3

Epidemiology and Prevention

Epidemiologic research assesses epilepsy’s risk factors, burden, comorbidities, and outcomes to identify opportunities for prevention efforts. Although data are incomplete, it is clear that epilepsy is one of the most common brain disorders and is likely to increase in prevalence with the aging population. Most cases of epilepsy result from unknown causes, but some cases with known causes—such as neurocysticercosis and other brain infections, traumatic brain injury, and stroke—could be avoided. Epilepsy is linked to numerous physical, neurological, mental health, and cognitive comorbidities, including heart disease, autism spectrum disorders, Alzheimer’s disease, depression, anxiety, and learning and memory problems. People with epilepsy are also more likely than others to have injuries, primarily seizure-related (e.g., fractures, burns, concussion), and to commit suicide. In addition to experiencing prejudice and discrimination, many people with epilepsy internalize feelings of stigma. Overall death rates, including from sudden unexpected death, are higher among people with epilepsy than in the general population. Actions needed to prevent epilepsy and its consequences include interventions to reduce the occurrence of epilepsy’s known risk factors, to eliminate seizures in people with epilepsy and mental health comorbidities, and to decrease felt stigma and epilepsy-related causes of death.

Epidemiologic research in epilepsy aims to assess the risk factors for developing the disorder; to evaluate its burden, comorbidities, and outcomes; and to identify opportunities for preventing epilepsy and its consequences. Chapter 2 explores the various methodological and



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3 Epidemiology and Prevention Epidemiologic research assesses epilepsy’s risk factors, burden, comorbidities, and outcomes to identify opportunities for prevention efforts. Although data are incomplete, it is clear that epilepsy is one of the most common brain dis- orders and is likely to increase in prevalence with the aging population. Most cases of epilepsy result from unknown causes, but some cases with known causes—such as neurocysticercosis and other brain infections, traumatic brain injury, and stroke—could be avoided. Epilepsy is linked to numerous physi- cal, neurological, mental health, and cognitive comorbidities, including heart disease, autism spectrum disorders, Alzheimer’s disease, depression, anxiety, and learning and memory problems. People with epilepsy are also more likely than others to have injuries, primarily seizure-related (e.g., fractures, burns, concussion), and to commit suicide. In addition to experiencing prejudice and discrimination, many people with epilepsy internalize feelings of stigma. Overall death rates, including from sudden unexpected death, are higher among people with epilepsy than in the general population. Actions needed to prevent epilepsy and its consequences include interventions to reduce the occurrence of epilepsy’s known risk factors, to eliminate seizures in people with epilepsy and mental health comorbidities, and to decrease felt stigma and epilepsy-related causes of death. E pidemiologic research in epilepsy aims to assess the risk factors for developing the disorder; to evaluate its burden, comorbidities, and outcomes; and to identify opportunities for preventing epilepsy and its consequences. Chapter 2 explores the various methodological and 109

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110 EPILEPSY ACROSS THE SPECTRUM measurement issues associated with epilepsy surveillance and describes sources for data collection. This chapter focuses on the gaps in epilepsy research in terms of what is known and not known related to incidence, prevalence, risk factors, comorbidities, and outcomes. These gaps suggest opportunities for prioritizing future epidemiologic studies in order to guide preventive and early intervention strategies. Improved epilepsy data collec- tion and measurement, as described in Chapter 2, are necessary for better epidemiologic research, along with well-designed and targeted studies to illuminate significant trends and inform health care providers, policy mak- ers, and the public. To improve knowledge regarding preventing epilepsy and its outcomes, the committee’s vision is for well-designed epidemiologic studies that high- light areas ripe for preventive efforts. Some, but by no means all, key focus areas are discussed here, including prevention of epilepsy, its comorbidities, and its consequences, including death. Before discussing these research ar- eas, the continuum of public health prevention is described as background. PUBLIC HEALTH AND PREVENTION In the context of public health, there are traditionally three levels of prevention: primary, secondary, and tertiary. Each aims to intervene at a different point along the continuum of a disease or disorder and involves different types of actions to ameliorate the condition or its impact. “Primary prevention” is the prevention of a disease or disorder before it begins, with the goal of decreasing its incidence in a population. For ex- ample, public health agencies, policy makers, and others work to eliminate environmental hazards (e.g., through sanitary measures such as ensuring clean drinking water), to improve disease resistance (e.g., through immuni- zation), and to decrease high-risk behavior (e.g., tobacco use) and promote healthy behavior (e.g., seatbelt use). In looking forward, future advances in biomedical research hold the promise of greater understanding of epilepto- genesis or possibly a cure; meanwhile, it may be possible to prevent some known causes of epilepsy, such as neurocysticercosis through education and sanitary measures, other brain infections through vaccines, traumatic brain injury (TBI) through seatbelt and helmet use, and stroke through reduction of known risk factors. “Secondary prevention” is the early identification and mitigation of a disease or disorder once it is present in the body but before it is symp- tomatic. For example, public health agencies collaborate with health pro- fessionals to screen a population (e.g., blood glucose or blood pressure screenings) and follow up to manage early symptoms and forestall the development of full-blown disease. Secondary prevention of epilepsy may be possible in the future, if biomarkers of epileptogenesis are identified and early intervention measures are developed.

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111 EPIDEMIOLOGY AND PREVENTION “Tertiary prevention” is the prevention of the progression of a disease or disorder and its outcomes after it has become symptomatic, in order to decrease the degree of resulting disability or impacts on health (i.e., to improve quality of life). For example, health professionals, together with public health agencies, work to minimize or eliminate exposures that make a disease or disorder worse (e.g., air pollution for people with asthma) and to screen for early detection of adverse outcomes (e.g., vision changes for people with diabetes). For chronic diseases and disorders, tertiary preven- tion is sometimes called disease management, although it should not be confused with medical treatment, and it may involve rehabilitation therapy, as after stroke. Some tertiary prevention efforts target the consequences of epilepsy (e.g., early identification of those who do not respond to seizure medications in order to identify options to prevent seizure recurrence), whereas others focus on its comorbidities (e.g., screening and interventions to identify and manage depression in people with epilepsy, described in Chapter 4). Future population health studies on comorbidities, including mental health conditions, and important outcomes (e.g., sudden unexpected death in epilepsy [SUDEP], injuries) may provide opportunities for success- ful interventions to promote optimal quality of life and avoid preventable deaths. INCIDENCE AND PREVALENCE Incidence Studies of the incidence of epilepsy describe the rate of new-onset epilepsy and the characteristics of newly diagnosed epilepsy. The annual incidence of epilepsy in the United States is estimated at approximately 48/100,000 people (Hirtz et al., 2007). This estimate represents the me- dian of a range of incidence estimates across all age groups. The hallmark longitudinal study of the epilepsies in the United States is the Rochester Epidemiology Project (described in Chapter 2), in which the incidence of epilepsy was examined in more than 2 million residents of Rochester, Min- nesota, across 5 decades from 1935 to 1984. The Rochester study found an age-adjusted incidence of 44/100,000 (Hauser et al., 1993). Based on the Rochester project, Hesdorffer and colleagues (2011a) estimated that 1 in 26 people (3.8 percent of people born today) will develop epilepsy over the course of their lifetime. However, this estimate is based on a nonrepresen- tative population from one community in the United States. Furthermore, diagnostic data from this study are out of date, given the advances in imag- ing and other medical technologies (e.g., none of the Rochester participants had available MRI [magnetic resonance imaging] data).

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112 EPILEPSY ACROSS THE SPECTRUM More recent studies have arrived at varying estimates of epilepsy incidence: • A population study in northern Manhattan reported an incidence of 41/100,000 (Benn et al., 2008). • Holden and colleagues (2005) looked at managed care organiza- tions and found an incidence of 47/100,000 for those who were continuously enrolled for 3 years and 71/100,000 for those en- rolled for 5 years. • In a health maintenance organization population, incidence for enrollees under age 65 was 35.5/100,000 (Annegers et al., 1999), although this age group would be expected to have a lower inci- dence than adults 65 years old or older, who have a high incidence of epilepsy (Thurman, 2011). Existing trend information suggests that the incidence of epilepsy may be declining in children and increasing among older adults (Hauser et al., 1993; Kotsopoulos et al., 2002; Sillanpää et al., 2011). However, it is not known whether these trends will continue or if changes in the distribution of risk factors for epilepsy (discussed later) are driving them. Research Gaps Epidemiologic research is needed in large, representative U.S. popula- tions to monitor trends in epilepsy incidence and related mortality and to track outcomes. Studies need to be conducted among the general popula- tion and in subpopulations at higher risk: children, for whom prognosis is a major concern; older adults, who have greater mortality associated with epilepsy; women, to track outcomes, including reproductive outcomes; as well as veterans and diverse racial/ethnic and socioeconomic groups, in order to assess any disparities in incidence, prognosis, and mortality and to determine opportunities for intervention. Within these subpopulations, sufficient numbers are needed to compare incidence by etiology, seizure type, syndrome, and the presence of comorbid conditions. With respect to treatment, these surveillance data could be used to monitor the outcomes of epilepsy care and provide feedback to health care providers (Box et al., 2010; Trevathan, 2011). As examples, specific populations for whom fur- ther research is needed—older adults, veterans, children, and people with epilepsy and associated comorbidities—are described below. Older adults The incidence of epilepsy is highest in children and older adults (Faught et al., 2012; Hauser et al., 1993; Kotsopoulos et al., 2002; Stephen and Brodie, 2000). By 2030, about 20 percent of the U.S. popula-

