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Clinical application of neuroimaging in epilepsy.

OBJECTIVE: To evaluate the use of neuroimaging in clinical practice and to assess the prevalence of detected structural abnormalities in epilepsy patients in a clinical set up. METHODS: 919 outpatients were identified and the scan results reviewed. A total of 677 patients had chronic active epilepsy (88 had idiopathic generalised epilepsy (IGE), 588 had localisation related epilepsy, one had symptomatic generalised epilepsy), 57 had a single epileptic seizure, 46 were in remission, and 139 had non-epileptic attacks. RESULTS: 391 patients had no scan (53 patients in this group had IGE, 182 had localisation related epilepsy, one had generalised symptomatic epilepsy, 18 had single epileptic attacks, 21 were in remission, 116 had non-epileptic attacks). Altogether 528 patients had a scan, the results were not available in 33, 163 had x ray computed tomography (CT) only, 178 had standard magnetic resonance imaging (MRI) (slice thickness 5 mm), and 154 had high resolution MRI (including a T1 weighted sequence with 1.5 mm thick slices). Some 252 of 495 scans (51%) were abnormal. Abnormalities were hippocampal sclerosis (n=128), atrophy or non-specific white matter lesions (n=35), vascular abnormalities (n=27), tumours (n=25), brain damage (n=24), malformations of cortical development (n=13). Excluding atrophy and non-specific white matter lesions the prevalence of detected abnormalities was 54% in localisation related epilepsy, 18% in single seizure patients, 16% in epilepsy in remission, and 0% in IGE and non-epileptic attacks. CONCLUSIONS: Abnormalities were detected in more than half of all patients with localisation related epilepsy, and in about one in five patients with single seizures or epilepsy in remission. Many patients had no scan or only CT or standard MRI. The true prevalence of structural abnormalities may be have been higher. Scanning did not add any information in patients with IGE or non-epileptic attacks.

Adolescent↗

Asthma and epilepsy: are they related? A retrospective study.

Numerous studies have suggested that epilepsy and asthma may be related conditions. There has, however, been little epidemiologic data published to support this association. We conducted a retrospective study to determine whether the prevalence of epilepsy is increased among children with asthma, and the prevalence of asthma is increased among children with epilepsy, in comparison with the general pediatric population. We reviewed the medical records, at a large city hospital, of two groups of pediatric outpatients: (1) 400 consecutive patients with asthma followed regularly at the asthma and allergy clinic; and (2) 201 consecutive patients with idiopathic epilepsy followed regularly at the pediatric neurology clinic. Patients with a history of birth prior to 36 weeks' gestational age were excluded. Among the 400 cases of asthma, there were three patients with idiopathic epilepsy (prevalence of 0.75%). The prevalence of epilepsy was similar in mild (0.79%) and moderate-to-severe (0.73%) asthma. Among the 201 cases of idiopathic epilepsy, there were 12 patients with asthma (prevalence of 5.97%). Similar percentages of epilepsy patients with and without asthma reported generalized tonic-clonic, complex partial, simple partial, and myoclonic seizures as their predominant type. The prevalence values in this study are consistent with the prevalence of epilepsy and asthma in the general pediatric population. Our findings therefore suggest that idiopathic epilepsy and asthma are not etiologically related or mutually predisposing conditions. Small samples, failure to exclude patients born prematurely, and the equation of electroencephalographic (EEG) abnormalities with epilepsy may account for the results of previous studies.

Asthma↗

An open, nonrandomized clinical comparative study evaluating the effect of epilepsy on learning.

