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Brian S Meldrum - One of the best experts on this subject based on the ideXlab platform.

  • genetically Epilepsy prone rats geprs and dba 2 mice two animal models of audiogenic Reflex Epilepsy for the evaluation of new generation aeds
    Epilepsy & Behavior, 2017
    Co-Authors: Giovambattista De Sarro, Emilio Russo, Rita Citraro, Brian S Meldrum
    Abstract:

    This review summarizes the current knowledge about DBA/2 mice and genetically Epilepsy-prone rats (GEPRs) and discusses the contribution of such animal models on the investigation of possible new therapeutic targets and new anticonvulsant compounds for the treatment of Epilepsy. Also, possible chemical or physical agents acting as proconvulsant agents are described. Abnormal activities of enzymes involved in catecholamine and serotonin synthesis and metabolism were reported in these models, and as a result of all these abnormalities, seizure susceptibility in both animals is greatly affected by pharmacological manipulations of the brain levels of monoamines and, prevalently, serotonin. In addition, both genetic epileptic models permit the evaluation of pharmacodynamic and pharmacokinetic interactions among several drugs measuring plasma and/or brain level of each compound. Audiogenic models of Epilepsy have been used not only for Reflex Epilepsy studies, but also as animal models of epileptogenesis. The seizure predisposition (epileptiform response to sound stimulation) and substantial characterization of behavioral, cellular, and molecular alterations in both acute and chronic (kindling) protocols potentiate the usefulness of these models in elucidating ictogenesis, epileptogenesis, and their mechanisms. This article is part of a Special Issue entitled "Genetic and Reflex Epilepsies, Audiogenic Seizures and Strains: From Experimental Models to the Clinic".

  • Genetically Epilepsy-prone rats (GEPRs) and DBA/2 mice: Two animal models of audiogenic Reflex Epilepsy for the evaluation of new generation AEDs
    Epilepsy & Behavior, 2017
    Co-Authors: Giovambattista De Sarro, Emilio Russo, Rita Citraro, Brian S Meldrum
    Abstract:

    This review summarizes the current knowledge about DBA/2 mice and genetically Epilepsy-prone rats (GEPRs) and discusses the contribution of such animal models on the investigation of possible new therapeutic targets and new anticonvulsant compounds for the treatment of Epilepsy. Also, possible chemical or physical agents acting as proconvulsant agents are described. Abnormal activities of enzymes involved in catecholamine and serotonin synthesis and metabolism were reported in these models, and as a result of all these abnormalities, seizure susceptibility in both animals is greatly affected by pharmacological manipulations of the brain levels of monoamines and, prevalently, serotonin. In addition, both genetic epileptic models permit the evaluation of pharmacodynamic and pharmacokinetic interactions among several drugs measuring plasma and/or brain level of each compound. Audiogenic models of Epilepsy have been used not only for Reflex Epilepsy studies, but also as animal models of epileptogenesis. The seizure predisposition (epileptiform response to sound stimulation) and substantial characterization of behavioral, cellular, and molecular alterations in both acute and chronic (kindling) protocols potentiate the usefulness of these models in elucidating ictogenesis, epileptogenesis, and their mechanisms. This article is part of a Special Issue entitled "Genetic and Reflex Epilepsies, Audiogenic Seizures and Strains: From Experimental Models to the Clinic".

  • anticonvulsant effects of 7 nitroindazole in rodents with Reflex Epilepsy may result from l arginine accumulation or a reduction in nitric oxide or l citrulline formation
    British Journal of Pharmacology, 1996
    Co-Authors: S.e. Smith, Ellen Tang, Astrid G Chapman, Brian S Meldrum
    Abstract:

    1. To investigate the role of nitric oxide in Epilepsy we have studied the effects of agents which affect nitric oxide synthesis in sound-induced seizures in DBA/2 mice and in genetically Epilepsy-prone (GEP) rats. 2. The neuronal selective nitric oxide synthase inhibitor, 7-nitroindazole (7-NI) is anticonvulsant in these models with ED50 values against clonic seizures in mg kg-1 i.p. (times following injection) of: 74 (+0.25 h), 120 (+1 h) in DAB/2 mice, and 56 (+0.25 h), 42 (+0.5 h), 36 (+1 h), 28 (+2 h), 38 (+4 h), 93 (+8 h) in GEP rats. 3. Therapeutic indices (locomotor deficit ED50/anticonvulsant ED50) for 7-NI are low, ranging from 0.6 to 1.1 at +0.25 h to +1 h after administration in GEP rats, but are more favourable at later times (1.6 at +2 h and 2.9 at +4 h). 4. The substrate for nitric oxide synthase, L-arginine (500-5000 mg kg-1, i.p. or 100-300 micrograms, i.c.v.) but not D-arginine (300 micrograms i.c.v.) is anticonvulsant in DBA/2 mice. L-Arginine (500-5000 mg kg-1, i.p. or 1800-6000 micrograms, i.c.v.) is a more potent anticonvulsant than D-arginine (1500-2500 mg kg-1, i.p. or 6000 micrograms, i.c.v.) in GEP rats. 5. In DBA/2 mice, L-arginine (30 micrograms i.c.v.) reverses the anticonvulsant effect of 7-NI (50 mg kg-1, i.p.). 6. In GEP rats, low dose L-arginine (25-50 mg kg-1, i.p.) but not D-arginine (50 mg kg-1, i.p.) reverses the anticonvulsant effect of low dose 7-NI (25 mg kg-1, i.p.). A higher dose of L-arginine (500 mg kg-1, i.p.) or 7-NI (50 mg kg-1, i.p.) produces summation of anticonvulsant effect. 7. The product for nitric oxide synthase, L-citrulline (250-831 micrograms i.c.v.), is convulsant in DBA/2 mice. 8. The anticonvulsant effect of the neuronal selective nitric oxide synthase inhibitor, 7-nitroindazole, may therefore be mediated by L-arginine accumulation, as well as by a reduction in nitric oxide and L-citrulline formation in rodent models of Reflex Epilepsy.

  • the effects of ampa receptor antagonists on kindled seizures and on Reflex Epilepsy in rodents and primates
    Epilepsy research. Supplement, 1992
    Co-Authors: Brian S Meldrum, Nick Durmuller, Stuart E Smith, Astrid G Chapman
    Abstract:

    : Two potent glutamate antagonists, NBQX and GYKI 52466, that act selectively on non-NMDA receptors, have been tested for anticonvulsant activity in 3 models of Reflex Epilepsy (sound-induced seizures in DBA/2 mice and in genetically Epilepsy-prone rats and photically-induced myoclonus in Papio papio) and in amygdala kindled rats. Both compounds potently but transiently suppress Reflexly-induced epileptic responses. GYKI 52466 also reduces behavioral seizures and afterdischarge duration in amygdala kindled rats, but with a lower potency than it suppresses Reflex Epilepsy. These data are similar to earlier results with antagonists acting selectively on NMDA receptors; they do not support a specific involvement of enhanced AMPA receptor sensitivity as a major factor in the expression of kindled seizures.

Robert Naquet - One of the best experts on this subject based on the ideXlab platform.

  • Epilepsy Caused by an Abnormal Alternative Splicing with Dosage Effect of the SV2A Gene in a Chicken Model
    2016
    Co-Authors: Marine Douaud, Carlo Batini, Robert Naquet, Katia Feve, Fabienne Pituello, David Gourichon, Simon Boitard, Eric Leguern, Agathe Vieaud, Alain Vignal
    Abstract:

    Photosensitive Reflex Epilepsy is caused by the combination of an individual’s enhanced sensitivity with relevant light stimuli, such as stroboscopic lights or video games. This is the most common Reflex Epilepsy in humans; it is characterized by the photoparoxysmal response, which is an abnormal electroencephalographic reaction, and seizures triggered by intermittent light stimulation. Here, by using genetic mapping, sequencing and functional analyses, we report that a mutation in the acceptor site of the second intron of SV2A (the gene encoding synaptic vesicle glycoprotein 2A) is causing photosensitive Reflex Epilepsy in a unique vertebrate model, the Fepi chicken strain, a spontaneous model where the neurological disorder is inherited as an autosomal recessive mutation. This mutation causes an aberrant splicing event and significantly reduces the level of SV2A mRNA in homozygous carriers. Levetiracetam, a second generation antiepileptic drug, is known to bind SV2A, and SV2A knock-out mice develop seizures soon after birth and usually die within three weeks. The Fepi chicken survives to adulthood and responds to levetiracetam, suggesting that the low-level expression of SV2A in these animals is sufficient to allow survival, but does not protect against seizures. Thus, the Fepi chicken model shows that the role of the SV2A pathway in the brain is conserved between birds and mammals, in spite of a large phylogenetic distance