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113 EPIDEMIOLOGY AND PREVENTION tion will be age 65 or older, an increase from approximately 13 percent in 2010 (Census Bureau, 2011; IOM, 2008). Due to the aging of the popu- lation and increases in life expectancy, the number of older adults who develop or have epilepsy will increase. Some of the increase will be from known causes, such as stroke, dementia, and TBI, which is often due to falls. Better medical management of stroke has increased survival rates and, thus, the number of survivors at risk for epilepsy; the number of people with aging-related dementia also is increasing; and the incidence of fall- induced TBI is rising in older adults (Annegers et al., 1995; Broderick et al., 1989; Fuster and Bansilal, 2010; Kannus et al., 2007; Ramanathan et al., 2012; Tartaglia et al., 2011; Watson and Mitchell, 2011). Older adults with epilepsy may experience greater disability because of deteriorations in health due to advanced age, comorbid conditions, and greater likelihood of side effects from seizure medications due to altered pharmacokinetics and interactions with other medications (Faught, 1999). The resultant impair- ments can decrease quality of life and increase the need for health services and long-term care (Guralnik et al., 1996). In anticipation of a growing number of older adults with epilepsy, additional research is needed that fo- cuses on concerns specific to this population, including preventing adverse medication interactions and disability and maintaining independent living. Epilepsy takes freedom from those who suffer from it. We cannot allow our citizens who have fought for freedom to lose their own freedom. –Kevin Malone Veterans Returning service members from Operation Enduring Freedom (OEF) and Operation Iraqi Freedom (OIF) are a specific population in which research on epilepsy incidence is needed, because TBI, the most com- mon injury of OEF-OIF (U.S. Army Traumatic Brain Injury Task Force, 2007), is associated with up to a 53-percent risk for posttraumatic epi- lepsy, depending on the severity of the injury (Salazar et al., 1985). The number of service members who survive after sustaining a serious injury is higher now than for any previous war (Goldberg, 2010; Lowenstein, 2009). Between 2001 and 2007, an estimated 1.6 million U.S. military personnel were deployed to Afghanistan and Iraq (Tanielian et al., 2008). Among a study population of approximately 868,000 service members, approximately 1,300 were hospitalized with a severe TBI, 1,550 with a moderate TBI, and 133 with a mild TBI (Wojcik et al., 2010). However, most people who sustain a mild TBI are not hospitalized, and many do not go to the emergency department (U.S. Army Traumatic Brain Injury Task Force, 2007), and mild TBIs comprise approximately three-quarters of all TBI cases in OEF-OIF service members (Armed Forces Health Surveillance Center, 2012). A report of the Armed Forces Epidemiological Board (2006) found that the Department of Defense (DOD) did not have a system-wide

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114 EPILEPSY ACROSS THE SPECTRUM approach for identifying, treating, and monitoring TBIs, especially mild cases. Since that report, the DOD has established and is working to imple- ment guidelines for the identification and treatment of mild TBI (U.S. Army Traumatic Brain Injury Task Force, 2007). Similarly, the Department of Veterans Affairs has also dedicated efforts to recognizing and managing mild TBI in OEF-OIF veterans (GAO, 2008). The emphasis on improved surveillance and care of mild TBI in today’s conflicts contrasts with earlier eras, when attention focused on more severe, penetrating TBI (Evans, 1962; Salazar et al., 1985). Studies of returning veterans require validated diagnosis of the severity of TBI and follow-up to monitor a range of potential outcomes, includ- ing the onset of epilepsy. Questions about the validity of the diagnosis of mild TBI have arisen in connection with a study of 2,525 service members answering a questionnaire after 1 year of deployment in Iraq, where symp- toms of mild TBI were reported by 15.2 percent (Hoge et al., 2008). An accompanying New England Journal of Medicine editorial highlighted the difficulty of separating symptoms of mild TBI from posttraumatic stress disorder (PTSD) and other psychological reactions due to the emotional trauma of wartime (Bryant, 2008). Because TBI among returning veterans may be associated with an increased risk for developing epilepsy, work to distinguish mild TBI from PTSD is crucial. PTSD itself is associated with the occurrence of seizure-like events that are not epilepsy (D’Alessio et al., 2006). Recently, Salinsky and colleagues (2011) found that there is a sig- nificant delay in the diagnosis of seizure-like events with a psychological basis in veterans treated with seizure medications, suggesting a presump- tive diagnosis of epilepsy. Among veterans with seizure-like events with a psychological basis, the delay in diagnosis was nearly five times as long as for civilians, and the cumulative treatment with seizure medications was four times higher. Progress in distinguishing between mild TBI and PTSD as well as between epilepsy and seizure-like events with a psychological basis is needed to determine the incidence and prevalence of TBI-related epilepsy among veterans and to provide optimal care. Children The most catastrophic forms of epilepsy occur in children, par- ticularly young children. Previous incidence studies have not assembled a sufficiently large incidence cohort of children with epilepsy to study the prognosis of most individual syndromes. However, it has been possible to study risk factors for poor seizure prognosis in childhood onset epilepsy overall, the risk for status epilepticus (SE), and the risk for early refractory epilepsy1 in different etiologic categories (Arts et al., 2004; Berg et al., 1 As noted in Chapter 1, refractory epilepsy is defined as the failure to control seizures after two seizure medications (whether as monotherapies or in combination) have been appropri- ately chosen and used (Kwan et al., 2010) (see also Chapter 4).

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115 EPIDEMIOLOGY AND PREVENTION 2001a,b; Camfield et al., 2002; Sillanpää and Shinnar, 2002, 2010). How- ever, studies have focused on common syndromes, and studies that have elucidated risk factors for poor prognosis within specific syndromes have been rare (Wirrell et al., 1996). Future studies of unselected incident cohorts of children with epilepsy are needed to assemble large enough cohorts with rare syndromes to study factors affecting prognosis. Epilepsy accompanied by comorbidities There is some evidence (see the discussion below on comorbidities) that the prognosis for epilepsy is worse in the presence of comorbidities that predate the diagnosis of epilepsy. Because comorbidities may influence epilepsy prognosis and are known to affect quality of life, studies of the incidence of epilepsy in people with comorbidities at or before the onset of epilepsy will permit greater under- standing of the consequences of the disorder when it is accompanied by comorbidities. For example, case-control studies of people with newly di- agnosed epilepsy could be conducted retrospectively to identify preexisting comorbidities, or prospective cohort studies of individuals with depression or migraine could look at the incidence of epilepsy in these groups. These studies may provide a greater understanding of how the timing of epilepsy onset in relation to its comorbidities affects prognosis. Prevalence Studies of the prevalence of epilepsy provide information on its burden in the population. Prevalence data encompass the number of newly diag- nosed cases of epilepsy as well as cases of epilepsy that persist over time, which includes people with continued seizures and people who are in remis- sion but who take seizure medications. Except for rapidly fatal conditions, prevalence is greater than incidence, because it accounts for the accumula- tion of cases over time. Prevalence thus reflects the incidence, chronicity, and related mortality of epilepsy. Similar to incidence, there is a range of estimates of prevalence of epi- lepsy in the United States: • Hirtz and colleagues (2007) estimate annual prevalence at 7.1/ 1,000 people. • The Rochester Epidemiology Project found that prevalence in- creased from 2.7/1,000 in 1940 to 6.8/1,000 in 1980 (Hauser et al., 1991). • Kelvin and colleagues (2007) found a 5/1,000 prevalence in New York City. • The Centers for Disease Control and Prevention’s (CDC’s) Behav- ioral Risk Factor Surveillance System (BRFSS), which depends on

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116 EPILEPSY ACROSS THE SPECTRUM self-reporting, estimated 8.4/1,000 cases of active epilepsy2 (Kobau et al., 2008). If lifetime prevalence (i.e., ever having epilepsy) is considered, the BRFSS estimate increases to 16.5/1,000 (1.7 per- cent of respondents) (Kobau et al., 2008). Research Gaps More studies have been done on the prevalence of epilepsy than on its incidence because prevalence studies are easier and faster to conduct. Prevalence data are used to inform planning for resources and services to meet the health care and social needs of people with epilepsy. To obtain a complete picture of epilepsy, prevalence studies should be conducted us- ing the same data sources as those in which long-term studies of epilepsy incidence are conducted. Socioeconomic status (SES) and race/ethnicity are discussed below as examples of two areas in which further research on incidence and prevalence is needed. Socioeconomic status Low SES is associated with a higher incidence of epilepsy (Heaney et al., 2002). Hesdorffer and colleagues (2005) studied adults in Iceland and found that people with epilepsy are more likely to have low SES in comparison to age- and gender-matched controls without epilepsy. This association exists in a society with universal health care where everyone has health insurance, and it also persists in adults with epilepsy of unknown etiology, even after adjustment for cumulative alco- hol consumption, which could be a confounding factor. Furthermore, low SES is also associated with an increased prevalence of epilepsy (Morgan et al., 2000; Shamansky and Glaser, 1979). Reasons for this are not well understood because these studies did not distinguish between epilepsy of unknown etiology and epilepsy of known etiology, which is problematic because some known etiologies of epilepsy (e.g., TBI, stroke) may them- selves be associated with low SES (Chang et al., 2002; Cubbin et al., 2000). While associations between SES and the etiology of epilepsy is one possible explanation for the association between SES and prevalence, existing treat- ment gaps may play a role as well, since people of lower SES are less likely to obtain seizure medications or to be under the care of a neurologist than people of higher SES (Begley et al., 2009), making them more likely to experience persistent seizures (Chapter 4). Race/ethnicity A study in the Harlem neighborhood of New York City found epilepsy prevalence to be higher in Hispanics than in non-Hispanics 2 Defined as “a history of epilepsy and currently taking medication or reporting one or more seizures during the past 3 months” (Kobau et al., 2008, p. 1).

