gamma-aminobutyric acid and Aura studies

gamma-Aminobutyric Acid: The most common inhibitory neurotransmitter in the central nervous system.
gamma-aminobutyric acid : A gamma-amino acid that is butanoic acid with the amino substituent located at C-4.

Research Excerpts

Excerpt	Relevance	Reference
"To assess tolerability and short-term efficacy of oral administration of pregabalin as an adjunct to phenobarbital, potassium bromide, or a combination of phenobarbital and potassium bromide for treatment of dogs with poorly controlled suspected idiopathic epilepsy."	9.14	Pregabalin as an adjunct to phenobarbital, potassium bromide, or a combination of phenobarbital and potassium bromide for treatment of dogs with suspected idiopathic epilepsy. ( Badgley, BL; Cerda-Gonzalez, S; Cooper, JJ; Dewey, CW; Ducoté, JM; Lavely, JA; Levine, JM; Packer, RA; Silver, GM, 2009)
"11 client-owned dogs suspected of having idiopathic epilepsy that was inadequately controlled with phenobarbital, potassium bromide, or a combination of these 2 drugs."	9.14	Pregabalin as an adjunct to phenobarbital, potassium bromide, or a combination of phenobarbital and potassium bromide for treatment of dogs with suspected idiopathic epilepsy. ( Badgley, BL; Cerda-Gonzalez, S; Cooper, JJ; Dewey, CW; Ducoté, JM; Lavely, JA; Levine, JM; Packer, RA; Silver, GM, 2009)
"To evaluate bodyweight gain during pregabalin therapy for epilepsy and the utility of a short counseling program to prevent this side effect."	9.13	Bodyweight gain under pregabalin therapy in epilepsy: mitigation by counseling patients? ( Elger, CE; Hoffmann, JM; Hoppe, C; Rademacher, M; Schmidt, D, 2008)
"Randomized controlled trial on the effects of extended versus standard patient counseling on the risk of bodyweight gain with 3- and 6-month follow-up including a consecutive sample of adult outpatients with epilepsy eligible for pregabalin add-on treatment (N=98)."	9.13	Bodyweight gain under pregabalin therapy in epilepsy: mitigation by counseling patients? ( Elger, CE; Hoffmann, JM; Hoppe, C; Rademacher, M; Schmidt, D, 2008)
"Pregabalin treatment is associated with a high risk for bodyweight gain which in part depends on total anticonvulsant drug load."	9.13	Bodyweight gain under pregabalin therapy in epilepsy: mitigation by counseling patients? ( Elger, CE; Hoffmann, JM; Hoppe, C; Rademacher, M; Schmidt, D, 2008)
"To evaluate the efficacy and safety of gabapentin (GBP) in idiopathic or crypto/symptomatic partial epilepsy in adults."	9.12	[Efficacy, safety and effect on the quality of life of gabapentin in adult epilepsy--results of a prospective open-label quasi naturalistic Hungarian multicenter study (phase human-IV)]. ( Rajna, P; Szíjártó, E, 2006)
"To determine the relative tolerability and efficacy of two newer antiepileptic drugs, lamotrigine (LTG) and gabapentin (GBP), as compared to carbamazepine (CBZ) in older patients with epilepsy."	9.11	New onset geriatric epilepsy: a randomized study of gabapentin, lamotrigine, and carbamazepine. ( Boardman, KD; Carter, GS; Collins, JF; Felicetta, J; Frederick, T; Marks, W; Pryor, F; Ramsay, RE; Rowan, AJ; Spitz, M; Tomyanovich, ML; Towne, A; Uthman, BM, 2005)
"This randomised, double-blind study compared the newer antiepileptic drugs (AEDs) gabapentin (GBP) and lamotrigine (LTG) as monotherapy in newly diagnosed epilepsy."	9.10	Gabapentin versus lamotrigine monotherapy: a double-blind comparison in newly diagnosed epilepsy. ( Anhut, H; Brodie, MJ; Chadwick, DW; Garofalo, EA; Maton, S; Messmer, SL; Murray, G; Otte, A; Sauermann, W, 2002)
"A retrospective audit of the perceived efficacy and tolerability of adjunctive gabapentin (GBT) therapy in patients with intractable epilepsy was carried out."	9.09	An audit of the perceived efficacy and tolerability of gabapentin therapy in an out-patient cohort with chronic epilepsy. ( Duncan, JS; Langan, Y; Sander, JW, 1999)
"The aim of the present prospective study was to evaluate changes in plasma GABA concentration in relation to clinical response during vigabatrin treatment of epilepsy."	9.09	Changes in plasma GABA concentration during vigabatrin treatment of epilepsy: a prospective study. ( Alving, J; Erdal, J; Gram, L; Löscher, W, 1999)
"Vigabatrin (gamma-vinyl gamma aminobutyric acid), a recently developed antiepileptic drug, has been extensively evaluated in the treatment of drug-resistant epilepsy."	9.09	Aminoaciduria resulting from vigabatrin administration in children with epilepsy. ( Ben-Zeev, B; Lahat, E; Sela, BA; Zlotnik, J, 1999)
"To evaluate the efficacy and safety of gabapentin (GBP) in partial epilepsy in children."	9.09	Gabapentin in childhood epilepsy: a prospective evaluation of efficacy and safety. ( Boenigk, HE; Borusiak, P; Korn-Merker, E, 2000)
"The aim of this study was to evaluate the efficacy and safety of gabapentin in patients with learning disabilities and resistant epilepsy, comparing the effects of gabapentin with lamotrigine on efficacy, behaviour and mood."	9.09	A randomized open-label study of gabapentin and lamotrigine in adults with learning disability and resistant epilepsy. ( Brown, S; Crawford, P; Kerr, M, 2001)
"To evaluate the efficacy, safety, and cognitive effects of initial vigabatrin monotherapy compared with initial carbamazepine monotherapy in patients with newly diagnosed epilepsy."	9.08	Vigabatrin vs carbamazepine monotherapy in patients with newly diagnosed epilepsy. A randomized, controlled study. ( Aikiä, M; Kälviäinen, R; Mervaala, E; Riekkinen, PJ; Saukkonen, AM, 1995)
"Vigabatrin seems to be an effective and safe antiepileptic drug as primary monotherapy for epilepsy with fewer cognitive side effects than carbamazepine."	9.08	Vigabatrin vs carbamazepine monotherapy in patients with newly diagnosed epilepsy. A randomized, controlled study. ( Aikiä, M; Kälviäinen, R; Mervaala, E; Riekkinen, PJ; Saukkonen, AM, 1995)
" Global improvement data from five double-blind clinical trials of gabapentin as add-on therapy in patients with epilepsy were reviewed to assess the effects of gabapentin on mood."	9.08	Effect of gabapentin (Neurontin) [corrected] on mood and well-being in patients with epilepsy. ( Dimond, KR; Lamoreaux, L; Pande, AC; Pierce, MW, 1996)
"The effect of hepatic enzyme-inducing antiepilepsy drugs (AEDs) on the clinical pharmacokinetics of tiagabine, a new AED, was studied in the steady-state condition."	9.08	Pharmacokinetics of tiagabine as add-on therapy in patients taking enzyme-inducing antiepilepsy drugs. ( Cascino, GD; Graves, NM; Gustavson, LE; Leppik, IE; Pixton, GC; So, EL; Wolff, D, 1995)
"Patients with newly diagnosed localization-related epilepsy who participated in a VGB-carbamazepine (CBZ) monotherapy trial were included."	9.08	A comparison of the neuropathological effects of vigabatrin and carbamazepine in patients with newly diagnosed localization-related epilepsy using MR-based cerebral T2 relaxation time measurements. ( Connelly, A; Duncan, JS; Van Paesschen, W, 1998)
"To determine whether vigabatrin (VGB) causes an increase in T2 relaxation time in patients with newly diagnosed localization-related epilepsy over 1 year."	9.08	A comparison of the neuropathological effects of vigabatrin and carbamazepine in patients with newly diagnosed localization-related epilepsy using MR-based cerebral T2 relaxation time measurements. ( Connelly, A; Duncan, JS; Van Paesschen, W, 1998)
"To study the interaction between gabapentin (GBP) and high-protein meals, 12 patients with epilepsy were administered this drug both while in a fasting state and after a high-protein meal."	9.08	Oral gabapentin disposition in patients with epilepsy after a high-protein meal. ( Baraldo, M; Benetello, P; Fortunato, M; Furlanut, M; Pea, F; Testa, G; Tognon, A, 1997)
"The effect of gabapentin on cognition and quality of life (QoL) in patients with epilepsy was investigated using a controlled pre- and post-treatment design."	9.08	Effects of gabapentin on cognition and quality of life in patients with epilepsy. ( Emmers, E; Mortimore, C; Trimble, M, 1998)
"The short- and long-term clinical efficacy of add-on vigabatrin treatment was evaluated in a group of 36 patients with intellectual disability and drug-refractory epilepsy."	9.08	Antiepileptic efficacy of vigabatrin in people with severe epilepsy and intellectual disability. ( Ylinen, A, 1998)
"Progabide, an experimental GABA-ergic antiepileptic drug, was given in a placebo-controlled double-blind cross-over trial to 19 adult patients with chronic partial epilepsy refractory to previous high-dose antiepileptic drug therapy."	9.06	Progabide for refractory partial epilepsy: a controlled add-on trial. ( Schmidt, D; Utech, K, 1986)
"Data from the MEDLINE database were searched using algorithms to identify relevant economic evaluations published in English or Spanish on pregabalin for the management of neuropathic pain, generalized anxiety disorder (GAD), and epilepsy in Spanish patients over the last 10 years."	8.90	Pharmacoeconomic outcomes for pregabalin: a systematic review in neuropathic pain, generalized anxiety disorder, and epilepsy from a Spanish perspective. ( Álvarez, E; Darbà, J; Kaskens, L; Navarro-Artieda, R; Pérez, C; Sicras-Mainar, A, 2014)
"The majority of published evidence supports the possibility that pregabalin could be a cost-effective and/or cost-saving alternative for the treatment of refractory epilepsy, GAD, and neuropathic pain, in both treatment-naïve patients and in those who have demonstrated inadequate response or intolerance to previous therapy."	8.90	Pharmacoeconomic outcomes for pregabalin: a systematic review in neuropathic pain, generalized anxiety disorder, and epilepsy from a Spanish perspective. ( Álvarez, E; Darbà, J; Kaskens, L; Navarro-Artieda, R; Pérez, C; Sicras-Mainar, A, 2014)
"The higher intrinsic potency of pregabalin compared to gabapentin is associated with an increased antiepileptic efficacy both in animal models of epilepsy and in clinical applications."	8.89	Pharmacokinetic and pharmacodynamic profile of pregabalin and its role in the treatment of epilepsy. ( Schulze-Bonhage, A, 2013)
" Controlled trials in elderly patients with epilepsy demonstrate efficacy and tolerability comparable to gabapentin."	8.84	Lamotrigine therapy in elderly patients with epilepsy, bipolar disorder or dementia. ( Nanry, K; Ramsay, E; Sajatovic, M; Thompson, T, 2007)
"Reports of lamotrigine therapy in elderly patients with epilepsy, bipolar disorder (BD), or dementia were identified by conducting an electronic search of major publication databases."	8.84	Lamotrigine therapy in elderly patients with epilepsy, bipolar disorder or dementia. ( Nanry, K; Ramsay, E; Sajatovic, M; Thompson, T, 2007)
"Review of the available literature suggests lamotrigine is effective and well tolerated in elderly patients with epilepsy and relatively well-tolerated and may be effective in delaying mood relapse, particularly in the depressive pole, in patients with BD."	8.84	Lamotrigine therapy in elderly patients with epilepsy, bipolar disorder or dementia. ( Nanry, K; Ramsay, E; Sajatovic, M; Thompson, T, 2007)
" However, a MEDLINE search using the search terms gabapentin and epilepsy, spanning back to the year 1986, produced numerous published reports from randomized, placebo-controlled and open-label trials, as well as case reports."	8.82	Gabapentin dosing in the treatment of epilepsy. ( Gidal, BE; McLean, MJ, 2003)
"Genetic disorders of gamma-aminobutyric acid (GABA), glycine, and serine metabolism and of the GABA and glycine receptors are causes of epilepsy with variable responsiveness to treatment."	8.81	Genetic disorders of gamma-aminobutyric acid, glycine, and serine as causes of epilepsy. ( Jaeken, J, 2002)
"To provide a qualitative, systematic update and review of the pharmacology, pharmacokinetics, efficacy in mood disorders, adverse effects, and costs of lamotrigine."	8.81	Lamotrigine update and its use in mood disorders. ( Hurley, SC, 2002)
" Hence, the methanol extract was further explored for its anticonvulsant potential in pentylenetetrazole (PTZ) induced acute seizures in mice."	8.31	Anticonvulsant potential of Grewia tiliaefolia in pentylenetetrazole induced epilepsy: insights from in vivo and in silico studies. ( Arora, S; Kaur, S; Kumar, N; Rajput, A; Sharma, P; Singh Bedi, PM; Singh, B; Singh, H; Singh, S; Singh, T, 2023)
" He had been administered phenytoin and gabapentin for the treatment of symptomatic traumatic epilepsy 8 years before."	7.88	Hypothyroidism induced by phenytoin and gabapentin: A Case Report. ( Ishii, K; Miyake, Z; Tamaoka, A, 2018)
"To characterize and quantify the variability of serial gabapentin concentrations in elderly patients with epilepsy."	7.85	Factors in Variability of Serial Gabapentin Concentrations in Elderly Patients with Epilepsy. ( Birnbaum, AK; Collins, JF; Conway, JM; Eberly, LE; Leppik, IE; Macias, FM; Ramsay, RE, 2017)
"Substantial intrapatient variability in serial gabapentin concentration was noted in elderly patients with epilepsy."	7.85	Factors in Variability of Serial Gabapentin Concentrations in Elderly Patients with Epilepsy. ( Birnbaum, AK; Collins, JF; Conway, JM; Eberly, LE; Leppik, IE; Macias, FM; Ramsay, RE, 2017)
"Pregabalin was mainly used as a second-line drug for the treatment of GAD or neuropathic pain and to a lesser extent as add-on therapy in epilepsy."	7.80	Pregabalin is increasingly prescribed for neuropathic pain, generalised anxiety disorder and epilepsy but many patients discontinue treatment. ( Bodén, R; Brandt, L; Kieler, H; Wettermark, B, 2014)
"These data indicate that MSCs were superior to gabapentin in ameliorating PTZ-induced epileptogenesis and verified the potential use of MSCs in seizure control, motor and cognitive impairments, oxidative stress, and the impairing GABA level in experimentally induced epilepsy."	7.80	Effects of intravenous human umbilical cord blood mesenchymal stem cell therapy versus gabapentin in pentylenetetrazole-induced chronic epilepsy in rats. ( Essawy, SS; Ewais, MM; Mohammed, AS; Tawfik, MK, 2014)
"To analyze the survival and the changes of proportions of Calbindin, Calretinin and Parvalbumin positive neurons in mouse hippocampal CA area at chronic stage of Pilocarpine-induced epilepsy."	7.79	[Survival of calbindin, calretinin and parvalbumin positive neurons in mouse hippocampal CA area at chronic stage of pilocarpine-induced epilepsy]. ( Liu, J; Liu, Y; Tang, F, 2013)
"Calbindin, Calretinin and Parvalbumin immunofluoresence staining were done 2 months after Pilocarpine-induced epilepsy in mice or saline injection."	7.79	[Survival of calbindin, calretinin and parvalbumin positive neurons in mouse hippocampal CA area at chronic stage of pilocarpine-induced epilepsy]. ( Liu, J; Liu, Y; Tang, F, 2013)
"The changes of proportions of Calbindin, Calretinin and Parvalbumin positive neurons in the CA area of mouse hippocampus may be a factor in the ongoing epileptic activity at chronic stage of Pilocarpine-induced epilepsy."	7.79	[Survival of calbindin, calretinin and parvalbumin positive neurons in mouse hippocampal CA area at chronic stage of pilocarpine-induced epilepsy]. ( Liu, J; Liu, Y; Tang, F, 2013)
"An open pilot study to evaluate the effect of pregabalin (PGB) as add-on therapy on seizure control, quality of life, and anxiety in patients with brain tumour-related epilepsy (BTRE)."	7.78	Effect of pregabalin add-on treatment on seizure control, quality of life, and anxiety in patients with brain tumour-related epilepsy: a pilot study. ( Carapella, CM; Dinapoli, L; Fabi, A; Maschio, M; Pace, A; Pompili, A; Sperati, F; Vidiri, A, 2012)
"Epileptiform discharges recorded in the 4-aminopyridine (4-AP) in vitro epilepsy model are mediated by glutamatergic and GABAergic signaling."	7.77	The 4-aminopyridine in vitro epilepsy model analyzed with a perforated multi-electrode array. ( Avoli, M; Dzakpasu, R; Gonzalez-Sulser, A; Motamedi, GK; Vicini, S; Wang, J, 2011)
"Vigabatrin was specifically designed to enhance gamma-aminobutyric acid (GABA) function in the CNS."	7.77	Vigabatrin. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in epilepsy and disorders of motor control. ( Grant, SM; Heel, RC, 1991)
"The incidence of constipation as an adverse effect of pregabalin has previously been reported as low, with all cases described as either mild or moderate."	7.76	Severe and disabling constipation: an adverse effect of pregabalin. ( Cook, MJ; D'Souza, WJ; Kamel, JT, 2010)
"The purpose of this study was to estimate the gamma-aminobutyric acid (GABA) and glutamate plus glutamine (Glx) concentrations in the cortical tubers of patients with tuberous sclerosis complex (TSC) using the MEGA-editing J-difference method and a stimulated echo-acquisition mode with a short echo time, and to determine which abnormality was more dominant between GABA and Glx in patients with TSC with epilepsy."	7.75	High gamma-aminobutyric acid level in cortical tubers in epileptic infants with tuberous sclerosis complex measured with the MEGA-editing J-difference method and a three-Tesla clinical MRI Instrument. ( Harada, M; Kubo, H; Matsuda, T; Mori, K; Nishitani, H; Nose, A; Taki, MM, 2009)
"Pregabalin (PGB) is a newer antiepileptic drug (AED) licensed as add-on treatment for partial epilepsy in adults."	7.75	Retention rate of pregabalin in drug-resistant epilepsy: 1-year follow-up, single-centre observation in 105 consecutive, adult patients. ( Brandt, C; Ebner, A; Elsner, H; May, TW; Nieder, E; Pohlmann-Eden, B; Schuermann, I; Witte-Boelt, K, 2009)
"In a retrospective evaluation of 32 inpatients with therapy-resistant epilepsy and intellectual disability, the efficacy of pregabalin (PGB) treatment was assessed after 6 and 12 months."	7.74	Efficacy and tolerability of pregabalin in patients with difficult-to-treat epilepsy and intellectual disability. ( Bocchicchio, M; Feuerbaum, E; Huber, B; May, T; Meinert, T; Robertson, E; Schorlemmer, H; Seidel, M; Wagner, W; Wilking, E, 2008)
"To assess whether there is a change in seizure activity in dogs with refractory epilepsy that are receiving appropriate doses of phenobarbitone and/or potassium bromide, when gabapentin is added to the therapeutic regimen."	7.73	Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent. ( Govendir, M; Malik, R; Perkins, M, 2005)
"A mechanism for the alleviation of the malfunction of a mutated (gamma2(K289M)) epilepsy-linked gamma-aminobutyric acid (GABA) neurotransmitter receptor by phenobarbital is presented."	7.73	On the mechanism of alleviation by phenobarbital of the malfunction of an epilepsy-linked GABA(A) receptor. ( Hess, GP; Krivoshein, AV, 2006)
"We report two patients with refractory epilepsy who developed unilateral painful gynecomastia and lower extremity pain (one of them localized and the other one diffuse), shortly after receiving Pregabalin (PGB)."	7.73	Two cases of painful gynecomastia and lower extremity pain in association with pregabalin therapy. ( Málaga, I; Sanmarti, FX, 2006)
"The objective of this study was to assess the safety of gabapentin (Neurontin) exposure in human pregnancy."	7.72	Gabapentin exposure in human pregnancy: results from the Gabapentin Pregnancy Registry. ( Montouris, G, 2003)
" Chronic seizures were induced by amygdalar injection of kainic acid 60 days before death."	7.71	Collapse of extracellular glutamate regulation during epileptogenesis: down-regulation and functional failure of glutamate transporter function in rats with chronic seizures induced by kainic acid. ( Doi, T; Kamada, H; Mitsuyama, Y; Nakajima, A; Ohya-Nishiguchi, H; Tokumaru, J; Ueda, Y; Willmore, LJ; Yokoyama, H, 2001)
"Pyridoxine-dependent epilepsy is a disease inherited as an autosomal recessive trait, characterized by rapid response to pharmacological dosages of pyridoxine."	7.70	Mutation and polymorphic marker analyses of 65K- and 67K-glutamate decarboxylase genes in two families with pyridoxine-dependent epilepsy. ( Hoshino, H; Kure, S; Matsubara, Y; Miyabayashi, S; Narisawa, K; Sakata, Y; Shinka, T; Takahashi, K, 1998)
"New antiepileptic drugs designed for enhancing GABAergic inhibition, such as vigabatrin (VGB) may be effective in Angelman syndrome (AS), because associated convulsions could be related to a reduced GABA-receptor density or receptor abnormality."	7.70	Adverse effects of vigabatrin in Angelman syndrome. ( Boltshauser, E; Kuenzle, C; Schmitt, B; Steinlin, M; Wohlrab, G, 1998)
"To measure the effects of topiramate on brain gamma-aminobutyric acid (GABA) in patients with epilepsy."	7.70	Topiramate increases brain GABA, homocarnosine, and pyrrolidinone in patients with epilepsy. ( Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 1999)
"To compare the long-term retention of gabapentin (GBP), lamotrigine (LTG), and vigabatrin (VGB) by patients with chronic epilepsy and the reasons for treatment discontinuation."	7.70	The long-term use of gabapentin, lamotrigine, and vigabatrin in patients with chronic epilepsy. ( Chadwick, DW; Fenwick, PB; Mawer, GE; Sander, JW; Wong, IC, 1999)
" We reported that daily dosing increased brain gamma-aminobutyric acid (GABA) in patients with epilepsy."	7.70	Effects of gabapentin on brain GABA, homocarnosine, and pyrrolidinone in epilepsy patients. ( Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 2000)
"The purpose of the present investigation was to determine whether the sensitivity to systemic toxic effects of cocaine is altered in genetically epilepsy-prone rats (GEPRs)."	7.70	Phenotypic expression of the systemic toxicity of cocaine in genetically epilepsy-prone rats. ( Heavner, JE; Kao, YJ; Kaye, AD; Reigel, CE; Shi, B, 2000)
"Infusion of the K(+) channel blocker 4-aminopyridine in the hippocampus induces the release of glutamate, as well as seizures and neurodegeneration."	7.70	Seizures and neurodegeneration induced by 4-aminopyridine in rat hippocampus in vivo: role of glutamate- and GABA-mediated neurotransmission and of ion channels. ( Peña, F; Tapia, R, 2000)
"We sought to determine the long-term retention rates of lamotrigine (LTG), gabapentin (GBP), and topiramate (TPM) therapy for patients at a tertiary referral clinic for chronic, refractory epilepsy."	7.70	Long-term retention rates of lamotrigine, gabapentin, and topiramate in chronic epilepsy. ( Lhatoo, SD; Polizzi, G; Sander, JW; Wong, IC, 2000)
