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PubMed2002

Association of family history of epilepsy with earlier age at seizure onset in patients with focal cortical dysplasia.

OBJECTIVE: To establish the contribution of family history of epilepsy to seizure onset in patients with focal cortical dysplasia (FCD). PATIENTS AND METHODS: From January 1998 to January 2001, we prospectively evaluated 19 consecutive patients (10 male, 9 female) with a diagnosis of FCD based on magnetic resonance imaging. All patients and at least 1 family member were directly interviewed by the same observer after completion of a semistructured questionnaire. Initially, we classified patients into 2 groups: presence or absence of family history of epilepsy. Patients with a family history of epilepsy were subdivided into 2 groups: patients with a family history of epilepsy in first-degree relatives or multiple relatives (n=5) and patients with a family history of epilepsy in relatives who were not first-degree (n=4). Statistical analysis was performed with use of the nonparametric tests Kruskal-Wallis and Kaplan-Meier (survival analysis). P=.05 was considered statistically significant. RESULTS: The ages of the patients ranged from 3 to 41 years (mean, 15.6 years). All patients had similar type and extent of cortical dysgenesis. Ages at seizure onset varied from 1 month to 22 years, with a mean of 5.8 years. Nine patients had a family history of epilepsy. The mean age at the first seizure in patients with a family history of epilepsy was 2.6 years compared with 8.5 years in those with no relatives having epilepsy (P=.02). When patients with a family history of epilepsy were classified further, the mean age at first seizure was 1.9 years for patients with a family history of epilepsy in first-degree or multiple relatives and 3.9 years for patients with a family history of epilepsy in relatives who were not first-degree compared with 8.5 years for patients with no family history of epilepsy (P=.04). CONCLUSION: Our results show that a family history of epilepsy is associated with an earlier age at seizure onset in patients with FCD. Although this is a preliminary finding and a larger sample is needed to confirm these results, we believe these observations provide evidence that genetic modifiers could become an important issue in the clinical presentation of patients with dysplastic lesions.

Adolescent↗
PubMed1999

A study of newly diagnosed epilepsy in Malaysia.

BACKGROUND/AIM OF STUDY: To determine the characteristics of newly diagnosed epilepsy in the multiracial population of Malaysia. METHODS: This is a prospective study of 165 consecutive newly diagnosed cases of epilepsy presenting to the neurology laboratory of the University Hospital, Kuala Lumpur. The inclusion criteria were: two or more seizures with interval of > 24 hours, age > 1 month, residents of Klang Valley. All the patients underwent an awake and sleep EEG. RESULTS: One hundred and sixty-five cases were collected over 1992-1994. Their ethnic origin was: Chinese (36%), Indian (35%), Malay (29%). The mean age of onset of epilepsy was 18.7 years. Localisation related epilepsies accounted for 57.6% of cases while the remaining 42.4% were generalised epilepsies. Of the generalised epilepsies, subclassification was as follows: idiopathic generalised epilepsy 28.5%, juvenile myoclonic epilepsy 5.5%, childhood absence epilepsy 3.6%, West syndrome 3%, Lennox Gastaut syndrome 1.2% and photosensitive epilepsy 0.6%. Twenty-two percent of the cases were symptomatic and 78% were cryptogenic/idiopathic. The patients had a mean of 3.9 other siblings. Only 0.76% of the close relatives (parents and siblings) had a history of epilepsy. CONCLUSION: The characteristics of epilepsy in Malaysia is largely similar to those reported elsewhere. Genetic factors may be playing a relatively minor role in causing epilepsy in this community.

Adolescent↗
PubMed1999

Epilepsy in women: the science of why it is special.

