The purpose of this study was to investigate the relationship between early and late age of seizure onset with the level of academic achievement for two groups of primary generalized epileptic children who were enrolled in the regular classroom setting, Furthermore, the study sought to determine if intelligence, spatial organization ability and sequencing ability influenced the level of achievement of these two groups.As per definition, the primary generalized epileptic children chosen for this study evidenced no focal electroencephalographic abnormality. The electroencephalographic patterns were bilateral, synchronous symmetrical spike and wave activity varying in frequency from two to six cycles per second. Subject selection was based primarily upon a neurologist's interpretation of the subject's electroencephalographic record.Subject selection was made from either a survey of 85 epileptic children within two Indiana school systems or from approximately 1,000 patients of an outpatient epileptic clinic. All subjects demonstrated right hand dominance and no one manifested any form of physical handicap or was diagnosed as having a primary emotional disturbance, The chronological age at time of testing ranged from nine years to 16 years 11 months, Also required was a Full Scale IQ greater than 70, as measured by standardized instruments of intelligence.The 61 subjects were divided into groups based upon the age of seizure onset, Group I consisted of 30 subjects whose age of seizure onset was birth to four years 11 months, inclusively and Group II consisted of 31 subjects whose age of seizure onset was six years to 15 years 11 months, inclusively. The age span specified for early age of seizure onset corresponded to interruption within the first half of the perceptual maturation span and the age span designated for late age of seizure onset involved interruption within the latter half of the perceptual maturation span and beyond.All subjects were administered equivalent test batteries. Achievement was determined by grade level scores obtained in reading recognition and arithmetic. The reading recognition grade level scores were obtained from either the Wide Range Achievement Test r Reading Subtest or the Woodcock Reading Mastery Tests - Word Identification Subtest. The arithmetic grade level scores were obtained from the Wide Range Achievement Test Arithmetic Subtest. The Wechsler Intelligence Scale for Children or the Wechsler Adult Intelligence Scale were used in assessing Full Scale IQ, Spatial organization was defined by the location scoreobtained from the Tactile Performance Test divided by the total number of stimulus blocks on the form-board. The difference i_n time scores obtained from Part B minus Part A of the Trail Making Test defined the sequencing ability score.In order to determine statistical significance between the dependent and independent variables simultaneously, a multivariate discriminant analysis of variance or analysis of covariance was applied, A .05 level of significance was set in testing the statistical significance of each null hypothesis.No significant differences were found between the two primary generalized epileptic groups for any of the hypotheses tested. Consequently, this research did not support the notion that primary generalized epileptics of early seizure onset perform significantly lower academically when compared with primary generalized epileptics of late seizure onset.. Even when Full Scale IQ, spatial organization ability and sequencing ability were assigned as covariates, no significant differences were found.From inspection of coefficients of the multiple correlation squared, results indicated that academic achievement was predicted as accurately from Full Scale IQ alone as when spatial organization ability and/or sequencing ability were used as additional predictors.

Introduction: One potential new therapy for epilepsy involves the omega-3 polyunsaturated fatty acids (PUFAs), and more specifically docosahexaenoic acid (DHA).   Methods: The anticonvulsant properties of the n-3 PUFAs were assessed in a series of different experiments. Subjects received chronic dietary supplementation, sub-chronic and acute injections of either fish oil (chronic) or DHA (sub-chronic, acute). Animals were tested in the electrical afterdischarge thresholds (ADTs) model in the amygdale and the maximal pentylenetetrazol (PTZ) model.   Results: Chronic, sub-chronic, and acute administrations of n-3 PUFAs were anticonvulsant in both the electrical stimulation and maximal PTZ models. In chronic experiments, amygala ADTs increased following 3 months of fish oil administration. Fourteen days of DHA i.p. injections increased latencies to maximal PTZ seizures. Acute injection of DHA s.c. and i.v. increased unesterified serum DHA and seizure latency. Conclusions: The present research suggests that n-3 PUFAs, and more specifically DHA, have anticonvulsant effects in vivo.

Introduction: One potential new therapy for epilepsy involves the omega-3 polyunsaturated fatty acids (PUFAs), and more specifically docosahexaenoic acid (DHA).   Methods: The anticonvulsant properties of the n-3 PUFAs were assessed in a series of different experiments. Subjects received chronic dietary supplementation, sub-chronic and acute injections of either fish oil (chronic) or DHA (sub-chronic, acute). Animals were tested in the electrical afterdischarge thresholds (ADTs) model in the amygdale and the maximal pentylenetetrazol (PTZ) model.   Results: Chronic, sub-chronic, and acute administrations of n-3 PUFAs were anticonvulsant in both the electrical stimulation and maximal PTZ models. In chronic experiments, amygala ADTs increased following 3 months of fish oil administration. Fourteen days of DHA i.p. injections increased latencies to maximal PTZ seizures. Acute injection of DHA s.c. and i.v. increased unesterified serum DHA and seizure latency. Conclusions: The present research suggests that n-3 PUFAs, and more specifically DHA, have anticonvulsant effects in vivo.