"Pyridoxine-dependent epilepsy is a rare autosomal recessive disorder."	7.69	Glutamate in pyridoxine-dependent epilepsy: neurotoxic glutamate concentration in the cerebrospinal fluid and its normalization by pyridoxine. ( Baumeister, FA; Egger, J; Gsell, W; Shin, YS, 1994)
"To assess the role of glutamate as an excitatory neurotransmitter and neurotoxin in pyridoxine-dependent epilepsy."	7.69	Glutamate in pyridoxine-dependent epilepsy: neurotoxic glutamate concentration in the cerebrospinal fluid and its normalization by pyridoxine. ( Baumeister, FA; Egger, J; Gsell, W; Shin, YS, 1994)
"The results indicate that control of epilepsy might not suffice as the therapeutic aim in treating of pyridoxine dependency."	7.69	Glutamate in pyridoxine-dependent epilepsy: neurotoxic glutamate concentration in the cerebrospinal fluid and its normalization by pyridoxine. ( Baumeister, FA; Egger, J; Gsell, W; Shin, YS, 1994)
"To determine the efficacy of a new anti-epileptic medication vigabatrin in adults and children with drug-resistant epilepsy."	7.69	Vigabatrin use in 72 patients with drug-resistant epilepsy. ( Buchanan, N, 1994)
"In an retrospective uncontrolled long-term study in 30 children with intractable epilepsy, it was found that treatment with vigabatrin resulted in a seizure reduction of more than 50% at 1-year follow-up in 40% of the children."	7.69	Vigabatrin in childhood epilepsy: a 5-year follow-up study. ( Alving, J; Gram, L; Høgenhaven, H; Uldall, P, 1995)
"We present the results of treatment with vigabatrin in the polytherapy of resistant infantile epilepsy."	7.69	[Treatment of refractory infantile epilepsy with vigabatrin in a series of 55 patients]. ( Hernández-Laín, A; López-Valdés, E; Mateos, F; Porta, J; Simón, R, 1996)
"A case of a patient with medically intractable epilepsy, who developed obstructive sleep apnoea (OSA), and an increase in seizure frequency, as a consequence of weight gain following treatment with vigabatrin is described."	7.69	Obstructive sleep apnoea following rapid weight gain secondary to treatment with vigabatrin (Sabril). ( Bird, JM; Lambert, MV, 1997)
"A retrospective survey was carried out of add-on treatment with lamotrigine (LTG) and vigabatrin (GVG) in 109 children with severe epilepsy, treated between 1987 and 1994, identified from a total population of 300 patients seen annually, in a tertiary referral outpatient clinic in Cardiff, Wales."	7.69	A survey of lamotrigine and vigabatrin treatment in children with severe epilepsy. ( Gordon, GS; Schapel, GJ; Wallace, SJ, 1997)
"The anticonvulsant action of progabide, an agonist of gamma-aminobutyric acid (GABA)A and GABAB receptors, was investigated in the kindling model of epilepsy in rats."	7.68	An analysis of anticonvulsant actions of GABA agonists (progabide and baclofen) in the kindling model of epilepsy. ( Morimoto, K; Nakamura, Y; Okamoto, M; Otsuki, S; Sato, K; Sato, M, 1990)
"The involvement of intranigral gamma-aminobutyric acid (GABA) receptors in the control of generalized non-convulsive epilepsy was investigated in the rat in 3 models of petit mal epilepsy induced by systemic administration of gamma-butyrolactone, pentylenetetrazol and 4,5,6,7-tetrahydroisoxazolo [5,4-c]pyridin 3-ol (THIP)."	7.67	Suppressive effects of intranigral injection of muscimol in three models of generalized non-convulsive epilepsy induced by chemical agents. ( Depaulis, A; Marescaux, C; Snead, OC; Vergnes, M, 1989)
"A long-term open multicenter trial was carried out in 15 European centers with therapy-resistant epileptics to evaluate the efficacy and safety of progabide, a new antiepileptic GABA receptor agonist; 187 patients, suffering from partial epilepsy (57%), primary generalized epilepsy (20%), secondary generalized epilepsy (21%), and unclassified generalized epilepsy (2%), participated in the study."	7.67	Long-term treatment of epilepsy: open multicenter trial with progabide in epileptic patients. ( Beaussart, M; Benoit, C; Broglin, D; Cambier, J; Cenraud, M; Chatel, M; Deville, MC; Fournier, V; Loiseau, P; Musch, B, 1987)
"The development of bicuculline- and allylglycine-induced epilepsy has been studied in developing rats (6 to 30 days old)."	7.67	Bicuculline- and allylglycine-induced epilepsy in developing rats. ( de Feo, MR; Mecarelli, O; Ricci, GF, 1985)
"One of the defects in human epilepsy appears to be the suboptimal functioning of at least certain central gamma-aminobutyric acid (GABA)-mediated synapses."	7.66	Transport and metabolism of gamma-aminobutyric acid in neurons and glia: implications for epilepsy. ( Krogsgaard-Larsen, P; Larsson, OM; Schousboe, A; Wood, JD, 1983)
"Epilepsy was symptomatic in 58%, and 74% exhibited associated cognitive deficits."	6.74	Pregabalin: preliminary experience in intractable childhood epilepsy. ( Alsaihati, BA; Jan, MM; Zuberi, SA, 2009)
"Seizures were mixed in nine (47%), and four (21%) manifested Lennox-Gastaut syndrome."	6.74	Pregabalin: preliminary experience in intractable childhood epilepsy. ( Alsaihati, BA; Jan, MM; Zuberi, SA, 2009)
"Most (74%) had daily seizures that failed multiple drugs (mean, 5)."	6.74	Pregabalin: preliminary experience in intractable childhood epilepsy. ( Alsaihati, BA; Jan, MM; Zuberi, SA, 2009)
" However, patients on the same PGB dosage per body weight had rather different PGB trough concentrations, which could be explained only in part by age and comedication."	6.73	Serum concentrations of pregabalin in patients with epilepsy: the influence of dose, age, and comedication. ( Jürgens, U; May, TW; Neb, R; Rambeck, B, 2007)
"Bodyweight gain was correlated with number of anticonvulsant drugs (r=."	6.73	Bodyweight gain under pregabalin therapy in epilepsy: mitigation by counseling patients? ( Elger, CE; Hoffmann, JM; Hoppe, C; Rademacher, M; Schmidt, D, 2008)
" There was no need to decrease of the dosage of GBP and the side effects were mild and of transitory nature."	6.72	[Efficacy, safety and effect on the quality of life of gabapentin in adult epilepsy--results of a prospective open-label quasi naturalistic Hungarian multicenter study (phase human-IV)]. ( Rajna, P; Szíjártó, E, 2006)
"The most common etiology was cerebral infarction."	6.71	New onset geriatric epilepsy: a randomized study of gabapentin, lamotrigine, and carbamazepine. ( Boardman, KD; Carter, GS; Collins, JF; Felicetta, J; Frederick, T; Marks, W; Pryor, F; Ramsay, RE; Rowan, AJ; Spitz, M; Tomyanovich, ML; Towne, A; Uthman, BM, 2005)
" During 2- and 6-week titration periods, respectively, GBP dosage reached 1,800 mg/day, and LTG, 150 mg/day."	6.70	Gabapentin versus lamotrigine monotherapy: a double-blind comparison in newly diagnosed epilepsy. ( Anhut, H; Brodie, MJ; Chadwick, DW; Garofalo, EA; Maton, S; Messmer, SL; Murray, G; Otte, A; Sauermann, W, 2002)
"Vigabatrin (VGB) is a new antiepileptic drug that increases the human brain gamma-aminobutyric acid (GABA) level by irreversibly inhibiting GABA transaminase."	6.70	Effects of vigabatrin on brain GABA+/CR signals in patients with epilepsy monitored by 1H-NMR-spectroscopy: responder characteristics. ( Boesiger, P; Duc, CO; Meier, D; Mueller, SG; Russ, W; Weber, B; Weber, OM; Wieser, HG, 2001)
"Gabapentin (GBP) is a non-metabolized antiepileptic drug that is eliminated by renal excretion and displays saturable, dose dependent absorption."	6.69	Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. ( Bockbrader, HN; DeCerce, J; Gidal, BE; Gonzalez, J; Kruger, S; Pitterle, ME; Ramsay, RE; Rutecki, P, 1998)
" At large daily doses, oral bioavailability (F) may be improved by giving the daily dose more frequently."	6.69	Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. ( Bockbrader, HN; DeCerce, J; Gidal, BE; Gonzalez, J; Kruger, S; Pitterle, ME; Ramsay, RE; Rutecki, P, 1998)
" The recommended dosing schedule for GBP is t."	6.69	Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. ( Bockbrader, HN; DeCerce, J; Gidal, BE; Gonzalez, J; Kruger, S; Pitterle, ME; Ramsay, RE; Rutecki, P, 1998)
"To evaluate whether switching GBP dosage regimen from t."	6.69	Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. ( Bockbrader, HN; DeCerce, J; Gidal, BE; Gonzalez, J; Kruger, S; Pitterle, ME; Ramsay, RE; Rutecki, P, 1998)
" dosing were 38."	6.69	Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. ( Bockbrader, HN; DeCerce, J; Gidal, BE; Gonzalez, J; Kruger, S; Pitterle, ME; Ramsay, RE; Rutecki, P, 1998)
"After 3 months, 42% of the patients with intellectual disability had experienced a reduction in seizure frequency of more than 50% (responders)."	6.69	Antiepileptic efficacy of vigabatrin in people with severe epilepsy and intellectual disability. ( Ylinen, A, 1998)
"Gabapentin was added to one other baseline drug and the efficacy was rated according to seizure type and frequency."	6.69	Gabapentin in childhood epilepsy: a prospective evaluation of efficacy and safety. ( Boenigk, HE; Borusiak, P; Korn-Merker, E, 2000)
"Although gabapentin seems also to be safe in children, the efficacy in refractory partial seizures was disappointing."	6.69	Gabapentin in childhood epilepsy: a prospective evaluation of efficacy and safety. ( Boenigk, HE; Borusiak, P; Korn-Merker, E, 2000)
"Vigabatrin seems to be an effective and safe antiepileptic drug as primary monotherapy for epilepsy with fewer cognitive side effects than carbamazepine."	6.68	Vigabatrin vs carbamazepine monotherapy in patients with newly diagnosed epilepsy. A randomized, controlled study. ( Aikiä, M; Kälviäinen, R; Mervaala, E; Riekkinen, PJ; Saukkonen, AM, 1995)
" We evaluated the cognitive and quality-of-life (QOL) effects of VGB in a double-blinded, add-on, placebo-controlled, parallel group dose-response study of patients with focal epilepsy whose complex partial seizures (CPS) were difficult to control."	6.68	Effects of differing dosages of vigabatrin (Sabril) on cognitive abilities and quality of life in epilepsy. ( Arnett, JL; Dodrill, CB; Sommerville, KW; Sussman, NM, 1995)
" Plasma tiagabine concentrations were determined by high-performance liquid chromatography; pharmacokinetic parameters were calculated using noncompartmental methods."	6.68	Pharmacokinetics of tiagabine as add-on therapy in patients taking enzyme-inducing antiepilepsy drugs. ( Cascino, GD; Graves, NM; Gustavson, LE; Leppik, IE; Pixton, GC; So, EL; Wolff, D, 1995)
"Vigabatrin was most effective in cryptogenic and symptomatic partial seizures (39% and 43%, respectively), and in infantile spasms (25%)."	6.68	Vigabatrin as add-on therapy in children and adolescents with refractory epilepsy: an open trial. ( Coppola, G; Pascotto, A; Terraciano, AM, 1997)
" The following kinetic parameters were calculated: area under the concentration time curve from zero time to 24 h after the dose, AUC 0-24 h; maximal serum concentration, Cmax; time to the maximal serum concentration, Tmax; absorption rate constant, ka; elimination rate constant, beta; elimination half-time, t1/2beta."	6.68	Oral gabapentin disposition in patients with epilepsy after a high-protein meal. ( Baraldo, M; Benetello, P; Fortunato, M; Furlanut, M; Pea, F; Testa, G; Tognon, A, 1997)
"Pregabalin , the S-enantiomer of 3-aminomethyl-5-methylhaxanoic acid, is a second-generation antiepileptic drug (AED) developed after gabapentin with improved pharmacokinetic and pharmacodynamics properties."	6.49	Pharmacokinetic and pharmacodynamic profile of pregabalin and its role in the treatment of epilepsy. ( Schulze-Bonhage, A, 2013)
" The article also looks at its clinical application as a combination therapy with particular respect to its pharmacokinetic profile."	6.49	Pharmacokinetic and pharmacodynamic profile of pregabalin and its role in the treatment of epilepsy. ( Schulze-Bonhage, A, 2013)
" Pregabalin has a linear uptake without transporter saturation at therapeutic dosages, high bioavailability with rapid absorption independent of food intake."	6.49	Pharmacokinetic and pharmacodynamic profile of pregabalin and its role in the treatment of epilepsy. ( Schulze-Bonhage, A, 2013)
"Levetiracetam (Keppra) is an antiepileptic drug (AED) characterized by a novel mechanism of action, unique profile of activity in seizure models, and broad-spectrum clinical efficacy."	6.45	Benefit of combination therapy in epilepsy: a review of the preclinical evidence with levetiracetam. ( Kaminski, RM; Klitgaard, H; Matagne, A; Patsalos, PN, 2009)
"Gabapentin is an antiepileptic drug (AED) by design expected to mimic the action of the neurotransmitter gamma-aminobutyric acid (GABA)."	6.44	Gabapentin: a Ca2+ channel alpha 2-delta ligand far beyond epilepsy therapy. ( Striano, P; Striano, S, 2008)
"The purposes of this review were to assess the gabapentin titration and dosing regimens that have been published in peer-reviewed journals, to develop dosing recommendations to maximize antiseizure efficacy without compromising tolerability, and to formulate guidelines for an adequate therapeutic assessment of gabapentin dosage efficacy."	6.42	Gabapentin dosing in the treatment of epilepsy. ( Gidal, BE; McLean, MJ, 2003)
" These were reviewed to assess the range of dosing and titration schedules reported."	6.42	Gabapentin dosing in the treatment of epilepsy. ( Gidal, BE; McLean, MJ, 2003)
" Side effects occurred around the onset of dosing and were reported in some studies to be transient."	6.42	Gabapentin dosing in the treatment of epilepsy. ( Gidal, BE; McLean, MJ, 2003)
"Based in the literature here, in most adult patients, gabapentin may be initiated at a dosage of 900 mg/d and titrated to maintenance dosages > or = 3600 mg/d."	6.42	Gabapentin dosing in the treatment of epilepsy. ( Gidal, BE; McLean, MJ, 2003)
"Epilepsy is a major symptom in succinic semialdehyde dehydrogenase deficiency."	6.41	Genetic disorders of gamma-aminobutyric acid, glycine, and serine as causes of epilepsy. ( Jaeken, J, 2002)
"Although epilepsy is fundamentally a circuit phenomenon, the most basic manifestation of the hyperexcitability characteristic of epilepsy must be evident at the level of a single neuron."	6.41	Epilepsy-associated plasticity in gamma-aminobutyric acid receptor expression, function, and inhibitory synaptic properties. ( Coulter, DA, 2001)
"Lamotrigine has positive effects on cognitive function, but occasionally produces insomnia."	6.41	Lamotrigine update and its use in mood disorders. ( Hurley, SC, 2002)
" A slow upward dose titration is recommended to reduce the incidence of serious rash, but this may delay the attainment of adequate dosage for 6 weeks."	6.41	Lamotrigine update and its use in mood disorders. ( Hurley, SC, 2002)
"Gabapentin is a recently introduced antiepileptic drug for the treatment of partial seizures."	6.40	Gabapentin for treatment of epilepsy in children. ( Holmes, GL, 1997)
"Gabapentin appears to be a useful new AED."	6.39	Gabapentin: a new agent for the management of epilepsy. ( Andrews, CO; Fischer, JH, 1994)
"Gabapentin's potential role in the treatment of epilepsy also was assessed."	6.39	Gabapentin: a new agent for the management of epilepsy. ( Andrews, CO; Fischer, JH, 1994)
"Vigabatrin is a specific and irreversible inhibitor of the enzyme gamma-amino-butyric-acid (GABA) transferase."	6.39	[Vigabatrin and lamotrigin: experiences with 2 new anticonvulsants in the Swiss epilepsy clinic]. ( Krämer, G; Vogt, H, 1995)
"Felbamate was licensed in 1993 for use as adjunctive therapy or monotherapy in adults with partial or tonic-clonic seizures and as adjunctive therapy for children with the Lennox-Gastaut syndrome."	6.39	Guidelines for treating epilepsy in the age of felbamate, vigabatrin, lamotrigine, and gabapentin. ( Laxer, KD, 1994)
"Gabapentin was approved January 1994 as adjunctive therapy in patients 12 years or older with partial seizures, with or without secondary generalization."	6.39	Guidelines for treating epilepsy in the age of felbamate, vigabatrin, lamotrigine, and gabapentin. ( Laxer, KD, 1994)
"Gabapentin is an antiepileptic drug with an unknown mechanism of action apparently dissimilar to that of other antiepileptic agents, and possessing some desirable pharmacokinetic traits."	6.38	Gabapentin. A review of its pharmacological properties and clinical potential in epilepsy. ( Goa, KL; Sorkin, EM, 1993)
"The average number of seizures per month during the previous 3 months before CNB treatment was 19."	5.91	Cenobamate and Clobazam Combination as Personalized Medicine in Autoimmune-Associated Epilepsy With Anti-Gad65 Antibodies. ( Aguilar-Castillo, MJ; Cabezudo-García, P; Carreño, M; Ciano-Petersen, NL; Estivill-Torrús, G; García-Martín, G; Gutierrez-Cardo, AL; López-Moreno, Y; Oliver, B; Ortega-Pinazo, J; Ramírez-García, T; Rodríguez-Uranga, JJ; Romero-Godoy, J; Sanchez-Godoy, L; Serrano-Castro, PJ, 2023)
"Neuropeptide Y (NPY) is a polypeptide sequence useful in regulating physiological functions like homeostasis, feeding, etc."	5.72	β-Cyclodextrin-crosslinked synthetic neuropeptide Y-based nanosponges in epilepsy by contributing GABAergic signal. ( Desai, D; Shende, P, 2022)
"Anandamide (AEA) content was downregulated after repeated seizures, and pharmacological enhancement of AEA signaling rescued seizure-induced anxiety by restoring the tonic control of the eCB signaling over glutamatergic transmission."	5.56	Anandamide Signaling Augmentation Rescues Amygdala Synaptic Function and Comorbid Emotional Alterations in a Model of Epilepsy. ( Colangeli, R; Hill, MN; Morena, M; Pittman, QJ; Teskey, GC, 2020)
"Epilepsy is often associated with emotional disturbances and the endocannabinoid (eCB) system tunes synaptic transmission in brain regions regulating emotional behavior."	5.56	Anandamide Signaling Augmentation Rescues Amygdala Synaptic Function and Comorbid Emotional Alterations in a Model of Epilepsy. ( Colangeli, R; Hill, MN; Morena, M; Pittman, QJ; Teskey, GC, 2020)
"Epilepsy is associated with increased morbidity and mortality together and places a large financial burden on individuals and society."	5.48	Anticonvulsive effects of protodioscin against pilocarpine-induced epilepsy. ( Chen, Y; Fajol, A; Ren, B; Shi, S; Song, S, 2018)
"In six-hertz-seizure test the MeCO (25, 50, 100 and 200mg/kg) and AeCO (50, 100, 200, 400 and 800mg/kg) showed significant protection compared to control group, and MeCO was more potent than AeCO."	5.46	Ameliorative potential of Colebrookea oppositifolia methanolic root extract against experimental models of epilepsy: Possible role of GABA mediated mechanism. ( Prasad, NBL; Venkataranganna, MV; Viswanatha, GL, 2017)
"Pretreatment with spermine, considerably, reversed the PTZ induced alterations."	5.46	Protective effect of spermine against pentylenetetrazole kindling epilepsy induced comorbidities in mice. ( Kumar, M; Kumar, P, 2017)
"Spermine is an endogenous polyamine; possesses anti-oxidant property and has ability to modulate ion channels and NO synthase activity."	5.46	Protective effect of spermine against pentylenetetrazole kindling epilepsy induced comorbidities in mice. ( Kumar, M; Kumar, P, 2017)
"Pre-treatment with liraglutide (75 and 150 μg/kg) significantly prevented the seizure severity, restored behavioural activity, oxidative defence enzymes, and altered level of neurochemicals in mice brain."	5.43	Neurochemical modulation involved in the beneficial effect of liraglutide, GLP-1 agonist on PTZ kindling epilepsy-induced comorbidities in mice. ( Koshal, P; Kumar, P, 2016)
"Epilepsy is a neurological disorder which occurs due to excessive firing of excitatory neurons in specific region of brain and associated with cognitive impairment and depression."	5.43	Neurochemical modulation involved in the beneficial effect of liraglutide, GLP-1 agonist on PTZ kindling epilepsy-induced comorbidities in mice. ( Koshal, P; Kumar, P, 2016)
"Gamma-aminobutyric acid-expressing (GABAergic) neurons are implicated in a variety of neuropsychiatric disorders, such as epilepsy, anxiety, autism, and other pathological processes, including cerebral ischemia injury and drug addiction."	5.41	GABAergic neurons maturation is regulated by a delicate network. ( Gao, M; Wang, K; Zhao, H, 2023)
"Vigabatrin is an inhibitor of γ-aminobutyric acid transaminase."	5.40	Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms. ( Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014)
"Vigabatrin pharmacokinetic data from six randomized controlled clinical trials and one open-label study were analyzed using nonlinear mixed-effects modeling."	5.40	Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms. ( Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014)
" Covariate analysis indicated that age, creatinine clearance (CLCR), and body weight were important predictors of vigabatrin pharmacokinetic parameters."	5.40	Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms. ( Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014)
"The model adequately described vigabatrin pharmacokinetic and enabled predictions of systemic exposures in pediatric patients 1-12 months of age."	5.40	Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms. ( Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014)
"1 %) and relative bioavailability (F) (26."	5.40	Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms. ( Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014)
" Mean PGB dosage was 279 mg/day."	5.38	Effect of pregabalin add-on treatment on seizure control, quality of life, and anxiety in patients with brain tumour-related epilepsy: a pilot study. ( Carapella, CM; Dinapoli, L; Fabi, A; Maschio, M; Pace, A; Pompili, A; Sperati, F; Vidiri, A, 2012)
"The incidence of constipation as an adverse effect of pregabalin has previously been reported as low, with all cases described as either mild or moderate."	5.36	Severe and disabling constipation: an adverse effect of pregabalin. ( Cook, MJ; D'Souza, WJ; Kamel, JT, 2010)
"Constipation was the most frequent adverse effect that required pregabalin to be withdrawn (6."	5.36	Severe and disabling constipation: an adverse effect of pregabalin. ( Cook, MJ; D'Souza, WJ; Kamel, JT, 2010)
"Epilepsy is a serious neurological disorder in human beings and the long-term pathological events remain largely obscure."	5.35	Time-course of neuronal death in the mouse pilocarpine model of chronic epilepsy using Fluoro-Jade C staining. ( Chen, LW; Huang, YG; Liu, YH; Wang, L, 2008)