Epilepsy is a common neurological disorder that may be affected by reproductive hormones and may complicate reproductive health. Many women with epilepsy experience changes in seizure frequency and severity with changes in reproductive cycles, including at puberty, over the menstrual cycle, with pregnancy and at menopause. Ovarian steroids alter neuronal excitability at the membrane and in the genome. Altered protein synthesis as a consequence of changes in RNA mediated gene transcription is one mechanism for steroid mediated effects on excitability. These genomic effects are delayed and sustained. In contrast, membrane effects are immediate and short duration. These effects are mediated at both the GABA-A and NMDA receptors. Estrogen also dynamically alters synaptic connectivity. Estrogen enhances excitability and lowers the seizure threshold, whereas progesterone enhances inhibition and increases the seizure threshold. In experimental models of epilepsy, estrogen is proconvulsant and progesterone is anticonvulsant. The net effect of these steroid actions is to alter neuronal excitability over physiological cycles. Some epilepsy syndromes are expressed or worsened at puberty. One third to one half of women with epilepsy have catamenial seizure patterns, with seizures most likely to occur in the perimenstrual period and at ovulation. More research is needed to understand the effects of menopause on epilepsy. Antiepileptic drugs may exacerbate the risk of reproductive endocrine disorders in women with epilepsy. Fertility rates are lower for women with epilepsy. Women with epilepsy are more likely to have anovulatory menstrual cycles, abnormal pituitary LH release and altered ovarian steroid concentrations. Polycystic ovaries are detected more often in women with epilepsy, particularly those on valproate. Treatment of hormone sensitive seizures relies on standard AEDs. Small trials suggest that adjunctive progesterone therapy is sometimes helpful. The newer AEDs, gabapentin and lamotrigine may have some advantages for women with epilepsy. These drugs do not alter levels of steroid hormones and do not interfere with effectiveness of hormonal contraception. Experience in pregnancy is limited. The dynamic effects of hormones on seizure expression and of seizures on reproductive health complicate the management of epilepsy in women. Newer AEDs may offer advantages for women with epilepsy in the reproductive years.

Epilepsy↗
PubMedDate not supplied

[Myoclonus and myoclonic epilepsies in childhood].

Myoclonic jerks occur in a number of different syndromes. There is many classifications of myoclonus. It is preferred the Fejerman classification, slightly modified that present the following five groups: 1. Myoclonus without encephalopathy and without epilepsy, which includes physiological myoclonus; 2. Encephalopathies with non epileptic myoclonus, which includes Kinsbourne syndrome and certain types of hyperekplexia which pose differential diagnosis problems with reflex myoclonic epilepsy; 3. Progressive encephalopathies with myoclonic seizures which includes typical and atypical progressive myoclonus epilepsies; 4. Epilepsies and epileptic encephalopathies with myoclonic seizures, which includes severe epilepsies which leads to mental retardation, as Otahara syndrome, West syndrome and Lennox-Gastaut syndrome, and other epilepsies which present sometimes myoclonic seizures, as Landau-Kleffner syndrome, 5. Comprises true myoclonic epilepsies, differentiating syndromes recognized as idiopathic, -benign myoclonic epilepsy of infancy, reflex form of benign myoclonic epilepsy in infancy, eyelid myoclonic with absences, perioral myoclonic with absences and juvenile myoclonic epilepsy-, cryptogenic-severe myoclonic epilepsy of infancy, myoclonic-astatic epilepsy and epilepsy with myoclonic absences-, and symptomatic as the generalized myoclonus in children with static encephalopathies. The epileptic syndromes of the last group are described. Despite this classification, apparently clear, there is still a great deal of confusion and in clinical practice, many cases are difficult to classify.

Child, Preschool↗
PubMed2001

[New antiepileptic drugs in childhood epilepsies: indications and limits].

Regarding the antiepileptic drugs (AEDs) in children, it was recently shown that they have a specific profile of efficacy and also of worsening according to the different epilepsy syndromes. However, the therapeutic profile of the most recent compounds is still not completely established in children because of the high number of syndromes and the difficulty to perform controlled studies in this age range. Controlled studies are most often first performed in adults and they begin in children whereas the new drug is already approved. However, some new AEDs dramatically improved seizure control, particularly in some severe epilepsy syndromes such as West syndrome and Lennox-Gastaut syndrome. Vigabatrin demonstrated a remarkable efficiency in infantile spasms whereas it tends to worsen myoclonic epilepsies, absence epilepsy and idiopathic partial epilepsy. Lamotrigine is efficient in absence epilepsy and symptomatic or cryptogenic generalized epilepsies such as Lennox-Gastaut syndrome and myoclonic astatic epilepsy. By contrast, lamotrigine increases the frequency of seizures in severe myoclonic epilepsy in infancy (Dravet syndrome) as well as in some cases of idiopathic partial epilepsy. Felbamate remains indicated as third line drug in refractory Lennox-Gastaut syndrome provided blood parameters are controlled. The therapeutic profile of oxcarbazepine is closed to that of carbamazepine. The efficacy of topiramate was demonstrated in partial epilepsy, but the other indications remain to be précised. Pediatric studies using gabapentin and tiagabine disclosed encouraging results in partial epilepsy. Clinical trials with stiripentol represent an example of strategy for developing a new AED in children; it recently demonstrated, in association with clobazaru, efficacy in a severe myoclonique epilepsy in infancy.