Lacosamide (LCM) is a new antiepileptic drug with a previously unknown mode of action. Using electrophysiological recording techniques in a range of in vitro preparations I have determined a mechanism of action of the new drug. In a 4-aminopyridine model of tonic-clonic seizures in rat visual cortex in vitro, LCM stereoselectively reduced maximal frequency and duration of tonic activity with EC[50�s] of 71 and 41 [mu]M respectively. LCM (100 [mu]M) significantly reduced excitability in whole cell patch clamped neurons producing non-selective reduction in the incidence of excitatory/inhibitory postsynaptic currents (EPSCs; LCM: 46.1 � 15.5 %, P <0.01, n = 4, IPSCs; LCM: 24.9 � 9.6 %, P <0.01, n = 4) and block of spontaneous action potentials (EC₅₀ 61 [mu]M). The inhibitory effects of LCM did not result from changes in passive membrane properties (including resting membrane potential or input resistance) as assessed by application of voltage ramps between -70 to +20 mV. LCM did not mimic the effects of diazepam as an allosteric modulator of GABA[A] receptor currents, nor did it inhibit evoked excitatory currents mediated by AMPA or NMDA receptors. Unlike phenytoin (DPH), carbamazepine (CBZ) or lamotrigine (LTG) that blocked sustained action potential firing evoked by brief depolarising steps (750 ms) or ramps (-70 to 20 mV, 90 mV.sec⁻�), LCM could weakly reduce the frequency of action potentials evoked by brief depolarisation suggesting a potential interaction with VGSCs. In accordance with this, the effect of LCM upon neurotransmission was negated in the presence of tetrodotoxin (200 nM, TTX). The frequency of miniature EPSCs was not altered by the drug (100 [mu]M). These results discounted some crucial potential anticonvulsant targets for LCM but implied a potential interaction with electrogenic VGSCs. When SRF duration was prolonged (10 s) LCM produced significant (P <0.01, n = 4-10, EC₅₀: 48 [mu]M) inhibition, but not within the first second of the burst EC₅₀: 640 [mu]M). Evoked TTX sensitive sodium currents in N1E-115 neuroblastoma cells were significantly reduced by LCM, CBZ, LTG and DPH when V[h]: -60 mV. Hyperpolarizing pulses (500 ms) to -100 mV could reverse block by CBZ, LTG and DPH but not LCM. The V₅₀ for steady state fast inactivation was more hyperpolarized by CBZ (-79.45 � 2.64 mV, n = 5, P < 0.001), LTG (-72.30 � 1.70 mV, n = 6, P <0.05) and DPH (-77.17 � 2.32 mV, n = 6, P <0.05) but not by LCM (-65.02 � 1.75 mV, n = 6, CONTROL: -65.84 � 0.86 mV). In contrast to CBZ, LCM did not slow recovery from fast inactivation or produce frequency dependent facilitation of block of a 3 s, 10 Hz pulse train. LCM (100 [mu]M) did produce a (V₅₀: CONTROL ~64 mV, LCM -57.47 � 4.53 mV, P <0.001, n = 4-8) hyperpolarizing shift in the voltage dependence of slow sodium channel inactivation and promoted channel entry into the slow inactivated state (P <0.001, n = 6) but did not alter the rate of recovery. I therefore conclude that LCM produces inhibition of epileptiform cellular activity, at least in part, via enhancement of voltage gated sodium channel slow inactivation and represents a molecule possessing a unique anticonvulsant mechanism of action.

An impression which has dominated both the clinical setting and research literature is that patients with temporal lobe epilepsy (TLE) not infrequently issue "bitter" complaints about their memory function. This observation has rarely been subjected to investigation, based as it is, on the implicit assumption that TLE subjects are "entitled" to a memory disturbance given the involvement of a critical memory structure (i.e, hippocampus) in the pathogenesis of the disorder. While it is almost axiomatic that clinicians become aware of memory difficulties because of the subjective complaints issued by patients, there is growing awareness that the relationship between complaint and objective memory disturbance is a complex and often counterintuitive one. This is particularly true of many patients with TLE who while complaining about their memory function often do so in the presence of objectively normal interictal memory function. / This thesis addressed the question: Why do patients with TLE complain about their memory? It was premised on the notion that memory self-report is not a unidimensional construct explicable in terms of an underlying memory dysfunction alone, but the perception and expression of memory may arise from seemingly disparate sources. The principal objective of the thesis was to systematically and comprehensively investigate the complaint in TLE, and to derive an understanding of the variables which contribute to the perception and expression of poor memory in members of this population. The variables selected for investigation emerged from a detailed review of the literature and can be grouped into five broad conceptual domains: demographic, epileptological, psychological, cognitive, and metacognitive. (For complete abstract open document)

Thesis (Ph.D.)--University of Missouri-Columbia, 2007. / The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on March 19, 2009) Vita. Includes bibliographical references.

Thesis (Ph.D.)--Virginia Commonwealth University, 2008. / Prepared for: Dept. of Anatomy and Neurobiology. Bibliography: leaves 164-205. Also available online via the Internet.

Thesis (Ph. D.)--University of Virginia, 1998. / Includes bibliographical references (109-122). Also available online through Digital Dissertations.

Thesis (Ph. D.)--UCLA, 2008. / Vita. Includes bibliographical references.

Thesis (Ph. D.)--West Virginia University, 1998. / Title from document title page. "September 1998." Document formatted into pages; contains x, 184 p. : ill. (some col.) Includes abstract. Includes bibliographical references (p. 161-184).