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117 EPIDEMIOLOGY AND PREVENTION and a higher prevalence of active epilepsy3 in whites than in blacks, although the prevalence of lifetime epilepsy4 was higher in blacks compared to whites (Kelvin et al., 2007). In this community, there were racial/ethnic disparities in care; blacks were more likely to receive care in the emergency department compared to whites and Hispanics. Similarly, Hope and colleagues (2009) found that blacks and Hispanics were more likely than whites to be diag- nosed in an emergency department, and blacks were more likely to receive a suboptimal seizure medication. Differences in care for prevalent epilepsy were also observed in residents of Alabama and surrounding states, where blacks were 60 percent less likely than non-Hispanic whites to undergo epilepsy surgery after receiving electroencephalograph (EEG) monitoring as part of a surgical evaluation, an association that persisted after control- ling for factors such as SES and medical insurance coverage (Burneo et al., 2005). The degree to which differences in epilepsy incidence and prevalence in different racial/ethnic groups reflect differences in socioeconomic status is unknown. Also unknown is the degree to which treatment gaps contribute to the higher epilepsy prevalence in some subgroups. Next Steps for Incidence and Prevalence Studies As described in Chapter 2, none of the recent estimates of incidence and prevalence are based on active and ongoing surveillance of epilepsy in the U.S. population over time. Updated and longitudinal data are needed from large, representative populations throughout the country to generate population-wide estimates of incidence and prevalence and allow subgroup analysis by severity and type of epilepsy, age, gender, race/ethnicity, geogra- phy, and SES. This information is necessary to have a complete understand- ing of the burden of epilepsy in the United States compared to other diseases and conditions, to show trends over time, and to learn whether specific populations carry a disproportionate amount of the epilepsy burden so that actions can be taken to provide needed health care and support services. Future studies of time trends in the incidence and prevalence of epi- lepsy conducted in large, representative cohorts will also be able to assess trends in remission, relapse, and refractory epilepsy. Although previous and ongoing prospective studies have examined these outcomes, the studies are mostly short term, outdated, and too small to enable subgroup analysis. A major contribution of the types of surveillance and population-based stud- ies suggested in this report would be the ability not only to report incidence and prevalence but also to examine the course of epilepsy overall and in 3 In this study, active epilepsy was defined as having ongoing seizures or taking a seizure medication within the previous 5 years. 4 In this study, lifetime epilepsy was defined as having a history of two or more unprovoked seizures.

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118 EPILEPSY ACROSS THE SPECTRUM subpopulations. Such data may allow assessment of how risk factors influ- ence the prevalence of epilepsy over time. Specific subgroups of interest include older adults, veterans, children, people with epilepsy accompanied by comorbidities, and diverse racial/ethnic and socioeconomic populations. These data are needed to know where and how to better focus epilepsy prevention and treatment efforts. RISK FACTORS Epilepsy Due to a Known Cause Cases of epilepsy that have a known etiology have a worse overall prognosis, more commonly involve persistent seizures, and have a higher mortality rate than cases in which the cause is unknown (Forsgren et al., 2005b; Hauser et al., 1998). Less than half of all newly diagnosed cases of epilepsy have a known structural or metabolic cause (Adelöw et al., 2009; Forsgren et al., 2005a; Hauser et al., 1993). Among people with newly diagnosed epilepsy, the predominant known causes are stroke, neurode- generative diseases such as dementia and multiple sclerosis, primary brain tumors or the spread of cancer from another site to the brain, and TBI (Annegers and Coan, 2000; Hauser et al., 1993; Herman, 2002; Hesdorffer et al., 1996a; Kelley and Rodriguez, 2009). Other known causes are rarer but confer a strong risk for developing epilepsy: brain infections, such as meningitis, encephalitis, and neurocysticercosis; pre- and perinatal in- jury; intellectual disability; cerebral palsy; and autism spectrum disorders (Annegers et al., 1988; Bergamasco et al., 1984; Carpio et al., 1998; Nelson and Ellenberg, 1987; Rocca et al., 1987; Tuchman and Rapin, 2002; Van der Berg and Yerushalmy, 1969). A recent study by Crump and colleagues (2011) found that preterm birth is associated with an increased risk of epilepsy in adulthood. Identifying causes of epilepsy is the first step in primary prevention. Prevention of posttraumatic epilepsy has been attempted through indirect means and planned interventions. Efforts to prevent epilepsy from devel- oping after TBI have involved randomized clinical trials of drug therapies; regrettably, these have not been successful (Temkin et al., 1990, 1999, 2007). Prevention of epilepsy after TBI is a complex problem, because the types, location, and extent of brain injury vary widely, and the process of epileptogenesis after TBI is not well understood. The heterogeneity of TBI has hindered the development of effective interventions to prevent poor functional outcomes in general. A systematic review of the literature found that only a third of randomized clinical trials of interventions to prevent negative health outcomes after TBI have been successful, underscoring the complexity of this injury (Hernández et al., 2005). Currently, the prevention of TBI itself allows the best opportunity to prevent posttraumatic epilepsy.

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119 EPIDEMIOLOGY AND PREVENTION Significant public health efforts have successfully increased the use of helmets and seatbelts to prevent TBI (Coronado et al., 2011). These measures to reduce the occurrence of TBI have likely led to a decrease in new cases of epilepsy associated with TBI, although this is undocumented. However, motor vehicle accidents are still among the leading causes of TBI (Bruns and Hauser, 2003; Coronado et al., 2011; Labi et al., 2003; Tagliaferri et al., 2006). Furthermore, in some populations, the incidence of TBI appears to be rising. For example, the number of visits to the emer- gency department because of TBI due to sports and recreational activities, in particular bicycling and football, increased from approximately 150,000 to 250,000 between 2001 and 2009 (Gilchrist et al., 2011). Therefore, TBI remains a significant public health problem, where people who participate in sports, especially children and adolescents, and members of the military and older adults (discussed earlier in the chapter) are at particularly high risk (Armed Forces Health Surveillance Center, 2012; Gilchrist et al., 2011; Ramanathan et al., 2012). The prevention of other risk factors for epilepsy could decrease the incidence of epilepsy as well. Prevention efforts for stroke often target its established risk factors, which include hypertension, cigarette smoking, and insufficient physical activity (Sacco et al., 1999). Results from the 2005 BRFSS found disparities in stroke prevalence among categories such as race/ ethnicity, age, and educational level (Neyer et al., 2007), indicating a need for targeted prevention programs. Prevention of brain infections such as meningitis through the use of childhood vaccines has proven to be effective (Robbins et al., 1996; Tsai et al., 2008) and should be continued. Among the known infectious etiologies of epilepsy, primary prevention associated with neurocysticercosis5 may be most likely to succeed. Neu- rocysticercosis is caused by infection of the nervous system by a type of tapeworm, Taenia solium, and is a major cause of epilepsy in many devel- oping countries throughout the world, including Latin America. Like other parasites that are transmitted through the digestive tract, tapeworms are spread to others through the consumption of food contaminated with the feces of an infected carrier, primarily due to poor sanitation, improper food handling practices, and inadequate hand washing. Neurocysticercosis is in- creasingly diagnosed in areas of the United States, especially the Southwest and other areas with large populations who travel to or immigrate from countries where the parasite is endemic (Del Brutto, 2012; Ong et al., 2002; White, 2000). For people who develop epilepsy from neurocysticercosis, 5 Cysticercosis is a parasitic infection with Taenia solium, an adult tapeworm, resulting from ingestion of the eggs of the tapeworm through consuming undercooked food (e.g., vegetables, pork) or water contaminated with the feces of a carrier of T. solium larvae. Cysticercosis that involves the central nervous system is termed neurocysticercosis and is the most common parasitic brain infection (DeGiorgio et al., 2004).