Anticonvulsants↗
PubMed2003

A prevalence study of epilepsy in Hong Kong.

OBJECTIVES: To examine epidemiological data on epilepsy for the Hong Kong west region. DESIGN. Descriptive study. SETTING: Epilepsy clinic, university teaching hospital, Hong Kong. PATIENTS AND METHODS: The epilepsy clinic of Queen Mary Hospital manages the majority of adult patients (aged 15 years or older) with chronic seizure disorders resident in the Hong Kong west area with an adult population of 475,900. All patients underwent electroencephalography examination and each subject was independently assessed by two epileptologists for diagnosis and classified according to the International League Against Epilepsy recommendations. RESULTS: Seven hundred and thirty-six patients (female, 42.9%; male, 57.1%; mean age, 40.8 years; standard deviation, 13.6 years) with epilepsy were enrolled in the study. The prevalence rate of active epilepsy in the population 15 years or older was estimated at 1.54 per 1000 on 1 January 2002. Two hundred and eighty-five (38.7%) patients had idiopathic epilepsy syndromes, 100 (13.6%) had cryptogenic epilepsy, and 285 (38.7%) had a remote symptomatic aetiology. Seizure type was partial in 408 (55.4%) patients and generalised in 285 (38.7%). Thirty-one (4.2%) patients had a positive family history. Idiopathic generalised epilepsy syndromes described as common in the literature, such as juvenile myoclonic epilepsy and childhood absence epilepsy, were infrequently seen at 0.68% and 0.95% of cases, respectively. CONCLUSIONS: This study provides baseline data for epilepsy service development and research in Hong Kong. The prevalence rate of active epilepsy in this Chinese, adult population was low compared with that reported in other developed countries. Further population-based epidemiological research is indicated to confirm the prevalence of seizure disorders in this locality.

Adolescent↗
PubMed2004

The mortality of epilepsy revisited.

Epilepsy carries a significant mortality that, on average, is 2-3 times higher than in the general population. Causes of death in epilepsy are presented. Mortality in epilepsy is assessed by means of particular parameters; the mortality rate, the standardised mortality ratio, and the proportional mortality rate. An overview of their use and significance is given here. A number of epidemiological studies have assessed mortality in people with epilepsy in the general population and in populations from hospitals, out-patient departments, and epilepsy centres. Methodological issues concerning the study of mortality in these populations are discussed. Epidemiological data are presented to describe the overall and cause-specific mortality, as well as determinants of mortality in epilepsy, such as epilepsy and seizure types, time from diagnosis, and age. It has become clear from population studies with long-term follow-up that epilepsy has a higher mortality in the first few years after diagnosis that tends to decrease over time. The pattern of mortality in epilepsy can reflect the underlying conditions causing epilepsy or be associated with the effect of seizures. Emphasis is given to preventable causes of death in epilepsy, such as sudden unexpected death in epilepsy and suicide, which are discussed more extensively. The size of the problem and measures to avoid more deaths in epilepsy are discussed in the light of recently published data.

Cause of Death↗
PubMed1995

Epilepsy and children's social and psychological adjustment.

This research investigates the effects of epilepsy on the social and psychological adjustment of the children studied in the National Health Interview Survey of 1988. Analyses examine the effect of epilepsy on four measures of adjustment--home behavior problems, school behavior problems, depressed mood, and impulsiveness. For each outcome, we address five questions: (1) Do children with currently active epilepsy have poorer adjustment than children with inactive epilepsy? (2) Do children with epilepsy fare worse than other children? (3) Do demographic background and family structure moderate the apparent effects of epilepsy? (4) Do family processes mediate the apparent effects of epilepsy? and (5) Do cooccurring conditions produce the apparent effects of epilepsy? Generally, we find that: (1) Children with active and inactive epilepsy fare about equally; (2) Children with any history of epilepsy fare worse than children without epilepsy; (3) Demographic and family background moderate only a small part of epilepsy's effect; and (4) A combination of family processes and cooccurring conditions appears to produce epilepsy's apparent effects.