  • Epilepsy caused by an abnormal alternative splicing with dosage effect of the SV2A gene in a chicken model.
    PLoS ONE, 2011
    Co-Authors: Marine Douaud, Carlo Batini, Katia Feve, Fabienne Pituello, David Gourichon, Simon Boitard, Eric Leguern, Gérard Coquerelle, Agathe Vieaud, Robert Naquet
    Abstract:

    Photosensitive Reflex Epilepsy is caused by the combination of an individual's enhanced sensitivity with relevant light stimuli, such as stroboscopic lights or video games. This is the most common Reflex Epilepsy in humans; it is characterized by the photoparoxysmal response, which is an abnormal electroencephalographic reaction, and seizures triggered by intermittent light stimulation. Here, by using genetic mapping, sequencing and functional analyses, we report that a mutation in the acceptor site of the second intron of SV2A (the gene encoding synaptic vesicle glycoprotein 2A) is causing photosensitive Reflex Epilepsy in a unique vertebrate model, the Fepi chicken strain, a spontaneous model where the neurological disorder is inherited as an autosomal recessive mutation. This mutation causes an aberrant splicing event and significantly reduces the level of SV2A mRNA in homozygous carriers. Levetiracetam, a second generation antiepileptic drug, is known to bind SV2A, and SV2A knock-out mice develop seizures soon after birth and usually die within three weeks. The Fepi chicken survives to adulthood and responds to levetiracetam, suggesting that the low-level expression of SV2A in these animals is sufficient to allow survival, but does not protect against seizures. Thus, the Fepi chicken model shows that the role of the SV2A pathway in the brain is conserved between birds and mammals, in spite of a large phylogenetic distance. The Fepi model appears particularly useful for further studies of physiopathology of Reflex Epilepsy, in comparison with induced models of Epilepsy in rodents. Consequently, SV2A is a very attractive candidate gene for analysis in the context of both mono- and polygenic generalized epilepsies in humans.

  • Transfer of an avian genetic Reflex Epilepsy by embryonic brain graft: a tissue autonomous process?
    The International Journal of Developmental Biology, 2005
    Co-Authors: M A Teillet, Robert Naquet, Carlo Batini
    Abstract:

    Electroencephalographic characteristics and clinical symptoms of an avian genetic Reflex Epilepsy have been transferred from Fayoumi epileptic (Fepi) chickens to non-epileptic chickens by embryonic homotopic grafts of brain neuroepithelium. Transplanted tissues belonging to the prosencephalic vesicle transferred epileptic electrical features while tissues from the mesencephalic vesicle were responsible for seizure motor manifestations of the disease. Thus each of these tissues can express their own specificity when grafted separately in a normal host, but they co-operate to produce the complete epileptic phenotype when grafted together.

  • An avian model of genetic Reflex Epilepsy.
    Archives Italiennes De Biologie, 2004
    Co-Authors: Carlo Batini, M A Teillet, Robert Naquet
    Abstract:

    The Fayoumi strain of chickens (Fepi) carries a recessive autosomal gene mutation in which homozygotes are afflicted with a photogenic and audiogenic Reflex Epilepsy. Seizures consist of stimulus-locked motor symptoms followed by generalized self sustained convulsions. EEG recordings show spikes and spike and waves patterns at rest which are suppressed during seizures and replaced by a desynchronized pattern of activity. Neurones of the prosencephalon discharge in bursts at rest, while neurones of the mesencephalon are bursting during seizures. Living neural chimeras were obtained by replacing specific embryonic brain vesicles in a normal chicken embryo with equivalent vesicles from a Fepi donor. These chimeras show that the epileptic phenotype can be totally or partially transferred from the Fepi to the normal chickens. Total transfer of photogenic and audiogenic seizures was obtained by substitution of both the prosencephalon and mesencephalon, while substitution of the prosencephalon alone resulted in transfer of interictal paroxysmal activity and substitution of the mesencephalon alone resulted principally in transfer of ictal motor symptoms. Increased expression of the c-fos protooncogene, as revealed by the western blot technique, confirmed the distinct encephalic localizations of the symptoms of the photogenic and audiogenic Reflex Epilepsy of the Fepi shown with the methods of electrophysiology and brain chimeras. We conclude that the Fepi is a good model of brain stem Reflex Epilepsy and suggest that the brain stem is a generator of some other animal and human genetic Reflex "epileptic syndromes".