" GBP plasma concentrations in the neonates declined with an estimated half-life of 14 h."	5.33	Pharmacokinetics of gabapentin during delivery, in the neonatal period, and lactation: does a fetal accumulation occur during pregnancy? ( Ohman, I; Tomson, T; Vitols, S, 2005)
"Patients were stabilised using phenobarbitone and/or potassium bromide to produce tolerable therapeutic serum concentrations and dosed additionally with gabapentin at 35 to 50 mg/kg/d (divided twice or three times daily) for 4 months."	5.33	Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent. ( Govendir, M; Malik, R; Perkins, M, 2005)
"To assess whether there is a change in seizure activity in dogs with refractory epilepsy that are receiving appropriate doses of phenobarbitone and/or potassium bromide, when gabapentin is added to the therapeutic regimen."	5.33	Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent. ( Govendir, M; Malik, R; Perkins, M, 2005)
"Owners recorded seizure activity and side effects during this period in a standardised diary."	5.33	Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent. ( Govendir, M; Malik, R; Perkins, M, 2005)
"In some dogs, seizures were prevented completely, while in others there was an increase in interictal period."	5.33	Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent. ( Govendir, M; Malik, R; Perkins, M, 2005)
"In vivo, it potently prevents seizures, pain-related behaviors and has anxiolytic-like activity in rodent models."	5.33	Activity profile of pregabalin in rodent models of epilepsy and ataxia. ( Bertram, E; Kinsora, JJ; Radulovic, LL; Serpa, KA; Taylor, CP; Vartanian, MG; Vergnes, M, 2006)
"The influence of age and administered daily dosage on the plasma concentrations of gabapentin (GBP) at steady state was evaluated in a group of 41 children and young adults (aged 3-30 years) receiving long-term adjunctive treatment with GBP for the management of refractory partial-onset seizures."	5.32	Plasma gabapentin concentrations in children with epilepsy: influence of age, relationship with dosage, and preliminary observations on correlation with clinical response. ( Bonanni, P; Bonomi, I; Ferrari, AR; Gatti, G; Guerrini, R; Perucca, E, 2003)
"p."	5.31	Guanosine and GMP prevent seizures induced by quinolinic acid in mice. ( da Silveira Perla, A; de Faria Maraschin, J; Lara, DR; Onofre Souza, D; Schmidt, AP, 2000)
"Bicuculline was used to investigate seizure susceptibility in pre- and peripubertal male and female rats exposed prenatally to morphine."	5.31	Prenatal morphine exposure alters susceptibility to bicuculline seizures in a sex- and age-specific manner. ( Schindler, CJ; Slamberová, R; Vathy, I; Velísková, J, 2000)
"Gabapentin (GBP) was introduced as an antiepileptic drug (AED) and has been used in the management of neuropathic pain."	5.31	Effects of gabapentin on brain GABA, homocarnosine, and pyrrolidinone in epilepsy patients. ( Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 2000)
" We reported that daily dosing increased brain gamma-aminobutyric acid (GABA) in patients with epilepsy."	5.31	Effects of gabapentin on brain GABA, homocarnosine, and pyrrolidinone in epilepsy patients. ( Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 2000)
"A significant decrease in seizure susceptibility could be observed in BCCA treated mice compared with sham-operated controls."	5.31	The influence of MK-801 on bicuculline evoked seizures in adult mice exposed to transient episode of brain ischemia. ( Kleinrok, Z; Rejdak, K; Rejdak, R; Sieklucka-Dziuba, M, 2000)
"The purpose of the present investigation was to determine whether the sensitivity to systemic toxic effects of cocaine is altered in genetically epilepsy-prone rats (GEPRs)."	5.31	Phenotypic expression of the systemic toxicity of cocaine in genetically epilepsy-prone rats. ( Heavner, JE; Kao, YJ; Kaye, AD; Reigel, CE; Shi, B, 2000)
"Moderate seizure (GEPR-3) and severe seizure (GEPR-9) rats, and the control strain, Sprague-Dawley rats, 10 weeks of age, were lightly anesthetized with halothane and nitrous oxide."	5.31	Phenotypic expression of the systemic toxicity of cocaine in genetically epilepsy-prone rats. ( Heavner, JE; Kao, YJ; Kaye, AD; Reigel, CE; Shi, B, 2000)
"Chronic seizures were induced by amygdalar injection of kainic acid 60 days before death."	5.31	Collapse of extracellular glutamate regulation during epileptogenesis: down-regulation and functional failure of glutamate transporter function in rats with chronic seizures induced by kainic acid. ( Doi, T; Kamada, H; Mitsuyama, Y; Nakajima, A; Ohya-Nishiguchi, H; Tokumaru, J; Ueda, Y; Willmore, LJ; Yokoyama, H, 2001)
"Epilepsy is a common condition in people with learning disabilities with many patients continuing to suffer from seizures despite antiepileptic drug (AED) treatment."	5.30	A naturalistic study of the use of vigabatrin, lamotrigine and gabapentin in adults with learning disabilities. ( Bhaumik, S; Branford, D; Duggirala, C; Ismail, IA, 1997)
"Lamotrigine caused increased seizures in 24% of patients, especially when prescribed at a higher dose."	5.30	A naturalistic study of the use of vigabatrin, lamotrigine and gabapentin in adults with learning disabilities. ( Bhaumik, S; Branford, D; Duggirala, C; Ismail, IA, 1997)
"Topiramate is a new antiepileptic medication with multiple putative mechanisms of action."	5.30	Topiramate increases brain GABA, homocarnosine, and pyrrolidinone in patients with epilepsy. ( Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 1999)
" In view of the evidence for the role of excitatory amino acids in destruction of CNS nerve cells, the optimal treatment must counteract the raised levels of CSF glutamate and the dosage of vitamin B6 must be adjusted accordingly."	5.29	Glutamate in pyridoxine-dependent epilepsy: neurotoxic glutamate concentration in the cerebrospinal fluid and its normalization by pyridoxine. ( Baumeister, FA; Egger, J; Gsell, W; Shin, YS, 1994)
"The development of mental retardation might theoretically be prevented by adjusting the dose of vitamin B6 to achieve not only remission of epilepsy but also normalization of CSF glutamate."	5.29	Glutamate in pyridoxine-dependent epilepsy: neurotoxic glutamate concentration in the cerebrospinal fluid and its normalization by pyridoxine. ( Baumeister, FA; Egger, J; Gsell, W; Shin, YS, 1994)
"Vigabatrin has a definite role to play in the management of persons with intractable complex partial seizures where standard anti-epileptic therapy has failed to achieve control."	5.29	Vigabatrin use in 72 patients with drug-resistant epilepsy. ( Buchanan, N, 1994)
"Progabide was administered at a mean daily dose of 30."	5.27	Long-term treatment of epilepsy: open multicenter trial with progabide in epileptic patients. ( Beaussart, M; Benoit, C; Broglin, D; Cambier, J; Cenraud, M; Chatel, M; Deville, MC; Fournier, V; Loiseau, P; Musch, B, 1987)
"By reducing neuronal excitability through selective binding to the α(2)δ subunit of voltage-dependent calcium channels, pregabalin effectively treats epilepsy, chronic pain, and anxiety disorders."	5.15	Pregabalin effect on steady-state pharmacokinetics of carbamazepine, lamotrigine, phenobarbital, phenytoin, topiramate, valproate, and tiagabine. ( Bockbrader, HN; Burger, P; Knapp, L, 2011)
"To assess tolerability and short-term efficacy of oral administration of pregabalin as an adjunct to phenobarbital, potassium bromide, or a combination of phenobarbital and potassium bromide for treatment of dogs with poorly controlled suspected idiopathic epilepsy."	5.14	Pregabalin as an adjunct to phenobarbital, potassium bromide, or a combination of phenobarbital and potassium bromide for treatment of dogs with suspected idiopathic epilepsy. ( Badgley, BL; Cerda-Gonzalez, S; Cooper, JJ; Dewey, CW; Ducoté, JM; Lavely, JA; Levine, JM; Packer, RA; Silver, GM, 2009)
"11 client-owned dogs suspected of having idiopathic epilepsy that was inadequately controlled with phenobarbital, potassium bromide, or a combination of these 2 drugs."	5.14	Pregabalin as an adjunct to phenobarbital, potassium bromide, or a combination of phenobarbital and potassium bromide for treatment of dogs with suspected idiopathic epilepsy. ( Badgley, BL; Cerda-Gonzalez, S; Cooper, JJ; Dewey, CW; Ducoté, JM; Lavely, JA; Levine, JM; Packer, RA; Silver, GM, 2009)
"To evaluate bodyweight gain during pregabalin therapy for epilepsy and the utility of a short counseling program to prevent this side effect."	5.13	Bodyweight gain under pregabalin therapy in epilepsy: mitigation by counseling patients? ( Elger, CE; Hoffmann, JM; Hoppe, C; Rademacher, M; Schmidt, D, 2008)
"Randomized controlled trial on the effects of extended versus standard patient counseling on the risk of bodyweight gain with 3- and 6-month follow-up including a consecutive sample of adult outpatients with epilepsy eligible for pregabalin add-on treatment (N=98)."	5.13	Bodyweight gain under pregabalin therapy in epilepsy: mitigation by counseling patients? ( Elger, CE; Hoffmann, JM; Hoppe, C; Rademacher, M; Schmidt, D, 2008)
"Pregabalin treatment is associated with a high risk for bodyweight gain which in part depends on total anticonvulsant drug load."	5.13	Bodyweight gain under pregabalin therapy in epilepsy: mitigation by counseling patients? ( Elger, CE; Hoffmann, JM; Hoppe, C; Rademacher, M; Schmidt, D, 2008)
"To evaluate the efficacy and safety of gabapentin (GBP) in idiopathic or crypto/symptomatic partial epilepsy in adults."	5.12	[Efficacy, safety and effect on the quality of life of gabapentin in adult epilepsy--results of a prospective open-label quasi naturalistic Hungarian multicenter study (phase human-IV)]. ( Rajna, P; Szíjártó, E, 2006)
"To compare clinicians' choice of one of the standard epilepsy drug treatments (carbamazepine or valproate) versus appropriate comparator new drugs."	5.12	A randomised controlled trial examining the longer-term outcomes of standard versus new antiepileptic drugs. The SANAD trial. ( Appleton, R; Baker, GA; Chadwick, DW; Doughty, J; Eaton, B; Gamble, C; Jacoby, A; Marson, AG; Shackley, P; Smith, DF; Tudur-Smith, C; Vanoli, A; Williamson, PR, 2007)
" We tested this hypothesis by reviewing the multiple mechanisms of action of topiramate (TPM) and levetiracetam (LEV) together with clinical behavioral side effects of patients who had been treated with TPM and LEV in a tertiary referral center for epilepsy."	5.11	Ketter's hypothesis of the mood effects of antiepileptic drugs coupled to the mechanism of action of topiramate and levetiracetam. ( Aldenkamp, AP; Bootsma, HP; Kessels, AG; Leenen, LA; Leonard, BE; Majoie, HJ; Roberts, GM, 2005)
"To determine the relative tolerability and efficacy of two newer antiepileptic drugs, lamotrigine (LTG) and gabapentin (GBP), as compared to carbamazepine (CBZ) in older patients with epilepsy."	5.11	New onset geriatric epilepsy: a randomized study of gabapentin, lamotrigine, and carbamazepine. ( Boardman, KD; Carter, GS; Collins, JF; Felicetta, J; Frederick, T; Marks, W; Pryor, F; Ramsay, RE; Rowan, AJ; Spitz, M; Tomyanovich, ML; Towne, A; Uthman, BM, 2005)
"This randomised, double-blind study compared the newer antiepileptic drugs (AEDs) gabapentin (GBP) and lamotrigine (LTG) as monotherapy in newly diagnosed epilepsy."	5.10	Gabapentin versus lamotrigine monotherapy: a double-blind comparison in newly diagnosed epilepsy. ( Anhut, H; Brodie, MJ; Chadwick, DW; Garofalo, EA; Maton, S; Messmer, SL; Murray, G; Otte, A; Sauermann, W, 2002)
"The aim of the study was to find out the percentage of patients with localization-related epilepsy achieving complete seizure control with gabapentin (GBP) add-on therapy."	5.09	Gabapentin add-on treatment: how many patients become seizure-free? An open-label multicenter study. ( Elger, CE; Mayer, T; Schütte, W; Wolf, P, 1999)
"A retrospective audit of the perceived efficacy and tolerability of adjunctive gabapentin (GBT) therapy in patients with intractable epilepsy was carried out."	5.09	An audit of the perceived efficacy and tolerability of gabapentin therapy in an out-patient cohort with chronic epilepsy. ( Duncan, JS; Langan, Y; Sander, JW, 1999)
"Ten patients with refractory partial epilepsy, previous mental retardation and psychosis or other significant psychiatric morbidity treated with vigabatrin were submitted periodically to specific tests (to quantify any possible change in behavioural parameters) and also to EEG recordings."	5.09	Vigabatrin use in psychotic epileptic patients: report of a prospective pilot study. ( Baldi, PL; De Agostini, G; Ferrari Ginevra, O; Lanzi, G; Muzio, C; Termine, C; Veggiotti, P, 1999)
"The aim of the present prospective study was to evaluate changes in plasma GABA concentration in relation to clinical response during vigabatrin treatment of epilepsy."	5.09	Changes in plasma GABA concentration during vigabatrin treatment of epilepsy: a prospective study. ( Alving, J; Erdal, J; Gram, L; Löscher, W, 1999)
"Vigabatrin (gamma-vinyl gamma aminobutyric acid), a recently developed antiepileptic drug, has been extensively evaluated in the treatment of drug-resistant epilepsy."	5.09	Aminoaciduria resulting from vigabatrin administration in children with epilepsy. ( Ben-Zeev, B; Lahat, E; Sela, BA; Zlotnik, J, 1999)
"To evaluate the efficacy and safety of gabapentin (GBP) in partial epilepsy in children."	5.09	Gabapentin in childhood epilepsy: a prospective evaluation of efficacy and safety. ( Boenigk, HE; Borusiak, P; Korn-Merker, E, 2000)
"Our objective was to determine, in three separate studies, the effects of controlled-release carbamazepine (CBZ-CR), lamotrigine (LTG), and gabapentin (GBP) on nocturnal sleep in epilepsy."	5.09	Effect of anticonvulsants on nocturnal sleep in epilepsy. ( Diomedi, M; Gigli, GL; Marciani, MG; Placidi, F; Romigi, A; Scalise, A, 2000)
"The aim of this study was to evaluate the efficacy and safety of gabapentin in patients with learning disabilities and resistant epilepsy, comparing the effects of gabapentin with lamotrigine on efficacy, behaviour and mood."	5.09	A randomized open-label study of gabapentin and lamotrigine in adults with learning disability and resistant epilepsy. ( Brown, S; Crawford, P; Kerr, M, 2001)
"Gabapentin was administered in single doses of 10 mg/kg (N=48 healthy subjects, age 1 month-12 years) or in multiple doses of 10-65 mg/kg per day (N=205 patients with epilepsy, age 2 months-13 years) at 08:00, 14:00, and 20:00."	5.09	Population pharmacokinetics of gabapentin in infants and children. ( Bockbrader, HN; Garofalo, E; Ouellet, D; Shapiro, DY; Wesche, DL, 2001)
"To evaluate the efficacy, safety, and cognitive effects of initial vigabatrin monotherapy compared with initial carbamazepine monotherapy in patients with newly diagnosed epilepsy."	5.08	Vigabatrin vs carbamazepine monotherapy in patients with newly diagnosed epilepsy. A randomized, controlled study. ( Aikiä, M; Kälviäinen, R; Mervaala, E; Riekkinen, PJ; Saukkonen, AM, 1995)
"Vigabatrin seems to be an effective and safe antiepileptic drug as primary monotherapy for epilepsy with fewer cognitive side effects than carbamazepine."	5.08	Vigabatrin vs carbamazepine monotherapy in patients with newly diagnosed epilepsy. A randomized, controlled study. ( Aikiä, M; Kälviäinen, R; Mervaala, E; Riekkinen, PJ; Saukkonen, AM, 1995)
" Global improvement data from five double-blind clinical trials of gabapentin as add-on therapy in patients with epilepsy were reviewed to assess the effects of gabapentin on mood."	5.08	Effect of gabapentin (Neurontin) [corrected] on mood and well-being in patients with epilepsy. ( Dimond, KR; Lamoreaux, L; Pande, AC; Pierce, MW, 1996)
"The effect of hepatic enzyme-inducing antiepilepsy drugs (AEDs) on the clinical pharmacokinetics of tiagabine, a new AED, was studied in the steady-state condition."	5.08	Pharmacokinetics of tiagabine as add-on therapy in patients taking enzyme-inducing antiepilepsy drugs. ( Cascino, GD; Graves, NM; Gustavson, LE; Leppik, IE; Pixton, GC; So, EL; Wolff, D, 1995)
"Patients with newly diagnosed localization-related epilepsy who participated in a VGB-carbamazepine (CBZ) monotherapy trial were included."	5.08	A comparison of the neuropathological effects of vigabatrin and carbamazepine in patients with newly diagnosed localization-related epilepsy using MR-based cerebral T2 relaxation time measurements. ( Connelly, A; Duncan, JS; Van Paesschen, W, 1998)
"To determine whether vigabatrin (VGB) causes an increase in T2 relaxation time in patients with newly diagnosed localization-related epilepsy over 1 year."	5.08	A comparison of the neuropathological effects of vigabatrin and carbamazepine in patients with newly diagnosed localization-related epilepsy using MR-based cerebral T2 relaxation time measurements. ( Connelly, A; Duncan, JS; Van Paesschen, W, 1998)
"To study the interaction between gabapentin (GBP) and high-protein meals, 12 patients with epilepsy were administered this drug both while in a fasting state and after a high-protein meal."	5.08	Oral gabapentin disposition in patients with epilepsy after a high-protein meal. ( Baraldo, M; Benetello, P; Fortunato, M; Furlanut, M; Pea, F; Testa, G; Tognon, A, 1997)
"The effect of gabapentin on cognition and quality of life (QoL) in patients with epilepsy was investigated using a controlled pre- and post-treatment design."	5.08	Effects of gabapentin on cognition and quality of life in patients with epilepsy. ( Emmers, E; Mortimore, C; Trimble, M, 1998)
"The short- and long-term clinical efficacy of add-on vigabatrin treatment was evaluated in a group of 36 patients with intellectual disability and drug-refractory epilepsy."	5.08	Antiepileptic efficacy of vigabatrin in people with severe epilepsy and intellectual disability. ( Ylinen, A, 1998)
"Progabide, an experimental GABA-ergic antiepileptic drug, was given in a placebo-controlled double-blind cross-over trial to 19 adult patients with chronic partial epilepsy refractory to previous high-dose antiepileptic drug therapy."	5.06	Progabide for refractory partial epilepsy: a controlled add-on trial. ( Schmidt, D; Utech, K, 1986)
"Data from the MEDLINE database were searched using algorithms to identify relevant economic evaluations published in English or Spanish on pregabalin for the management of neuropathic pain, generalized anxiety disorder (GAD), and epilepsy in Spanish patients over the last 10 years."	4.90	Pharmacoeconomic outcomes for pregabalin: a systematic review in neuropathic pain, generalized anxiety disorder, and epilepsy from a Spanish perspective. ( Álvarez, E; Darbà, J; Kaskens, L; Navarro-Artieda, R; Pérez, C; Sicras-Mainar, A, 2014)
"The majority of published evidence supports the possibility that pregabalin could be a cost-effective and/or cost-saving alternative for the treatment of refractory epilepsy, GAD, and neuropathic pain, in both treatment-naïve patients and in those who have demonstrated inadequate response or intolerance to previous therapy."	4.90	Pharmacoeconomic outcomes for pregabalin: a systematic review in neuropathic pain, generalized anxiety disorder, and epilepsy from a Spanish perspective. ( Álvarez, E; Darbà, J; Kaskens, L; Navarro-Artieda, R; Pérez, C; Sicras-Mainar, A, 2014)
"The higher intrinsic potency of pregabalin compared to gabapentin is associated with an increased antiepileptic efficacy both in animal models of epilepsy and in clinical applications."	4.89	Pharmacokinetic and pharmacodynamic profile of pregabalin and its role in the treatment of epilepsy. ( Schulze-Bonhage, A, 2013)
" Adenosine has inhibitory effect and play important role in epilepsy."	4.88	[Angiotensins as neuromodulators]. ( Kowalski, A; Kuśmirowska, K; Rebas, E, 2012)
"A systematic review of FORCTs and randomised controlled trials (RCT) of topiramate, levetiracetam and gabapentin as adjuvant therapy in refractory adult epilepsy was conducted."	4.84	Reporting and analysis of open-label extension studies of anti-epileptic drugs. ( Hemming, K; Hutton, JL; Maguire, MJ; Marson, AG, 2008)
" The USA guideline for epilepsy treatment recommends that patients with newly diagnosed epilepsy can be treated with gabapentin, lamotrigine, topiramate, and oxcarbazepine."	4.84	[Newer antiepileptic drugs]. ( Matsuura, M, 2007)
" Controlled trials in elderly patients with epilepsy demonstrate efficacy and tolerability comparable to gabapentin."	4.84	Lamotrigine therapy in elderly patients with epilepsy, bipolar disorder or dementia. ( Nanry, K; Ramsay, E; Sajatovic, M; Thompson, T, 2007)
"Reports of lamotrigine therapy in elderly patients with epilepsy, bipolar disorder (BD), or dementia were identified by conducting an electronic search of major publication databases."	4.84	Lamotrigine therapy in elderly patients with epilepsy, bipolar disorder or dementia. ( Nanry, K; Ramsay, E; Sajatovic, M; Thompson, T, 2007)
"Review of the available literature suggests lamotrigine is effective and well tolerated in elderly patients with epilepsy and relatively well-tolerated and may be effective in delaying mood relapse, particularly in the depressive pole, in patients with BD."	4.84	Lamotrigine therapy in elderly patients with epilepsy, bipolar disorder or dementia. ( Nanry, K; Ramsay, E; Sajatovic, M; Thompson, T, 2007)
" Finally, we consider the link between alpha2delta subunits and disease, both in terms of spontaneous and engineered mouse mutants that show cerebellar ataxia and spike-wave epilepsy, and in terms of neuropathic pain and the mechanism of action of the gabapentinoid drugs - small-molecule ligands of the alpha2delta-1 and alpha2delta-2 subunits."	4.84	Functional biology of the alpha(2)delta subunits of voltage-gated calcium channels. ( Davies, A; Dolphin, AC; Douglas, L; Hendrich, J; Van Minh, AT; Wratten, J, 2007)
" However, a MEDLINE search using the search terms gabapentin and epilepsy, spanning back to the year 1986, produced numerous published reports from randomized, placebo-controlled and open-label trials, as well as case reports."	4.82	Gabapentin dosing in the treatment of epilepsy. ( Gidal, BE; McLean, MJ, 2003)