Children with epilepsy, as a group, have a greater risk for developing learning problems as comorbid disorders. It is unknown which factors contribute to the development of such learning problems; therefore, our current knowledge does not allow the prediction of educational delay in an individual child with epilepsy. This study aimed at excluding as many factors as possible that could interfere with the analysis of the impact of epilepsy on learning. From patients referred to us in 1997 (N = 123), children were included with mild global learning impairment, defined as educational delay between 6 months and 1 year and no other apparent reason for learning impairment except for epilepsy (ie, excluding children with dyslexia, attention-deficit hyperactivity disorder, or mental handicap). A total of 44 patients fulfilled this criterion: 31 also had epilepsy (experimental group); the remaining 13 patients with similar mild learning impairment but without epilepsy were used as controls. In the experimental group two subgroups were distinguished on the basis of onset of learning impairment: in group A (n = 17) the learning problems are not unexpected as they were preceded by mild developmental delay; in group B (n = 14) the problems are unexpected and had a sudden onset. The two experimental groups differed from the control group on a number of variables, such as gender and the incidence of perinatal complications. More differences have been found between the two experimental groups: group B is selected from a larger group: all children with mild global learning impairment with sudden onset. In this group considerably more children with epilepsy have been found compared to the children with developmental delay; moreover the epilepsy is more often characterized in these children as "unexpected," that is, there was no previous established diagnosis of epilepsy, the symptoms were mostly unclear and behavioral in make-up (attentional lapses, etc); the electroencephalogram plays a much greater role in the diagnosis in this group, especially in demonstrating seizures; finally, the children in this group more frequently have neuropsychologic impairment. Children with epilepsy can have mild global learning difficulties, especially in the period after the onset of seizures. This group can be divided in a group with "trait-dependent learning difficulties," that is learning difficulties based on developmental delay, and a group with "state-dependent learning difficulties." The focus in our study was on this latter group, consisting of children with sudden and unexpected decline of results in school. The crucial finding in this group is the relatively frequent demonstration of difficult-to-detect seizures, demonstrating that an uncontrolled epilepsy can cause a decline in school results even when the seizures are of short duration and have subtle symptoms.

Attention Deficit Disorder with Hyperactivity↗

Prevalence and associated features of epilepsy in adults with Down's syndrome.

The aim of this study was to establish the prevalence of epilepsy in persons with Down's syndrome aged 19 years and over. A total of 191 adults with Down's syndrome were identified, giving a prevalence of 0.76/1000 (95% CI 0.75 to 0.77). Of these, 18 had epilepsy, giving a prevalence of 9.4% (95% CI 5.3% to 13.5%). The prevalence of epilepsy increased with age, reaching 46% in those over 50. The neurophysiological (EEG) findings of the epilepsy group were compared with those of a control group of Down's syndrome adults without epilepsy. Paroxysmal abnormalities consistent with a diagnosis of epilepsy were found in 80% of the epilepsy group, compared with only 13% of controls (P < 0.001). Epilepsy of late onset was associated with diffuse EEG abnormalities and clinical evidence of dementia. The age distribution and EEG findings suggest two independent processes in the causation of epilepsy: late-onset epilepsy associated with clinical evidence of dementia, and early-onset epilepsy in the absence of dementia.

Adolescent↗

The localizing value of ictal EEG in focal epilepsy.

OBJECTIVE: To investigate the lateralization and localization of ictal EEG in focal epilepsy. METHODS: A total of 486 ictal EEG of 72 patients with focal epilepsy arising from the mesial temporal, neocortical temporal, mesial frontal, dorsolateral frontal, parietal, and occipital regions were analyzed. RESULTS: Surface ictal EEG was adequately localized in 72% of cases, more often in temporal than extratemporal epilepsy. Localized ictal onsets were seen in 57% of seizures and were most common in mesial temporal lobe epilepsy (MTLE), lateral frontal lobe epilepsy (LFLE), and parietal lobe epilepsy, whereas lateralized onsets predominated in neocortical temporal lobe epilepsy and generalized onsets in mesial frontal lobe epilepsy (MFLE) and occipital lobe epilepsy. Approximately two-thirds of seizures were localized, 22% generalized, 4% lateralized, and 6% mislocalized/lateralized. False localization/lateralization occurred in 28% of occipital and 16% of parietal seizures. Rhythmic temporal theta at ictal onset was seen exclusively in temporal lobe seizures, whereas localized repetitive epileptiform activity was highly predictive of LFLE. Seizures arising from the lateral convexity and mesial regions were differentiated by a high incidence of repetitive epileptiform activity at ictal onset in the former and rhythmic theta activity in the latter. CONCLUSIONS: With the exception of mesial frontal lobe epilepsy, ictal recordings are very useful in the localization/lateralization of focal seizures. Some patterns are highly accurate in localizing the epileptogenic lobe. One limitation of ictal EEG is the potential for false localization/lateralization in occipital and parietal lobe epilepsies.

