As a group, the convulsive disorders are among the most frequently occurring neurologic conditions in children. In the United States, approximately 5% of children and adolescents experience a seizure of some type by the age of 20 (1). This proportion may be very different in other cultures—higher, for example, in Japanese and lower in Chinese or Asian Indians. The greatest proportion of these children experience convulsions only in association with a febrile illness. Only about a quarter of those experiencing seizures actually meet criteria for “epilepsy”—a condition characterized by recurrent unprovoked seizures (2–4).

Despite efforts of organizations such as the International League Against Epilepsy (ILAE) to develop standardized definitions for the convulsive disorders for epidemiologic uses, there remain differences in definitions that preclude direct comparison across studies. Population-based studies dealing specifically with children are few and suffer from difficulties with definitions and differences in methodology. Further, total-population studies of the epidemiology of convulsive disorders or epilepsy seldom provide sufficient detail regarding the specifics of seizure type and etiology in children.

In this chapter we concentrate on studies targeted toward children while integrating data from total-population studies. We focus on studies of incidence (newly diagnosed cases), since these are more useful in the assessment of etiology and outcome than prevalence studies. In addition, there is less variation in definitions of seizures and epilepsy in incidence studies than in prevalence studies, allowing some comparison across geographic areas.

DEFINITIONS

Epilepsy

Epilepsy is a condition characterized by recurrent (two or more) unprovoked seizures separated by more than 24 hours. Although epilepsy is the focus of this chapter, only a few of the cited studies limit cases to children with epilepsy using this definition. Rather, authors include various combinations of the other classes of convulsive disorders, so one must read papers carefully if cross-study comparisons are to be made.

Seizure

A seizure is the clinical manifestation of an abnormal and excessive activity of a set of cortical neurons.

Acute Symptomatic Seizure

Acute symptomatic seizures occur in close temporal association with a systemic or central nervous system (CNS) insult (5). About 5% of children with infections of the CNS have acute symptomatic seizures at the time of infection (6). About 10% of children who suffer traumatic brain injury experience seizures within one or two weeks after their injury (7). By age 20, 1% of all children will have experienced acute symptomatic seizures (8). Inclusion of children with acute symptomatic seizures as having epilepsy will double the reported incidence of epilepsy.

Febrile Seizure

A febrile seizure is a convulsive episode occurring in association with an acute febrile illness. This is actually a subcategory of acute symptomatic seizure, differing only in that all children are exposed to the risk factor. Some authors place restrictions for inclusion in this category based on age or clinical symptomatology.

In the United States and in northern European countries, between 2% and 4% of all children can be expected to experience a convulsion during a febrile illness by the age of 5 years (9–14,15) but there is striking variation in the frequency of occurrence of febrile convulsions worldwide (16–19). The high frequency reported in Japan (9%) has been attributed to recognition of symptoms. It is hypothesized that the typical sleeping arrangement, in which children tend to sleep with or in close proximity to parents, facilitates recognition of symptoms. However, this theory may not explain all geographic differences, because similar sleeping accommodations are common in China and India as well—regions where incidence is low. It is possible that a selective genetic predisposition for febrile convulsions and the accompanying generalized spike and wave electroencephalograph (EEG) pattern exist in the Japanese. The very high frequency of febrile seizures reported in African countries may be related to misclassification of children suffering from cerebral malaria, who probably have parasitemia (20). These children have temperature elevation, but probably do not have febrile seizures as defined in Western countries.

Most contemporary studies segregate febrile seizures from epilepsy, but a few series have included selected cases of febrile seizures, primarily those with “complex” features, with cases of epilepsy. Since such cases comprise 20% to 30% of all febrile convulsion cases, their inclusion may double the apparent incidence or prevalence of unprovoked seizures or epilepsy. People with febrile seizures are at an increased risk to develop epilepsy, and this increase in risk extends at least into the third decade of life (21–23).

Neonatal Seizures

Neonatal seizures are those that occur in the first 28 days of life. This definition, which is derived from concepts of mortality statistics, is conceivably in flux. Infants less than 32 weeks gestational age (a group with improving survivorship) are incapable of developing integrated cerebral electrical activity. In some studies of premature infants, convulsive events occurring between birth and 44 weeks gestational age have been considered a neonatal seizure. From the standpoint of the preceding classification, most neonatal seizures, particularly those occurring in the first few days of life, would fall into the acute symptomatic category. Epidemiologically, there seems little that is unique about seizures after the first 7 days of life in full-term infants when compared with seizures identified after the first month of life. There is likely considerable misclassification of cases, with the gold standard being seizures confirmed by EEG monitoring (24), because monitoring also identifies infants with only electrical paroxysms and no clinical features. There are no population-based studies of neonatal seizures using electrical confirmation of seizures.