Adaptation, Psychological↗
PubMedDate not supplied

Genetics of myoclonic and myoclonus epilepsies.

Mendelian forms of benign myoclonic epilepsies where a chromosomal locus has been defined include (1) the autosomal dominant (AD) juvenile myoclonic epilepsy (JME) in chr. 6p11, (2) the autosomal dominant childhood absence epilepsy which evolves to JME in chr. 1p, (3) familial adult myoclonic epilepsy of Yasuda and Inazuki, and (4) possibly JME within the idiopathic generalized epilepsy susceptibility gene in chr. 8 reported by Zara et al (1995). Other myoclonic epilepsy syndromes with onset in the first year of life (Aicardi's Neonatal (Early) Myoclonic Encephalopathy, West's Syndrome, Dravet's Severe Myoclonic Epilepsy, and Dravet's Benign Myoclonic Epilepsy of Infancy), in early childhood (Lennox-Gastaut-Dravet Syndrome, Myoclonic Variant of Lennox Gastaut Dravet Syndrome, Myoclonic-Astatic Epilepsy of Doose, Benign Myoclonic Epilepsies (BME), or even in late childhood (Childhood Absence Epilepsy with myoclonias, vs. Myoclonic Absence Epilepsy) are probably genetically complex diseases. Amongst the progressive myoclonus epilepsy syndromes, specific mutations have already been defined in Unverricht Lundborg disease, ceroid lipofuscinoses 3 or Spielmayer Voight syndrome within Battens disease, sialidosis, dentadorubropallidoluysian atrophy and the mitochondrial syndrome MERRF. Most recently our laboratories established the locus for Lafora's disease in chr. 6q and results are speedily moving towards the definition of its mutation.

Chromosome Mapping↗
PubMed2000

Cerebral and cerebellar volume reduction in children with intractable epilepsy.

PURPOSE: Adult epilepsy studies have demonstrated cerebral and cerebellar volume reduction beyond the epileptogenic zone, correlating this with an inferior surgical outcome. We determined whether brain volumes were reduced in childhood epilepsy and the significance of this. METHODS: Cerebral, cerebellar, and hippocampal volumes were measured by quantitative magnetic resonance imaging on 112 children (ages 4-18) with epilepsy syndrome determined by video-EEG telemetry. Eighty-seven had partial epilepsy and 25 had generalized epilepsy or indeterminate syndrome. Normative volumes were obtained from 44 child controls from the community. RESULTS: A significant reduction in cerebral (12.6%) and cerebellar (7.9%) volume was present in the epilepsy group compared with controls. Analysis of subgroups revealed that cerebral volume was significantly decreased in frontal lobe and nonlocalized partial epilepsies. The mean hippocampal ratio of 0.73 for mesial temporal lobe epilepsy was significantly less than for all other syndromes and controls. There was no difference in the rate of hippocampal volume reduction between syndromes. There was a significant correlation between IQ and cerebral and cerebellar volume, but not duration or age of onset of epilepsy. CONCLUSIONS: Cerebral and cerebellar volume reduction is common in intractable epilepsy syndromes of childhood. These cross-sectional data suggest that brain volume reduction is present at epilepsy onset and is not a result of intractable seizures. Hippocampal asymmetry is more sensitive than volume reduction as a marker for mesial temporal lobe epilepsy, but neither measure is specific.

Adolescent↗
PubMed2000

[Myoclonic epilepsies in infancy].

INTRODUCTION: The presence of myoclonus in a patient has different meanings: there exist myoclonus without encephalopathy or epilepsy (sleep myoclonus), encephalopathies with non-epileptic myoclonus (Kinsbourne's syndrome), encephalopathies with epileptic myoclonus (progressive or not), epileptic encephalopathies with myoclonic seizures (the classic West and Lennox-Gastaut syndromes) and myoclonic epilepsies. DEVELOPMENT: Main types of myoclonic epilepsies (benign childhood myoclonic epilepsy, severe-polymorphic-myoclonic epilepsy, juvenile myoclonic epilepsy, childhood familial myoclonic epilepsy, benign reflex myoclonic epilepsy, as well as progressive myoclonic epilepsies, among which progressive myoclonic epilepsy (PME) type 1 (Unverricht-Lundborg's disease) and PME2 (Lafora type) are prominent, whereas other entities, such as those related to neuronal ceroid lipofuscinosis or mitochondrial cytopathies are discussed more briefly) are reviewed, analyzing clinical, EEG and therapeutic issues, while the most recent contributions in the field of genetics are considered. CONCLUSIONS: Myoclonic epilepsies constitute a very heterogeneous type of epilepsy, both in their origin and in their prognosis, with favorable forms of course along with other progressive and refractory forms with an ill-fated prognosis.