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150 EPILEPSY ACROSS THE SPECTRUM Fernandes, P. T., P. C. Salgado, A. L. Noronha, F. D. Barbosa, E. A. Souza, J. W. Sander, and L. M. Li. 2007. Prejudice towards chronic diseases: Comparison among epilepsy, AIDS and diabetes. Seizure 16(4):320-323. Ferraro, T. N., D. J. Dlugos, and R. J. Buono. 2006. Role of genetics in the diagnosis and treatment of epilepsy. Expert Review of Neurotherapeutics 6(12):1789-1800. Ficker, D. M., E. L. So, W. K. Shen, J. F. Annegers, P. C. O’Brien, G. D. Cascino, and P. G. Belau. 1998. Population-based study of the incidence of sudden unexplained death in epilepsy. Neurology 51(5):1270-1274. Forsgren, L., and L. Nystrom. 1990. An incident case-referent study of epileptic seizures in adults. Epilepsy Research 6(1):66-81. Forsgren, L., S. O. Edvinsson, L. Nyström, and H. K. Blomquist. 1996. Influence of epilepsy on mortality in mental retardation: An epidemiologic study. Epilepsia 37(10):956-963. Forsgren, L., E. Beghi, A. Oun, and M. Sillanpää. 2005a. The epidemiology of epilepsy in Europe: A systematic review. European Journal of Neurology 12(4):245-253. Forsgren, L., W. A. Hauser, E. Olafsson, J. W. A. S. Sander, M. Sillanpää, and T. Tomson. 2005b. Mortality of epilepsy in developed countries: A review. Epilepsia 46(Suppl. 11):18-27. Fuster, V., and S. Bansilal. 2010. Promoting cardiovascular and cerebrovascular health. Stroke 41(6):1079-1083. Gaitatzis, A., K. Carroll, A. Majeed, and W. S. J. 2004a. The epidemiology of the comorbidity of epilepsy in the general population. Epilepsia 45(12):1613-1622. Gaitatzis, A., A. L. Johnson, D. W. Chadwick, S. D. Shorvon, and J. W. Sander. 2004b. Life expectancy in people with newly diagnosed epilepsy. Brain 127(Pt. 11):2427-2432. Gaitatzis, A., M. R. Trimble, and J. W. Sander. 2004c. The psychiatric comorbidity of epilepsy. Acta Neurologica Scandinavica 110(4):207-220. GAO (Government Accountability Office). 2008. VA health care: Mild traumatic brain injury screening and evaluation implemented for OEF/OIF veterans, but challenges remain. GAO-08-276. Washington, DC: GAO. Geerts, A., W. F. Arts, H. Stroink, E. Peeters, O. Brouwer, B. Peters, L. Laan, and C. van Donselaar. 2010. Course and outcome of childhood epilepsy: A 15-year follow-up of the Dutch Study of Epilepsy in Childhood. Epilepsia 51(7):1189-1197. George, J. R., and G. G. Davis. 1998. Comparison of anti-epileptic drug levels in different cases of sudden death. Journal of Forensic Sciences 43(3):598-603. Gilchrist, J., K. E. Thomas, L. Xu, L. C. McGuire, and V. Coronado. 2011. Nonfatal traumatic brain injuries related to sports and recreation activities among persons aged ≤ 19 years— United States, 2001-2009. Morbidity and Mortality Weekly Report 60(39):1337-1342. Gilliam, F., H. Hecimovic, and Y. Sheline. 2003. Psychiatric comorbidity, health, and function in epilepsy. Epilepsy and Behavior 4(Suppl. 4):S26-S30. Goldberg, M. S. 2010. Death and injury rates of U.S. military personnel in Iraq. Military Medicine 175(4):220-226. Goulden, K. J., S. Shinnar, H. Koller, M. Katz, and S. A. Richardson. 1991. Epilepsy in chil- dren with mental retardation: A cohort study. Epilepsia 32(5):690-697. Guralnik, J. M., L. P. Fried, and M. E. Salive. 1996. Disability as a public health outcome in the aging population. Annual Review of Public Health 17(1):25-46. Haglund, M. M., and D. W. Hochman. 2005. Furosemide and mannitol suppression of epilep- tic activity in the human brain. Journal of Neurophysiology 94(2):907-918. Harris, E. C., and B. Barraclough. 1997. Suicide as an outcome for mental disorders. A meta- analysis. British Journal of Psychiatry 170:205-228. Hauser, W. A., J. F. Annegers, and L. R. Elveback. 1980. Mortality in patients with epilepsy. Epilepsia 21(4):399-412. Hauser, W. A., J. F. Annegers, and L. T. Kurland. 1991. Prevalence of epilepsy in Rochester, Minnesota: 1940-1980. Epilepsia 32(4):429-445.

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151 EPIDEMIOLOGY AND PREVENTION ———. 1993. Incidence of epilepsy and unprovoked seizures in Rochester, Minnesota: 1935- 1984. Epilepsia 34(3):453-468. Hauser, W. A., S. S. Rich, J. R. Lee, J. F. Annegers, and V. E. Anderson. 1998. Risk of recurrent seizures after two unprovoked seizures. New England Journal of Medicine 338(7):429-434. Heaney, D. C., B. K. MacDonald, A. Everitt, S. Stevenson, G. S. Leonardi, P. Wilkinson, and J. W. Sander. 2002. Socioeconomic variation in incidence of epilepsy: Prospective com- munity based study in south east England. BMJ 325(7371):1013-1016. Helmstaedter, C. 2004. Neuropsychological aspects of epilepsy surgery. Epilepsy and Behavior 5(Suppl. 1):S45-S55. ———. 2007. Cognitive outcome of status epilepticus in adults. Epilepsia 48(Suppl. 8):85-90. Herman, S. T. 2002. Epilepsy after brain insult: Targeting epileptogenesis. Neurology 59(9 Suppl. 5):S21-S26. Hermann, B., and M. Seidenberg. 2007. Epilepsy and cognition. Epilepsy Currents 7(1):1-6. Hermann, B., J. Jones, R. Sheth, C. Dow, M. Koehn, and M. Seidenberg. 2006a. Children with new-onset epilepsy: Neuropsychological status and brain structure. Brain 129(Pt. 10):2609-2619. Hermann, B., M. Seidenberg, C. Dow, J. Jones, P. Rutecki, A. Bhattacharya, and B. Bell. 2006b. Cognitive prognosis in chronic temporal lobe epilepsy. Annals of Neurology 60(1):80-87. Hermann, B., M. Seidenberg, and J. Jones. 2008a. The neurobehavioural comorbidities of epilepsy: Can a natural history be developed? Lancet Neurology 7(2):151-160. Hermann, B., M. Seidenberg, M. Sager, C. Carlsson, B. Gidal, R. Sheth, P. Rutecki, and S. Asthana. 2008b. Growing old with epilepsy: The neglected issue of cognitive and brain health in aging and elder persons with chronic epilepsy. Epilepsia 49(5):731-740. Hermann, B., J. E. Jones, R. Sheth, M. Koehn, T. Becker, J. Fine, C. A. Allen, and M. Seidenberg. 2008c. Growing up with epilepsy: A two-year investigation of cognitive development in children with new onset epilepsy. Epilepsia 49(11):1847-1858. Hernández, A. V., E. W. Steyerberg, G. S. Taylor, A. Marmarou, J. D. F. Habbema, and A. I. R. Maas. 2005. Subgroup analysis and covariate adjustment in randomized clinical trials of traumatic brain injury: A systematic review. Neurosurgery 57(6):1244-1253. Hesdorffer, D. C., and A. M. Kanner. 2009. The FDA alert on suicidality and antiepileptic drugs: Fire or false alarm? Epilepsia 50(5):978-986. Hesdorffer, D. C., W. A. Hauser, J. F. Annegers, E. Kokmen, and W. A. Rocca. 1996a. Demen- tia and adult-onset unprovoked seizures. Neurology 46(3):727-730. Hesdorffer, D. C., W. A. Hauser, J. F. Annegers, and W. A. Rocca. 1996b. Severe, uncontrolled hypertension and adult-onset seizures: A case-control study in Rochester, Minnesota. Epilepsia 37(8):736-741. Hesdorffer, D. C., G. Logroscino, G. Cascino, J. F. Annegers, and W. A. Hauser. 1998. Incidence of status epilepticus in Rochester, Minnesota, 1965-1984. Neurology 50(3):735-741. Hesdorffer, D. C., W. A. Hauser, J. F. Annegers, and G. Cascino. 2000. Major depression is a risk factor for seizures in older adults. Annals of Neurology 47(2):246-249. Hesdorffer, D. C., J. P. Stables, W. A. Hauser, J. F. Annegers, and G. Cascino. 2001. Are certain diuretics also anticonvulsants? Annals of Neurology 50(4):458-462. Hesdorffer, D. C., P. Ludvigsson, E. Olafsson, G. Gudmundsson, O. Kjartansson, and W. A. Hauser. 2004. ADHD as a risk factor for incident unprovoked seizures and epilepsy in children. Archives of General Psychiatry 61(7):731-736. Hesdorffer, D. C., H. Tian, K. Anand, W. A. Hauser, P. Ludvigsson, E. Olafsson, and O. Kjartansson. 2005. Socioeconomic status is a risk factor for epilepsy in Icelandic adults but not in children. Epilepsia 46(8):1297-1303.