Definitional difficulties are superimposed upon differences in risk within economic groups and geographic areas. Among full-term infants, the reported frequency of neonatal seizures ranges from slightly over 1 per 1,000 live births to 8 per 1,000 live births (25–27). The incidence is lower in developed countries than in developing countries; the incidence may be higher in infants born to mothers of low social-economic class. The frequency is higher among those with low birth weight, and may be higher in children with intracerebral hemorrhage and those who are small for gestational age. There are definite temporal trends in incidence in recent years, with a reduced frequency among full-term infants in most but not all industrialized countries. There are also differences in causes over time. Metabolic insults such as hypoglycemia and hypocalcemia were important in the 1950s and 1960s, while in contemporary studies, hypoxic–ischemic insults account for the majority of cases.

Among survivors of neonatal seizures (about 75% of the total), one-third to one-half have adverse neurologic outcomes. Approximately one-fifth might be expected to experience subsequent unprovoked seizures, mostly in those with neonatal seizures attributable to anoxic insults (28). Given that the majority of these children experiencing anoxia have associated neurologic disability, their epilepsy may also be intractable. Children with “benign familial neonatal seizures” (BFNS) (29)—the first epilepsy syndrome for which genes were identified: one encoding a potassium channel KCNQ2 (on chromosome 20q) and another KCNQ3 (on chromosome 8q)—and children experiencing “fifth day” seizures (a syndrome which seems to have largely disappeared) (30,31), have a slightly increased risk for later seizures, but their long-term prognosis in general is quite good. While most epidemiologic studies of epilepsy exclude neonatal seizures unless the patients have subsequent unprovoked seizures, their inclusion would substantially increase the reported incidence of epilepsy, particularly incidence reported in the first year of life. Epilepsy syndromes starting in the neonatal period are generally considered to be epilepsy in current classification systems (32).

Unprovoked Seizures

Unprovoked seizures occur in the absence of an identified acute precipitant. In studies in the United States and Iceland, about 25% of newly diagnosed unprovoked seizures in children occur as a single event and never meet criteria for epilepsy (33–35). Half of newly identified unprovoked seizures in childhood in Japan (16) and Spain (36) were isolated events and did not recur.

THE EPIDEMIOLOGY OF EPILEPSY

Incidence cohorts are necessary if one wishes to understand the geographic distribution, causes, and prognosis of epilepsy. A number of recent studies of the incidence have used similar methodology and definition, allowing some comparison. These studies form the basis for most of the following discussion.

Incidence

Information about the incidence of epilepsy (recurrent unprovoked seizures) in children is derived from studies of total populations that provide age-specific information about incidence and from studies limited to children. Even in studies limited to children, there are difficulties in comparisons across studies because of the inclusion of different age groups as “children,” differences in inclusion criteria, and, in the case of the total-population studies that provide age-specific incidence, different age grouping.

Incidence rates in children have been estimated from many different populations over the past several decades and have been found to range from 35 per 100,000 in India (37) to 124 per 100, 000 in Chile (38) (Table 9.1). Methodological differences in case ascertainment may account for some variation in rate. The majority of studies have captured information using medical contacts. Some studies conducted in developing countries, however, have relied on door-to-door survey methodology and may have been able to capture cases in the community who did not seek medical attention.

Most recent incidence studies of all unprovoked seizures have been conducted in developed countries (Table 9.2). The incidence of “all unprovoked seizures” should be somewhat higher than the incidence of epilepsy. An examination of the studies that have provided incidence of all unprovoked seizures shows a reasonable similarity, with the exception of a study in Finland, representing the only outlier. In the most recent studies, the incidence in Tunisia (69) seems substantially higher than the incidence reported by the more recent studies in Iceland and in Sweden.