  • Brain chimeras in birds: application to the study of a genetic form of Reflex Epilepsy.
    Trends in Neurosciences, 1996
    Co-Authors: Carlo Batini, M A Teillet, Robert Naquet, Nicole M. Le Douarin
    Abstract:

    Abstract A strain of chicken, called here FEpi (for Fayoumi epileptic), bearing an autosomal recessive mutation, exhibits a form of Reflex Epilepsy with EEG interictal paroxysmal manifestations and generalized seizures in response to either light or sound stimulations. By using the brain chimera technology, we demonstrate here that the epileptic phenotype can be partially or totally transferred from an FEpi to a normal chick by grafting specific regions of the embryonic brain. The mesencephalon contains the generator of all epileptic manifestations whether they involve visual or auditory neuronal circuits, with the exception of the abnormal EEG which is transmitted exclusively by telencephalic grafts. This analysis supports the hypothesis that certain forms of human and mammalian epilepsies have a brainstem origin. Trends Neurosci . (1996) 19, 246–252

Cigdem Ozkara - One of the best experts on this subject based on the ideXlab platform.

  • Reflex Epilepsy: triggers and management strategies
    Neuropsychiatric disease and treatment, 2018
    Co-Authors: Zeynep Vildan Okudan, Cigdem Ozkara
    Abstract:

    Reflex epilepsies (REs) are identified as epileptic seizures that are consistently induced by identifiable and objective-specific triggers, which may be an afferent stimulus or by the patient's own activity. RE may have different subtypes depending on the stimulus characteristic. There are significant clinical and electrophysiologic differences between different RE types. Visual stimuli-sensitive or photosensitive epilepsies constitute a large proportion of the RE and are mainly related to genetic causes. Reflex epilepsies may present with focal or generalized seizures due to specific triggers, and sometimes seizures may occur spontaneously. The stimuli can be external (light flashes, hot water), internal (emotion, thinking), or both and should be distinguished from triggering precipitants, which most epileptic patients could report such as emotional stress, sleep deprivation, alcohol, and menstrual cycle. Different genetic and acquired factors may play a role in etiology of RE. This review will provide a current overview of the triggering factors and management of Reflex seizures.

  • orgasm induced seizures a study of six patients
    Epilepsia, 2006
    Co-Authors: Cigdem Ozkara, Samuray Ozdemir, Aynur Yilmaz, Mustafa Uzan, Naz Yeni, Mine Ozmen
    Abstract:

    Summary: Purpose: Reflexseizuresareknownastheepilepticseizures triggered by some specific stimuli in sensitive patients.They are often classified according to the stimuli that triggerthem rather than by the type of the seizure. Epileptic seizuresinduced by sexual orgasm are very rare in the literature. Methods: We report six patients with different epileptic syn-dromes who experienced seizures after sexual intercourse andorgasm. Results: All patients are women whose epileptogenic focuswas in the right temporal in four and left frontal in one patient.One patient had pure generalized Reflex Epilepsy. Conclusions: Seizures induced by orgasm are very rare, withfemale and right hemisphere dominance requiring complexmechanisms to occur. Key Words: Reflex seizures—Sexualorgasm—Reflex Epilepsy—Orgasmic Epilepsy. Reflex Epilepsy (RE) is a condition in which seizurescan be triggered habitually by an external stimulus or, lesscommonly, by internal mental processes. Individuals withREmayhaveseizuresexclusivelyinresponsetoaspecificstimulusaswellasspontaneouslyoccurringseizures.Pho-tosensitive Epilepsy is the most common type of this kindofEpilepsy.Lesscommonly,seizuresresultfromauditory,olfactory, or vestibular stimuli. Reflex seizures also mayoccur in response to more elaborate stimuli or mental pro-cesses. Examples of these include reading, music, eating,hotwater,orseizuresinducedbycognitiveprocesses,suchasmathematicalcalculation.However,seizuresevokedbysexual orgasm were reported in very few articles (Ban-caud et al., 1971; Remillard et al., 1983; Berthier et al.,1987; Toone, 1991). Here we describe six patients witha different type of epileptic syndrome who experiencedseizures induced by sexual orgasm. They were also ques-tionedabouttheimpactofseizuresontheirsexuallife,andthis exclusively uncommon type of trigger was discussedwithin the context of Reflex Epilepsy.

