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van Iterson L.,Epilepsy Institute in the Netherlands Foundation SEIN | van Iterson L.,Expertise Center for Education and Epilepsy | de Jong P.F.,University of Amsterdam | Zijlstra B.J.H.,University of Amsterdam
Epilepsy and Behavior | Year: 2015

Introduction: In pediatric epilepsy, comorbidities are reported to be frequent. The present study focusedon the cognitive patterns of children with isolated epilepsy, children with isolated neurodevelopmental disorders (reading disorders, math disorders, autism spectrum disorders), and children with epilepsy and these neurodevelopmental disorders as comorbidities. Methods: Based on two samples of referred children, one with epilepsy, reading disorders, math disorders, or ASDs occurring in ". isolation" (. n=. 117) and one with reading disorders, math disorders, and ASDs occurring comorbid with epilepsy (. n=. 171), cognitive patterns were compared. The patterns displayed by verbal and nonverbal abilities from the WISC series were studied with repeated measures ANOVA. Thereafter, an exploratory 2. *. 3. *. 2 factorial analysis was done to study the independent contribution of the type of comorbidity and of the presence or absence of epilepsy to the VIQ-PIQ pattern. Results: In isolated epilepsy, a VIQ. >. PIQ pattern was found, which was not seen in the other disorders. When epilepsy and another disorder co-occurred, patterns were altered. They resembled partly the pattern seen in isolated epilepsy and partly the pattern seen in the isolated neurodevelopmental disorder. In comorbid reading disorders, the VIQ. >. PIQ pattern was mitigated; in comorbid math disorders, it was exacerbated. In comorbid ASDs, no clear pattern emerged. In the presence of epilepsy, patterns characteristic of isolated disorders appeared systematically shifted toward relatively lowered performance abilities or relatively spared verbal abilities. The similar "impact" exerted by epilepsy on the patterns of the various conditions suggested shared mechanisms. © 2015 Elsevier Inc. Source


Baxendale S.,University College London | Donnachie E.,Epilepsy Society | Thompson P.,University College London | Sander J.W.,University College London | Sander J.W.,Epilepsy Institute in the Netherlands Foundation SEIN
Epilepsia | Year: 2013

Purpose Dysembryoplastic neuroepithelial tumors (DNTs) provide a unique model for studying the effects of seizures on cognitive development. Epilepsy and antiepileptic medications are prominent features in the lives and schooling of people who develop seizures in childhood. People with an adult onset share the same underlying brain pathology, but their childhood development is unaffected by seizures. Therefore, DNTs provide a model to examine the specific influence of seizures and their treatment on cognitive development, over and above the effects of the underlying pathology in epilepsy. Methods We examined the neuropsychological characteristics of 56 adults with DNT and medically intractable epilepsy (mean age 32.7 years). Twenty-two adults (39%) had an age of onset of epilepsy before the age of 12 years (childhood-onset group). Scores on tests of intelligence (Verbal IQ and Performance IQ), reading, working memory, verbal learning, verbal recall, visual learning, and expressive and receptive language ability were analyzed. Key Findings There were no significant localization effects (right vs. left vs. extratemporal) on any of the neuropsychological test scores. In the group as a whole, the neuropsychological test scores were significantly lower than healthy, age-matched controls on measures of Verbal IQ (p < 0.01), naming p < 0.01, verbal learning (p < 0.01), and working memory (p < 0.05). The childhood-onset group had significantly lower scores on the measures of Verbal IQ (p < 0.01), Performance IQ (p < 0.05), reading (p < 0.05), naming (p = 0.05), and verbal retention (p < 0.05) than those with an onset of seizures at the age of 12 or older. Significance The traditional pattern of lateralized memory deficits seen in people with hippocampal sclerosis may not be present in people with temporal lobe epilepsy associated with a DNT. The presence of seizures and their treatment in early childhood may adversely influence the development of these core cognitive abilities, resulting in patterns of cognitive deficits that remain apparent in adulthood.© 2013 International League Against Epilepsy. Source


Postnov A.,VU University Amsterdam | Froklage F.E.,VU University Amsterdam | Froklage F.E.,Epilepsy Institute in the Netherlands Foundation SEIN | Van Lingen A.,VU University Amsterdam | And 8 more authors.
Journal of Nuclear Medicine | Year: 2013

