Van Dyke DC, et al, Recent research on the etiologies of autism. Inf Young Child 11(3):1-8, 1999.

32. Rapin I, Autism. N Engl J Med 337(2):97-104, 1997.

33. Berney TP, Autism -- an evolving concept. Br J Psychiatry 176:20-5, 2000.

34. Rodier PM, The early origins of autism. Sci Am 282(2):56-63, 2000.

35. Miller MT, Ocular anomalies: embryological implications. Acta Ophthalmol Scand 73 Suppl 214:4-9, discussion 9-11, 1995.

36. Miller MT, Stromland K, et al, The puzzle of autism: an ophthalmologic contribution. Trans Am Ophthalmol Soc. 96(3):369-85; discussion 385-7, 1998.

37. Miller MT, Stromland K, Teratogen update: thalidomide: a review, with a focus on ocular findings and new potential uses. Teratology 60(5):306-21, 1999.

38. Kent L, Evans J, et al, Comorbidity of autistic spectrum disorders in children with Down syndrome. Devel Med Child Neurol 41:153-8, 1999.

39. Renner P, Klinger LG, Klinger MR, Implicit and explicit memory in autism: Is autism an amnesic disorder? J Aut Dev Disord 30(1):3-14, 2000.

40. Persson B, Brief report: a longitudianl study of quality of life and independence among adult men with autism. J Aut Dev Disord 30(1):61-6, 2000.

41. Backman B, Pilebro C, Visual pedagory in dentistry for children with autism. J Dent Child 66(5):325-31, 1999.

42. Kopel, HM, The autistic child in dental practice. J Dent Child 44(4):302-9, 1977.

43. Johnson CD, Matt CK, et al, Preventing factitious gingival injury in an autistic patient. J Am Dent Assoc 127(2):244-7,1996.

44. Luscre DM, Center DB, Procedures for reducing dental fear in children with autism. J Aut Dev Disord 26:547-56, 1996.

45. Lowe O, Lindemann R, Assessment of the autistic patient’s dental needs and ability to undergo dental examination. J Dent Child 3:29-35, 1985.

46. Kamen S, Skier J, Dental management of the autistic child. Spec Care Dent 5:20-3, 1985.

47. Klein U, Nowak AJ, Autistic disorder: A review for the pediatric dentist. Pediatr Dent 20:312-7, 1998.

48. Davilla JM, Jensen OE, Behavioral and pharmacological dental management of a patient with autism. Spec Care Dent 8(2):58-60, 1988.

To request a printed copy of this article, please contact/Stanley R. Surabian, DDS, JD, University Medical Center, Division of Dentistry, 445 S. Cedar Ave., Fresno, CA 93702, or at ssurabiandds@communitymedical.org.

Table 1. Seizure Classifications

Major motor seizures -- tonic-clonic (grand mal)
Minor motor seizures -- absence (petit mal)
Myoclonic seizures
Febrile seizures
Simple partial seizures
Complex partial seizures