"The known clinical disorders of GABA metabolism are pyridoxine dependent epilepsy, GABA-transaminase deficiency, SSADH deficiency, and homocarnosinosis."	4.82	Clinical aspects of the disorders of GABA metabolism in children. ( Gibson, KM; Pearl, PL, 2004)
" Pyridoxine dependent epilepsy is a treatable condition with a potentially widening clinical spectrum, but with a prognosis dependent on early intervention."	4.82	Clinical aspects of the disorders of GABA metabolism in children. ( Gibson, KM; Pearl, PL, 2004)
"The efficacy and safety of pregabalin as adjunctive therapy for patients with partial epilepsy with or without secondary generalization has been established by four randomized, 12-week, double-blind, placebo-controlled trials (n = 1396) and four long-term open-label studies (n = 1480)."	4.82	Defining success in clinical trials--profiling pregabalin, the newest AED. ( Ryvlin, P, 2005)
"To review pregabalin's pharmacology, pharmacokinetics, efficacy, and adverse effects in the treatment of neuropathic pain, epilepsy, and anxiety."	4.82	Pregabalin: a new neuromodulator with broad therapeutic indications. ( McAuley, JW; Shneker, BF, 2005)
" Key terms were anxiety, diabetic neuropathy, epilepsy, neuropathic pain, postherpetic neuralgia, pregabalin, and seizures."	4.82	Pregabalin: a new neuromodulator with broad therapeutic indications. ( McAuley, JW; Shneker, BF, 2005)
"Genetic disorders of gamma-aminobutyric acid (GABA), glycine, and serine metabolism and of the GABA and glycine receptors are causes of epilepsy with variable responsiveness to treatment."	4.81	Genetic disorders of gamma-aminobutyric acid, glycine, and serine as causes of epilepsy. ( Jaeken, J, 2002)
"The introduction of these new antiepileptic drugs, from felbamate to levetiracetam, raised hope of control of epilepsy with fewer adverse effects and improved quality of life."	4.81	New antiepileptic drug therapies. ( Bergin, AM; Connolly, M, 2002)
", gamma-aminobutyric acid (GABA) and glycine as the main inhibitory neurotransmitters in the brain play a crucial role in some forms of epilepsy."	4.81	The inhibitory neural circuitry as target of antiepileptic drugs. ( Böhme, I; Lüddens, H, 2001)
"To provide a qualitative, systematic update and review of the pharmacology, pharmacokinetics, efficacy in mood disorders, adverse effects, and costs of lamotrigine."	4.81	Lamotrigine update and its use in mood disorders. ( Hurley, SC, 2002)
"Gabapentin (GBP) is a antiepileptic drug (AED) indicated as adjunct therapy for treatment of partial seizures, with and without secondary generalization, in patients 12 and older with epilepsy."	4.80	Gabapentin. ( Morris, GL, 1999)
"Vigabatrin is undoubtedly one of the most exciting anti-epilepsy drugs in use today."	4.79	Vigabatrin: effect on brain GABA levels measured by nuclear magnetic resonance spectroscopy. ( Behar, K; Mattson, RH; Petroff, OA; Rothman, D, 1995)
"Vigabatrin is among the most promising of the new anti-epilepsy drugs, but two unrelated complications have been noted in patients receiving vigabatrin for chronic refractory epilepsy."	4.79	Behavioural abnormalities and retention rates of anti-epilepsy drugs during long-term treatment of epilepsy: a clinical perspective. ( Schmidt, D, 1995)
" More specifically, vigabatrin, which is a very useful and well tolerated new antiepileptic drug for refractory partial epilepsy, should be started at a low dosage of 0."	4.79	The new anticonvulsant drugs. Implications for avoidance of adverse effects. ( Krämer, G; Schmidt, D, 1994)
"A 7-year-old boy with intractable epilepsy developed acute psychosis 3 days after initiating a rapid vigabatrin dosage escalation."	4.79	Vigabatrin-associated reversible acute psychosis in a child. ( Beltrán Marqués, M; Cánovas Martínez, A; Delgado Cordón, F; Escrivá Aparisi, A; Ordovás Baines, JP, 1995)
"To evaluate the efficacy and tolerability of the newly developed antiepileptic drugs gabapentin, lamotrigine, tiagabine, topiramate, vigabatrin, and zonisamide in patients with refractory partial epilepsy."	4.79	New antiepileptic drugs: a systematic review of their efficacy and tolerability. ( Chadwick, DW; Kadir, ZA; Marson, AG, 1996)
"Gabapentin, lamotrigine, tiagabine, topiramate, vigabatrin, and zonisamide are all administered as add-on therapy for treatment of patients with refractory epilepsy."	4.79	Clinical administration of new antiepileptic drugs: an overview of safety and efficacy. ( Chadwick, DW; Kadir, Z; Marson, T, 1996)
"Since 1994, three new antiepileptic drugs, felbamate, lamotrigene, and gabapentin, have been released for the treatment of epilepsy."	4.79	A review of the newer antiepileptic drugs and the ketogenic diet. ( Barron, TF; Hunt, SL, 1997)
"Gabapentin (GBP), lamotrigine (LTG), tiagabine (TGB), topiramate (TPM), vigabatrin (VGB), and zonisamide (ZNS) are all in use as "add-on" treatment for patients with refractory epilepsy."	4.79	The new antiepileptic drugs: a systematic review of their efficacy and tolerability. ( Chadwick, DW; Hutton, JL; Kadir, ZA; Marson, AG, 1997)
" Felbamate (FBM) is effective in the treatment of partial seizures and Lennox-Gastaut epilepsy."	4.78	Advances in the pharmacotherapy of epilepsy. ( Ramsay, RE, 1993)
"Because of its abundance in the brain, its ability to produce hyperpolarizing inhibition of almost all neurons, its association with benzodiazepines, and the discovery that many convulsants inhibited its synthesis, gamma-aminobutyric acid (GABA) has often appeared to be the key to epilepsy."	4.78	GABA and epilepsy: their complex relationship and the evolution of our understanding. ( Snodgrass, SR, 1992)
"The substantia nigra has been identified as a critical site at which gamma-aminobutyric acid (GABA) agonist drugs act to reduce susceptibility to a number of types of experimentally induced generalized seizures."	4.77	Mechanisms of seizure control mediated by gamma-aminobutyric acid: role of the substantia nigra. ( Gale, K, 1985)
" Hence, the methanol extract was further explored for its anticonvulsant potential in pentylenetetrazole (PTZ) induced acute seizures in mice."	4.31	Anticonvulsant potential of Grewia tiliaefolia in pentylenetetrazole induced epilepsy: insights from in vivo and in silico studies. ( Arora, S; Kaur, S; Kumar, N; Rajput, A; Sharma, P; Singh Bedi, PM; Singh, B; Singh, H; Singh, S; Singh, T, 2023)
"Rats with hHCy developed more severe stages of behavioral patterns during flurothyl-induced epilepsy with shorter latency."	4.31	Maternal hyperhomocysteinemia increases seizures susceptibility of neonatal rats. ( Gataulina, E; Gerasimova, E; Khalilov, I; Kurmashova, E; Sitdikova, GF; Yakovlev, AV, 2023)
"Rare inherited missense variants in SLC32A1, the gene that encodes the vesicular gamma-aminobutyric acid (GABA) transporter, have recently been shown to cause genetic epilepsy with febrile seizures plus."	4.12	De Novo Missense Variants in SLC32A1 Cause a Developmental and Epileptic Encephalopathy Due to Impaired GABAergic Neurotransmission. ( Abou Jamra, R; Bilan, F; Brose, N; Bupp, C; Ganapathi, M; Henderson, LB; Le Guyader, G; Lemke, JR; Pereira, EM; Platzer, K; Sticht, H; Taschenberger, H; Wojcik, SM, 2022)
" OV329, a novel drug candidate for the treatment of epilepsy and addiction, has been shown in vitro to be substantially more potent as a GABA-AT inactivator than vigabatrin, an antiseizure drug approved as an add-on therapy for adult patients with refractory complex partial seizures and monotherapy for pediatric patients with infantile spasms."	4.02	OV329, a novel highly potent γ-aminobutyric acid aminotransferase inactivator, induces pronounced anticonvulsant effects in the pentylenetetrazole seizure threshold test and in amygdala-kindled rats. ( Deking, LS; During, MJ; Feja, M; Gernert, M; Kaczmarek, E; Meller, S; Silverman, RB, 2021)
"These results reveal an anticonvulsant profile of OV329 that appears to be superior in both potency and efficacy to vigabatrin and highlight OV329 as a highly promising candidate for the treatment of seizures and pharmacoresistant epilepsies."	4.02	OV329, a novel highly potent γ-aminobutyric acid aminotransferase inactivator, induces pronounced anticonvulsant effects in the pentylenetetrazole seizure threshold test and in amygdala-kindled rats. ( Deking, LS; During, MJ; Feja, M; Gernert, M; Kaczmarek, E; Meller, S; Silverman, RB, 2021)
"We therefore examined the effects of OV329 (5, 20, and 40 mg/kg ip) on the seizure threshold of female Wistar Unilever rats, using the timed intravenous pentylenetetrazole (ivPTZ) seizure threshold model as a seizure test particularly sensitive to GABA-potentiating manipulations, and amygdala-kindled rats as a model of difficult-to-treat temporal lobe epilepsy."	4.02	OV329, a novel highly potent γ-aminobutyric acid aminotransferase inactivator, induces pronounced anticonvulsant effects in the pentylenetetrazole seizure threshold test and in amygdala-kindled rats. ( Deking, LS; During, MJ; Feja, M; Gernert, M; Kaczmarek, E; Meller, S; Silverman, RB, 2021)
" He had been administered phenytoin and gabapentin for the treatment of symptomatic traumatic epilepsy 8 years before."	3.88	Hypothyroidism induced by phenytoin and gabapentin: A Case Report. ( Ishii, K; Miyake, Z; Tamaoka, A, 2018)
"To characterize and quantify the variability of serial gabapentin concentrations in elderly patients with epilepsy."	3.85	Factors in Variability of Serial Gabapentin Concentrations in Elderly Patients with Epilepsy. ( Birnbaum, AK; Collins, JF; Conway, JM; Eberly, LE; Leppik, IE; Macias, FM; Ramsay, RE, 2017)
"Substantial intrapatient variability in serial gabapentin concentration was noted in elderly patients with epilepsy."	3.85	Factors in Variability of Serial Gabapentin Concentrations in Elderly Patients with Epilepsy. ( Birnbaum, AK; Collins, JF; Conway, JM; Eberly, LE; Leppik, IE; Macias, FM; Ramsay, RE, 2017)
"Transplantation of progenitor cells from embryonic medial or caudal ganglionic eminence (MGE, CGE) were made in a well-characterized mouse model of status epilepticus-induced epilepsy (systemic pilocarpine)."	3.85	Persistent seizure control in epileptic mice transplanted with gamma-aminobutyric acid progenitors. ( Baraban, SC; Casalia, ML; Howard, MA, 2017)
"Pregabalin (PGB) is extensively prescribed to treat neurological and neuropsychiatrical conditions such as neuropathic pain, anxiety disorders, and epilepsy."	3.85	Chronic pregabalin treatment decreases excitability of dentate gyrus and accelerates maturation of adult-born granule cells. ( Coll, L; Lempel, AA; Piriz, J; Schinder, AF; Uchitel, OD, 2017)
" Here, we report changes in the concentrations of the neurotransmitters glutamate (Glu) and gamma-aminobutyric acid (GABA) in the HIPP and the AMG of patients with nonlesional temporal lobe epilepsy undergoing surgery for intracranial subdural and depth electrode implantation."	3.83	In vivo measurements of limbic glutamate and GABA concentrations in epileptic patients during affective and cognitive tasks: A microdialysis study. ( Buchanan, RJ; Gjini, K; Meier, KT; Modur, P; Nadasdy, Z; Robinson, JL, 2016)
"We compared persistence of antiepileptic drugs (AEDs) including carbamazepine, oxcarbazepine, gabapentin, lamotrigine, topiramate, valproic acid, and phenytoin in an Asian population with epilepsy."	3.83	Comparative persistence of antiepileptic drugs in patients with epilepsy: A STROBE-compliant retrospective cohort study. ( Hsieh, CY; Huang, CW; Lai, EC; Lin, SJ; Setoguchi, S; Su, CC; Yang, YK, 2016)
"Gabapentin and pregabalin are antiepileptic drugs (AEDs) with epilepsy and neuropathic pain indications."	3.81	Experience from therapeutic drug monitoring and gender aspects of gabapentin and pregabalin in clinical practice. ( Baftiu, A; Beiske, G; Burns, ML; Johannessen Landmark, C; Johannessen, SI, 2015)
"Anonymous data from routine TDM-service at the National Center for Epilepsy regarding serum concentration measurements of gabapentin and pregabalin, 2009-2013, were utilised."	3.81	Experience from therapeutic drug monitoring and gender aspects of gabapentin and pregabalin in clinical practice. ( Baftiu, A; Beiske, G; Burns, ML; Johannessen Landmark, C; Johannessen, SI, 2015)
"Gabapentin and pregabalin are more used in women than in men, and routine use of TDM is most common in patients with epilepsy."	3.81	Experience from therapeutic drug monitoring and gender aspects of gabapentin and pregabalin in clinical practice. ( Baftiu, A; Beiske, G; Burns, ML; Johannessen Landmark, C; Johannessen, SI, 2015)
" The maximal electroshock test (MES) and pentylenetertrazole (PTZ)-induced seizures in male mice were used to evaluate anticonvulsant activities of eudesmin, and sedative effects of eudesmin were evaluated by pentobarbital sodium-induced sleeping time (PST) and locomotor activity in mice."	3.81	Anticonvulsant and Sedative Effects of Eudesmin isolated from Acorus tatarinowii on mice and rats. ( He, J; Lei, JP; Liao, DG; Liu, F; Liu, H; Luo, K; Song, Z; Yang, L; Zhang, TY; Zhuang, K, 2015)
"Pregabalin was mainly used as a second-line drug for the treatment of GAD or neuropathic pain and to a lesser extent as add-on therapy in epilepsy."	3.80	Pregabalin is increasingly prescribed for neuropathic pain, generalised anxiety disorder and epilepsy but many patients discontinue treatment. ( Bodén, R; Brandt, L; Kieler, H; Wettermark, B, 2014)
"These data indicate that MSCs were superior to gabapentin in ameliorating PTZ-induced epileptogenesis and verified the potential use of MSCs in seizure control, motor and cognitive impairments, oxidative stress, and the impairing GABA level in experimentally induced epilepsy."	3.80	Effects of intravenous human umbilical cord blood mesenchymal stem cell therapy versus gabapentin in pentylenetetrazole-induced chronic epilepsy in rats. ( Essawy, SS; Ewais, MM; Mohammed, AS; Tawfik, MK, 2014)
"To analyze the survival and the changes of proportions of Calbindin, Calretinin and Parvalbumin positive neurons in mouse hippocampal CA area at chronic stage of Pilocarpine-induced epilepsy."	3.79	[Survival of calbindin, calretinin and parvalbumin positive neurons in mouse hippocampal CA area at chronic stage of pilocarpine-induced epilepsy]. ( Liu, J; Liu, Y; Tang, F, 2013)
"Calbindin, Calretinin and Parvalbumin immunofluoresence staining were done 2 months after Pilocarpine-induced epilepsy in mice or saline injection."	3.79	[Survival of calbindin, calretinin and parvalbumin positive neurons in mouse hippocampal CA area at chronic stage of pilocarpine-induced epilepsy]. ( Liu, J; Liu, Y; Tang, F, 2013)
"The changes of proportions of Calbindin, Calretinin and Parvalbumin positive neurons in the CA area of mouse hippocampus may be a factor in the ongoing epileptic activity at chronic stage of Pilocarpine-induced epilepsy."	3.79	[Survival of calbindin, calretinin and parvalbumin positive neurons in mouse hippocampal CA area at chronic stage of pilocarpine-induced epilepsy]. ( Liu, J; Liu, Y; Tang, F, 2013)
" NKCC1 or KCC2 expression changes have been demonstrated previously in the hippocampal neurons of mice with pilocarpine-induced status epilepticus (PISE)."	3.79	STE20/SPS1-related proline/alanine-rich kinase is involved in plasticity of GABA signaling function in a mouse model of acquired epilepsy. ( Cai, X; Chen, S; Chen, Y; Chen, Z; Fang, Z; Wang, Q; Yang, L; Zhou, J; Zhou, L, 2013)
"An open pilot study to evaluate the effect of pregabalin (PGB) as add-on therapy on seizure control, quality of life, and anxiety in patients with brain tumour-related epilepsy (BTRE)."	3.78	Effect of pregabalin add-on treatment on seizure control, quality of life, and anxiety in patients with brain tumour-related epilepsy: a pilot study. ( Carapella, CM; Dinapoli, L; Fabi, A; Maschio, M; Pace, A; Pompili, A; Sperati, F; Vidiri, A, 2012)
"Epileptiform discharges recorded in the 4-aminopyridine (4-AP) in vitro epilepsy model are mediated by glutamatergic and GABAergic signaling."	3.77	The 4-aminopyridine in vitro epilepsy model analyzed with a perforated multi-electrode array. ( Avoli, M; Dzakpasu, R; Gonzalez-Sulser, A; Motamedi, GK; Vicini, S; Wang, J, 2011)
" We have addressed this issue in the 4-aminopyridine model of epilepsy in vitro by comparing GABAergic epileptiform currents and their sensitivity to gap junction blockers in wild-type vs."	3.77	Is connexin36 critical for GABAergic hypersynchronization in the hippocampus? ( Beaumont, M; Maccaferri, G, 2011)
"To observe the dynamics of hippocampal release of glutamate (Glu) and gamma-aminobutyric acid (GABA) in epilepsy (TLE) after administration with high frequency stimulation (HFS)."	3.77	[The effect of high frequency stimulation of epileptic foci on the release of glutamate and gamma-aminobutyric acid in hippocampus of the kainic acid-kindled rats]. ( Chen, SG; Huang, HP; Lin, MX; Lin, WH, 2011)
"This study aims to determine the expression of Gamma-aminobutyric acid (GABA) following hypoxia in neonatal rats and explore how it may increase susceptibility to epilepsy later in life."	3.77	Downregulation of hippocampal GABA after hypoxia-induced seizures in neonatal rats. ( Li, K; Sun, W; Wang, Y; Xu, E; Xu, ZC; Zeng, W; Zhan, L, 2011)
"Vigabatrin was specifically designed to enhance gamma-aminobutyric acid (GABA) function in the CNS."	3.77	Vigabatrin. A review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in epilepsy and disorders of motor control. ( Grant, SM; Heel, RC, 1991)
"The incidence of constipation as an adverse effect of pregabalin has previously been reported as low, with all cases described as either mild or moderate."	3.76	Severe and disabling constipation: an adverse effect of pregabalin. ( Cook, MJ; D'Souza, WJ; Kamel, JT, 2010)
" The present study optimized the method to induce differentiation of gamma-aminobutyric acid-producing neurons (GABAergic neurons) from ES cell-derived neural stem/progenitor cells (NS/PCs), and transplanted these ES cell-derived GABAergic neurons producing neural progenitors into kindled epileptic mice, and analyzed the morphological and functional recovery from epilepsy."	3.76	Seizure suppression in amygdala-kindled mice by transplantation of neural stem/progenitor cells derived from mouse embryonic stem cells. ( Itano, T; Kawai, N; Matsumoto, Y; Nagao, S; Nakamura, T; Okano, H; Shindo, A; Tamiya, T, 2010)
" We have previously shown that postnatal administration of low doses of domoic acid (DOM) can produce many of the behavioral and morphological changes found in current animal models of temporal lobe epilepsy (TLE), as well as the human condition."	3.76	Selective reductions in subpopulations of GABAergic neurons in a developmental rat model of epilepsy. ( Gill, DA; Ramsay, SL; Tasker, RA, 2010)
"In this study of older adults with epilepsy, lamotrigine was the most effective AED as measured by 12-month retention and seizure freedom, with levetiracetam a close second."	3.76	Comparative effectiveness of 10 antiepileptic drugs in older adults with epilepsy. ( Arif, H; Bazil, CW; Buchsbaum, R; Hirsch, LJ; Pierro, J; Resor, SR; Sims, J; Whalen, M, 2010)
"Our study suggests that there are clinically significant differences among gabapentin, lamotrigine, levetiracetam, tiagabine, and topiramate as treatment for focal epilepsy in everyday practice."	3.75	Retention rates of new antiepileptic drugs in localization-related epilepsy: a single-center study. ( Auvinen, A; Fallah, M; Keränen, T; Peltola, J; Peltola, M; Raitanen, J, 2009)
"An 8-year-old boy with a neurodegenerative disease of unknown origin and an epilepsy disorder developed an urticarial rash and irritability 10 and 4 days, respectively, after the start of gabapentin 20 mg/kg 3 times a day for epilepsy control."	3.75	Probability of rash related to gabapentin therapy in a child. ( de Wildt, SN; Gijsen, VM; Ito, S, 2009)
"The purpose of this study was to estimate the gamma-aminobutyric acid (GABA) and glutamate plus glutamine (Glx) concentrations in the cortical tubers of patients with tuberous sclerosis complex (TSC) using the MEGA-editing J-difference method and a stimulated echo-acquisition mode with a short echo time, and to determine which abnormality was more dominant between GABA and Glx in patients with TSC with epilepsy."	3.75	High gamma-aminobutyric acid level in cortical tubers in epileptic infants with tuberous sclerosis complex measured with the MEGA-editing J-difference method and a three-Tesla clinical MRI Instrument. ( Harada, M; Kubo, H; Matsuda, T; Mori, K; Nishitani, H; Nose, A; Taki, MM, 2009)
"Pregabalin (PGB) is a newer antiepileptic drug (AED) licensed as add-on treatment for partial epilepsy in adults."	3.75	Retention rate of pregabalin in drug-resistant epilepsy: 1-year follow-up, single-centre observation in 105 consecutive, adult patients. ( Brandt, C; Ebner, A; Elsner, H; May, TW; Nieder, E; Pohlmann-Eden, B; Schuermann, I; Witte-Boelt, K, 2009)
"In a retrospective evaluation of 32 inpatients with therapy-resistant epilepsy and intellectual disability, the efficacy of pregabalin (PGB) treatment was assessed after 6 and 12 months."	3.74	Efficacy and tolerability of pregabalin in patients with difficult-to-treat epilepsy and intellectual disability. ( Bocchicchio, M; Feuerbaum, E; Huber, B; May, T; Meinert, T; Robertson, E; Schorlemmer, H; Seidel, M; Wagner, W; Wilking, E, 2008)
"We investigated efficacy of prolonged intraventricular gabapentin (GBP) infusion in the rat flurothyl epilepsy model."	3.74	Intraventricular administration of gabapentin in the rat increases flurothyl seizure threshold. ( Fisher, RS; Kraus, AC; Oommen, J, 2007)
" After 5 days of GBP infusion, seizures were induced by flurothyl dripped onto filter paper."	3.74	Intraventricular administration of gabapentin in the rat increases flurothyl seizure threshold. ( Fisher, RS; Kraus, AC; Oommen, J, 2007)
"GBP instilled into the lateral ventricles by pump for 5 days delays onset of generalized tonic-clonic seizures produced by flurothyl in the rat."	3.74	Intraventricular administration of gabapentin in the rat increases flurothyl seizure threshold. ( Fisher, RS; Kraus, AC; Oommen, J, 2007)