OCR for page 109
152 EPILEPSY ACROSS THE SPECTRUM Hesdorffer, D. C., W. A. Hauser, E. Olafsson, P. Ludvigsson, and O. Kjartansson. 2006. De- pression and suicide attempt as risk factors for incident unprovoked seizures. Annals of Neurology 59(1):35-41. Hesdorffer, D. C., P. Ludvigsson, W. A. Hauser, E. Olafsson, and O. Kjartansson. 2007. Co- occurrence of major depression or suicide attempt with migraine with aura and risk for unprovoked seizure. Epilepsy Research 75(2-3):220-223. Hesdorffer, D. C., A. T. Berg, and A. M. Kanner. 2010. An update on antiepileptic drugs and suicide: Are there definitive answers yet? Epilepsy Currents 10(6):137-145. Hesdorffer, D. C., G. Logroscino, E. K. T. Benn, N. Katri, G. Cascino, and W. A. Hauser. 2011a. Estimating risk for developing epilepsy: A population-based study in Rochester, Minnesota. Neurology 76(1):23-27. Hesdorffer, D. C., T. Tomson, E. Benn, J. W. Sander, L. Nilsson, Y. Langan, T. S. Walczak, E. Beghi, M. J. Brodie, and A. Hauser. 2011b. Combined analysis of risk factors for SUDEP. Epilepsia 52(6):1150-1159. Hesdorffer, D. C., T. Tomson, E. Benn, J. W. Sander, L. Nilsson, Y. Langan, T. S. Walczak, E. Beghi, M. J. Brodie, and W. A. Hauser. 2012. Do antiepileptic drugs or generalized tonic-clonic seizure frequency increase SUDEP risk? A combined analysis. Epilepsia 53(2):249-252. Hirtz, D., D. J. Thurman, K. Gwinn-Hardy, M. Mohamed, A. R. Chaudhuri, and R. Zalutsky. 2007. How common are the “common” neurologic disorders? Neurology 68(5):326-337. Hitiris, N., R. Mohanraj, J. Norrie, G. J. Sills, and M. J. Brodie. 2007a. Predictors of phar- macoresistant epilepsy. Epilepsy Research 75(2-3):192-196. Hitiris, N., S. Suratman, K. Kelly, L. J. Stephen, G. J. Sills, and M. J. Brodie. 2007b. Sud- den unexpected death in epilepsy: A search for risk factors. Epilepsy and Behavior 10(1):138-141. Hochman, D. W., S. C. Baraban, J. W. Owens, and P. A. Schwartzkroin. 1995. Dissociation of synchronization and excitability in furosemide blockade of epileptiform activity. Science 270(5233):99-102. Hoge, C. W., D. McGurk, J. L. Thomas, A. L. Cox, C. C. Engel, and C. A. Castro. 2008. Mild traumatic brain injury in U.S. soldiers returning from Iraq. New England Journal of Medicine 358(5):453-463. Holden, E. W., H. Thanh Nguyen, E. Grossman, S. Robinson, L. S. Nelson, M. J. Gunter, A. Von Worley, and D. J. Thurman. 2005. Estimating prevalence, incidence, and disease- related mortality for patients with epilepsy in managed care organizations. Epilepsia 46(2):311-319. Holmes, G. L., C. E. Stafstrom, and the Tuberous Sclerosis Study Group. 2007. Tuberous sclerosis complex and epilepsy: Recent developments and future challenges. Epilepsia 48(4):617–630. Holtmann, M., K. Becker, B. Kentner-Figura, and M. H. Schmidt. 2003. Increased frequency of Rolandic spikes in ADHD children. Epilepsia 44(9):1241-1244. Hope, O. A., J. E. Zeber, N. R. Kressin, B. G. Bokhour, A. C. Vancott, J. A. Cramer, M. E. Amuan, J. E. Knoefel, and M. J. Pugh. 2009. New-onset geriatric epilepsy care: Race, setting of diagnosis, and choice of antiepileptic drug. Epilepsia 50(5):1085-1093. Hotez, P. J. 2008. Neglected infections of poverty in the United States of America. PLoS Ne- glected Tropical Diseases 2(6):e256. Iivanainen, M., and J. Lehtinen. 1979. Causes of death in institutionalized epileptics. Epilepsia 20(5):485-491. IOM (Institute of Medicine). 2003. Priority areas for national action: Transforming health care quality. Washington, DC: The National Academies Press. ———. 2008. Retooling for an aging America: Building the health care workforce. Washing- ton, DC: The National Academies Press.

OCR for page 109
153 EPIDEMIOLOGY AND PREVENTION Jacoby, A. 1994. Felt versus enacted stigma: A concept revisited. Evidence from a study of people with epilepsy in remission. Social Science and Medicine 38(2):269-274. ———. 2002. Stigma, epilepsy, and quality of life. Epilepsy and Behavior 3(6S2):10-20. Jacoby, A., and J. K. Austin. 2007. Social stigma for adults and children with epilepsy. Epi- lepsia 48(Suppl. 9):6-9. Jacoby, A., and G. A. Baker. 2008. Quality-of-life trajectories in epilepsy: A review of the literature. Epilepsy and Behavior 12(4):557-571. Jacoby, A., G. A. Baker, N. Steen, P. Potts, and D. W. Chadwick. 1996. The clinical course of epilepsy and its psychosocial correlates: Findings from a UK community study. Epilepsia 37(2):148-161. Jones, J. E., B. P. Hermann, J. J. Barry, F. G. Gilliam, A. M. Kanner, and K. J. Meador. 2003. Rates and risk factors for suicide, suicidal ideation, and suicide attempts in chronic epi- lepsy. Epilepsy and Behavior 4(Suppl. 3):S31-S38. Jones, J. E., R. Watson, R. Sheth, R. Caplan, M. Koehn, M. Seidenberg, and B. Hermann. 2007. Psychiatric comorbidity in children with new onset epilepsy. Developmental Medi- cine and Child Neurology 49(7):493-497. Jorge, R. E., R. G. Robinson, S. Arndt, and S. Starkstein. 2003. Mortality and poststroke depression: A placebo-controlled trial of antidepressants. American Journal of Psychiatry 160(10):1823-1829. Kabore, J. K., J. W. Cabore, Z. Melaku, M. Druet-Cabanac, and P. M. Preux. 1996. Epilepsy in a focus of onchocerciasis in Burkina Faso. Lancet 347(9004):836. Kanner, A. M., R. Byrne, A. Chicharro, J. Wuu, and M. Frey. 2009. A lifetime psychiatric history predicts a worse seizure outcome following temporal lobectomy. Neurology 72(9):793-799. Kannus, P., S. Niemi, J. Parkkari, M. Palvanen, and H. Sievanen. 2007. Alarming rise in fall- induced severe head injuries among elderly people. Injury 38(1):81-83. Kelley, B. J., and M. Rodriguez. 2009. Seizures in patients with multiple sclerosis: Epidemiol- ogy, pathophysiology and management. CNS Drugs 23(10):805-815. Kelvin, E. A., D. C. Hesdorffer, E. Bagiella, H. Andrews, T. A. Pedley, T. T. Shih, L. Leary, D. J. Thurman, and W. A. Hauser. 2007. Prevalence of self-reported epilepsy in a multiracial and multiethnic community in New York City. Epilepsy Research 77(2-3):141-150. Kirsch, R., and E. Wirrell. 2001. Do cognitively normal children with epilepsy have a higher rate of injury than their nonepileptic peers? Journal of Child Neurology 16(2):100-104. Klenerman, P., J. W. Sander, and S. D. Shorvon. 1993. Mortality in patients with epilepsy: A study of patients in long term residential care. Journal of Neurology, Neurosurgery and Psychiatry 56(2):149-152. Kobau, R., H. Zahran, D. Grant, D. J. Thurman, P. H. Price, and M. M. Zack. 2007. Prevalence of active epilepsy and health-related quality of life among adults with self- reported epilepsy in California: California Health Interview Survey, 2003. Epilepsia 48(10):1904-1913. Kobau, R., H. Zahran, D. J. Thurman, M. M. Zack, T. R. Henry, S. C. Schachter, and P. H. Price. 2008. Epilepsy surveillance among adults—19 states, Behavioral Risk Factor Sur- veillance System, 2005. Morbidity and Mortality Weekly Report Surveillance Summaries 57(6):1-20. Kotila, M., and O. Waltimo. 1992. Epilepsy after stroke. Epilepsia 33(3):495-498. Kotsopoulos, I. A., T. van Merode, F. G. Kessels, M. C. de Krom, and J. A. Knottnerus. 2002. Systematic review and meta-analysis of incidence studies of epilepsy and unprovoked seizures. Epilepsia 43(11):1402-1409. Kozinska, J., K. M. Sawicka, A. Zadrozniak, E. Wojda, M. Andres-Mach, M. Dudra- Jastrzebska, and J. J. Luszczki. 2009. Indapamide enhances the protective action of carbamazepine, phenobarbital, and valproate against maximal electroshock-induced seizures in mice. Advances in Medical Sciences 54(1):66-74.