Several longitudinal studies in children have shown a reduction in the incidence of epilepsy over time. In a study in Rochester, Minnesota, incidence of epilepsy fell by about 40% between 1935 and 1975; however, this trend seems to have reversed after 1975 in this community (64,71) (Table 9.3). Among the studies that included all afebrile seizures (Table 9.4), a study of a British general practice reported that incidence under age 20 fell from 154 per 100,000 between 1975 and 1984 to 61 per 100,000 in the years from 1985 to 1994 (74). In Finland the incidence of epilepsy in children declined by about 20% between 1986 and 2002 (77). In studies in Copparo, Italy, done some 30 years apart, the incidence of epilepsy fell from 97 per 100,000 in the period 1964 to 1978 to 59 per 100,000 in the period from 1996 to 2005. The fall in the middle decades of the past century is largely unexplained, but the increase in Rochester after 1975 may be related to increased survivorship of very low-birth-weight infants.

Interpretation of studies reporting frequency of afebrile seizures is difficult, since there seems to be wide variation (Table 9.4). Again, some differences in incidence may be due to definition or methodology. For example, the high incidence in Ecuador is likely due to the inclusion of acute symptomatic seizures.

Some studies have used other definitions of “epilepsy” (Table 9.5). In general, these studies seem consistent with studies from the same geographic area, taking into consideration the age structure studied. There are also some studies using computerized population-based data recorded for other purposes. In general, these computer-based studies have relied on algorithms with positive predictive values of 90% or better, but are less accurate than direct record review. While there are a number of studies that report global incidence, there are few studies that provide data on gender, age, etiology, or seizure type. The following sections summarize results available from studies that do report such data.

Age-Specific Incidence

In all studies providing separate information regarding the incidence by detailed age groups, the incidence is highest in the first year of life (82). The most recent studies report incidence in the first year of life of about 100 per 100,000 children. Incidence falls after age 1 year, although the rate of the fall varies. In Canada, for example, incidence appears to be stable from ages 1 through 10 years at about 40 per 100,000, and in early adolescence incidence is similar to that reported in adult years of life (20 per 100,000) (48).

In many studies, incidence is typically provided only for 5- or 10-year age groups. In developing countries, incidence may be higher in adolescence than in early childhood, whereas in developed countries, incidence is lower in the second decade of life than in the first decade. The exception is a British study from which one can calculate age-specific incidence: the incidence seems highest in the late teenage years (78). Although this study used a unique definition of “epilepsy,” internal comparisons should be consistent, assuming that there is no bias in identification related to age group. As a result, these investigators’ observations may be valid.

Gender-Specific Incidence

For most recent studies that report gender, gender-specific incidence in children is higher in males, although seldom significantly so. This seems to be true regardless of study definition. Only one Swedish study demonstrates a clearly higher incidence in females (68).

Race-Specific Incidence

One may make broad comparisons across studies of different races, but these are unreliable because of different definitions across studies. In one study of children that used broad definitions of epilepsy and allowed direct comparison by race, the incidence in African American children was higher than that in Caucasian children (83). This study did not control for socioeconomic status.

TABLE 9.1

TABLE 9.2

TABLE 9.3

Seizure Type

Most recent studies of epilepsy in developed countries report a predominance of partial seizure disorders over generalized seizure disorders. One must consider the age distribution being studied as well as seizures classified. Generalized-onset seizures seem to predominate in the first year of life. The preponderance of generalized seizures in the first year of life may be in part due to the classification of children with infantile spasms as “generalized.” Spasms account for up to 40% of incident epilepsy in the first year of life and they should probably be separately classified. After the first year, partial seizures seem to predominate. Some studies seem to find exceptions to this, however, notably older studies from Tokyo, Japan (16), and Copparo, Italy (43), where 80% to 85% of new cases were considered generalized. Because both areas would be expected to have access to modern diagnostic techniques, the predominance is puzzling, and a later study from the Copparo region shows a less dramatic difference in epilepsy by seizure type (62). When seizure type is reported, studies in developing countries seem to have a predominance of generalized epilepsy. Whether this represents misclassification related to limited evaluation of incidence cases remains uncertain. An excess of generalized-onset seizures may account for the higher incidence in some countries such as Chile. Studies of “all unprovoked seizures” and studies using more inclusive definitions for cases of “epilepsy” (eg, “all afebrile seizures”) tend to report a preponderance of generalized seizures. It is likely that in children both single, unprovoked seizures and acute symptomatic seizures are predominantly generalized. This should account for the apparent difference in distribution by seizure type based upon study inclusion criteria.