Adult↗
PubMed2006

[Sudden death and mortality in epilepsy].

Mortality in epilepsy is 2-3 times higher than in the age- and sex-matched general population. It is the highest in young male epilepsy patients with generalised tonic-clonic seizures living in low socio-economical situation. The main factors of early mortality unrelated to seizures are the neurological conditions underlying epilepsy. Suicide is an important factor first of all in temporal lobe epilepsy. The group of mortality directly related to epilepsy is made up of the high-mortality grand mal status epilepticus rarely seen in treated epilepsy; the accidents related to seizures and sudden unexpected death (SUDEP). The reasons directly related to epilepsy make up about 40 per cent of epilepsy mortality. There is a 20-24-fold increase of the risk of sudden death in epilepsy compared to sudden death in the general population. The main risk of SUDEP is the "severity" of epilepsy signaled by generalized tonic-clonic seizures, resistance to antiepileptic drugs, polytherapy and frequent drug-modifications in adulthood epilepsy. Seizure-dependent autonomic changes as cardiac rhythm and breathing disturbances as well as some antiepileptic drugs and treatment modifications may contribute to the development of SUDEP. The data suggest that the main tools helping to decrease mortality in epilepsy nowadays are as follows: optimal seizure control, effective treatment of concomitant psychiatric conditions and monitoring for potentially dangerous heart dysrhythmias as well as respiration disorders.

Anticonvulsants↗
PubMed1996

Epilepsy in children.

Childhood epilepsies comprise a broad range of disorders which vary from benign to progressive and disabling. Accurate diagnosis of epilepsy type and determination of aetiology, when possible, are essential for appropriate treatment. The most common seizure type encountered in children is febrile seizures. These represent a benign condition which is not, in fact, epilepsy and usually does not require antiepileptic medication. When partial seizures occur in childhood, benign syndromes with spontaneous remission, such as rolandic epilepsy, must be distinguished from symptomatic epilepsies which may be refractory to medical management. Complex partial seizures in young children may appear different than in adults. The adverse effect profiles and dosing regimens of antiepileptic drugs in children are also different than in adults, and influence the choice of treatment. Epilepsy surgery should be considered for some children with intractible partial seizures. Generalized epilepsies also have a broader spectrum in children. The idiopathic generalized absence epilepsies are usually easy to control with medication. They range from childhood absence epilepsy which tends to remit in adolescence to juvenile myoclonic epilepsy which is a lifelong condition. In contrast, the seizures of West syndrome and Lennox-Gastaut syndrome are difficult to control, and treatment involves therapeutic modalities rarely used in adults such as ACTH and the ketogenic diet. Many childhood epilepsy syndromes have a familial predisposition, and the genetic bases for several disorders have been described.

Anticonvulsants↗
PubMed2000

Neurophysiologic and neuroradiologic features of intractable epilepsy after traumatic brain injury in adults.

BACKGROUND: There is controversy regarding the precise mechanism by which epilepsy results after traumatic brain injury (TBI). Previous reports have suggested that mesial temporal lobe epilepsy may result from TBI only in young children, while neocortical epilepsy arises from TBI in later life. These conclusions were based on surgical series and may be biased because of patient selection. OBJECTIVE: To determine the frequency of mesial temporal lobe as opposed to neocortical epilepsy in patients with intractable epilepsy resulting from TBI after the age of 10 years. PATIENTS AND METHODS: We identified 23 patients with intractable epilepsy who had TBI after the age of 10 years, preceding the onset of epilepsy. Patients were studied by simultaneous videotape and scalp electroencephalographic recording of typical seizures; magnetic resonance imaging; neuropsychologic studies; and, when appropriate, intracarotid amobarbital testing. Two patients underwent anterior temporal lobectomies. RESULTS: Of the 23 patients, 8 (35%) had mesial temporal lobe epilepsy, based on the finding of hippocampal sclerosis on a magnetic resonance imaging scan, consistent interictal and ictal electroencephalographic recordings, evidence of temporal lobe dysfunction on neuropsychologic testing, and characteristic seizure semiology. Two of these patients underwent anterior temporal lobectomies with clinical benefit, and hippocampal sclerosis was confirmed pathologically. In 2 cases, patients were not treated surgically because of bilateral temporal lobe dysfunction noted on intracarotid amobarbital testing. Eleven patients had neocortical epilepsy; 1 had primary generalized epilepsy; and, in 3, the site of seizure onset was not localized. CONCLUSIONS: Mesial temporal lobe epilepsy can result from TBI in adolescents and adults as well as in children, and can often be bilateral and associated with multifocal injury. This information may be useful in developing prophylactic therapy for posttraumatic epilepsy.