OCR for page 109
154 EPILEPSY ACROSS THE SPECTRUM Krohn, W. 1963. Causes of death among epileptics. Epilepsia 4:315-322. Kumari, P., D. Ram, S. Haque Nizamie, and N. Goyal. 2009. Stigma and quality of life in individuals with epilepsy: A preliminary report. Epilepsy and Behavior 15(3):358-361. Kwan, P., and M. J. Brodie. 2000. Early identification of refractory epilepsy. New England Journal of Medicine 342(5):314-319. Kwan, P., A. Arzimanoglou, A. T. Berg, M. J. Brodie, W. Allen Hauser, G. Mathern, S. L. Moshe, E. Perucca, S. Wiebe, and J. French. 2010. Definition of drug resistant epilepsy: Consensus proposal by the ad hoc task force of the ILAE Commission on Therapeutic Strategies. Epilepsia 51(6):1069-1077. Labi, M. L., M. Brentjens, M. L. Coad, W. J. Flynn, and M. Zielezny. 2003. Development of a longitudinal study of complications and functional outcomes after traumatic brain injury. Brain Injury 17(4):265-278. Lamberts, R. J., R. D. Thijs, A. Laffan, Y. Langan, and J. W. Sander. 2012. Sudden unex- pected death in epilepsy: People with nocturnal seizures may be at highest risk. Epilepsia 53(2):253-257. Langan, Y., L. Nashef, and J. W. Sander. 2000. Sudden unexpected death in epilepsy: A series of witnessed deaths. Journal of Neurology, Neurosurgery and Psychiatry 68(2):211-213. ———. 2005. Case-control study of SUDEP. Neurology 64(7):1131-1133. Leaffer, E. B., A. Jacoby, E. Benn, W. A. Hauser, T. Shih, P. Dayan, R. Green, H. Andrews, D. J. Thurman, and D. Hesdorffer. 2011. Associates of stigma in an incident epilepsy popula- tion from northern Manhattan, New York City. Epilepsy and Behavior 21(1):60-64. Lee, M. A. 1998. EEG video recording of sudden unexpected death in epilepsy (SUDEP) [ab- stract]. Epilepsia 39(Suppl. 6):123-124. Lim, L. L., N. Foldvary, E. Mascha, and J. Lee. 2001. Acetazolamide in women with catame- nial epilepsy. Epilepsia 42(6):746-749. Logroscino, G., D. C. Hesdorffer, G. Cascino, J. F. Annegers, and W. A. Hauser. 1997. Short- term mortality after a first episode of status epilepticus. Epilepsia 38(12):1344-1349. ———. 2001. Time trends in incidence, mortality, and case-fatality after first episode of status epilepticus. Epilepsia 42(8):1031-1035. Logroscino, G., D. C. Hesdorffer, G. D. Cascino, J. F. Annegers, E. Bagiella, and W. A. Hauser. 2002. Long-term mortality after a first episode of status epilepticus. Neurology 58(4):537-541. Logroscino, G., D. C. Hesdorffer, G. Cascino, and W. A. Hauser. 2008. Status epilepticus without an underlying cause and risk of death: A population-based study. Archives of Neurology 65(2):221-224. Loring, D. W., and K. J. Meador. 2001. Cognitive and behavioral effects of epilepsy treatment. Epilepsia 42(Suppl. 8):24-32. Lowenstein, D. H. 2009. Epilepsy after head injury: An overview. Epilepsia 50(Suppl. 2):4-9. Ludvigsson, P., D. Hesdorffer, E. Olafsson, O. Kjartansson, and W. A. Hauser. 2006. Migraine with aura is a risk factor for unprovoked seizures in children. Annals of Neurology 59(1):210-213. Maa, E. H., K. T. Kahle, B. P. Walcott, M. C. Spitz, and K. J. Staley. 2011. Diuretics and epilepsy: Will the past and present meet? Epilepsia 52(9):1559-1569. MacAllister, W. S., H. A. Bender, L. Whitman, A. Welsh, S. Keller, Y. Granader, and E. M. Sherman. 2011. Assessment of executive functioning in childhood epilepsy: The Tower of London and BRIEF. Child Neuropsychology (in press). Mann, J. J., A. Apter, J. Bertolote, A. Beautrais, D. Currier, A. Haas, U. Hegerl, J. Lonnqvist, K. Malone, A. Marusic, L. Mehlum, G. Patton, M. Phillips, W. Rutz, Z. Rihmer, A. Schmidtke, D. Shaffer, M. Silverman, Y. Takahashi, A. Varnik, D. Wasserman, P. Yip, and H. Hendin. 2005. Suicide prevention strategies: A systematic review. JAMA 294(16):2064-2074.

OCR for page 109
155 EPIDEMIOLOGY AND PREVENTION Martinovic, Z., P. Simonovic, and R. Djokic. 2006. Preventing depression in adolescents with epilepsy. Epilepsy and Behavior 9(4):619-624. Mazarati, A., P. Siddarth, R. A. Baldwin, D. Shin, R. Caplan, and R. Sankar. 2008. Depression after status epilepticus: Behavioural and biochemical deficits and effects of fluoxetine. Brain 131(Pt. 8):2071-2083. McLean, B. N., and S. Wimalaratna. 2007. Sudden death in epilepsy recorded in ambulatory EEG. Journal of Neurology, Neurosurgery and Psychiatry 78(12):1395-1397. Morgan, C. L., Z. Ahmed, and M. P. Kerr. 2000. Social deprivation and prevalence of epi- lepsy and associated health usage. Journal of Neurology, Neurosurgery, and Psychiatry 69(1):13-17. Murphy, C. C., E. Trevathan, and M. Yeargin-Allsopp. 1995. Prevalence of epilepsy and epileptic seizures in 10-year-old children: Results from the Metropolitan Atlanta Devel- opmental Disabilities Study. Epilepsia 36(9):866-872. Nashef, L., E. L. So, P. Ryvlin, and T. Tomson. 2012. Unifying the definitions of sudden un- expected death in epilepsy. Epilepsia 53(2):227-233. Nelson, K. B., and J. H. Ellenberg. 1987. Predisposing and causative factors in childhood epilepsy. Epilepsia 28(Suppl. 1):S16-S24. Neyer, J. R., K. J. Greenlund, C. H. Denny, N. L. Keenan, M. Casper, D. R. Labarthe, and J. B. Croft. 2007. Prevalence of stroke—United States, 2005. Morbidity and Mortality Weekly Report 56(19):469-474. Ng, S. K., W. A. Hauser, J. C. Brust, and M. Susser. 1993. Hypertension and the risk of new- onset unprovoked seizures. Neurology 43(2):425-428. Nicoletti, A., A. Bartoloni, A. Reggio, F. Bartalesi, M. Roselli, V. Sofia, J. Rosado Chavez, H. Gamboa Barahona, F. Paradisi, G. Cancrini, V. C. Tsang, and A. J. Hall. 2002. Epilepsy, cysticercosis, and toxocariasis: A population-based case-control study in rural Bolivia. Neurology 58(8):1256-1261. Nicoletti, A., A. Bartoloni, V. Sofia, A. Mantella, G. Nsengiyumva, G. Frescaline, and P. M. Preux. 2007. Epilepsy and toxocariasis: A case-control study in Burundi. Epilepsia 48(5):894-899. Nicoletti, A., V. Sofia, A. Mantella, G. Vitale, D. Contrafatto, V. Sorbello, R. Biondi, P. M. Preux, H. H. Garcia, M. Zappia, and A. Bartoloni. 2008. Epilepsy and toxocariasis: A case-control study in Italy. Epilepsia 49(4):594-599. Nicoletti, A., V. Sofia, G. Vitale, S. I. Bonelli, V. Bejarano, F. Bartalesi, D. S. Tran, P. M. Preux, M. Zappia, and A. Bartoloni. 2009. Natural history and mortality of chronic epilepsy in an untreated population of rural Bolivia: A follow-up after 10 years. Epilepsia 50(10):2199-2206. Nilsson, L., T. Tomson, B. Y. Farahmand, V. Diwan, and P. G. Persson. 1997. Cause-specific mortality in epilepsy: A cohort study of more than 9,000 patients once hospitalized for epilepsy. Epilepsia 38(10):1062-1068. Nilsson, L., B. Y. Farahmand, P. G. Persson, I. Thiblin, and T. Tomson. 1999. Risk factors for sudden unexpected death in epilepsy: A case-control study. Lancet 353(9156):888-893. Nobili, L., P. Proserpio, G. Rubboli, N. Montano, G. Didato, and C. A. Tassinari. 2011. Sudden unexpected death in epilepsy (SUDEP) and sleep. Sleep Medicine Reviews 15(4): 237-246. Nuyen, J., F. G. Schellevis, W. A. Satariano, P. M. Spreeuwenberg, M. D. Birkner, G. A. van den Bos, and P. P. Groenewegen. 2006. Comorbidity was associated with neurologic and psychiatric diseases: A general practice-based controlled study. Journal of Clinical Epidemiology 59(12):1274-1284. O’Callaghan, F. J., C. Osmond, and C. N. Martyn. 2000. Trends in epilepsy mortality in England and Wales and the United States, 1950-1994. American Journal of Epidemiol- ogy 151(2):182-189.