Adolescent↗

Role of genetics in the diagnosis and treatment of epilepsy.

Epilepsy is a heterogeneous group of multifactorial diseases, the vast majority determined by interactions between many genes and environmental factors; however, there are rare epilepsy syndromes that can be caused by a single gene mutation and are inherited according to classical mendelian genetic principles. Finding disease-causing genetic mutations in epilepsy has provided new opportunities for aiding diagnosis and developing therapies. Thus, the discovery of KCNQ2 mutations in benign familial neonatal convulsions, SCN1A mutations in severe myoclonic epilepsy of infancy and in generalized epilepsy with febrile seizures plus, and CHRA4 and CHRB2 mutations in autosomal-dominant nocturnal frontal lobe epilepsy, has led to the establishment of epilepsy as a disorder of ion channel function and, furthermore, has led to the introduction of genetic tests that are available clinically to aid in diagnosis and treatment. At the present time, clinical use of genetic testing in epilepsy is greatest in suspected cases of severe myoclonic epilepsy of infancy, generalized epilepsy with febrile seizures plus, atypical cases of benign familial neonatal convulsions and 'occult' cases of autosomal-dominant nocturnal frontal lobe epilepsy without a family history. Overall, clinical use is limited by the low number of documented disease-associated mutations and the uncertain clinical significance of many test results. Further elucidation of the relationship between gene mutations and channel function will add value to genetic testing in the future, as will better characterization of the association between gene mutations and clinical phenotypes.

Biomarkers↗

Ion channels and epilepsy.

The role of voltage-gated and ligand-gated ion channels in epileptogenesis of both genetic and acquired epilepsies, and as targets in the development of new antiepileptic drugs (AEDs) is reviewed. Voltage-gated Na+ channels are essential for action potentials, and their mutations are the substrate for generalised epilepsy with febrile seizures plus and benign familial neonatal infantile seizures; Na+ channel inhibition is the primary mechanism of carbamazepine, phenytoin and lamotrigine, and is a probable mechanism for many other classic and novel AEDs. Voltage-gated K+ channels are essential in the repolarisation and hyperpolarisation that follows paroxysmal depolarisation shifts (PDSs), and their mutations are the substrate for the benign neonatal epilepsy and episodic ataxia type 1; they are new targets for AEDs such as retigabine. Voltage-gated Ca2+ channels are involved in neurotransmitter release, in the sustained depolarisation-phase of PDSs, and in the generation of absence seizures; their mutations are a substrate for juvenile myoclonic epilepsy and the absence-like pattern seen in some mice; the antiabsence effect of ethosuximide is due to the inhibition of thalamic T-type Ca2+ channels. Voltage-gated Cl- channels are implicated in GABA(A) transmission, and mutations in these channels have been described in some families with juvenile myoclonic epilepsies, epilepsy with grand mal seizures on awakening or juvenile absence epilepsy. Hyperpolarisation-activated cation channels have been implicated in spike-wave seizures and in hippocampal epileptiform discharges. The Cl- ionophore of the GABA(A) receptor is responsible for the rapid post-PDS hyperpolarisation, it has been involved in epileptogenesis both in animals and humans, and mutations in these receptors have been found in families with juvenile myoclonic epilepsy or generalised epilepsy with febrile seizures plus; enhancement of GABA(A) inhibitory transmission is the primary mechanism of benzodiazepines and phenobarbital and is a mechanistic approach to the development of novel AEDs such as tiagabine or vigabatrin. Altered GABA(B)-receptor function is implicated in spike-wave seizures. Ionotropic glutamate receptors are implicated in the sustained depolarisation phase of PDS and in epileptogenesis both in animals and humans; felbamate, phenobarbital and topiramate block these receptors, and attenuation of glutamatergic excitatory transmission is another new mechanistic approach. Mutations in the nicotinic acetylcholine receptor are the substrates for the nocturnal frontal lobe epilepsy. The knowledge of the role of the ion channels in the epilepsies is allowing the design of new and more specific therapeutic strategies.