Adult↗
PubMed1998

Severe idiopathic generalized epilepsy of infancy with generalized tonic-clonic seizures.

PURPOSE: While the literature on infantile epilepsies with minor and major seizures is extensive, little consideration has been given to infantile epilepsy with generalized tonic-clonic seizures (GTCS) alone. The aim of the present study was to analyze the data of a large group of patients and their families to obtain further insight into the clinical picture and pathogenesis of this type of epilepsy. METHODS: The 101 children (58 boys, 43 girls) met the following inclusion criteria: onset of the epilepsy with febrile or afebrile GTCS in the first 5 years of life, absence of primary organic brain lesion or progressive brain disease, severe course with frequent febrile and/or afebrile GTCS, failure of conventional anticonvulsive therapy. RESULTS: The epilepsy predominantly afflicts normally developed infants, boys and girls being about equally affected. The epilepsy begins with frequent febrile or afebrile GTCS, characteristically of long duration and often with alternating lateralization. In half of the cases additional myoclonic or myoclonic astatic seizures and/or absences occur. The initial GTCS phase is the same in epilepsies with and without minor seizures. Erratic myoclonias are especially characteristic. With advancing age, the symptomatology becomes increasingly polymorphic due to the occurrence of additional simple and complex focal and tonic seizures. Severe impairment of mental development soon after onset is a leading symptom. The overall death rate was 9%. Only 11% of the patients had been seizure-free for at least two years at final examination. The EEG was initially normal and subsequently exhibited diffuse 4-7/s rhythms, and only later spikes and waves of irregular shape (87%). Focal sharp waves occurred transiently in 26%. The family history and EEG of probands and relatives showed the pathogenesis to be decisively determined by genetic factors. CONCLUSION: Early infantile GTCS epilepsy represents a genetically determined (idiopathic) epileptic encephalopathy. It overlaps with other forms of early childhood epilepsy such as severe myoclonic epilepsy, severe type of myoclonic astatic epilepsy, as well as early childhood absence epilepsy with GTCS.

Age of Onset↗
PubMed2005

Motor cortex excitability in focal epilepsies not including the primary motor area--a TMS study.

It is unclear whether focal epilepsies chronically influence the processing of cortex distant to the epileptogenic zone. Therefore, motor cortex excitability was analysed in patients with temporal and extratemporal epilepsies whose epileptogenic zones did not include the primary motor area. Single and paired-pulse transcranial magnetic stimulation (TMS) was applied to the primary motor cortex in 20 healthy controls and 23 patients with focal epilepsy (39.4 +/- 13.2 years; 12 left, 11 right; 14 temporal, nine extratemporal: six frontal, three parieto-occipital) ipsi- and contralateral to the epileptogenic zone. In all patients, the epileptogenic zone did not include the primary motor cortex. The resting motor threshold (RMT), the cortical silent period (CSP), the intracortical inhibition [ICI; combined interstimulus intervals (ISI) 2 and 3 ms] and the intracortical facilitation (ICF; combined ISI 10 and 15 ms) were determined. The measures obtained ipsilateral to the epileptogenic zone were compared with those elicited in contralateral hemispheres and, in exploratory analyses, with controls using non-parametric tests, including Hodges-Lehmann estimates of median differences (HLE) with 95% confidence intervals (CI). In the patient group, the CSP elicited in the ipsilateral motor cortex (median 162.3 ms) was shortened compared with the contralateral CSP (median 174.6 ms; HLE 15.9 ms; CI 6.2, 27.0 ms; P = 0.002). This interhemispheric difference was more pronounced in extratemporal epilepsies (HLE 23.4 ms; CI -3.2, 67.6 ms) compared with temporal epilepsies (HLE 14.3 ms; CI 4.7, 26.2 ms). Patients with parieto-occipital epilepsies showed the greatest interhemispheric differences in CSP (HLE 33.5 ms) and patients with mesial temporal epilepsies the smallest (HLE 9.9 ms). No significant differences were found between ipsi- and contralateral RMT, ICI or ICF. In analyses of subgroups, the CSP was shorter in epileptic hemispheres of patients with extratemporal epilepsies (141.4 ms) than in controls (173.4 ms; HLE 40.0 ms; CI 3.2, 83.4 ms; P = 0.029). ICF was increased in epileptic hemispheres of extratemporal epilepsies (147.6%) compared with temporal epilepsies (114.6%; HLE 33.0%; CI 4.1, 68.3%; P = 0.038). The results suggest that focal epilepsies influence chronically distant cortex, leading to decreased inhibition and increased facilitation in the ipsilateral motor cortex even when the epileptogenic zone is apart from it. This alteration may be due to synaptic reorganization and appears to be more pronounced in extratemporal and neocortical temporal than in mesial temporal epilepsies. This may have diagnostic implications.