Udaya Seneviratne - One of the best experts on this subject based on the ideXlab platform.

  • seizures triggered by eating a rare form of Reflex Epilepsy
    Epileptic Disorders, 2020
    Co-Authors: Nirosen Vijiaratnam, Christine Girges, Jacqueline Idaszak, Udaya Seneviratne
    Abstract:

    Eating Epilepsy is rare and comprises Reflex seizures induced by food intake presenting with broad clinical manifestations. Despite this heterogeneity, a unique focal impaired awareness seizure semiology localizing to specific brain regions has been noted. Here, we present a case with video-EEG depicting this characteristic clinical presentation and its informative electrographic correlate. [Published with video sequence].

  • Reflex epilepsies; clinical and demographic characteristics in a tropical country.
    Journal of Clinical Neuroscience, 2005
    Co-Authors: Udaya Seneviratne
    Abstract:

    Summary Background This study is aimed at defining the clinical spectrum and demographic aspects of Reflex Epilepsy in a tropical country in Asia. Methods We studied 526 consecutive patients with Epilepsy. Details of seizure provoking factors were obtained from direct interviews and medical records. Results Of the 526 patients, 47(8.9%) were found to be having Reflex Epilepsy. There were 25(53.2%) males and 22(46.8%) females. Family history of Epilepsy and Reflex Epilepsy were found in 8(17%) and 3(6.4%) respectively. Provoking factors were, eating (34%), higher cerebral functions (17%), bathing (10.6%), photosensitivity (8.5%), startle induced (4.3%), and mixed (more than one of the above: 25.5%). Seizures were provoked by above factors, exclusively in 10 (21.3%), mostly (more than 50% occasions) in 10 (21.3%), and sometimes (less than 50% occasions) in 27 (57.4%) patients. The type of seizure was complex partial evolving to generalized in 23 (48.9%), complex partial in 10 (21.3%), and generalized in 14 (29.8%). Conclusion Our study highlights geographical differences in the spectrum of Reflex Epilepsy.

J Kawasaki - One of the best experts on this subject based on the ideXlab platform.

  • rub Epilepsy a somatosensory evoked Reflex Epilepsy induced by prolonged cutaneous stimulation
    Journal of Neurology Neurosurgery and Psychiatry, 2001
    Co-Authors: Kousuke Kanemoto, Y Watanabe, T Tsuji, M Fukami, J Kawasaki
    Abstract:

    TO DELINEATE RUB Epilepsy a type of Reflex Epilepsy induced by prolonged or repetitive cutaneous stimulation in a circumscribed area of the body—three cases are presented, as well as one of tooth brushing Epilepsy for comparison. In all three cases of rub Epilepsy, cutaneous stimuli in a particular body area on the left side initially induced a sensory jacksonian march in the middle of, or in close vicinity to, the trigger zone, which led to subsequent unilateral tonic contractions with intact consciousness. By contrast, a motor jacksonian seizure without sensory aura was induced in the patient with tooth brushing Epilepsy. A review of cases with rub Epilepsy, including those in this paper, disclosed a striking consistency in clinical manifestations. The symptomatology of the induced seizures indicates a propagation of epileptic discharges from the postcentral gyrus to the supplementary motor area. Rub Epilepsy is proposed as a separate clinical entity, clearly demarcated from other somatosensory evoked Reflex epilepsies such as startle and tooth brushing Epilepsy.