Action Potentials↗

[Benign epilepsy in children and adolescents].

THE CONCEPT OF BENIGN EPILEPSY: The benign nature of epilepsy is difficult to establish. The diagnosis of epilepsy often has an effect disproportionate to the severity. In everyday practice, most cases of epilepsy follow a benign course. A benign evolution is the rule in certain syndromes which are usually diagnosed early. In other cases however, the benign prognosis cannot be determined except after long-term follow-up. BENIGN EPILEPSY: There are 3 large categories of benign epilepsy: partial idiopathic epilepsy, generalized idiopathic epilepsy, occasional seizures. They are particularly frequent in children and adolescents, but can be observed in the neonatal period and in older patients. DIAGNOSIS OF BENIGN EPILEPSY: A syndromic approach to the problem is required. The patient's history, clinical signs, electroencephalographic data, and in certain cases neuroimaging findings are required for diagnosis. Confirmation of the benign nature of the epilepsy is reassuring for the patient and the family and can avoid unnecessary explorations. The appropriate therapeutic attitude is usually abstention from long-term antiepileptic treatment. It is importance for all clinicians to be familiar with "benign" epilepsy.

Adolescent↗

[Severity and epidemiology of myoclonic epilepsy].

The author first reviews the definition of myoclonia as an epileptic crisis differentiated from tonic crises and infantile spasms. He reviews the prevalence and incidence found in bibliographic data, under the following headings 1. Early myoclonic encephalopathy or neonatal myoclonic encephalopathy 2. Early epileptic syndrome with bursts of suppression or Otahara's syndrome. 3. West's syndrome. 4. The benign myoclonic epilepsy syndrome of children. 6. Syndrome of myoclonic epilepsy in non-progressive encephalopathy. 7. Early myoclonic epilepsy of children or Dose's syndrome. 8. Lennox-Gastaut syndrome. 9. Syndrome of epilepsy with absences in children. 10. Myoclonic absence epilepsy syndrome. 11. Landau-Kleffner syndrome and the syndrome of continuous slow spike-and-wave epilepsy during slow sleep. 12. Photosensitive epilepsy. 13. Absence epilepsy in young patients. 14. Juvenile myoclonic epilepsy. 15. Syndrome of gran mal epilepsy on waking. 16. Progressive myoclonic epilepsies. The author reviews 6,450 cases, 408 patients who had myoclonic crises, that is 6.3%. The differences seen in this total group of patients were: the myoclonic crises which presented alone, myoclonic crises accompanied by simple typical absences, those initially accompanied by generalized tonic-clonic crises and those presenting typical absences, tonic-clonic generalized crises and myoclonus simultaneously. The course of the different groups is analyzed.

Epilepsies, Myoclonic↗

[Vigabatrin in the treatment of intractable focal epilepsy in children and adolescents. Two-year study].