OCR for page 109
156 EPILEPSY ACROSS THE SPECTRUM O’Donoghue, M. F., D. M. Goodridge, K. Redhead, J. W. Sander, and J. S. Duncan. 1999. Assessing the psychosocial consequences of epilepsy: A community-based study. British Journal of General Practice 49(440):211-214. Ong, S., D. A. Talan, G. J. Moran, W. Mower, M. Newdow, V. C. Tsang, and R. W. Pinner. 2002. Neurocysticercosis in radiographically imaged seizure patients in U.S. emergency departments. Emerging Infectious Diseases 8(6):608-613. Ottman, R., and R. B. Lipton. 1994. Comorbidity of migraine and epilepsy. Neurology 44(11):2105-2110. Ottman, R., R. B. Lipton, A. B. Ettinger, J. A. Cramer, M. L. Reed, A. Morrison, and G. J. Wan. 2011. Comorbidities of epilepsy: Results from the Epilepsy Comorbidities and Health (EPIC) survey. Epilepsia 52(2):308-315. Pack, A. 2008. Bone health in people with epilepsy: Is it impaired and what are the risk fac- tors? Seizure 17(2):181-186. Pion, S. D., C. Kaiser, F. Boutros-Toni, A. Cournil, M. M. Taylor, S. E. O. Meredith, A. Stufe, I. Bertocchi, W. Kipp, P.-M. Preux, and M. Boussinesq. 2009. Epilepsy in onchocerciasis endemic areas: Systematic review and meta-analysis of population-based surveys. PLoS Neglected Tropical Diseases 3(6):e461. Qin, P., H. Xu, T. M. Laursen, M. Vestergaard, and P. B. Mortensen. 2005. Risk for schizo- phrenia and schizophrenia-like psychosis among patients with epilepsy: Population based cohort study. BMJ 331(7507):23-25. Rafnsson, V., E. Olafsson, W. A. Hauser, and G. Gudmundsson. 2001. Cause-specific mortality in adults with unprovoked seizures. A population-based incidence cohort study. Neuro- epidemiology 20(4):232-236. Ramanathan, D. M., N. McWilliams, P. Schatz, and F. G. Hillary. 2012. Epidemiological shifts in elderly TBI: 18-year trends in Pennsylvania. Journal of Neurotrauma 29(7):1371-1378. Reisinger, E. L., and C. DiIorio. 2009. Individual, seizure-related, and psychosocial predic- tors of depressive symptoms among people with epilepsy over six months. Epilepsy and Behavior 15(2):196-201. Richardson, S. A., H. Koller, M. Katz, and J. McLaren. 1980. Seizures and epilepsy in a mentally retarded population over the first 22 years of life. Applied Research in Mental Retardation 1(1-2):123-138. Robbins, J. B., R. Schneerson, P. Anderson, and D. H. Smith. 1996. Prevention of sys- temic infections, especially meningitis, caused by Haemophilus influenzae type b. Im- pact on public health and implications for other polysaccharide-based vaccines. JAMA 276(14):1181-1185. Rocca, W. A., F. W. Sharbrough, W. A. Hauser, J. F. Annegers, and B. S. Schoenberg. 1987. Risk factors for complex partial seizures: A population-based case-control study. Annals of Neurology 21(1):22-31. Rodenburg, R., G. J. Stams, A. M. Meijer, A. P. Aldenkamp, and M. Dekovic. 2005. Psycho- pathology in children with epilepsy: A meta-analysis. Journal of Pediatric Psychology 30(6):453-468. Rutter, M. 1994. Comorbidity: Meanings and mechanisms. Clinical Psychology: Science and Practice 1(1):100-103. Ryvlin, P., M. Cucherat, and S. Rheims. 2011. Risk of sudden unexpected death in epilepsy in patients given adjunctive antiepileptic treatment for refractory seizures: A meta-analysis of placebo-controlled randomised trials. Lancet Neurology 10(11):961-968. Sacco, R. L., P. A. Wolf, and P. B. Gorelick. 1999. Risk factors and their management for stroke prevention: Outlook for 1999 and beyond. Neurology 53(7 Suppl. 4):S15-S24. Saemundsen, E., P. Ludvigsson, and V. Rafnsson. 2008. Risk of autism spectrum disorders after infantile spasms: A population-based study nested in a cohort with seizures in the first year of life. Epilepsia 49(11):1865-1870.

OCR for page 109
157 EPIDEMIOLOGY AND PREVENTION Salazar, A. M., B. Jabbari, S. C. Vance, J. Grafman, D. Amin, and J. D. Dillon. 1985. Epilepsy after penetrating head injury. I. Clinical correlates: A report of the Vietnam Head Injury Study. Neurology 35(10):1406-1414. Salinsky, M., D. Spencer, E. Boudreau, and F. Ferguson. 2011. Psychogenic nonepileptic sei- zures in U.S. veterans. Neurology 77(10):945-950. Santo, A. H. 2007. Cysticercosis-related mortality in the state of Sao Paulo, Brazil, 1985-2004: A study using multiple causes of death. Cadernos de Saude Publica 23(12):2917-2927. Serpa, J. A., E. A. Graviss, J. S. Kass, and A. C. White, Jr. 2011. Neurocysticercosis in Hous- ton, Texas: An update. Medicine 90(1):81-86. Shackleton, D. P., R. G. Westendorp, D. G. Trenite, and J. P. Vandenbroucke. 1999. Mortal- ity in patients with epilepsy: 40 years of follow up in a Dutch cohort study. Journal of Neurology, Neurosurgery and Psychiatry 66(5):636-640. Shamansky, S. L., and G. H. Glaser. 1979. Socioeconomic characteristics of childhood seizure disorders in the New Haven area: An epidemiologic study. Epilepsia 20(5):457-474. Shinton, R. A., J. S. Gill, A. V. Zezulka, and D. G. Beevers. 1987. The frequency of epilepsy preceding stroke. Case-control study in 230 patients. Lancet 1(8523):11-13. Sillanpää, M. 2004. Learning disability: Occurrence and long-term consequences in childhood- onset epilepsy. Epilepsy and Behavior 5(6):937-944. Sillanpää, M., and S. Shinnar. 2002. Status epilepticus in a population-based cohort with childhood-onset epilepsy in Finland. Annals of Neurology 52(3):303-310. ———. 2010. Long-term mortality in childhood-onset epilepsy. New England Journal of Medicine 363(26):2522-2529. Sillanpää, M., S. Lastunen, H. Helenius, and D. Schmidt. 2011. Regional differences and secular trends in the incidence of epilepsy in Finland: A nationwide 23-year registry study. Epilepsia 52(10):1857-1867. So, E. L., M. C. Sam, and T. L. Lagerlund. 2000. Postictal central apnea as a cause of SUDEP: Evidence from near-SUDEP incident. Epilepsia 41(11):1494-1497. Sorvillo, F. J., C. DeGiorgio, and S. H. Waterman. 2007. Deaths from cysticercosis, United States. Emerging Infectious Diseases 13(2):230-235. Sorvillo, F., P. Wilkins, S. Shafir, and M. Eberhard. 2011. Public health implications of cysti- cercosis acquired in the United States. Emerging Infectious Diseases 17(1):1-6. Sotelo, J. 2011. Clinical manifestations, diagnosis, and treatment of neurocysticercosis. Cur- rent Neurology and Neuroscience Reports 11(6):529-535. Spencer, S. S., A. T. Berg, B. G. Vickrey, M. R. Sperling, C. W. Bazil, S. Shinnar, J. T. Langfitt, T. S. Walczak, and S. V. Pacia. 2005. Predicting long-term seizure outcome after resective epilepsy surgery: The multicenter study. Neurology 65(6):912-918. Sperling, M. R., H. Feldman, J. Kinman, J. D. Liporace, and M. J. O’Connor. 1999. Seizure control and mortality in epilepsy. Annals of Neurology 46(1):45-50. Stephen, L. J., and M. J. Brodie. 2000. Epilepsy in elderly people. Lancet 355(9213):1441-1446. Surges, R., R. D. Thijs, H. L. Tan, and J. W. Sander. 2009. Sudden unexpected death in epilepsy: Risk factors and potential pathomechanisms. Nature Reviews Neurology 5(9):492-504. Tagliaferri, F., C. Compagnone, M. Korsic, F. Servadei, and J. Kraus. 2006. A systematic review of brain injury epidemiology in Europe. Acta Neurochirurgica 148(3):255-268. Talan, D. A., G. J. Moran, W. R. Mower, M. Newdow, S. Ong, L. Slutsker, W. R. Jarvis, L. A. Conn, and R. W. Pinner. 1998. EMERGEncy ID NET: An emergency department-based emerging infections sentinel network. The EMERGEncy ID NET study group. Annals of Emergency Medicine 32(6):703-711. Tanielian, T., L. H. Jaycox, T. L. Schell, G. N. Marshall, M. A. Burnam, C. Eibner, B. R. Karney, L. S. Meredith, J. S. Ringel, and M. E. Vaiana. 2008. Invisible wounds of war: Summary and recommendations for addressing psychological and cognitive injuries. Arlington, VA: RAND Corporation.