TABLE 9.4

TABLE 9.5

Etiology

When reported, between 60% and 80% of all new cases in children have no obvious antecedent to explain the condition. This is true even with the use of magnetic resonance imaging. A small proportion of new cases can be attributed to trauma, infection, postnatal vascular lesions, or CNS degenerative conditions. About 20% of cases are associated with neurologic handicaps presumed present from birth, intellectual disability (ID), defined as IQ less than 70, cerebral palsy (CP), or a combination thereof. Whereas most cases of ID or CP in and of themselves usually lack obvious causes, a more appropriate estimate for the proportion with identified cause may be 3%, as reported in a study from Sweden (69). Much has been made of the relationship between migration disorders and epilepsy. This pathology is more readily identified with MRI examinations. Although no systematic population-based studies have been undertaken to evaluate the burden of migration disorders on the incidence of epilepsy, such cases are likely to account for at best 1% to 2% of all cases of childhood epilepsy, and many of these cases would have previously been categorized as being associated with neurologic handicaps presumed present from birth.

Familial (genetic) predisposition certainly plays a role in the risk for developing epilepsy (84,85). The offspring or sibling of a person with epilepsy has a threefold increase in risk of developing epilepsy. Although familial aggregation consistent with Mendelian inheritance is rare, there are several childhood-onset syndromes with clear genetic patterns of inheritance; for some, a specific gene anomaly has been identified. Examples of these include benign familial neonatal seizures, benign infantile epilepsy, and Baltic myoclonic epilepsy, febrile seizures plus, and Dravet syndrome. A localization on chromosome 6 and other chromosomal localizations for juvenile-onset epilepsies remains controversial, and the mode of inheritance is not understood (86,87). A linkage for the EEG pattern (not the epilepsy) has been reported for Rolandic epilepsy with central temporal spikes (88,89).

It is important to point out factors that are not causal for epilepsy. Once cases of CP are accounted for, there has been no evidence of an association between adverse pre- and perinatal factors and the development of epilepsy. The concept of “birth trauma” or of “pregnancy complications” being a cause of epilepsy has not been supported in a variety of studies (90–92). From a similar standpoint, febrile seizures are not “causal” for epilepsy. They are more likely a marker for a preexisting susceptibility—in some cases genetic, and in other cases “structural.”

EPILEPSY SYNDROMES

Considerable emphasis has been placed on epilepsy syndromes in recent years (32,93). The classification to date is most useful in children, but, even in epidemiologic studies in children, a substantial proportion of cases fall into nonspecific categories (34). Syndrome classification has generally not been useful for classification in population-based studies, although its failure may occur primarily in studies of adults. Detailed and sophisticated information is necessary to appropriately categorize cases, and this information is seldom available in population-based studies. Even when available and specifically sought after, only 40% to 60% of children with incident epilepsy meet criteria for specific syndromes (34,64). Most individual epilepsy syndromes are rare; thus, there is substantial variation in incidence across studies because of small numbers of cases. Despite limitations in these and other population-based studies, some information regarding the frequency of epilepsy syndromes is available.

Few population-based incidence studies of all ages classified all cases according to specific epilepsy syndromes as opposed to broad categories separated by mode of seizure onset and by etiology. There are also a few incidence studies limited to children that have provided detailed breakdown by epilepsy syndromes. There are case series and some prevalence cohorts reporting proportions of cases with specific syndromes, but these studies may give a biased sample of syndrome frequency.

The incidence of epileptic syndromes for the period between 1980 and 1984 was investigated for the population of Rochester, Minnesota. In this study approximately 20% of childhood cases fell into nonspecific categories, and about one-third were considered localization-related cryptogenic epilepsies without further localization. In Spain, in a study limited to children through age 14, a detailed distribution of epilepsy syndromes (as of the 1989 classification) was presented. Generalized idiopathic epilepsies accounted for 24% of incidence cases, and idiopathic localization-related (focal) epilepsies accounted for 18%. In two studies, conducted in Bordeaux, France (94), and Iceland (34), data on the incidence of seizure and epilepsy syndromes were not presented separately for children (30,76). In France, approximately 1% of the population with newly diagnosed epilepsy had juvenile myoclonic epilepsy, grand mal on awakening, or West syndrome, and 2% had pyknolepsy. The incidence of idiopathic localization-related epilepsy was 1.7 per 100,000 (7% of all cases, adults and children). These proportions correspond to those reported for studies in children alone. In the population-based, prospective study of epilepsy in Iceland, juvenile myoclonic epilepsy, West syndrome, and childhood absence epilepsy each accounted for 1% of all newly diagnosed cases, with an incidence of 0.7 per 100,000 person years. Benign Rolandic epilepsy accounted for 20% of new-onset cases in children and 5% of cases in the total population, providing an incidence rate of 2.8 per 100,000 person years. In summary, most population studies show that specific syndromes are rare, with few exceptions, and most individually would meet criteria for a “rare disease” based upon FDA and EMEA criteria. The exception would seem to be juvenile myoclonic epilepsy, which has a very low incidence but also a very low rate of remission; hence, it has a high prevalence in studies of all ages (95).