UNLABELLED: Vigabatrin VGB is the drug of III generation applied for a long time to patients in Poland. In Polish literature there were many reports published concerning the efficacy of VGB, however, most are short-term examinations. The AIM OF THE STUDY WAS: 1. the analysis of VGB efficacy in long term treatment of intractable focal epilepsies in children and adolescents; 2. stating if efficacy of VGB treatment depends on localization of epileptic focus; 3. answering if the effect of tolerance is developed in relation to VGB. MATERIALS AND METHODS: There were 50 patients between 4 to 20 years of age (average 12.7 +/- 4.8) with intractable focal epilepsy in the examined group. partial complex seizures were the dominant type of seizures at 74% of the examined patients. Time of observation amounted to 24 months. The patients were administered with VGB as add-on therapy. 37 patients (74%) were diagnosed with temporal lobe epilepsy, 11 (22%) with frontal lobe epilepsy, 1 patient (2%) with parietal lobe epilepsy and 1 (2%) with occipital lobe epilepsy. Patients who did not complain of seizures for a period of at least one year were classified as those with "seizure free". RESULTS: The examination was completed for 36 patients (76%). The treatment was discontinued in 12 patients (24%) as there was not a sufficient seizure control. One patient with temporal lobe epilepsy stopped the drug as three occurred the epileptic state of atypic generalised absence seizures induced by VGB. The final evaluation comprised all 50 examined patients. 9 patients (18%) achieved complete seizure control, 24 (48%) reduction to 50-99%. There was no change in 17 patients (34%). The examined patients with frontal localisation of epileptic focus presented significantly worse results of treatment, i.e. (reduction in the number of seizures over 35.3-36.5%) than the patients with temporal lobe epilepsy (reduction over 63.8 +/- 37.2%--p < 0.001). No significant difference in the average number of seizures in the 5th and 24th month of treatment was reported in the whole examined group. This contradicts the existence of the effect of tolerance in relation to VGB. CONCLUSIONS: 1. Vigabatrin is a very efficient drug in long-term treatment of patients with intractable focal epilepsies. 2. Patients with temporal lobe epilepsy present statistically better treatment results than patients with frontal lobe epilepsy. 3. No effect of tolerance to VGB was recorded during a 2-year observation.

Adolescent↗

[Neuroepidemiology of epilepsy in Senegalese school milieu].

The authors proceeded to a 7 month long prevalence survey on epilepsy in the schools of the regions of Dakar and Thies in Senegal, West africa. It consisted to a cross sectional descriptive study targeting the children between 3 and 10 years old. The W.H.O. questionnaire on epilepsy was used for data collection. Among the 2803 children of the population study, 58 were detected suffering from epilepsy, realizing a prevalence rate of 21%. The males were more represented (62% of the epilepsies). All the epileptic children presented generalized seizures represented either by "Grand Mal" generalized tonic-clonic form (84.4% of the epilepsies), or by "Petit Mal" absences (15.6% of the epilepsies). The etiological forms were dominated by idiopathic epilepsies. Secondary generalized cases represented 31% of the epilepsy and were essentially detected in rural areas. They were usually related to obstetrical traumas (61.1% of the secondary generalized epilepsies) or to child encephalopathy with seizure attacks (38.9% of the secondary generalized epilepsies). It appears also from this study that epilepsy remains a dramatic public health reality and is more frequent among low economy income people who have less access to the health care system.

Child↗

Epilepsy in contemporary fiction: fates of patients.

Fictional accounts of epilepsy are of interest because they may convey information on images and public views of epilepsy which are not contained in medical texts. Thus, medical and nonmedical traditions together form the cultural history of epilepsy. Of the numerous possible aspects of epilepsy in fiction, this paper looks especially at the writers' background of knowledge about epilepsy: epilepsy as a handicap and a reason for social rejection, with special reference to epilepsy under the Nazi rule; threats to patients' lives; the motive of the child with epilepsy as a divine child; and epilepsy as a fate, and a reason for distinction. Literary writers may help their readers understand that a person's suffering and fighting a condition like epilepsy very much deserves our attention and sympathy. Without being exclusive, the paper pays special attention to epilepsy in the writings of Canadian authors.

Adult↗

Health-related quality of life among persons with epilepsy--Texas, 1998.

Epilepsy is a central nervous system disorder characterized by unprovoked, recurrent seizures that may affect physical, mental, or behavioral functioning. In 1995, approximately 2.3 million persons residing in the United States had epilepsy. Approximately 181,000 new cases of epilepsy are diagnosed each year, with annual estimated costs of $12.5 billion in medical care and lost productivity. Because epilepsy has a substantial impact on health (e.g., physical and psychosocial difficulties, side effects of anticonvulsant therapy, lifestyle restrictions, and perceived stigmatization), self-reported physical and mental health-related quality of life (HRQOL) measures are useful in gauging the impact of epilepsy on persons with the disorder. Persons with chronic health disorders are at risk for impaired HRQOL. Few studies have examined the HRQOL of persons with epilepsy, and none has used a representative sample of adults residing in the United States. This report examines data from the 1998 Texas Behavioral Risk Factor Surveillance System (BRFSS) that included a question about epilepsy; findings indicate that persons with epilepsy reported substantially worse HRQOL than persons without epilepsy. Community-based interventions such as the Sepulveda Epilepsy Education Program that address medication self-management, psychosocial self-management, and other education interventions can improve the quality of life for persons with epilepsy.