OCR for page 109
158 EPILEPSY ACROSS THE SPECTRUM Tartaglia, M. C., H. J. Rosen, and B. L. Miller. 2011. Neuroimaging in dementia. Neurothera- peutics 8(1):82-92. Taylor, J., R. Kolamunnage-Dona, A. G. Marson, P. E. Smith, A. P. Aldenkamp, and G. A. Baker. 2010. Patients with epilepsy: Cognitively compromised before the start of antiepi- leptic drug treatment? Epilepsia 51(1):48-56. Téllez-Zenteno, J. F., R. Dhar, L. Hernandez-Ronquillo, and S. Wiebe. 2007a. Long-term outcomes in epilepsy surgery: Antiepileptic drugs, mortality, cognitive and psychosocial aspects. Brain 130(Pt. 2):334-345. Téllez-Zenteno, J. F., S. B. Patten, N. Jetté, J. Williams, and S. Wiebe. 2007b. Psychiatric co- morbidity in epilepsy: A population-based analysis. Epilepsia 48(12):2336-2344. Temkin, N. R., S. S. Dikmen, A. J. Wilensky, J. Keihm, S. Chabal, and H. R. Winn. 1990. A randomized, double-blind study of phenytoin for the prevention of post-traumatic seizures. New England Journal of Medicine 323(8):497-502. Temkin, N. R., S. S. Dikmen, G. D. Anderson, A. J. Wilensky, M. D. Holmes, W. Cohen, D. W. Newell, P. Nelson, A. Awan, and H. R. Winn. 1999. Valproate therapy for prevention of posttraumatic seizures: A randomized trial. Journal of Neurosurgery 91(4):593-600. Temkin, N. R., G. D. Anderson, H. R. Winn, R. G. Ellenbogen, G. W. Britz, J. Schuster, T. Lucas, D. W. Newell, P. N. Mansfield, J. E. Machamer, J. Barber, and S. S. Dikmen. 2007. Magnesium sulfate for neuroprotection after traumatic brain injury: A randomised controlled trial. Lancet Neurology 6(1):29-38. Temkin, O. 1971. The falling sickness: A history of epilepsy from the Greeks to the beginnings of modern neurology. 2nd ed. Baltimore, MD: Johns Hopkins University Press. Thompson, N. J., E. R. Walker, N. Obolensky, A. Winning, C. Barmon, C. DiIorio, and M. T. Compton. 2010. Distance delivery of mindfulness-based cognitive therapy for depression: Project UPLIFT. Epilepsy and Behavior 19(3):247-254. Thorup, A., B. L. Waltoft, C. B. Pedersen, P. B. Mortensen, and M. Nordentoft. 2007. Young males have a higher risk of developing schizophrenia: A Danish Register Study. Psycho- logical Medicine 37(4):479-484. Thurman, D. 2011. Epidemiologic research and surveillance of the epilepsies: A systems-level perspective. PowerPoint presented at the IOM Meeting on Public Health Dimensions of the Epilepsies, January 10. http://iom.edu/~/media/Files/Activity%20Files/Disease/ Epilepsy/Thurman%202.pdf (accessed October 19, 2011). Thurman, D. J., E. Beghi, C. E. Begley, A. T. Berg, J. R. Buchhalter, D. Ding, D. C. Hesdorffer, W. A. Hauser, L. Kazis, R. Kobau, B. Kroner, D. Labiner, K. Liow, G. Logroscino, M. T. Medina, C. R. Newton, K. Parko, A. Paschal, P.-M. Preux, J. W. Sander, A. Selassie, W. Theodore, T. Tomson, and S. Wiebe. 2011. Standards for epidemiologic studies and surveillance of epilepsy. Epilepsia 52(Suppl. 7):2-26. Tomson, T., E. Beghi, A. Sundqvist, and S. I. Johannessen. 2004. Medical risks in epilepsy: A review with focus on physical injuries, mortality, traffic accidents and their prevention. Epilepsy Research 60(1):1-16. Tomson, T., L. Nashef, and P. Ryvlin. 2008. Sudden unexpected death in epilepsy: Current knowledge and future directions. Lancet Neurology 7(11):1021-1031. Tonini, C., E. Beghi, A. T. Berg, G. Bogliun, L. Giordano, R. W. Newton, A. Tetto, E. Vitelli, D. Vitezic, and S. Wiebe. 2004. Predictors of epilepsy surgery outcome: A meta-analysis. Epilepsy Research 62(1):75-87. Trevathan, E. 2011. “Flying blind” without epilepsy surveillance data. Neurology 76(1):10-11. Trimble, M. R., and E. H. Reynolds. 1976. Anticonvulsant drugs and mental symptoms: A review. Psychological Medicine 6(2):169-178. Tsai, C. J., M. R. Griffin, J. P. Nuorti, and C. G. Grijalva. 2008. Changing epidemiology of pneumococcal meningitis after the introduction of pneumococcal conjugate vaccine in the United States. Clinical Infectious Diseases 46(11):1664-1672.

OCR for page 109
159 EPIDEMIOLOGY AND PREVENTION Tsiropoulos, I., M. Andersen, T. Nymark, J. Lauritsen, D. Gaist, and J. Hallas. 2008. Expo- sure to antiepileptic drugs and the risk of hip fracture: A case-control study. Epilepsia 49(12):2092-2099. Tuchman, R., and I. Rapin. 2002. Epilepsy in autism. Lancet Neurology 1(6):352-358. U.S. Army Traumatic Brain Injury Task Force. 2007. Report to the Surgeon General. http:// www.armymedicine.army.mil/reports/tbi/TBITaskForceReportJanuary2008.pdf (accessed January 4, 2012). Valmadrid, C., C. Voorhees, B. Litt, and C. R. Schneyer. 2001. Practice patterns of neurologists regarding bone and mineral effects of antiepileptic drug therapy. Archives of Neurology 58(9):1369-1374. Van der Berg, B. J., and J. Yerushalmy. 1969. Studies on convulsive disorders in young chil- dren. I. Incidence of febrile and nonfebrile convulsions by age and other factors. Pediatric Research 3(4):298-304. Velioğlu, S. K., C. Boz, and M. Ozmenoğlu. 2005. The impact of migraine on epilepsy: A prospective prognosis study. Cephalalgia 25(7):528-535. Vestergaard, M., C. B. Pedersen, J. Christensen, K. M. Madsen, J. Olsen, and P. B. Mortensen. 2005. Febrile seizures and risk of schizophrenia. Schizophrenia Research 73(2-3):343-349. Vestergaard, P. 2008. Changes in bone turnover, bone mineral and fracture risk induced by drugs used to treat epilepsy. Current Drug Safety 3(3):168-172. Vestergaard, P., S. Tigaran, L. Rejnmark, C. Tigaran, M. Dam, and L. Mosekilde. 1999. Frac- ture risk is increased in epilepsy. Acta Neurologica Scandinavica 99(5):269-275. Vingerhoets, G. 2006. Cognitive effects of seizures. Seizure 15(4):221-226. Walczak, T. S., I. E. Leppik, M. D’Amelio, J. Rarick, E. So, P. Ahman, K. Ruggles, G. D. Cascino, J. F. Annegers, and W. A. Hauser. 2001. Incidence and risk factors in sudden unexpected death in epilepsy: A prospective cohort study. Neurology 56(4):519-525. Walker, E. R., N. Obolensky, S. Dini, and N. J. Thompson. 2010. Formative and process evaluations of a cognitive-behavioral therapy and mindfulness intervention for people with epilepsy and depression. Epilepsy and Behavior 19(3):239-246. Wallace, S. J. 2001. Epilepsy in cerebral palsy. Developmental Medicine and Child Neurology 43(10):713-717. Wallin, M. T., and J. F. Kurtzke. 2004. Neurocysticercosis in the United States: Review of an important emerging infection. Neurology 63(9):1559-1564. Watson, W. L., and R. Mitchell. 2011. Conflicting trends in fall-related injury hospital- isations among older people: Variations by injury type. Osteoporosis International 22(10):2623-2631. White, A. C., Jr. 2000. Neurocysticercosis: Updates on epidemiology, pathogenesis, diagnosis, and management. Annual Review of Medicine 51:187-206. Williams, J., M. L. Griebel, and R. A. Dykman. 1998. Neuropsychological patterns in pediatric epilepsy. Seizure 7(3):223-228. Williams, J., E. G. Schulz, and M. L. Griebel. 2001. Seizure occurrence in children diagnosed with ADHD. Clinical Pediatrics 40(4):221-224. Wirrell, E. C., C. S. Camfield, P. R. Camfield, K. E. Gordon, and J. M. Dooley. 1996. Long- term prognosis of typical childhood absence epilepsy: Remission or progression to juve- nile myoclonic epilepsy. Neurology 47(4):912-918. Wirrell, E. C., B. R. Grossardt, E. L. So, and K. C. Nickels. 2011. A population-based study of long-term outcomes of cryptogenic focal epilepsy in childhood: Cryptogenic epilepsy is probably not symptomatic epilepsy. Epilepsia 52(4):738-745. Wojcik, B. E., C. R. Stein, K. Bagg, R. J. Humphrey, and J. Orosco. 2010. Traumatic brain injury hospitalizations of U.S. Army soldiers deployed to Afghanistan and Iraq. American Journal of Preventive Medicine 38(1 Suppl.):S108-S116.

OCR for page 109