"To use proton magnetic resonance spectroscopy (MRS) to measure concentrations of gamma-aminobutyric acid (GABA) and glutamate plus glutamine (GLX) in adult patients with refractory epilepsy associated with malformations of cortical development (MCD)."	3.74	Proton magnetic resonance spectroscopy of malformations of cortical development causing epilepsy. ( Barker, GJ; Duncan, JS; McLean, MA; Simister, RJ, 2007)
"To explore the mechanism of epilepsy induced by IL-1beta and IL-6, the changes of glutamic acid (Glu) and GABA immunoreaction in the cerebral cortex and hippocampus of rats with seizure induced by IL-1beta or IL-6 were studied."	3.73	Changes in behavior and amino acid neurotransmitters in the brain of rats with seizure induced by IL-1beta or IL-6. ( Changgeng, Z; Li, L; Xiaojing, W; Xiaoqin, Z; Zhengli, L, 2005)
"To assess whether there is a change in seizure activity in dogs with refractory epilepsy that are receiving appropriate doses of phenobarbitone and/or potassium bromide, when gabapentin is added to the therapeutic regimen."	3.73	Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent. ( Govendir, M; Malik, R; Perkins, M, 2005)
"Thirty patients were enrolled: 10 on gabapentin, 10 on lamotrigine and 10 on carbamazepine monotherapy for epilepsy."	3.73	Measuring the effects of antiepileptic medications on balance in older people. ( Blum, D; Fife, TD; Fisher, RS, 2006)
" Although the sample size is small, this study suggests that lamotrigine may induce less disequilibrium than does carbamazepine in older people on monotherapy for epilepsy."	3.73	Measuring the effects of antiepileptic medications on balance in older people. ( Blum, D; Fife, TD; Fisher, RS, 2006)
"A mechanism for the alleviation of the malfunction of a mutated (gamma2(K289M)) epilepsy-linked gamma-aminobutyric acid (GABA) neurotransmitter receptor by phenobarbital is presented."	3.73	On the mechanism of alleviation by phenobarbital of the malfunction of an epilepsy-linked GABA(A) receptor. ( Hess, GP; Krivoshein, AV, 2006)
"We report two patients with refractory epilepsy who developed unilateral painful gynecomastia and lower extremity pain (one of them localized and the other one diffuse), shortly after receiving Pregabalin (PGB)."	3.73	Two cases of painful gynecomastia and lower extremity pain in association with pregabalin therapy. ( Málaga, I; Sanmarti, FX, 2006)
" Mice which underwent 10 s but not 5 s seizures episode subsequently exhibited significantly increased seizure susceptibility to low doses (equal ED(16)) of bicuculline (BCC) and NMDA during a 3-week observation period."	3.72	The epileptogenic effect of seizures induced by hypoxia: the role of NMDA and AMPA/KA antagonists. ( Rubaj, A; Sieklucka-Dziuba, M; Zgodziński, W, 2003)
"The objective of this study was to assess the safety of gabapentin (Neurontin) exposure in human pregnancy."	3.72	Gabapentin exposure in human pregnancy: results from the Gabapentin Pregnancy Registry. ( Montouris, G, 2003)
") showing that activation of the cannabinoid receptor CB1 by the endocannabinoid anandamide protects against excitotoxic damage in a mouse model of kainic acid-induced epilepsy."	3.72	Neuroscience. Stout guards of the central nervous system. ( Lichtman, AH; Mechoulam, R, 2003)
" Hence, the standard of care for older patients with epilepsy should be reevaluated, although the vast use of phenytoin in this population suggests that change in practice patterns may be difficult."	3.72	Potentially inappropriate antiepileptic drugs for elderly patients with epilepsy. ( Berlowitz, D; Charbonneau, A; Cramer, J; Kazis, L; Knoefel, J; Mandell, A; Pugh, MJ, 2004)
"Gabapentin (1-(aminomethyl)cyclohexane acetic acid, CAS 601 42-96-3, GBP, Neurontin) and its derivative gabapentin-lactam (8-aza-spiro[5,4]decan-9-one, GBP-L) were determined by HPLC in the serum of patients with focal epilepsy treated with GBP."	3.72	Determination of gabapentin-lactam in serum of patients under gabapentin therapy. ( Feuerstein, TJ; Knörle, R; Schulze-Bonhage, A, 2004)
" Chronic seizures were induced by amygdalar injection of kainic acid 60 days before death."	3.71	Collapse of extracellular glutamate regulation during epileptogenesis: down-regulation and functional failure of glutamate transporter function in rats with chronic seizures induced by kainic acid. ( Doi, T; Kamada, H; Mitsuyama, Y; Nakajima, A; Ohya-Nishiguchi, H; Tokumaru, J; Ueda, Y; Willmore, LJ; Yokoyama, H, 2001)
"This postmarketing surveillance study of lamotrigine (LTG) was performed to provide complementary data to large-scale Prescription-Event Monitoring study with a retrospective case records survey in five tertiary referral epilepsy centres in the United Kingdom."	3.71	Adverse event monitoring in lamotrigine patients: a pharmacoepidemiologic study in the United Kingdom. ( Mawer, GE; Sander, JW; Wong, IC, 2001)
"Vigabatrin (VGB) treatment is neuroprotective in various models of status epilepticus (SE) and delays the development of kindling via mechanisms that are assumed to relate to the elevation of GABA levels in the brain."	3.71	Chronic elevation of brain GABA levels beginning two days after status epilepticus does not prevent epileptogenesis in rats. ( Halonen, T; Nissinen, J; Pitkänen, A, 2001)
" To test whether GABA transport is compromised in both the forward (uptake) and reverse (heterotransport) direction in the sclerotic epileptic dentate gyrus, the physiological effects of microapplied GABA and nipecotic acid (NPA; a compound that induces heterotransport) were examined in granule cells in hippocampal slices from kainate (KA)-induced epileptic rats and patients with temporal lobe epilepsy (TLE)."	3.71	GABA uptake and heterotransport are impaired in the dentate gyrus of epileptic rats and humans with temporal lobe sclerosis. ( Patrylo, PR; Spencer, DD; Williamson, A, 2001)
"Vigabatrin use in some epilepsy patients has been associated with persistent visual field constriction and retinal dysfunction."	3.71	GABA and the ornithine delta-aminotransferase gene in vigabatrin-associated visual field defects. ( Felice, K; Hisama, FM; Lee, HH; Mattson, RH; Petroff, OA, 2001)
" In the last decade, pregnancy registries have been activated by collaborative groups of physicians in Europe (EURAP), North America (NAREP), Australia and India (the latter two recently merged into EURAP), to enroll a large number of exposed women to be monitored prospectively with standardized methods, and by three pharmaceutical companies marketing lamotrigine, gabapentin and vigabatrin, as part of their post-marketing surveillance."	3.71	Pregnancy registries in epilepsy. ( Annegers, JF; Beghi, E, 2001)
"Pyridoxine-dependent epilepsy is a disease inherited as an autosomal recessive trait, characterized by rapid response to pharmacological dosages of pyridoxine."	3.70	Mutation and polymorphic marker analyses of 65K- and 67K-glutamate decarboxylase genes in two families with pyridoxine-dependent epilepsy. ( Hoshino, H; Kure, S; Matsubara, Y; Miyabayashi, S; Narisawa, K; Sakata, Y; Shinka, T; Takahashi, K, 1998)
" Gabapentin is a new antiepileptic drug not appreciably metabolized by the liver in humans, and it appears to be safe and effective in the maintenance therapy of epilepsy in these patients."	3.70	Treatment of seizures in acute intermittent porphyria: safety and efficacy of gabapentin. ( Brambilla, A; Erli, LC; Grandi, R; Mirabile, D; Zadra, M, 1998)
"New antiepileptic drugs designed for enhancing GABAergic inhibition, such as vigabatrin (VGB) may be effective in Angelman syndrome (AS), because associated convulsions could be related to a reduced GABA-receptor density or receptor abnormality."	3.70	Adverse effects of vigabatrin in Angelman syndrome. ( Boltshauser, E; Kuenzle, C; Schmitt, B; Steinlin, M; Wohlrab, G, 1998)
"To measure the effects of topiramate on brain gamma-aminobutyric acid (GABA) in patients with epilepsy."	3.70	Topiramate increases brain GABA, homocarnosine, and pyrrolidinone in patients with epilepsy. ( Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 1999)
"This report describes the long-term follow-up of 56 patients with refractory partial epilepsy who, within 3 months of vigabatrin add-on therapy (3 g/day), showed a reduction in monthly seizure frequency of more than 50%."	3.70	Long-term treatment with vigabatrin - 10 years of clinical experience. ( Mumford, JP; Riekkinen, PJ; Salmenperä, T; Ylinen, A, 1999)
"To compare the long-term retention of gabapentin (GBP), lamotrigine (LTG), and vigabatrin (VGB) by patients with chronic epilepsy and the reasons for treatment discontinuation."	3.70	The long-term use of gabapentin, lamotrigine, and vigabatrin in patients with chronic epilepsy. ( Chadwick, DW; Fenwick, PB; Mawer, GE; Sander, JW; Wong, IC, 1999)
"To report on the occurrence of myoclonus in patients receiving gabapentin (GBP) for the treatment of epilepsy."	3.70	Myoclonus associated with the use of gabapentin. ( Asconapé, J; DellaBadia, J; Diedrich, A, 2000)
" We reported that daily dosing increased brain gamma-aminobutyric acid (GABA) in patients with epilepsy."	3.70	Effects of gabapentin on brain GABA, homocarnosine, and pyrrolidinone in epilepsy patients. ( Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 2000)
"The purpose of the present investigation was to determine whether the sensitivity to systemic toxic effects of cocaine is altered in genetically epilepsy-prone rats (GEPRs)."	3.70	Phenotypic expression of the systemic toxicity of cocaine in genetically epilepsy-prone rats. ( Heavner, JE; Kao, YJ; Kaye, AD; Reigel, CE; Shi, B, 2000)
"Infusion of the K(+) channel blocker 4-aminopyridine in the hippocampus induces the release of glutamate, as well as seizures and neurodegeneration."	3.70	Seizures and neurodegeneration induced by 4-aminopyridine in rat hippocampus in vivo: role of glutamate- and GABA-mediated neurotransmission and of ion channels. ( Peña, F; Tapia, R, 2000)
"We sought to determine the long-term retention rates of lamotrigine (LTG), gabapentin (GBP), and topiramate (TPM) therapy for patients at a tertiary referral clinic for chronic, refractory epilepsy."	3.70	Long-term retention rates of lamotrigine, gabapentin, and topiramate in chronic epilepsy. ( Lhatoo, SD; Polizzi, G; Sander, JW; Wong, IC, 2000)
"In the treatment of children with epilepsy, the role of topiramate has been expanding gradually."	3.70	Pharmacokinetics and pharmacodynamics of topiramate. ( Bourgeois, BF, 2000)
"One hundred and twenty-seven patients with uncontrolled epilepsy have been treated in an open add-on study with vigabatrin with a mean follow up of ten months."	3.69	Vigabatrin in unsatisfactory controlled epilepsies. Swiss Vigabatrin Study Group. ( Russ, W, 1995)
"Bursting activities were investigated under conditions of reduced outward K+ currents in neocortical slices obtained from rats presenting the gamma-aminobutyric acid (GABA)-withdrawal syndrome (GWS), a focal epilepsy consecutive to the interruption of a chronic intracortical GABA infusion into the somatomotor cortex."	3.69	A potassium current controls burst termination in rat neocortical neurons after GABA withdrawal. ( Champagnat, J; Silva-Barrat, C, 1995)
"Gabapentin represents a significant advance in the management of epilepsy."	3.69	Gabapentin (NEURONTIN)--a novel anticonvulsant. ( Murdoch, LA, 1994)
"Pyridoxine-dependent epilepsy is a rare autosomal recessive disorder."	3.69	Glutamate in pyridoxine-dependent epilepsy: neurotoxic glutamate concentration in the cerebrospinal fluid and its normalization by pyridoxine. ( Baumeister, FA; Egger, J; Gsell, W; Shin, YS, 1994)
"To assess the role of glutamate as an excitatory neurotransmitter and neurotoxin in pyridoxine-dependent epilepsy."	3.69	Glutamate in pyridoxine-dependent epilepsy: neurotoxic glutamate concentration in the cerebrospinal fluid and its normalization by pyridoxine. ( Baumeister, FA; Egger, J; Gsell, W; Shin, YS, 1994)
"The results indicate that control of epilepsy might not suffice as the therapeutic aim in treating of pyridoxine dependency."	3.69	Glutamate in pyridoxine-dependent epilepsy: neurotoxic glutamate concentration in the cerebrospinal fluid and its normalization by pyridoxine. ( Baumeister, FA; Egger, J; Gsell, W; Shin, YS, 1994)
"To determine the efficacy of a new anti-epileptic medication vigabatrin in adults and children with drug-resistant epilepsy."	3.69	Vigabatrin use in 72 patients with drug-resistant epilepsy. ( Buchanan, N, 1994)
"In an retrospective uncontrolled long-term study in 30 children with intractable epilepsy, it was found that treatment with vigabatrin resulted in a seizure reduction of more than 50% at 1-year follow-up in 40% of the children."	3.69	Vigabatrin in childhood epilepsy: a 5-year follow-up study. ( Alving, J; Gram, L; Høgenhaven, H; Uldall, P, 1995)
"We report two cases of unusual movement disorders associated with the use of gabapentin (GBP) in patients being treated for epilepsy who were otherwise neurologically intact."	3.69	Movement disorders associated with the use of gabapentin. ( Krahn, LE; Reeves, AL; Sharbrough, FW; So, EL, 1996)
"In order to identify lasting alterations in gamma-aminobutyric acid (GABA) neurons in the kindling model of epilepsy, immunocytochemical techniques were used to quantify the number of GABA-immunoreactive (IR) neurons in different regions of the hippocampal formation (HCF) of amygdala-kindled rats, 40 days after the last fully kindled seizure."	3.69	Immunocytochemical localization of GABA immunoreactivity in dentate granule cells of normal and kindled rats. ( Ebert, U; Lehmann, H; Löscher, W, 1996)
"The purpose of this study was to measure changes in brain GABA after a single oral dose (50 mg/kg) of vigabatrin in patients with intractable epilepsy."	3.69	Human brain GABA levels rise rapidly after initiation of vigabatrin therapy. ( Behar, KL; Collins, TL; Mattson, RH; Petroff, OA; Rothman, DL, 1996)
"We present the results of treatment with vigabatrin in the polytherapy of resistant infantile epilepsy."	3.69	[Treatment of refractory infantile epilepsy with vigabatrin in a series of 55 patients]. ( Hernández-Laín, A; López-Valdés, E; Mateos, F; Porta, J; Simón, R, 1996)
"In order to determine whether changes in synaptic inhibition are involved in chronic models of epilepsy, it is necessary to understand the factors which determine the kinetics of fast gamma-aminobutyric acid (GABA)ergic inhibition."	3.69	Analysis of the kinetics of synaptic inhibition points to a reduction in GABA release in area CA1 of the genetically epileptic mouse, El. ( Andreasen, M; Fueta, Y; Lambert, JD; Roepstorff, A, 1996)
"A case of a patient with medically intractable epilepsy, who developed obstructive sleep apnoea (OSA), and an increase in seizure frequency, as a consequence of weight gain following treatment with vigabatrin is described."	3.69	Obstructive sleep apnoea following rapid weight gain secondary to treatment with vigabatrin (Sabril). ( Bird, JM; Lambert, MV, 1997)
"To evaluate the relationship of gabapentin therapy with choreoathetotic movements in mentally retarded patients treated with intractable epilepsy."	3.69	Choreoathetosis as a side effect of gabapentin therapy in severely neurologically impaired patients. ( Chudnow, RS; Dewey, RB; Lawson, CR, 1997)
"We suggest that, in patients with mental retardation and epilepsy, involuntary movements may either occur as reversible side effects of gabapentin therapy or result from a previously undescribed adverse drug interaction with other antiepileptic agents."	3.69	Choreoathetosis as a side effect of gabapentin therapy in severely neurologically impaired patients. ( Chudnow, RS; Dewey, RB; Lawson, CR, 1997)
"The relationship between the ratio of vigabatrin concentration to dosage (VGB C/D) and both patient age and the presence of other antiepileptic drugs (AEDs) was analyzed retrospectively by bivariate and multivariate methods in 179 patients with epilepsy (114 children and 65 adults)."	3.69	Vigabatrin serum concentration to dosage ratio: influence of age and associated antiepileptic drugs. ( Armijo, JA; Arteaga, R; Bravo, J; Cuadrado, A, 1997)
"5 months of pregnancy then carbamazepine 400 mg LP x 2/day, raised to 600 mg LP x 2/day at the 25th week of gestation because of epileptic crisis."	3.69	[Carbamazepine and vigabatrin in epileptic pregnant woman and side effects in the newborn infant]. ( Aboulghit, H; Beust, M; Kayemba Kay'S, S; Mourtada, A; Voisin, M, 1997)
"Newborns of epileptic mothers treated with carbamazepine and/or vigabatrin during pregnancy should be placed under clinical observation during their first postnatal week."	3.69	[Carbamazepine and vigabatrin in epileptic pregnant woman and side effects in the newborn infant]. ( Aboulghit, H; Beust, M; Kayemba Kay'S, S; Mourtada, A; Voisin, M, 1997)
"A retrospective survey was carried out of add-on treatment with lamotrigine (LTG) and vigabatrin (GVG) in 109 children with severe epilepsy, treated between 1987 and 1994, identified from a total population of 300 patients seen annually, in a tertiary referral outpatient clinic in Cardiff, Wales."	3.69	A survey of lamotrigine and vigabatrin treatment in children with severe epilepsy. ( Gordon, GS; Schapel, GJ; Wallace, SJ, 1997)
"We studied the CSF amino acid levels of 42 patients with newly diagnosed epilepsy before treatment with antiepileptic medication and during monotherapy with either vigabatrin or carbamazepine."	3.68	Amino acid levels in the cerebrospinal fluid of newly diagnosed epileptic patients: effect of vigabatrin and carbamazepine monotherapies. ( Halonen, T; Kälviäinen, R; Pitkänen, A; Riekkinen, PJ, 1993)
"The anticonvulsant action of progabide, an agonist of gamma-aminobutyric acid (GABA)A and GABAB receptors, was investigated in the kindling model of epilepsy in rats."	3.68	An analysis of anticonvulsant actions of GABA agonists (progabide and baclofen) in the kindling model of epilepsy. ( Morimoto, K; Nakamura, Y; Okamoto, M; Otsuki, S; Sato, K; Sato, M, 1990)
"The temporal sequence of electrophysiological and biochemical correlates of epilepsy induced by systemic injection of kainic acid (15 mg/kg i."	3.67	Altered time course of changes in the hippocampal concentration of excitatory and inhibitory amino acids during kainate-induced epilepsy. ( Berretta, S; De Simone, D; Di Giorgio, RM; Nicoletti, F; Patti, F; Perciavalle, V; Polizzi, MC; Scapagnini, U; Sortino, MA; Speciale, C, 1984)
" Vigabatrin, 50 mg kg-1, was administered orally as add-on therapy to 11 patients with drug-resistant complex partial epilepsy as a single dose, then once every third day for 2 months, every other day for 2 months and daily for 1 month."	3.67	The effect of different vigabatrin treatment regimens on CSF biochemistry and seizure control in epileptic patients. ( Ben-Menachem, E; Dahlgren, L; Haegele, KD; Hardenberg, J; Huebert, N; Mumford, JP; Persson, LI; Schechter, PJ, 1989)
" Antiepileptic drugs such as vigabatrin [gamma vinyl GABA (GVG)], a drug rationally developed to treat resistant epilepsy, can enhance GABA transmission in these regions and may thereby afford seizure protection."	3.67	GABA in epilepsy: the pharmacologic basis. ( Gale, K, 1989)
"The involvement of intranigral gamma-aminobutyric acid (GABA) receptors in the control of generalized non-convulsive epilepsy was investigated in the rat in 3 models of petit mal epilepsy induced by systemic administration of gamma-butyrolactone, pentylenetetrazol and 4,5,6,7-tetrahydroisoxazolo [5,4-c]pyridin 3-ol (THIP)."	3.67	Suppressive effects of intranigral injection of muscimol in three models of generalized non-convulsive epilepsy induced by chemical agents. ( Depaulis, A; Marescaux, C; Snead, OC; Vergnes, M, 1989)
"The effects of GABAergic agents on non-convulsive epilepsy were studied by intracerebroventricular injections of muscimol and bicuculline in WAG/Rij rats."	3.67	Effects of GABA-ergic agents on spontaneous non-convulsive epilepsy, EEG and behaviour, in the WAG/RIJ inbred strain of rats. ( Coenen, AM; Peeters, BW; van Rijn, CM; Vossen, JM, 1989)
"Three drugs which increase GABA-mediated inhibitory neurotransmission in the brain, namely the GABA degradation inhibitors aminooxyacetic acid (AOAA) and gamma-acetylenic GABA (GAG), and the GABA receptor agonist THIP (gaboxadol), were administered to epilepsy-prone gerbils via subcutaneously implanted osmotic minipumps for 2 weeks."	3.67	Development of tolerance to the anticonvulsant effect of GABAmimetic drugs in genetically epilepsy-prone gerbils. ( Löscher, W, 1986)
"The effect of the combined administration of gamma-aminobutyric acid (GABA) and phosphatidylserine was evaluated in a pilot study of 42 patients with drug-resistant epilepsy."	3.67	Preliminary evaluation of the effect of GABA and phosphatidylserine in epileptic patients. ( Benassi, E; Bo, GP; Cocito, L; Loeb, C; Maffini, M; Scotto, P, 1987)
"Levels of total gamma-aminobutyric acid (TGABA), free GABA (FGABA), and homocarnosine (HC) were studied in CSF taken from 12 controls and 28 patients with drug-refractory epilepsy before and during 7 months of gamma-vinyl-GABA (GVG) administration."	3.67	Levels of total gamma-aminobutyric acid (GABA), free GABA and homocarnosine in cerebrospinal fluid of epileptic patients before and during gamma-vinyl-GABA (vigabatrin) treatment. ( Matilainen, R; Pitkänen, A; Riekkinen, P; Ruutiainen, T, 1988)
"To assess the relationships between the efficacy and blood levels of progabide (PGB) and its active acidic metabolite (PGA) in epileptics, observations were carried out on 89 adult patients with epilepsy of different types and severity in two groups at Paris and Genoa."	3.67	Blood levels of progabide and its active metabolite in epileptic patients: relationships to the therapeutic outcome. ( Benassi, E; Besio, G; Bianchetti, G; Loeb, C; Morselli, PL, 1988)
"A long-term open multicenter trial was carried out in 15 European centers with therapy-resistant epileptics to evaluate the efficacy and safety of progabide, a new antiepileptic GABA receptor agonist; 187 patients, suffering from partial epilepsy (57%), primary generalized epilepsy (20%), secondary generalized epilepsy (21%), and unclassified generalized epilepsy (2%), participated in the study."	3.67	Long-term treatment of epilepsy: open multicenter trial with progabide in epileptic patients. ( Beaussart, M; Benoit, C; Broglin, D; Cambier, J; Cenraud, M; Chatel, M; Deville, MC; Fournier, V; Loiseau, P; Musch, B, 1987)