Adult↗
PubMed2005

Three to four years after diagnosis: cognition and behaviour in children with 'epilepsy only'. A prospective, controlled study.

A 3.5-year follow-up study of cognition and behaviour in 42 children with newly diagnosed idiopathic or cryptogenic epilepsy ('epilepsy only') attending mainstream education and 30 healthy gender-matched classmate controls was carried out to identify differences between groups, to detect factors that contribute to the difference and its change over time, and to establish the proportion of poorly performing children. The neuropsychological battery covered the major domains of cognition, mental and motor speed and academic language skills. Children were tested at the time of diagnosis (before any anti-epileptic drug treatment started) and 3, 12 and approximately 42 months later. Parents and teachers completed behaviour checklists, for which the scoring was adapted to prevent any influence of epilepsy-related ambiguity. Based on parental interviews at the time of diagnosis, children with epilepsy were categorized as having longstanding behavioural and/or learning problems, as belonging to a troubled family, as being exposed to 'off-balance' parenting starting at the time of epilepsy onset and/or as reacting maladaptively to the changes in relation to the onset of epilepsy. Throughout follow-up, the group of children with epilepsy only performed less well than healthy classmates on measures of learning, memory span for words, attention and behaviour. After controlling for school delay, proactive interference (number of responses to the same images as in the learning trials, but now presented in reordered locations) was the only remaining variable that distinguished the group of children with epilepsy only. Group-wise, no changes in cognitive and behavioural differences over time were found, but instability in individual performances appeared to characterize children with epilepsy only. Rather than intrinsically epilepsy-related variables, such as idiopathic versus cryptogenic aetiology, seizure control or anti-epileptic drug treatment, the child's prediagnostic learning and behavioural histories and the parents' ability to continue their habitual parenting in the face of the diagnosis of epilepsy only were shown by both group-wise and case-by-case analyses to be important for understanding the cognitive and behavioural functioning of the children with epilepsy only.

Adaptation, Psychological↗
PubMedDate not supplied

Likelihood of pregnancy in individuals with idiopathic/cryptogenic epilepsy: social and biologic influences.

We interviewed 1,558 adults with idiopathic/cryptogenic epilepsy ascertained from voluntary organizations and 316 of their siblings without epilepsy to determine their personal history of marriage and pregnancy. We examined the effects of seizure type, age at onset, and family history of epilepsy on the sex-specific likelihood of pregnancy in individuals with idiopathic/cryptogenic epilepsy as compared with their same-sex siblings. Overall, men with idiopathic/cryptogenic epilepsy were only 36% as likely as male unaffected siblings ever to have fathered a pregnancy. In men, the reduced likelihood of fathering a pregnancy was associated with partial-onset seizures, early age at onset (< 20 years), and a negative family history of epilepsy, and the effects of these epilepsy characteristics appeared to be mediated through reduced marriage rates. Among men with epilepsy who had ever been married, reproductive disadvantage was confined to those with early-onset (< 10 years) partial epilepsy. Overall, women with idiopathic/cryptogenic epilepsy were only 37% as likely ever to have had a pregnancy as female unaffected siblings; this effect was not strongly influenced by seizure type, age at onset, or family history of epilepsy. In women who had ever been married, unlike in men, reduced likelihood of pregnancy persisted, regardless of seizure type, age at onset, or family history of epilepsy.

Adult↗