Resistance to current drug therapy is an important issue in the treatment of epilepsy. Inadequate access of central nervous system drugs to their targets in the brain may be caused by overexpression or overactivity of multidrug transporters, such as P-glycoprotein (P-gp), at the blood-brain barrier. Laniquidar, an inhibitor of P-gp, has been labeled with 11C for use in PET studies of P-gp expression in humans. Given potential interspecies differences in biodistribution, the purpose of this study was to ensure safe use of 11C-laniquidar by determining the dosimetry of 11C-laniquidar using whole-body PET studies. Methods: Six healthy volunteers were subjected to a series of 10 whole-body PET scans within approximately 70 min. Five blood samples were taken during the series. Results: High uptake of 11Claniquidar was seen in liver, spleen, kidneys, and lung, whereas brain uptake was low. The effective dose for 11C- laniquidar was 4.76 ± 0.13 and 3.69 ± 0.01 μSv MBq-1 for women and men, respectively. Conclusion: Biodistribution and measured effective dose indicate that 11C-laniquidar is a safe tracer for PET imaging, with a total dose of about 2 mSv for a brain PET/CT protocol. COPYRIGHT © 2013 by the Society of Nuclear Medicine and Molecular Imaging, Inc. Source


Qiao X.,University of Amsterdam | Werkman T.R.,University of Amsterdam | Gorter J.A.,University of Amsterdam | Gorter J.A.,Epilepsy Institute in the Netherlands Foundation SEIN | And 4 more authors.
Epilepsy Research | Year: 2013

Voltage-gated Na+ channels control neuronal excitability and are the primary target for the majority of anti-epileptic drugs. This study investigates the (sub)cellular expression patterns of three important brain-associated Na+ channel α subunits: NaV1.1, NaV1.2 and NaV1.6 during epileptogenesis (induced by kainic acid) using time points that cover the period from induction to the chronic phase of epilepsy.NaV1.1 immunoreactivity was persistently reduced at 1 day, 3 weeks and 2 months after SE in CA1 and CA3. About 50% of the NaV1.1-positive interneurons was lost at one day after SE in all regions investigated. In the hilus a similar reduction in NeuN-positive neurons was found, while in the CA1 and CA3 region the loss in NeuN-positive neurons only reached 15% in the chronic phase of epilepsy. This implies a stronger shift in the balance between excitation and inhibition toward excitation in the CA1 and CA3 region than in the hilus. NaV1.2 immunoreactivity in the inner molecular layer of the dentate gyrus was lower than control at 1 day after SE. It increased at 3 weeks and 2 months after SE in the inner molecular layer and overlapped with sprouted mossy fibers. NaV1.6 immunoreactivity in the dendritic region of CA1 and CA3 was persistently reduced at all time-points during epileptogenesis. Some astrocytes expressed NaV1.1 and NaV1.6 at 3 weeks after SE.Expression data alone are not sufficient to explain changes in network stability, or infer causality in epileptogenesis. These results demonstrate that hippocampal sub-regional expression of NaV1.1, NaV1.2 and NaV1.6 Na+ channel α subunits is altered during epileptogenesis in a time and location specific way. This implies that understanding epileptogenesis has to take into account several distinct and type-specific changes in sodium channel expression. © 2013 Elsevier B.V. Source


Holtman L.,University of Amsterdam | Van Vliet E.A.,University of Amsterdam | Van Vliet E.A.,Epilepsy Institute in the Netherlands Foundation SEIN | Edelbroek P.M.,Epilepsy Institute in the Netherlands Foundation SEIN | And 3 more authors.
Epilepsy Research | Year: 2010

Purpose: Status epilepticus (SE) leads to upregulation of pro-inflammatory proteins including cyclooxygenase-2 (cox-2) which could be implicated in the epileptogenic process and epileptic seizures. Recent studies show that cox-2 can regulate expression of P-glycoprotein (P-gp) during epileptogenesis and epilepsy. P-gp could cause pharmacoresistance by reducing brain entry of anti-epileptic drugs such as phenytoin (PHT). Here we have investigated the effects of cox-2 inhibition on epileptogenesis, spontaneous seizures and PHT treatment in a rat model for temporal lobe epilepsy (TLE). Methods: A 3-day treatment with the cox-2 inhibitor SC-58236 (SC) was started 1 day before electrically induced SE. Chronic epileptic rats were treated with SC for 14 days, which was followed by a 7-day period of SC/PHT combination treatment. Seizure activity was monitored continuously using electroencephalography. Results: SC treatment did not affect SE duration, but led to an increased number of rats that died during the first 2 weeks after SE. Cox-2 inhibition during the chronic period led to an increased number of seizures in the 2nd week of treatment in 50% of the rats. SC/PHT treatment reduced seizures significantly for only 2 days. Conclusions: Both SC treatment that started before SE and the 14-day treatment in chronic epileptic rats led to adverse effects in the TLE rat model. Despite a temporal reduction in seizure frequency with SC/PHT treatment, SC does not seem to be a suitable approach for anti-epileptogenic or anti-epileptic therapy. © 2010 Elsevier B.V. Source

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