"Roles for melatonin, taurine, and the pineal gland in epilepsy are examined."	3.67	Could supplementary dietary tryptophan and taurine prevent epileptic seizures? ( Maurizi, CP, 1985)
"The lumbar cerebrospinal fluid (CSF) gamma-aminobutyric acid (GABA) levels were measured in 27 patients with epilepsy, another three epileptic patients with status epilepticus and three epileptic patients with chronic cerebellar ataxia."	3.67	GABA levels in cerebrospinal fluid of patients with epilepsy. ( Hosokawa, K; Kugoh, T; Ogawa, N; Otsuki, S; Takahashi, S; Yamamoto, M, 1985)
"The development of bicuculline- and allylglycine-induced epilepsy has been studied in developing rats (6 to 30 days old)."	3.67	Bicuculline- and allylglycine-induced epilepsy in developing rats. ( de Feo, MR; Mecarelli, O; Ricci, GF, 1985)
"Alterations in gamma-aminobutyric acid (GABA) metabolism have been investigated in the kindling model of epilepsy."	3.67	Absence of modifications in gamma-aminobutyric acid metabolism after repeated generalized seizures in amygdala-kindled rats. ( Biziere, K; Heaulme, M; Lerner-Natoli, M; Leyris, R; Rondouin, G, 1985)
"In 14 children with epilepsy, 51 with febrile convulsions and 22 with meningitis gamma-aminobutyric acid (GABA) concentrations in lumbar CSF were determined."	3.66	Low CSF GABA concentration in children with febrile convulsions, untreated epilepsy, and meningitis. ( Löscher, W; Rating, D; Siemes, H, 1983)
"One of the defects in human epilepsy appears to be the suboptimal functioning of at least certain central gamma-aminobutyric acid (GABA)-mediated synapses."	3.66	Transport and metabolism of gamma-aminobutyric acid in neurons and glia: implications for epilepsy. ( Krogsgaard-Larsen, P; Larsson, OM; Schousboe, A; Wood, JD, 1983)
"Gamma-Aminobutyric acid (GABA) has been implicated in the neurochemistry of epilepsy."	3.66	Low cerebrospinal fluid gamma-aminobutyric acid content in seizure patients. ( Ballenger, JC; Glaeser, BS; Hare, TA; Post, RM; Wood, JH, 1979)
"Epilepsy is a neurological disease affected by an imbalance of inhibitory and excitatory signaling in the brain."	3.01	Epileptic Targets and Drugs: A Mini-Review. ( de Moura, JP; Dos Santos, AMF; Lopes, SM; Monteiro, AFM; Rodrigues, TCML; Scotti, L; Scotti, MT, 2023)
"Epilepsy is a common neurological disorder associated with alterations of excitation-inhibition balance within brain neuronal networks."	3.01	Fundamental Neurochemistry Review: GABA ( Bryson, A; Petrou, S; Reid, C, 2023)
"Epilepsy is a neurological disease with high global prevalence."	2.87	The beneficial effect of probiotics as a supplementary treatment in drug-resistant epilepsy: a pilot study. ( Blanco, JR; Gómez-Eguílaz, M; Pérez-Martínez, L; Ramón-Trapero, JL, 2018)
"Epilepsy is a paroxysmal brain disorder that results from an imbalance between neuronal excitation and inhibition."	2.82	Genetic variations in GABA metabolism and epilepsy. ( Deng, YC; Feng, Y; Gan, YJ; Li, GY; Liu, C; Qiao, XZ; Wei, ZH; Zhang, CC, 2022)
"All children were diagnosed with cryptogenic epilepsy and symptomatic epilepsy."	2.80	[Diagnosis and correction of cognitive impairment in preschool age children with epilepsy]. ( Guzeva, OV; Guzeva, VI; Guzeva, VV; Okhrim, IV; Zgoda, VN, 2015)
"In patients with brain tumors, the choice of antiepileptic medication is guided by tolerability and pharmacokinetic interactions."	2.79	Levetiracetam and pregabalin for antiepileptic monotherapy in patients with primary brain tumors. A phase II randomized study. ( Jeckelmann, S; Novy, J; Rossetti, AO; Roth, P; Stupp, R; Weller, M, 2014)
" To evaluate if pregabalin coadministration affects pharmacokinetics of other antiepileptic drugs, population pharmacokinetic analyses using NONMEM software were performed on data from three epilepsy trials involving seven antiepileptic drugs with pregabalin as add-on therapy."	2.76	Pregabalin effect on steady-state pharmacokinetics of carbamazepine, lamotrigine, phenobarbital, phenytoin, topiramate, valproate, and tiagabine. ( Bockbrader, HN; Burger, P; Knapp, L, 2011)
"Epilepsy was symptomatic in 58%, and 74% exhibited associated cognitive deficits."	2.74	Pregabalin: preliminary experience in intractable childhood epilepsy. ( Alsaihati, BA; Jan, MM; Zuberi, SA, 2009)
"Seizures were mixed in nine (47%), and four (21%) manifested Lennox-Gastaut syndrome."	2.74	Pregabalin: preliminary experience in intractable childhood epilepsy. ( Alsaihati, BA; Jan, MM; Zuberi, SA, 2009)
"Most (74%) had daily seizures that failed multiple drugs (mean, 5)."	2.74	Pregabalin: preliminary experience in intractable childhood epilepsy. ( Alsaihati, BA; Jan, MM; Zuberi, SA, 2009)
" However, patients on the same PGB dosage per body weight had rather different PGB trough concentrations, which could be explained only in part by age and comedication."	2.73	Serum concentrations of pregabalin in patients with epilepsy: the influence of dose, age, and comedication. ( Jürgens, U; May, TW; Neb, R; Rambeck, B, 2007)
"Bodyweight gain was correlated with number of anticonvulsant drugs (r=."	2.73	Bodyweight gain under pregabalin therapy in epilepsy: mitigation by counseling patients? ( Elger, CE; Hoffmann, JM; Hoppe, C; Rademacher, M; Schmidt, D, 2008)
"Epilepsy is a neurologicaldisorder characterized by persistent predisposition to recurrent seizurescaused by abnormal neuronal activity in the brain."	2.72	Revisiting the role of neurotransmitters in epilepsy: An updated review. ( Akyuz, E; Angelopoulou, E; Eroglu, E; Kullu, I; Paudel, YN; Polat, AK, 2021)
"Epilepsy is a neurological condition characterized by synchronous neuronal oscillations (seizures) in the electroencephalogram."	2.72	5-HT/GABA interaction in epilepsy. ( Crunelli, V; Deidda, G; Di Giovanni, G, 2021)
"Epilepsy is characterized by recurrent seizures due to abnormal hyperexcitation of neurons."	2.72	The Role of Phospholipase C in GABAergic Inhibition and Its Relevance to Epilepsy. ( Kim, HY; Kim, JI; Suh, PG, 2021)
" There was no need to decrease of the dosage of GBP and the side effects were mild and of transitory nature."	2.72	[Efficacy, safety and effect on the quality of life of gabapentin in adult epilepsy--results of a prospective open-label quasi naturalistic Hungarian multicenter study (phase human-IV)]. ( Rajna, P; Szíjártó, E, 2006)
" It has been suggested that this transportation is capacity limited, thus decreasing GBP bioavailability at higher doses."	2.71	The absorption of gabapentin following high dose escalation. ( Beran, RG; Berry, DJ; Clarke, LA; Hung, WT; Plunkeft, MJ, 2003)
" After stabilising at each dosage, a sequence of serum and saliva samples were collected within the dosage interval; GBP and co-medication concentrations were determined and the results subjected to PK modelling."	2.71	The absorption of gabapentin following high dose escalation. ( Beran, RG; Berry, DJ; Clarke, LA; Hung, WT; Plunkeft, MJ, 2003)
"The most common etiology was cerebral infarction."	2.71	New onset geriatric epilepsy: a randomized study of gabapentin, lamotrigine, and carbamazepine. ( Boardman, KD; Carter, GS; Collins, JF; Felicetta, J; Frederick, T; Marks, W; Pryor, F; Ramsay, RE; Rowan, AJ; Spitz, M; Tomyanovich, ML; Towne, A; Uthman, BM, 2005)
" During 2- and 6-week titration periods, respectively, GBP dosage reached 1,800 mg/day, and LTG, 150 mg/day."	2.70	Gabapentin versus lamotrigine monotherapy: a double-blind comparison in newly diagnosed epilepsy. ( Anhut, H; Brodie, MJ; Chadwick, DW; Garofalo, EA; Maton, S; Messmer, SL; Murray, G; Otte, A; Sauermann, W, 2002)
"Vigabatrin (VGB) is a new antiepileptic drug that increases the human brain gamma-aminobutyric acid (GABA) level by irreversibly inhibiting GABA transaminase."	2.70	Effects of vigabatrin on brain GABA+/CR signals in patients with epilepsy monitored by 1H-NMR-spectroscopy: responder characteristics. ( Boesiger, P; Duc, CO; Meier, D; Mueller, SG; Russ, W; Weber, B; Weber, OM; Wieser, HG, 2001)
"Gabapentin was administered in single doses of 10 mg/kg (N=48 healthy subjects, age 1 month-12 years) or in multiple doses of 10-65 mg/kg per day (N=205 patients with epilepsy, age 2 months-13 years) at 08:00, 14:00, and 20:00."	2.70	Population pharmacokinetics of gabapentin in infants and children. ( Bockbrader, HN; Garofalo, E; Ouellet, D; Shapiro, DY; Wesche, DL, 2001)
" Intersubject variability was approximately 30% for oral clearance and volume of distribution and was larger for the absorption rate constant and lag time."	2.70	Population pharmacokinetics of gabapentin in infants and children. ( Bockbrader, HN; Garofalo, E; Ouellet, D; Shapiro, DY; Wesche, DL, 2001)
"Gabapentin (GBP) is a non-metabolized antiepileptic drug that is eliminated by renal excretion and displays saturable, dose dependent absorption."	2.69	Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. ( Bockbrader, HN; DeCerce, J; Gidal, BE; Gonzalez, J; Kruger, S; Pitterle, ME; Ramsay, RE; Rutecki, P, 1998)
" At large daily doses, oral bioavailability (F) may be improved by giving the daily dose more frequently."	2.69	Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. ( Bockbrader, HN; DeCerce, J; Gidal, BE; Gonzalez, J; Kruger, S; Pitterle, ME; Ramsay, RE; Rutecki, P, 1998)
" The recommended dosing schedule for GBP is t."	2.69	Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. ( Bockbrader, HN; DeCerce, J; Gidal, BE; Gonzalez, J; Kruger, S; Pitterle, ME; Ramsay, RE; Rutecki, P, 1998)
"To evaluate whether switching GBP dosage regimen from t."	2.69	Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. ( Bockbrader, HN; DeCerce, J; Gidal, BE; Gonzalez, J; Kruger, S; Pitterle, ME; Ramsay, RE; Rutecki, P, 1998)
" dosing were 38."	2.69	Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. ( Bockbrader, HN; DeCerce, J; Gidal, BE; Gonzalez, J; Kruger, S; Pitterle, ME; Ramsay, RE; Rutecki, P, 1998)
"Patients obtaining complete seizure control of all seizures or any partial seizure type during the last 8 weeks were calculated."	2.69	Gabapentin add-on treatment: how many patients become seizure-free? An open-label multicenter study. ( Elger, CE; Mayer, T; Schütte, W; Wolf, P, 1999)
"After 3 months, 42% of the patients with intellectual disability had experienced a reduction in seizure frequency of more than 50% (responders)."	2.69	Antiepileptic efficacy of vigabatrin in people with severe epilepsy and intellectual disability. ( Ylinen, A, 1998)
"Vigabatrin (VGB) has been approved in Europe and is prescribed for either once or twice-daily administration."	2.69	Once-daily versus twice-daily vigabatrin: is there a difference? The results of a double-blind pilot study. ( Blankenhorn, V; Krämer, G; Mumford, JP; Richens, A; Stefan, H; Thümler, R; Zahner, B, 1999)
"This clinical study provides support for the pharmacological evidence that this preparation may be administered on a once or twice daily basis, depending on the individual patient's preference, total dosage and co-medication."	2.69	Once-daily versus twice-daily vigabatrin: is there a difference? The results of a double-blind pilot study. ( Blankenhorn, V; Krämer, G; Mumford, JP; Richens, A; Stefan, H; Thümler, R; Zahner, B, 1999)
" Two analyses of adverse events are presented: tolerability and safety."	2.69	Safety and tolerability of gabapentin as adjunctive therapy in a large, multicenter study. ( Bernstein, P; Faught, RE; Holmes, GL; Magnus-Miller, L; McLean, MJ; Morrell, MJ; Privitera, MD; Rose-Legatt, A; Willmore, LJ, 1999)
" Within these 281 patients, two mutually exclusive groups were compared (a) those reporting adverse events at only < or =1,800 mg/day (low dose); and (b) those reporting adverse events at only >1,800 mg/day (high dose)."	2.69	Safety and tolerability of gabapentin as adjunctive therapy in a large, multicenter study. ( Bernstein, P; Faught, RE; Holmes, GL; Magnus-Miller, L; McLean, MJ; Morrell, MJ; Privitera, MD; Rose-Legatt, A; Willmore, LJ, 1999)
"Gabapentin doses >1,800 mg/day were as well tolerated as doses < or =1,800 mg/day and were not associated with more adverse events."	2.69	Safety and tolerability of gabapentin as adjunctive therapy in a large, multicenter study. ( Bernstein, P; Faught, RE; Holmes, GL; Magnus-Miller, L; McLean, MJ; Morrell, MJ; Privitera, MD; Rose-Legatt, A; Willmore, LJ, 1999)
"Gabapentin was added to one other baseline drug and the efficacy was rated according to seizure type and frequency."	2.69	Gabapentin in childhood epilepsy: a prospective evaluation of efficacy and safety. ( Boenigk, HE; Borusiak, P; Korn-Merker, E, 2000)
"Although gabapentin seems also to be safe in children, the efficacy in refractory partial seizures was disappointing."	2.69	Gabapentin in childhood epilepsy: a prospective evaluation of efficacy and safety. ( Boenigk, HE; Borusiak, P; Korn-Merker, E, 2000)
"Vigabatrin seems to be an effective and safe antiepileptic drug as primary monotherapy for epilepsy with fewer cognitive side effects than carbamazepine."	2.68	Vigabatrin vs carbamazepine monotherapy in patients with newly diagnosed epilepsy. A randomized, controlled study. ( Aikiä, M; Kälviäinen, R; Mervaala, E; Riekkinen, PJ; Saukkonen, AM, 1995)
" We evaluated the cognitive and quality-of-life (QOL) effects of VGB in a double-blinded, add-on, placebo-controlled, parallel group dose-response study of patients with focal epilepsy whose complex partial seizures (CPS) were difficult to control."	2.68	Effects of differing dosages of vigabatrin (Sabril) on cognitive abilities and quality of life in epilepsy. ( Arnett, JL; Dodrill, CB; Sommerville, KW; Sussman, NM, 1995)
"Vigabatrin (VGB) is an effective add-on anti-epileptic drug."	2.68	Retrospective study of vigabatrin and psychiatric behavioural disturbances. ( Wong, IC, 1995)
" Discontinuation resulting from adverse events were infrequent, occurring in 15% of patients receiving TGB compared to 5% receiving placebo."	2.68	Tiagabine: the safety landscape. ( Leppik, IE, 1995)
" Plasma tiagabine concentrations were determined by high-performance liquid chromatography; pharmacokinetic parameters were calculated using noncompartmental methods."	2.68	Pharmacokinetics of tiagabine as add-on therapy in patients taking enzyme-inducing antiepilepsy drugs. ( Cascino, GD; Graves, NM; Gustavson, LE; Leppik, IE; Pixton, GC; So, EL; Wolff, D, 1995)
"Vigabatrin was most effective in cryptogenic and symptomatic partial seizures (39% and 43%, respectively), and in infantile spasms (25%)."	2.68	Vigabatrin as add-on therapy in children and adolescents with refractory epilepsy: an open trial. ( Coppola, G; Pascotto, A; Terraciano, AM, 1997)
" The following kinetic parameters were calculated: area under the concentration time curve from zero time to 24 h after the dose, AUC 0-24 h; maximal serum concentration, Cmax; time to the maximal serum concentration, Tmax; absorption rate constant, ka; elimination rate constant, beta; elimination half-time, t1/2beta."	2.68	Oral gabapentin disposition in patients with epilepsy after a high-protein meal. ( Baraldo, M; Benetello, P; Fortunato, M; Furlanut, M; Pea, F; Testa, G; Tognon, A, 1997)
"Safety and efficacy studies of new antiepileptic drugs require strict adherence to prescribed dosage regimens."	2.66	Compliant populations: variability in serum concentrations. ( Graves, NM; Holmes, GB; Leppik, IE, 1988)
"Epilepsy is a common neurological disease characterized by recurrent unpredictable seizures."	2.61	Use and Future Prospects of in Vivo Microdialysis for Epilepsy Studies. ( Kennedy, RT; Luna-Munguia, H; Stacey, WC; Zestos, AG, 2019)
"Epilepsy is a common neurological condition with a worldwide prevalence of around 1%."	2.55	Antiepileptic drug monotherapy for epilepsy: a network meta-analysis of individual participant data. ( Marson, AG; Nevitt, SJ; Sudell, M; Tudur Smith, C; Weston, J, 2017)
"Epilepsy is a common neurological condition with a worldwide prevalence of around 1%."	2.55	Antiepileptic drug monotherapy for epilepsy: a network meta-analysis of individual participant data. ( Marson, AG; Nevitt, SJ; Sudell, M; Tudur Smith, C; Weston, J, 2017)
"Autism and epilepsy are two associated disorders that are highly prevalent, share common developmental origins, and demonstrate substantial heritability."	2.53	Cortical interneuron dysfunction in epilepsy associated with autism spectrum disorders. ( Jacob, J, 2016)
"Although epilepsy has traditionally been thought of as a disease caused by changes in neuronal properties exclusively, these new findings challenge us to consider the contribution of glial cells as drivers of epileptogenesis in acquired epilepsies."	2.53	Glia as drivers of abnormal neuronal activity. ( Robel, S; Sontheimer, H, 2016)
"Epilepsy is a heterogeneous family of neurological disorders that manifest as seizures, i."	2.50	Physiological bases of the K+ and the glutamate/GABA hypotheses of epilepsy. ( DiNuzzo, M; Giove, F; Mangia, S; Maraviglia, B, 2014)
"Epilepsy is characterised by the propensity of the brain to generate spontaneous recurrent bursts of excessive neuronal activity, seizures."	2.49	Cortical inhibition, pH and cell excitability in epilepsy: what are optimal targets for antiepileptic interventions? ( Kaila, K; Kullmann, DM; Miles, R; Pavlov, I, 2013)
"Pregabalin , the S-enantiomer of 3-aminomethyl-5-methylhaxanoic acid, is a second-generation antiepileptic drug (AED) developed after gabapentin with improved pharmacokinetic and pharmacodynamics properties."	2.49	Pharmacokinetic and pharmacodynamic profile of pregabalin and its role in the treatment of epilepsy. ( Schulze-Bonhage, A, 2013)
" The article also looks at its clinical application as a combination therapy with particular respect to its pharmacokinetic profile."	2.49	Pharmacokinetic and pharmacodynamic profile of pregabalin and its role in the treatment of epilepsy. ( Schulze-Bonhage, A, 2013)
" Pregabalin has a linear uptake without transporter saturation at therapeutic dosages, high bioavailability with rapid absorption independent of food intake."	2.49	Pharmacokinetic and pharmacodynamic profile of pregabalin and its role in the treatment of epilepsy. ( Schulze-Bonhage, A, 2013)
"Adenosine has inhibitory effect and play important role in epilepsy."	2.48	[Angiotensins as neuromodulators]. ( Kowalski, A; Kuśmirowska, K; Rebas, E, 2012)
"Epilepsy or seizure disorder is one of the most common neurological diseases in humans."	2.48	Methylmercury: a potential environmental risk factor contributing to epileptogenesis. ( Yuan, Y, 2012)
"Problematic compounds may cause seizures either acutely or on withdrawal: Their use may reduce effectiveness of antiepileptic drugs, or may simply promote and enhance chaotic lifestyles."	2.48	Alcohol and drugs in epilepsy: pathophysiology, presentation, possibilities, and prevention. ( Borland, W; Leach, JP; Mohanraj, R, 2012)
"In animal experiments, seizures were found to increase NKCC1 expression, lower the KCC2 expression and accelerate neuronal differentiation."	2.47	Alterations in the expression of neuronal chloride transporters may contribute to schizophrenia. ( Kalkman, HO, 2011)
" We aimed at identifying treatment emergent adverse events (AEs) associated with pregabalin through a systematic review and meta-analysis of all available RCTs."	2.47	The adverse event profile of pregabalin: a systematic review and meta-analysis of randomized controlled trials. ( Gangemi, P; Perucca, P; Specchio, L; Zaccara, G, 2011)
" We also assessed the association between serious AEs and pregabalin, and investigated whether pregabalin AEs display a dose-response relationship."	2.47	The adverse event profile of pregabalin: a systematic review and meta-analysis of randomized controlled trials. ( Gangemi, P; Perucca, P; Specchio, L; Zaccara, G, 2011)
" We used relative risks (RRs) to assess the association of any [99% confidence intervals (CIs)] or serious AEs (95% CIs) with pregabalin, and risk differences (RDs, 95% CIs) to investigate dose-response relationships of pregabalin AEs."	2.47	The adverse event profile of pregabalin: a systematic review and meta-analysis of randomized controlled trials. ( Gangemi, P; Perucca, P; Specchio, L; Zaccara, G, 2011)
" There was a selective dose-response pattern in the onset of pregabalin AEs, with certain AEs appearing at lower doses than others."	2.47	The adverse event profile of pregabalin: a systematic review and meta-analysis of randomized controlled trials. ( Gangemi, P; Perucca, P; Specchio, L; Zaccara, G, 2011)
" Pregabalin AEs appear according to a selective dose-response pattern, possibly reflecting the severity of dysfunction of distinct anatomic structures."	2.47	The adverse event profile of pregabalin: a systematic review and meta-analysis of randomized controlled trials. ( Gangemi, P; Perucca, P; Specchio, L; Zaccara, G, 2011)
"Epilepsy is one of the most impactful diseases on social life."	2.47	Temporal lobe epilepsy and anti glutamic acid decarboxylase autoimmunity. ( Errichiello, L; Striano, P; Striano, S; Zara, F, 2011)
"The incidence of seizures is particularly high in the early ages of life."	2.47	Altered GABA signaling in early life epilepsies. ( Briggs, SW; Galanopoulou, AS, 2011)
"Familial febrile seizures is caused by mild loss-of-function mutations in NaV1."	2.46	NaV1.1 channels and epilepsy. ( Catterall, WA; Kalume, F; Oakley, JC, 2010)
"Generalized epilepsy with febrile seizures plus (GEFS+) is caused by missense mutations in NaV1."	2.46	NaV1.1 channels and epilepsy. ( Catterall, WA; Kalume, F; Oakley, JC, 2010)
"The causes of epilepsies and epileptic seizures are multifactorial."	2.46	Mutations affecting GABAergic signaling in seizures and epilepsy. ( Galanopoulou, AS, 2010)
"Pediatric epilepsy is a common, chronic, and challenging physical illness for children and their families."	2.46	Psychiatric concerns in pediatric epilepsy. ( Bujoreanu, IS; DeMaso, DR; Ibeziako, P, 2010)
"Levetiracetam (Keppra) is an antiepileptic drug (AED) characterized by a novel mechanism of action, unique profile of activity in seizure models, and broad-spectrum clinical efficacy."	2.45	Benefit of combination therapy in epilepsy: a review of the preclinical evidence with levetiracetam. ( Kaminski, RM; Klitgaard, H; Matagne, A; Patsalos, PN, 2009)