West Syndrome

The incidence of West syndrome has been evaluated in several geographic areas and seems consistent across studies. Incidence ranges from 2 to 8 per 10,000 live births (Table 9.6). In all studies reporting gender-specific incidence, there is a male preponderance.

The clinical perception of West syndrome is that the prognosis is poor, but population-based studies in Iceland and Minnesota suggest an excellent prognosis in idiopathic cases (107). These findings underscore the need for more population-based incidence cohorts examining West syndrome.

Lennox–Gastaut Syndrome

The incidence of Lennox–Gastaut syndrome is between 2 and 5 per 100,000 (Table 9.7), and there probably is little variation in frequency worldwide. The syndrome typically accounts for 2% to 3% of new cases of epilepsy in children. However, in Kiel, Germany, this syndrome accounts for about 3 per 100,000 cases in those age 8 and under, and in Spain, about 5% of all cases (64).

Severe Myoclonic Epilepsy of Infancy (Dravet Syndrome)

The majority of cases of Dravet syndrome have been associated with a de novo mutation of the gene sodium channel 1a (SCN1A). Based upon one case identified clinically in the National Perinatal Collaborative Project (54,000 live births), and on five cases identified from clinics in western Texas, the cumulative risk through age 7 has been suggested to be approximately 1 in 40,000 (108). In more recent studies, the incidence has been reported to be about 1 per 15,000 live births, with about 80% being attributed to a genetic mutation (109). A lower proportions of cases attributable to the mutation have been reported from Japan (110). About 300 new cases will occur in the United States in 2015.

TABLE 9.6

Absence Epilepsy: Childhood Absence (Pyknolepsy) and Juvenile Absence Epilepsy

Epilepsies characterized by absence seizures are separated into childhood absence (pyknolepsy) and juvenile absence epilepsy. Although these syndromes are considered to be distinct, they are difficult to distinguish clinically and epidemiologically. As a result, they are lumped together in most epidemiologic studies. In Sweden, Finland, and Rochester, Minnesota, absence epilepsy comprised approximately 8% of all childhood-onset epilepsies, and the incidence was about 7 per 100,000 (Table 9.8). Incidence was somewhat lower in the Faeroes and another Finnish study (less than 2 per 100,000) and highest in Copporo, Italy (15 per 100,000). Overall, there seems to be considerable consistency for this combined epilepsy syndrome category. Only two studies distinguish the two syndromes, and this seems to have been based primarily on age of onset.

TABLE 9.7

Juvenile Myoclonic Epilepsy

Juvenile myoclonic epilepsy (JME) has received a considerable amount of attention and is perceived as a frequent epilepsy syndrome in children. Most of the studies reporting this syndrome in children have been performed in Scandinavian countries (Table 9.9).

In Sweden, five children under the age of 15 had a diagnosis of JME, with an incidence of 6 per 100,000. In the studies in Iceland and Rochester, Minnesota, most cases were identified between the ages of 15 and 24. If these age groups are included, the incidence under age 25 is approximately 6 per 100,000. In both Rochester and Iceland, between 5% and 10% of newly diagnosed epilepsy in children may meet criteria for this syndrome. This contrasts with the study in Bordeaux, France, in which 30% of cases were diagnosed at age 5.

Benign Rolandic Epilepsy

Benign Rolandic epilepsy is among the more common childhood epilepsy syndromes, according to studies from Scandinavia, Italy, and other countries (Table 9.10). In Italy and Iceland, this syndrome accounts for approximately 25% of incidence cases of epilepsy in children from birth through age 15 (34,41). In Sweden, the incidence in those under age 15 is 10.7 per 100,000, and this syndrome accounts for about 14% of childhood epilepsy.