Epilepsy↗

[Cases of symptomatic epilepsy at a regional reference neuropediatric unit].

OBJECTIVE: The objective of this study was to analyze, from an aetiological angle, the cases seen with symptomatic epilepsy by the Seccion de Neuropaediatria del Hospital Miguel Servet de Zaragoza. PATIENTS AND METHODS: We studied the cases diagnosed as having symptomatic epilepsy between May 1990 and November 1999. RESULTS: Of a total of 4,466 children assessed during the study period, the diagnosis of epilepsy was established in 461 children (10.3% of the total). This included idiopathic epilepsy in 110 cases (23.9%), cryptogenic epilepsy in 119 cases (25.8%) and symptomatic epilepsy in 232 cases (50.3%). The aetiologies of the symptomatic epilepsies were: prenatal encephalopathies in 137 cases (59%), perinatal encephalopathies in 33 (14.3%), postnatal encephalopathies (due to accidents, acquired infections and postnatal cerebrovascular accidents) in 20 (9%), tumours ( including the post-operative period) in 14 (6%), neurocutaneous syndromes in 13 (5.6%), metabolic and degenerative disorders in 13 (5.6%) and one case of vascular malformation. CONCLUSIONS: The symptomatic epilepsies make up half the epilepsies evaluated by the department of neuropaediatrics. In 59% the cause was prenatal. Other causes of symptomatic epilepsy were also represented in the series. A detailed study of these should help us to understand and manage them better. We consider aetiological aspects to be very important in the study of epilepsy, since the aetiology is one of the most important factors in prognosis.

Adolescent↗

Idiopathic generalised epilepsies with 3 Hz and faster spike wave discharges: a population-based study with evaluation and long-term follow-up in 71 patients.

For several years we have been following patients with intractable, childhood-onset idiopathic generalised epilepsies with > or = 3 Hz spike-wave discharges. Our need to find explanations for their intractability was the starting point for this study. We were interested in identifying characteristics, which would predict intractability; evaluating how these patients were treated and whether polytherapy was useful. We identified patients with > or = 3 Hz spike-wave discharges by reviewing EEG reports recorded between 1983 and 1992. Data were collected from medical records and through personal interviews. We identified 82 patients with tentative idiopathic generalised epilepsy. Eleven were excluded. Thirty-eight patients had childhood absence epilepsy, 18 had juvenile absence epilepsy, 13 had juvenile myoclonic epilepsy and two had eyelid myoclonia with absences: 89.5, 78, 38 and 0% of the patients in each group, respectively, had been seizure free for more than 2 years. Twenty percent of the patients had intractable seizures. All intractable patients with juvenile absence epilepsy had rhythmic, random eyelid blinking and generalised tonic-clonic seizures. A history of more than ten generalised tonic-clonic seizures was associated with intractability in juvenile myoclonic patients. Monotherapy with ethosuximide or valproate resulted in seizure control in 65% of patients. Seventeen patients (24%) were treated with polytherapy, six achieved remission. These six patients had childhood absence epilepsy and juvenile absence epilepsy. Positive outcome was found in childhood absence epilepsy and juvenile absence epilepsy. Intractable seizures were more frequent among patients with juvenile myoclonic epilepsy. None of them benefited from polytherapy with conventional anti-epileptic drugs.

Adolescent↗

Psychopathology and quality of life: psychogenic non-epileptic seizures versus epilepsy.