"In particular, interictal spikes and seizures, especially if prolonged or frequent, may cause acute or long-lasting effects on brain functioning and development, which may impair performance in a variety of behavioral tests."	2.45	The epileptic hypothesis: developmentally related arguments based on animal models. ( Galanopoulou, AS; Moshé, SL, 2009)
"The incidence of epilepsy is significantly higher in children than adults."	2.45	The 2008 Judith Hoyer lecture: epilepsy in children: listening to mothers. ( Holmes, GL, 2009)
"Studies on mechanisms of seizure generation and propagation have identified new potential targets for AEDs."	2.45	New antiepileptic drugs: molecular targets. ( Mula, M, 2009)
"Gabapentin is an antiepileptic drug (AED) by design expected to mimic the action of the neurotransmitter gamma-aminobutyric acid (GABA)."	2.44	Gabapentin: a Ca2+ channel alpha 2-delta ligand far beyond epilepsy therapy. ( Striano, P; Striano, S, 2008)
"Gabapentin was at length approved in 2006."	2.44	[Newer antiepileptic drugs]. ( Matsuura, M, 2007)
"A rationale for their use in migraine prophylaxis is the hypothesis that migraine and epilepsy share several common pathogenetic mechanisms."	2.44	Antiepileptic drugs in migraine: from clinical aspects to cellular mechanisms. ( Calabresi, P; Cupini, LM; Galletti, F; Rossi, C; Sarchielli, P, 2007)
"Brief postictal and alternating psychoses provide an opportunity to understand the complex relationships between epilepsy and schizophrenia-like brief psychotic episodes, and this understanding can assist in their management."	2.44	Alternating and postictal psychoses: review and a unifying hypothesis. ( Sachdev, PS, 2007)
" Individualization of dosage and avoidance of unnecessary polypharmacy are essential for safe utilization of anti-epileptic drugs."	2.44	[Epilepsy in the elderly]. ( Yoshino, A, 2007)
"Although epilepsy was believed to have the highest incidence in childhood, recent epidemiologic studies revealed that the incidence increases markedly in elderly."	2.44	[Epilepsy in the elderly]. ( Yoshino, A, 2007)
"Although seizures are very common during early brain development, consequences of seizures during this age period are less severe than in the mature brain."	2.44	Neurobiological mechanisms of developmental epilepsy: translating experimental findings into clinical application. ( Stafstrom, CE, 2007)
"Epilepsy is the most common primary neurological disorder known."	2.43	The GABA shunt: an attractive and potential therapeutic target in the treatment of epileptic disorders. ( Sriram, D; Vaigundaragavendran, J; Yogeeswari, P, 2005)
" Responder rates across the effective doses (150-600 mg/day) ranged from 14% to 51% and demonstrated a significant dose-response relationship."	2.43	Defining success in clinical trials--profiling pregabalin, the newest AED. ( Ryvlin, P, 2005)
"Epilepsy is a common and devastating neurological disorder."	2.43	Molecular and cellular mechanisms of pharmacoresistance in epilepsy. ( Beck, H; Remy, S, 2006)
"However, specific types of seizures, such as myoclonic seizures or distinctive electroencephalographic patterns, such as suppression burst patterns, epileptic syndrome or early myoclonic encephalopathy, may suggest a specific metabolic disease."	2.43	[Neonatal epilepsy and inborn errors of metabolism]. ( Bahi-Buisson, N; de Lonlay, P; Desguerre, I; Dulac, O; Kaminska, A; Léger, PL; Mention, K; Nabbout, R; Plouin, P; Valayanopoulos, V, 2006)
" For drugs that are eliminated renally completely unchanged (gabapentin, pregabalin and vigabatrin) or mainly unchanged (levetiracetam and topiramate), the pharmacokinetic variability is less pronounced and more predictable."	2.43	Pharmacokinetic variability of newer antiepileptic drugs: when is monitoring needed? ( Johannessen, SI; Tomson, T, 2006)
" For these older drugs it has been common practice to adjust the dosage to achieve a serum drug concentration within a predefined 'therapeutic range', representing an interval where most patients are expected to show an optimal response."	2.43	Pharmacokinetic variability of newer antiepileptic drugs: when is monitoring needed? ( Johannessen, SI; Tomson, T, 2006)
"The purposes of this review were to assess the gabapentin titration and dosing regimens that have been published in peer-reviewed journals, to develop dosing recommendations to maximize antiseizure efficacy without compromising tolerability, and to formulate guidelines for an adequate therapeutic assessment of gabapentin dosage efficacy."	2.42	Gabapentin dosing in the treatment of epilepsy. ( Gidal, BE; McLean, MJ, 2003)
" These were reviewed to assess the range of dosing and titration schedules reported."	2.42	Gabapentin dosing in the treatment of epilepsy. ( Gidal, BE; McLean, MJ, 2003)
" Side effects occurred around the onset of dosing and were reported in some studies to be transient."	2.42	Gabapentin dosing in the treatment of epilepsy. ( Gidal, BE; McLean, MJ, 2003)
"Based in the literature here, in most adult patients, gabapentin may be initiated at a dosage of 900 mg/d and titrated to maintenance dosages > or = 3600 mg/d."	2.42	Gabapentin dosing in the treatment of epilepsy. ( Gidal, BE; McLean, MJ, 2003)
"The pharmacokinetic properties of a drug are the primary deter-minant of the extent and duration of drug action, and influence susceptibility to clinically important drug interactions."	2.42	The ideal pharmacokinetic properties of an antiepileptic drug: how close does levetiracetam come? ( Johannessen, SI; Perucca, E, 2003)
" Although its half-life is relatively short (6 to 8 hours), its duration of action is longer than anticipated from its pharmacokinetics in plasma, and a twice-daily dosing regimen is adequate to produce the desired response."	2.42	The ideal pharmacokinetic properties of an antiepileptic drug: how close does levetiracetam come? ( Johannessen, SI; Perucca, E, 2003)
"3 h, and dose-proportional maximal plasma concentrations and total exposures predict a dose-response relationship in clinical practice and allow an effective starting dose of 150 mg/day in clinical practice without need for titration."	2.42	Pregabalin pharmacology and its relevance to clinical practice. ( Ben-Menachem, E, 2004)
"Many forms of epilepsy are intractable to current therapies and there is a pressing need to develop agents and strategies to not only suppress seizures, but also cure epilepsy."	2.41	Ca2+ channels and epilepsy. ( Jones, OT, 2002)
"The epilepsies encompass diverse seizure disorders afflicting as many as 50 million people worldwide."	2.41	Ca2+ channels and epilepsy. ( Jones, OT, 2002)
"Gabapentin is a drug that shares a similar structure to that of GABA, although its mechanism of action cannot be explained solely by a direct gaba mimetic effect."	2.41	[Characteristics and indications of gabapentin]. ( Sancho-Rieger, J, 2002)
" It is well absorbed when administered orally and displays linear kinetics up to doses of 1,800 mg/day."	2.41	[Characteristics and indications of gabapentin]. ( Sancho-Rieger, J, 2002)
"Tiagabine (TGB) is an anti epileptic drug whose mechanism of action is due to a reduction in the neurone and astrocyte uptake of gamma aminobutyric acid (GABA), causing its concentration at the synapse to be increased."	2.41	[Characteristics and indications of tiagabine]. ( Casas-Fernández, C; Domingo-Jiménez, R, 2002)
"Although antiepileptic drugs (AEDs) are commonly used to control and prevent seizures, their long-term use carries a considerable risk of morbidity."	2.41	Antiepileptic drug therapy for adults: when to initiate and how to choose. ( Sirven, JI, 2002)
"Epilepsy is a major symptom in succinic semialdehyde dehydrogenase deficiency."	2.41	Genetic disorders of gamma-aminobutyric acid, glycine, and serine as causes of epilepsy. ( Jaeken, J, 2002)
" However, on rare occasions, they can progress to more severe cutaneous disorders, including Stevens-Johnson syndrome and toxic epidermal necrolysis."	2.41	Therapeutic safety monitoring: what to look for and when to look for it. ( Harden, CL, 2000)
"Although epilepsy is fundamentally a circuit phenomenon, the most basic manifestation of the hyperexcitability characteristic of epilepsy must be evident at the level of a single neuron."	2.41	Epilepsy-associated plasticity in gamma-aminobutyric acid receptor expression, function, and inhibitory synaptic properties. ( Coulter, DA, 2001)
"Epilepsy affects 1."	2.41	New antiepileptic drugs and preparations. ( Jagoda, A; Yoon, Y, 2000)
"Lamotrigine has positive effects on cognitive function, but occasionally produces insomnia."	2.41	Lamotrigine update and its use in mood disorders. ( Hurley, SC, 2002)
" A slow upward dose titration is recommended to reduce the incidence of serious rash, but this may delay the attainment of adequate dosage for 6 weeks."	2.41	Lamotrigine update and its use in mood disorders. ( Hurley, SC, 2002)
"Knowledge of these syndromes has important treatment and prognostic implications, which usually extend into adulthood."	2.41	Adolescent seizures and epilepsy syndromes. ( Kim, HL; Wheless, JW, 2002)
"The characteristic clinical history, seizure semiology, and magnetic resonance imaging findings have allowed a discrete epilepsy syndrome to be established."	2.41	Adolescent seizures and epilepsy syndromes. ( Kim, HL; Wheless, JW, 2002)
"Standard antiepileptic drugs (AEDs) have a number of pharmacokinetic shortcomings, and AEDs with more favorable profiles would be preferred."	2.40	Pharmacokinetics and interaction profile of topiramate: review and comparison with other newer antiepileptic drugs. ( Johannessen, SI, 1997)
"Standard antiepileptic drugs (AEDs) are associated with a wide variety of acute and chronic adverse events and with many interactions with each other and with non-AEDs that complicate patient management."	2.40	Overview of the safety of newer antiepileptic drugs. ( Shorvon, S; Stefan, H, 1997)
"Vigabatrin is a structural analogue of gamma amino butyric acid (GABA), which binds irreversibly to GABA-transaminase causing increased brain levels of GABA."	2.40	Vigabatrin. ( Sankar, R; Shields, WD, 1997)
"Felbamate, however, has been linked with substantially increased incidence of aplastic anemia, and the other new AEDs have been studied for relatively short periods of time."	2.40	Pharmacologic and dietary therapies in epilepsy: conventional treatments and recent advances. ( Chapman, DP; Giles, WH, 1997)
"Gabapentin is a recently introduced antiepileptic drug for the treatment of partial seizures."	2.40	Gabapentin for treatment of epilepsy in children. ( Holmes, GL, 1997)
"Gamma-aminobutyric acid (GABA) plays a pivotal role in suppressing the origin and spread of seizure activity."	2.40	Measuring human brain GABA in vivo: effects of GABA-transaminase inhibition with vigabatrin. ( Petroff, OA; Rothman, DL, 1998)
"Epilepsy is a disorder of recurrent seizures that are neural in origin."	2.40	Seizures: classification, etiologies, and pathophysiology. ( March, PA, 1998)
"Partial seizures are usually due to a structural cerebrocortical lesion and may be simple or complex."	2.40	Seizures: classification, etiologies, and pathophysiology. ( March, PA, 1998)
"Successful treatment of seizure disorders in small animals requires proper patient assessment, understanding the principles of antiepileptic drug (AED) therapy, designing a strategy for pharmacotherapy, and plans for emergency treatment."	2.40	Antiepileptic drug therapy. ( Podell, M, 1998)
"Gabapentin is an antiepileptic drug used in the treatment of partial and generalized tonic-clonic seizures."	2.40	Gabapentin. Antiepileptic mechanism of action. ( Kelly, KM, 1998)
" Because dosing is often modest, cost should rarely be the overriding factor in choosing a drug for a patient with newly diagnosed epilepsy in the developed world."	2.40	Monostars: an aid to choosing an antiepileptic drug as monotherapy. ( Brodie, MJ, 1999)
"Gabapentin has few drug-drug interactions, none of which is clinically limiting."	2.40	Gabapentin in the management of convulsive disorders. ( McLean, MJ, 1999)
" Therefore, gabapentin dosing must be optimized on an individual basis to achieve an adequate trial of the drug and obtain the best seizure control."	2.40	Gabapentin in the management of convulsive disorders. ( McLean, MJ, 1999)
"Tiagabine (TGB) is a recently approved antiepileptic drug (AED) that inhibits y-aminobutyric acid (GABA) reuptake into neurons and glia, a mechanism of action that is specific and unique among the AEDs."	2.40	Tiagabine. ( Schachter, SC, 1999)
" Conversion to TGB monotherapy can be achieved in patients with medically refractory epilepsy, although additional controlled studies are needed to confirm the efficacy of TGB as monotherapy and to establish the effective dosage range."	2.40	Tiagabine. ( Schachter, SC, 1999)
"Gabapentin (GBP) is a antiepileptic drug (AED) indicated as adjunct therapy for treatment of partial seizures, with and without secondary generalization, in patients 12 and older with epilepsy."	2.40	Gabapentin. ( Morris, GL, 1999)
"To most effectively treat children with epilepsy syndromes, further research must be completed to validate the positive effects described in case reports, open-label clinical trials, and early controlled clinical trials."	2.40	Managing pediatric epilepsy syndromes with new antiepileptic drugs. ( Pellock, JM, 1999)
" For all drugs that are metabolized, half-life is shortened and clearance is increased when patients receive concomitant enzyme-inducing agents such as barbiturates, phenytoin, and carbamazepine."	2.40	The clinical pharmacokinetics of the new antiepileptic drugs. ( Perucca, E, 1999)
" After oral administration, absorption is rapid and relatively efficient for the new AEDs, the most notable exception being gabapentin, whose bioavailability decreases with increasing dosage."	2.40	The clinical pharmacokinetics of the new antiepileptic drugs. ( Perucca, E, 1999)
"Vigabatrin acts to increase GABA levels in the presynaptic nerve terminal by inhibiting the activity of GABA-transaminase."	2.39	Vigabatrin: effect on brain GABA levels measured by nuclear magnetic resonance spectroscopy. ( Behar, K; Mattson, RH; Petroff, OA; Rothman, D, 1995)
" Although there appears to be a clear dose-response relationship up to 3 g/day, it is not well documented if higher doses result in proportionately higher brain GABA levels."	2.39	Vigabatrin: effect on brain GABA levels measured by nuclear magnetic resonance spectroscopy. ( Behar, K; Mattson, RH; Petroff, OA; Rothman, D, 1995)
" Pharmacodynamic interactions take place at the level of receptor sites, where they may have additive or potentiating effects."	2.39	Pharmacokinetic and pharmacodynamic drug interactions during treatment with vigabatrin. ( Richens, A, 1995)
" Finally, gabapentin is a very safe add-on medication."	2.39	The new anticonvulsant drugs. Implications for avoidance of adverse effects. ( Krämer, G; Schmidt, D, 1994)
" More specifically, vigabatrin, which is a very useful and well tolerated new antiepileptic drug for refractory partial epilepsy, should be started at a low dosage of 0."	2.39	The new anticonvulsant drugs. Implications for avoidance of adverse effects. ( Krämer, G; Schmidt, D, 1994)
"Gabapentin appears to be a useful new AED."	2.39	Gabapentin: a new agent for the management of epilepsy. ( Andrews, CO; Fischer, JH, 1994)
"Gabapentin's potential role in the treatment of epilepsy also was assessed."	2.39	Gabapentin: a new agent for the management of epilepsy. ( Andrews, CO; Fischer, JH, 1994)
"Vigabatrin is a specific and irreversible inhibitor of the enzyme gamma-amino-butyric-acid (GABA) transferase."	2.39	[Vigabatrin and lamotrigin: experiences with 2 new anticonvulsants in the Swiss epilepsy clinic]. ( Krämer, G; Vogt, H, 1995)
"Epilepsy is one of the most common neurological disorders."	2.39	Newer antiepileptic drugs. Towards an improved risk-benefit ratio. ( Patsalos, PN; Sander, JW, 1994)
"Felbamate was licensed in 1993 for use as adjunctive therapy or monotherapy in adults with partial or tonic-clonic seizures and as adjunctive therapy for children with the Lennox-Gastaut syndrome."	2.39	Guidelines for treating epilepsy in the age of felbamate, vigabatrin, lamotrigine, and gabapentin. ( Laxer, KD, 1994)
"Gabapentin was approved January 1994 as adjunctive therapy in patients 12 years or older with partial seizures, with or without secondary generalization."	2.39	Guidelines for treating epilepsy in the age of felbamate, vigabatrin, lamotrigine, and gabapentin. ( Laxer, KD, 1994)
"With the introduction of three new anti-epileptic drugs (AEDs) in the UK during the past 4 years as adjunctive add-on therapy, the possibility of AED pharmacokinetic interactions has become a relevant consideration."	2.39	Phenobarbitone to gabapentin: a guide to 82 years of anti-epileptic drug pharmacokinetic interactions. ( Patsalos, PN, 1994)
"Gabapentin is a new, water-soluble, antiepileptic agent with properties of an amino acid."	2.39	Clinical pharmacokinetics of gabapentin. ( McLean, MJ, 1994)
" The elimination half-life is approximately 5 to 9 hours."	2.39	Clinical pharmacokinetics of gabapentin. ( McLean, MJ, 1994)
" This drug is rapidly absorbed and exhibits dose-dependent bioavailability as a result of a saturable transport mechanism."	2.39	Clinical pharmacokinetics of gabapentin. ( McLean, MJ, 1994)
" Plasma concentrations are essentially proportional to dosages up to 1,800 mg daily, which is the highest dosage used in double-blind, placebo-controlled clinical trials."	2.39	Clinical pharmacokinetics of gabapentin. ( McLean, MJ, 1994)
"Gabapentin, has shown significant promise in the treatment of patients with refractory partial seizures and secondarily generalized tonic-clonic seizures."	2.39	Clinical efficacy and safety of gabapentin. ( Ramsay, RE, 1994)
" Although adverse events occur in most patients receiving gabapentin as adjunctive therapy, they are transient and mild to moderate in severity."	2.39	Clinical efficacy and safety of gabapentin. ( Ramsay, RE, 1994)
"Vigabatrin was designed to increase the levels of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) in the brain."	2.39	A risk-benefit assessment of vigabatrin in the treatment of neurological disorders. ( Richens, A; Srinivasan, J, 1994)
"Vigabatrin (VGB, Sabril) is a new antiepileptic drug used for treatment of partial and secondarily generalized tonic-clonic seizures."	2.39	Vigabatrin: effects on human brain GABA levels by nuclear magnetic resonance spectroscopy. ( Behar, K; Mattson, RH; Petroff, O; Rothman, D, 1994)
" GABA elevation in brain closely parallels VGB dosage and reaches concentrations 2-3 times control values at daily dosage of 3 g."	2.39	Vigabatrin: effects on human brain GABA levels by nuclear magnetic resonance spectroscopy. ( Behar, K; Mattson, RH; Petroff, O; Rothman, D, 1994)
" ZNS daily dosage is 400-600 mg."	2.39	Antiepileptic drugs in development: prospects for the near future. ( Leppik, IE, 1994)
"A 7-year-old boy with intractable epilepsy developed acute psychosis 3 days after initiating a rapid vigabatrin dosage escalation."	2.39	Vigabatrin-associated reversible acute psychosis in a child. ( Beltrán Marqués, M; Cánovas Martínez, A; Delgado Cordón, F; Escrivá Aparisi, A; Ordovás Baines, JP, 1995)
"Antiepileptic drugs (AEDs) in broad use today have a number of pharmacokinetic liabilities, including a propensity for clinically meaningful drug interactions."	2.39	Pharmacokinetic profile of topiramate in comparison with other new antiepileptic drugs. ( Perucca, E, 1996)
"gamma-Aminobutyric acid (GABA) was first proposed as a putative inhibitory neurotransmitter by Elliot and van Gelder in 1958."	2.39	Vigabatrin. ( Ben-Menachem, E, 1995)
"Vigabatrin (VGB) was designed specifically to inhibit GABA transaminase and thereby increase the availability of GABA in the brain."	2.39	Vigabatrin. ( Ben-Menachem, E, 1995)
" Adverse effects of antiepileptic treatment may affect the patient's quality of life to an even greater extent than the occurrence of seizures."	2.39	Adverse effects of established and new antiepileptic drugs: an attempted comparison. ( Gram, L; Rogvi-Hansen, B, 1995)
" However, the pharmacokinetic properties of an AED determine its ease of use, i."	2.39	Important pharmacokinetic properties of antiepileptic drugs. ( Bourgeois, BF, 1995)
" This may be related to dosage and speed of introduction."	2.39	Psychotic and severe behavioural reactions with vigabatrin: a review. ( Ferrie, CD; Panayiotopoulos, CP; Robinson, RO, 1996)
"This article surveys the pharmacokinetic parameters for the new antiepileptic drugs (AEDs): felbamate, gabapentin, lamotrigine, oxcarbazepine, tiagabine, topiramate, and vigabatrin."	2.39	Pharmacokinetics of new antiepileptic drugs. ( Gram, L, 1996)
"Epilepsy is common in individuals who are mentally retarded and/or otherwise multiply handicapped."	2.39	The role of the old and the new antiepileptic drugs in special populations: mental and multiple handicaps. ( Mattson, RH, 1996)
"For many years, the medical treatment of epilepsy was based on the use of the same few drugs, which were chosen according to the seizure type in a fairly standardized manner."	2.39	New antiepileptic drugs. ( Bourgeois, BF, 1996)
"Vigabatrin is an irreversible inhibitor of GABA transaminase."	2.39	[Antiepileptic drugs: mechanism of action]. ( Mercadé Cerdá, JM, 1996)
" Specific indications and dosage schedules have been provided."	2.39	New antiepileptic drugs. ( Brodie, MJ; Wilson, EA, 1996)
"Epilepsy is a common condition with a prevalence of just 1% in a given population."	2.39	New drugs and vagal stimulation for treatment of epilepsy--the Israeli experience. ( Korczyn, AD; Neufeld, MY, 1996)
"Gabapentin is an antiepileptic drug with an unknown mechanism of action apparently dissimilar to that of other antiepileptic agents, and possessing some desirable pharmacokinetic traits."	2.38	Gabapentin. A review of its pharmacological properties and clinical potential in epilepsy. ( Goa, KL; Sorkin, EM, 1993)
"Epilepsy is a disorder of the central nervous system in which the clinical symptoms are recurrent seizures."	2.38	Advances in pharmacotherapy: recent developments in the treatment of epilepsy. ( Graves, NM; Leppik, IE, 1993)