PREVALENCE OF CHILDHOOD EPILEPSY

Prevalence provides little information beyond that required for health service needs. Prevalence data are virtually useless for prognosis or etiology. Furthermore, differences in methodology and definitions frequently preclude the ability to make comparisons across studies. Nonetheless, a presentation regarding the epidemiology of epilepsy would not be complete without some discussion of prevalence. The definitions of prevalence vary as extensively as the definitions of incidence. Prevalence rates in various studies worldwide are usually confounded by a dizzying array of definitions. Tables 9.11, 9.12, and 9.13 stratify studies according to definition. When definitions are comparable, there seems to be little variation in the prevalence of epilepsy, except for a moderately higher prevalence in developing countries such as Tanzania (114) or Zambia (123). An outlier is found in two studies in Egypt that show quite unusual lifetime prevalence patterns (125,126). The lifetime prevalence of epilepsy in those age 0 to 4 was over 6%, but was only 2.5% in the 10 to 14 years age group and around 2 to 3 per 1000 in adults—prevalence in the low range for adults. This is particularly remarkable and would suggest an exceedingly high incidence and an exceedingly high mortality for childhood epilepsy. These findings are in stark contrast to the findings in another recent study in Egypt, which seem more consistent with findings from European countries and report an eight-fold lower lifetime prevalence in young children (66). Compared with the studies in the United States and Europe, the prevalence of epilepsy may be higher in South America and lower in some parts of Asia.

TABLE 9.8

TABLE 9.9

TABLE 9.10

In studies that have defined prevalence as seizures or medication use in the 5 years prior to prevalence determination, estimates remain between 3 and 7 per 1,000 in developed countries and in the range of 9 to 22 per 1,000 in developing countries (Table 9.12). Prevalence should be slightly lower if the requisite time period is shorter (Table 9.11). It is hypothesized that the increased prevalence in some of these regions is a result of parasitic infections. In some studies, prevalence seems to increase with age. Studies that have measured lifetime prevalence (Table 9.13) within the same population at different points in time show that prevalence of epilepsy has decreased (74). Recently there has been a tendency in reports from developing countries to report the prevalence (or incidence) of convulsive epilepsy (159,160,161). While this may be useful for regional comparisons, the high proportion of children with nonconvulsive epilepsy in more complete studies of incidence or prevalence renders these studies inappropriate for comparison—particularly of children. Further, a definition of “convulsive seizure” is seldom provided, although one simplistically assumes that the authors mean seizures characterized only by generalized major motor seizures. Studies of convulsive epilepsy will not be discussed further.

Tables 9.11, 9.12, and 9.13 summarize numerous studies of the prevalence of epilepsy worldwide.

Prevalence by Seizure Type

Most prevalence studies find a preponderance of generalized-onset seizures. This appears to be true regardless of study site, although the proportion with partial seizures is higher in studies from developed countries.

Etiology

When etiology is reported in incidence studies, between 60% and 80% of cases are of unknown cause. When prevalence studies report etiology in children, epilepsy is most commonly associated with neurologic handicap present from birth (eg, MR or CP), but few studies provide quantitative data. Several studies report the frequency of developmental delay (independent of ID) and other handicap that occurs in up to 25% of cases.

Gender

Except for the British general practice study (42), which used broad definitions of epilepsy, there is a male excess in virtually all studies, although it seldom reaches statistical significance. When age or gender breakdown is provided, females have a higher prevalence in the teenage years in some studies (133,144).

TABLE 9.11

TABLE 9.12

TABLE 9.13

TABLE 9.14

Race

Prevalence by racial subgroups can be compared in some studies in the United States. Prevalence is higher in African Americans than in Caucasians. These studies do not address whether this difference is attributable to racial or socioeconomic factors.

Cumulative Incidence

A concept more useful than prevalence in terms of epidemiologic measurements is “cumulative incidence,” which is the risk of developing a convulsive disorder through to a specific age. It is the cumulative incidence, not prevalence, that is important for comparisons of risk for epilepsy.

Cumulative incidence alone is reported from several studies (Table 9.14) and has been reported in or may be calculated from data provided in many papers reporting incidence. If there is no mortality attributable to epilepsy (mortality is negligible in children without handicap), cumulative incidence of epilepsy and lifetime prevalence of epilepsy at age 20 should be similar. The cumulative incidence for all convulsive disorders through age 20 was slightly more than 4% in Rochester, Minnesota; that for epilepsy was slightly more than 1%; and that for all afebrile seizures was about 2%. These proportions should be similar to the lifetime prevalence for these same definitions.

CONCLUSION

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