BACKGROUND: HRQOL is lower in patients with psychogenic non-epileptic seizures (PNES) than in epilepsy patients. Although psychopathology may reduce HRQOL, it is not known whether patients with PNES and epilepsy are similarly affected. We aimed to compare the relationship between psychopathology and HRQOL in PNES and treatment resistant epilepsy. MATERIAL/METHODS: 106 patients with definite diagnosis of PNES or epilepsy were recruited from Epilepsy Monitoring Unit. Patients completed QOLIE-89, Profile of Mood States (POMS), and Adverse Events Profile (AEP). Total Mood Disturbance (TMD) was derived from POMS. We used chi-square and t tests and hierarchical multiple regression to compare HRQOL and its mental status correlates in patients with PNES and epilepsy. RESULTS: Psychiatric history was more prevalent and depression/dejection and TMD were higher in PNES than epilepsy (P<=0.003). PNES patients had a lower adjusted mean HRQOL than epilepsy patients (P<0.01). Mood problems and AEP were strong predictors of HRQOL (P<0.001) and explained the lower HRQOL in PNES vis-l-vis epilepsy. Decreases in HRQOL due to mood problems were similar in both groups. The model explained 62% of the variation in HRQOL. CONCLUSIONS: Although more severe psychopathology in PNES explains the lower HRQOL in PNES relative to epilepsy, the negative association between psychopathology and HRQOL remains stable across the groups. PNES patients with severe mood problems show similar, low levels of HRQOL as patients with severe mood problems who have epilepsy. Future studies should examine causal linkages between psychopathology and PNES and other explanations in seizure-related QOL.

Adult↗

Myoclonic-astatic epilepsy.

Myoclonic-astatic epilepsy (MAE) belongs to the group of epilepsies with primarily generalized seizures as absence epilepsies, and juvenile myoclonic epilepsy, as well as infantile and juvenile idiopathic epilepsy with generalized tonic-clonic seizures. Like these types of epilepsy, MAE is polygenically determined with little non-genetic variability. The disease is characterized by the following criteria: genetic predisposition (high incidence of seizures and/or genetic EEG patterns in relatives); mostly normal development and no neurological deficits before onset; primarily generalized myoclonic, astatic or myoclonic-astatic seizures, short absences and mostly generalized tonic-clonic seizures; no tonic seizures or tonic drop attacks during daytime (except for some rare cases with a most unfavourable course); generalized EEG patterns (spikes and waves, photosensitivity, 4-7/sec rhythms), no multifocal EEG abnormalities (but often pseudofoci). There is a partial overlap with other 'syndromes', such as benign and severe myoclonic epilepsy in infants (Dravet et al., 1985a, b), myoclonic epilepsy of infancy and early childhood (Aicardi and others). In differential diagnosis the Lennox-Gastaut syndrome in its stricter sense has to be considered, and also atypical benign partial epilepsy or pseudo-Lennox syndrome. Discussion is presented of possible pitfalls in the classical syndromic approach to classifying epilepsies of early childhood, and of the advantages of a neurobiological view for understanding the immense variability of clinical manifestations of epilepsy.

Brain Mapping↗

Knowledge of epilepsy and attitudes towards the condition among schoolteachers in Bobo-Dioulasso (Burkina Faso).

Epilepsy is one of the stigmatising afflictions still common in Africa. The attitudes toward people with epilepsy are influenced by the degree of knowledge of the condition. This study was conducted to assess 260 teachers' knowledge and attitude towards epilepsy. They answered a semi-structured questionnaire in order to quantify their knowledge of and attitude towards epilepsy in Bobo-Dioulasso. Teachers were chosen at random. Almost all the teachers had heard about epilepsy, with 43.2% of them linking epilepsy to a central nervous system disturbance. Some teachers still thought that epilepsy was contagious or hereditary, and 15.4% objected to having epileptic children in their classes. Their knowledge of the clinical characteristics and first aid for a person during a seizure was unsatisfactory, and 56.5% of teachers who believed that epilepsy could be cured, thought that this disease should be treated by both modern and traditional medicines. The majority of teachers were interested in training involving clinical manifestations, aetiology of epilepsy and first aid procedures. Schools should offer some kind of information and assistance in health matters, and physicians should ensure that teachers have sufficient knowledge of epilepsy. More knowledge among primary school teachers should avoid discrimination against pupils with epilepsy.

Adult↗