"The diagnosis of myoclonus was more difficult than those of epilepsy, because the clarification of pathogenesis and definition of diagnosis was lacked."	2.38	[Diagnosis and therapy of epilepsy and myoclonus]. ( Okamoto, Y; Ota, K, 1993)
"Gabapentin (GBP) was designed to be a structured analogue of gamma-aminobutyric acid (GABA)."	2.38	Advances in the pharmacotherapy of epilepsy. ( Ramsay, RE, 1993)
"Baclofen was shown also to increase the incidence of seizures evoked by pentylenetetrazole without increasing seizures due to local injections of excitatory amino acids."	2.38	GABA and epilepsy: their complex relationship and the evolution of our understanding. ( Snodgrass, SR, 1992)
"Vigabatrin is an enzyme-activated, irreversible inhibitor of gamma-aminobutyric acid (GABA) aminotransferase, which causes a marked increase in cerebral GABA concentration and a resulting anticonvulsant action."	2.38	Pharmacology and clinical pharmacology of vigabatrin. ( Richens, A, 1991)
" Their beneficial effects decline with chronic administration because of drug tolerance, and the theoretical basis for BDZ responses remains unclear."	2.38	Myoclonus: analysis of monoamine, GABA, and other systems. ( Snodgrass, SR, 1990)
"Not until patients with myoclonus and major functional disability were reported in the 1960s was attention given to understanding its basis and pharmacotherapy."	2.38	Myoclonus: analysis of monoamine, GABA, and other systems. ( Snodgrass, SR, 1990)
"Myoclonus is a clinical term meaning a quick involuntary jerk, seen in normal subjects under certain circumstances, including sleep, and in certain disease states."	2.38	Myoclonus: analysis of monoamine, GABA, and other systems. ( Snodgrass, SR, 1990)
"Among psychiatric disorders the acute symptoms of schizophrenia are exacerbated by enhanced GABA-ergic function."	2.36	Pharmacology of GABA. ( Meldrum, B, 1982)
"Valproic acid is a new antiepileptic drug."	2.36	Valproic acid. Review of a new antiepileptic drug. ( Bruni, J; Wilder, BJ, 1979)
"Epilepsy is a chronic neurological disorder characterized by recurrent unprovoked seizures."	1.91	Role of long noncoding RNAs; BDNF-AS and 17A and their relation to GABAergic dysfunction in Egyptian epileptic patients. ( Darwish, HA; Seleem, MM; Shaheen, AA; Zayed, AA, 2023)
"The treatment of epilepsy is associated with the inhibition of γ-aminobutyric acid-aminotransferase (GABA-AT), which suppresses the concentration of a key neurotransmitter GABA."	1.91	Identification of novel C-15 fluoro isosteviol derivatives for GABA-AT inhibition by in silico investigations. ( Akshinthala, P; Kapavarapu, R; M, AR; Salaria, P, 2023)
"Epilepsy is highly prevalent in SSADHD, and its onset and severity correlate with an age-related decline in GABA and GABA-related metabolite levels as well as TMS markers of reduced cortical inhibition."	1.91	The presence and severity of epilepsy coincide with reduced γ-aminobutyrate and cortical excitatory markers in succinic semialdehyde dehydrogenase deficiency. ( Arning, E; Aygun, D; Bertoldi, M; DiBacco, ML; García-Cazorla, À; Gibson, KM; Jeltsch, K; Lee, HHC; MacMullin, P; Opladen, T; Pearl, PL; Rotenberg, A; Roullet, JB; Sachee, D; Tokatly Latzer, I; Tsuboyama, M, 2023)
"Neonatal seizures commonly caused by hypoxia can lead to long-term neurological outcomes."	1.91	Fingolimod Administration Following Hypoxia Induced Neonatal Seizure Can Restore Impaired Long-term Potentiation and Memory Performance in Adult Rats. ( Ali Mard, S; Farbood, Y; Ghafouri, S; Hajipour, S; Khombi Shooshtari, M; Moradi Chameh, H; Sarkaki, A; Sistani Karampour, N, 2023)
"Seizure was induced in 24 male and female pups (6 in each experimental group) at postnatal day 10 (P10) by premixed gas (5% oxygen/ 95% nitrogen) in a hypoxic chamber for 15 minutes."	1.91	Fingolimod Administration Following Hypoxia Induced Neonatal Seizure Can Restore Impaired Long-term Potentiation and Memory Performance in Adult Rats. ( Ali Mard, S; Farbood, Y; Ghafouri, S; Hajipour, S; Khombi Shooshtari, M; Moradi Chameh, H; Sarkaki, A; Sistani Karampour, N, 2023)
"Neonatal seizures are severe pathologies which may result in long-term neurological consequences."	1.91	Maternal hyperhomocysteinemia increases seizures susceptibility of neonatal rats. ( Gataulina, E; Gerasimova, E; Khalilov, I; Kurmashova, E; Sitdikova, GF; Yakovlev, AV, 2023)
"The higher susceptibility to seizures in rats with prenatal hHCy due to a shift in the balance of excitation/inhibition toward excitation may underlie the clinical evidence about the association of hHCy with an increased risk of epilepsy."	1.91	Maternal hyperhomocysteinemia increases seizures susceptibility of neonatal rats. ( Gataulina, E; Gerasimova, E; Khalilov, I; Kurmashova, E; Sitdikova, GF; Yakovlev, AV, 2023)
"Meanwhile, it decreased the seizure severity and reduced seizure-caused anxious behavior in the PTZ-kindling mice, suggesting a significant antiepileptic activity and anxiolytic/anxiogenic potential."	1.91	Herb pair of Polygala tenuifolia Willd and Acorus tatarinowii Schott decoction attenuates seizures and alleviates anxiety in mice: Evidence for modulating inflammation, alleviating oxidative stress and mediating GABA pathway. ( He, X; Liu, Y; Xie, Y; Yang, Y; Yuan, X, 2023)
"Mean seizure class did not differ between the treatment groups."	1.91	E2730, an uncompetitive γ-aminobutyric acid transporter-1 inhibitor, suppresses epileptic seizures in a rat model of chronic mesial temporal lobe epilepsy. ( Ali, I; Brady, RD; Braine, E; Casillas-Espinosa, PM; Cheng, JY; Fukushima, K; Haskali, MB; Hudson, MR; Jones, NC; Jupp, B; Kwan, P; Major, B; Mychasiuk, R; O'Brien, TJ; Sachdev, P; Shultz, SR; Silva, J; Thergarajan, P; Vivash, L; Wright, DK; Yamakawa, GR, 2023)
"The average number of seizures per month during the previous 3 months before CNB treatment was 19."	1.91	Cenobamate and Clobazam Combination as Personalized Medicine in Autoimmune-Associated Epilepsy With Anti-Gad65 Antibodies. ( Aguilar-Castillo, MJ; Cabezudo-García, P; Carreño, M; Ciano-Petersen, NL; Estivill-Torrús, G; García-Martín, G; Gutierrez-Cardo, AL; López-Moreno, Y; Oliver, B; Ortega-Pinazo, J; Ramírez-García, T; Rodríguez-Uranga, JJ; Romero-Godoy, J; Sanchez-Godoy, L; Serrano-Castro, PJ, 2023)
"Neuropeptide Y (NPY) is a polypeptide sequence useful in regulating physiological functions like homeostasis, feeding, etc."	1.72	β-Cyclodextrin-crosslinked synthetic neuropeptide Y-based nanosponges in epilepsy by contributing GABAergic signal. ( Desai, D; Shende, P, 2022)
"Epilepsy is a common neurological disorder characterized by recurrent unprovoked seizures."	1.72	De novo Y1460C missense variant in Na ( Appendino, JP; Au, PYB; Chahine, M; Ebdalla, A; Plumereau, Q; Poulin, H; Scantlebury, MH, 2022)
"OV329, a novel drug candidate for the treatment of epilepsy and addiction, has been shown in vitro to be substantially more potent as a GABA-AT inactivator than vigabatrin, an antiseizure drug approved as an add-on therapy for adult patients with refractory complex partial seizures and monotherapy for pediatric patients with infantile spasms."	1.62	OV329, a novel highly potent γ-aminobutyric acid aminotransferase inactivator, induces pronounced anticonvulsant effects in the pentylenetetrazole seizure threshold test and in amygdala-kindled rats. ( Deking, LS; During, MJ; Feja, M; Gernert, M; Kaczmarek, E; Meller, S; Silverman, RB, 2021)
"Focal cortical dysplasia (FCD) is a major cause of drug-resistant epilepsy; however the underlying epileptogenic mechanisms of FCD metabolism in epilepsy patients remain unclear."	1.62	Focal corticarl dysplasia in epilepsy is associated with GABA increase. ( Chen, Y; Gong, T; Lin, L; Lin, Y; Liu, Y; Wang, G, 2021)
"We performed EEG recordings and autism diagnostic interview."	1.56	Endoplasmic reticulum retention and degradation of a mutation in SLC6A1 associated with epilepsy and autism. ( Cai, K; Delpire, E; Eissman, J; Flamm, C; Kang, JQ; Li, BM; Li, ZY; Liao, WP; Mermer, F; Nwosu, G; Poliquin, S; Shen, W; Shi, YW; Wang, J; Xu, D, 2020)
"Anandamide (AEA) content was downregulated after repeated seizures, and pharmacological enhancement of AEA signaling rescued seizure-induced anxiety by restoring the tonic control of the eCB signaling over glutamatergic transmission."	1.56	Anandamide Signaling Augmentation Rescues Amygdala Synaptic Function and Comorbid Emotional Alterations in a Model of Epilepsy. ( Colangeli, R; Hill, MN; Morena, M; Pittman, QJ; Teskey, GC, 2020)
"Epilepsy is often associated with emotional disturbances and the endocannabinoid (eCB) system tunes synaptic transmission in brain regions regulating emotional behavior."	1.56	Anandamide Signaling Augmentation Rescues Amygdala Synaptic Function and Comorbid Emotional Alterations in a Model of Epilepsy. ( Colangeli, R; Hill, MN; Morena, M; Pittman, QJ; Teskey, GC, 2020)
"Status epilepticus is defined as a state of unrelenting seizure activity."	1.51	Excitatory GABAergic signalling is associated with benzodiazepine resistance in status epilepticus. ( Akerman, CJ; Burman, RJ; Calin, A; Codadu, NK; Katz, AA; Lee, JH; Newey, SE; Parrish, RR; Raimondo, JV; Selfe, JS; Trevelyan, AJ; van den Berg, M; Wilmshurst, JM; Wright, R, 2019)
"Generalized convulsive status epilepticus is associated with a rapidly rising mortality rate, and thus constitutes a medical emergency."	1.51	Excitatory GABAergic signalling is associated with benzodiazepine resistance in status epilepticus. ( Akerman, CJ; Burman, RJ; Calin, A; Codadu, NK; Katz, AA; Lee, JH; Newey, SE; Parrish, RR; Raimondo, JV; Selfe, JS; Trevelyan, AJ; van den Berg, M; Wilmshurst, JM; Wright, R, 2019)
"Epilepsy is a prevalent neurological disorder that was reported to affect about 56 million people in the world."	1.51	The Anticonvulsant Effects of Baldrinal on Pilocarpine-Induced convulsion in Adult Male Mice. ( Guo, F; Li, X; Liu, N; Ma, L; Sun, T; Yu, J; Zhang, X; Zheng, P; Zhou, R, 2019)
"Spontaneous and evoked seizures were evaluated from EEG recordings, and their severity was tested by the Racine scale."	1.51	The Anticonvulsant Effects of Baldrinal on Pilocarpine-Induced convulsion in Adult Male Mice. ( Guo, F; Li, X; Liu, N; Ma, L; Sun, T; Yu, J; Zhang, X; Zheng, P; Zhou, R, 2019)
"Epilepsy is a group of neurological disorders which affects millions of people worldwide."	1.51	Electrophoretic Delivery of γ-aminobutyric Acid (GABA) into Epileptic Focus Prevents Seizures in Mice. ( Kaszas, A; Malliaras, GG; Proctor, CM; Slezia, A; Williamson, A, 2019)
"Gamma-aminobutyric acid (GABA) is a major modulator in brain maturation and its role in many different neurodevelopmental disorders has been widely reported."	1.48	Gamma-aminobutyric acid levels in cerebrospinal fluid in neuropaediatric disorders. ( Armstrong-Morón, J; Artuch, R; Casado, M; Cortès-Saladelafont, E; Cuadras, D; García-Cazorla, À; Molero-Luis, M; Montoya, J; Yubero, D, 2018)
"Epilepsy is associated with increased morbidity and mortality together and places a large financial burden on individuals and society."	1.48	Anticonvulsive effects of protodioscin against pilocarpine-induced epilepsy. ( Chen, Y; Fajol, A; Ren, B; Shi, S; Song, S, 2018)
"In six-hertz-seizure test the MeCO (25, 50, 100 and 200mg/kg) and AeCO (50, 100, 200, 400 and 800mg/kg) showed significant protection compared to control group, and MeCO was more potent than AeCO."	1.46	Ameliorative potential of Colebrookea oppositifolia methanolic root extract against experimental models of epilepsy: Possible role of GABA mediated mechanism. ( Prasad, NBL; Venkataranganna, MV; Viswanatha, GL, 2017)
"Levetiracetam treatment did not affect bone strength, bone mass, and bone turnover."	1.46	Effects of the Antiepileptic Drugs Phenytoin, Gabapentin, and Levetiracetam on Bone Strength, Bone Mass, and Bone Turnover in Rats. ( Izumo, N; Kanda, J; Kobayashi, Y; Onodera, K; Shimakura, T; Takahashi, HE; Wakabayashi, H; Yamamoto, N, 2017)
" To prevent the risk of bone fractures, patients prescribed a long-term administration of gabapentin should be regularly monitored for changes in bone mass."	1.46	Effects of the Antiepileptic Drugs Phenytoin, Gabapentin, and Levetiracetam on Bone Strength, Bone Mass, and Bone Turnover in Rats. ( Izumo, N; Kanda, J; Kobayashi, Y; Onodera, K; Shimakura, T; Takahashi, HE; Wakabayashi, H; Yamamoto, N, 2017)
"To prevent the risk of bone fractures, patients prescribed a long-term administration of gabapentin should be regularly monitored for changes in bone mass."	1.46	Effects of the Antiepileptic Drugs Phenytoin, Gabapentin, and Levetiracetam on Bone Strength, Bone Mass, and Bone Turnover in Rats. ( Izumo, N; Kanda, J; Kobayashi, Y; Onodera, K; Shimakura, T; Takahashi, HE; Wakabayashi, H; Yamamoto, N, 2017)
"Pretreatment with spermine, considerably, reversed the PTZ induced alterations."	1.46	Protective effect of spermine against pentylenetetrazole kindling epilepsy induced comorbidities in mice. ( Kumar, M; Kumar, P, 2017)
"Spermine is an endogenous polyamine; possesses anti-oxidant property and has ability to modulate ion channels and NO synthase activity."	1.46	Protective effect of spermine against pentylenetetrazole kindling epilepsy induced comorbidities in mice. ( Kumar, M; Kumar, P, 2017)
", ip) indicate that the liver is the primary site of biotransformation of the compound, suggesting that both 22a and its metabolite(s) are active, compensating probably low bioavailability of the parent molecule."	1.43	Design, physico-chemical properties and biological evaluation of some new N-[(phenoxy)alkyl]- and N-{2-[2-(phenoxy)ethoxy]ethyl}aminoalkanols as anticonvulsant agents. ( Bednarski, M; Gunia-Krzyżak, A; Marona, H; Nitek, W; Pękala, E; Powroźnik, B; Słoczyńska, K; Walczak, M; Waszkielewicz, AM; Żesławska, E, 2016)
"Pre-treatment with liraglutide (75 and 150 μg/kg) significantly prevented the seizure severity, restored behavioural activity, oxidative defence enzymes, and altered level of neurochemicals in mice brain."	1.43	Neurochemical modulation involved in the beneficial effect of liraglutide, GLP-1 agonist on PTZ kindling epilepsy-induced comorbidities in mice. ( Koshal, P; Kumar, P, 2016)
"Epilepsy is a neurological disorder which occurs due to excessive firing of excitatory neurons in specific region of brain and associated with cognitive impairment and depression."	1.43	Neurochemical modulation involved in the beneficial effect of liraglutide, GLP-1 agonist on PTZ kindling epilepsy-induced comorbidities in mice. ( Koshal, P; Kumar, P, 2016)
"Weight gain and alopecia were the most common patient-reported CSEs in this study, and weight gain was the most likely cosmetic side effect to result in dosage adjustment or medication discontinuation."	1.42	Cosmetic side effects of antiepileptic drugs in adults with epilepsy. ( Buchsbaum, R; Chen, B; Choi, H; Detyniecki, K; Hirsch, LJ; Javed, A; Kato, K; Legge, A; Moeller, J, 2015)
" We compared the overall rate of CSEs and intolerable CSEs (ICSEs-CSEs that led to dosage reduction or discontinuation) between different AEDs in both monotherapy and polytherapy."	1.42	Cosmetic side effects of antiepileptic drugs in adults with epilepsy. ( Buchsbaum, R; Chen, B; Choi, H; Detyniecki, K; Hirsch, LJ; Javed, A; Kato, K; Legge, A; Moeller, J, 2015)
" Cosmetic side effects leading to dosage change or discontinuation occurred most frequently with pregabalin and valproic acid compared with all other AEDs (13."	1.42	Cosmetic side effects of antiepileptic drugs in adults with epilepsy. ( Buchsbaum, R; Chen, B; Choi, H; Detyniecki, K; Hirsch, LJ; Javed, A; Kato, K; Legge, A; Moeller, J, 2015)
"Weight gain was the most commonly reported CSE (68/1903, 3."	1.42	Cosmetic side effects of antiepileptic drugs in adults with epilepsy. ( Buchsbaum, R; Chen, B; Choi, H; Detyniecki, K; Hirsch, LJ; Javed, A; Kato, K; Legge, A; Moeller, J, 2015)
"Hair loss was most commonly reported among patients taking valproic acid (24/270; 8."	1.42	Cosmetic side effects of antiepileptic drugs in adults with epilepsy. ( Buchsbaum, R; Chen, B; Choi, H; Detyniecki, K; Hirsch, LJ; Javed, A; Kato, K; Legge, A; Moeller, J, 2015)
"Epilepsy was assumed as indication when other AEDs were also measured (50% of patients)."	1.42	Experience from therapeutic drug monitoring and gender aspects of gabapentin and pregabalin in clinical practice. ( Baftiu, A; Beiske, G; Burns, ML; Johannessen Landmark, C; Johannessen, SI, 2015)
"CNS inflammation is characterized by a disturbance of glial cell functions."	1.40	Glia and epilepsy: experimental investigation of antiepileptic drugs in an astroglia/microglia co-culture model of inflammation. ( Dambach, H; Faustmann, PM; Haase, CG; Hinkerohe, D; Hufnagel, A; Moinfar, Z; Prochnow, N; Stienen, MN, 2014)
"Brain gliomas are highly epileptogenic."	1.40	Cortical GABAergic excitation contributes to epileptic activities around human glioma. ( Baulac, M; Bielle, F; Capelle, L; Chazal, G; Cresto, N; Devaux, B; Duyckaerts, C; Huberfeld, G; Kourdougli, N; Le Van Quyen, M; Miles, R; Pallud, J; Pellegrino, C; Rivera, C; Varlet, P, 2014)
"Gabapentin has been shown to disrupt the interaction of thrombospondin (TSP) with α2δ-1, an auxiliary calcium channel subunit."	1.40	Gabapentin attenuates hyperexcitability in the freeze-lesion model of developmental cortical malformation. ( Andresen, L; Dulla, CG; Hampton, D; Maguire, J; Morel, L; Taylor-Weiner, A; Yang, Y, 2014)
"Vigabatrin is an inhibitor of γ-aminobutyric acid transaminase."	1.40	Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms. ( Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014)
"Vigabatrin pharmacokinetic data from six randomized controlled clinical trials and one open-label study were analyzed using nonlinear mixed-effects modeling."	1.40	Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms. ( Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014)
" Covariate analysis indicated that age, creatinine clearance (CLCR), and body weight were important predictors of vigabatrin pharmacokinetic parameters."	1.40	Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms. ( Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014)
"The model adequately described vigabatrin pharmacokinetic and enabled predictions of systemic exposures in pediatric patients 1-12 months of age."	1.40	Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms. ( Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014)
"1 %) and relative bioavailability (F) (26."	1.40	Population pharmacokinetics analysis of vigabatrin in adults and children with epilepsy and children with infantile spasms. ( Karim, A; Kowalski, KG; Nielsen, JC; Patel, M; Tolbert, D; Wesche, DL, 2014)
"Early treatment of epilepsy is warranted to avoid possible severe consequences."	1.39	Epilepsy and brain injury: a case report of a dramatic neuropsychiatric vicious circle. ( Angeletti, G; Carbonetti, P; Del Casale, A; Fensore, C; Ferracuti, S; Girardi, P; Kotzalidis, GD; Lazanio, S; Muzi, A; Rapinesi, C; Savoja, V; Scatena, P; Serata, D; Tatarelli, R, 2013)
"Long-term untreated epilepsy may expose to accident proneness and further psychiatric deterioration."	1.39	Epilepsy and brain injury: a case report of a dramatic neuropsychiatric vicious circle. ( Angeletti, G; Carbonetti, P; Del Casale, A; Fensore, C; Ferracuti, S; Girardi, P; Kotzalidis, GD; Lazanio, S; Muzi, A; Rapinesi, C; Savoja, V; Scatena, P; Serata, D; Tatarelli, R, 2013)
"Understanding how seizures spread throughout the brain is an important problem in the treatment of epilepsy, especially for implantable devices that aim to avert focal seizures before they spread to, and overwhelm, the rest of the brain."	1.39	Mechanisms of seizure propagation in 2-dimensional centre-surround recurrent networks. ( Hall, D; Kuhlmann, L, 2013)
"Gabapentin (GAB) is a newer second-line antiepileptic drug (AED) used in children."	1.38	Retention rate of Gabapentin in children with intractable epilepsies at 1 year. ( Ali, I; Gupta, R; Lewis, TG; Mills, JK; Mordekar, SR; Mughal, K; Ruslan, NE; Sasidharan, L; Sharma, R; Siddiqua, A; Ugar, A; Wassmer, E; Whitehouse, WP, 2012)
"Bacopa monnieri and Bacoside-A treatment reverses epilepsy associated changes to near control suggesting that decreased GABA receptors in the cerebral cortex have an important role in epileptic occurrence; Bacopa monnieri and Bacoside-A have therapeutic application in epilepsy management."	1.38	Decreased GABA receptor in the cerebral cortex of epileptic rats: effect of Bacopa monnieri and Bacoside-A. ( Abraham, PM; Antony, S; Balakrishnan, S; Mathew, J; Paulose, CS, 2012)
"Depression, epilepsy, post traumatic stress disorder (PTSD), and chronic pain exemplify medical conditions that are exacerbated by stress, have low heart rate variability (HRV) and low GABAergic activity, respond to pharmacologic agents that increase activity of the GABA system, and show symptom improvement in response to yoga-based interventions."	1.38	Effects of yoga on the autonomic nervous system, gamma-aminobutyric-acid, and allostasis in epilepsy, depression, and post-traumatic stress disorder. ( Brown, RP; Ciraulo, DA; Gerbarg, PL; Saper, RB; Streeter, CC, 2012)
" Mean PGB dosage was 279 mg/day."	1.38	Effect of pregabalin add-on treatment on seizure control, quality of life, and anxiety in patients with brain tumour-related epilepsy: a pilot study. ( Carapella, CM; Dinapoli, L; Fabi, A; Maschio, M; Pace, A; Pompili, A; Sperati, F; Vidiri, A, 2012)
"Focal cortical dysplasia (FCD), which is characterized histologically by disorganized cortical lamination and large abnormal cells, is one of the major causes of intractable epilepsies."	1.37	KCC2 was downregulated in small neurons localized in epileptogenic human focal cortical dysplasia. ( Fujiwara, T; Fukuda, A; Inoue, Y; Matsuda, K; Mihara, T; Okabe, A; Sato, K; Shimizu-Okabe, C; Tanaka, M; Yagi, K, 2011)
"Epilepsy affects half of patients."	1.37	Epilepsy in succinic semialdehyde dehydrogenase deficiency, a disorder of GABA metabolism. ( Jakobs, C; Michael Gibson, K; Pearl, PL; Shukla, L; Theodore, WH, 2011)
"Epilepsy is a neurological disorder associated with excitatory and inhibitory imbalance within the underlying neural network."	1.37	Reduced hippocampal GABAergic function in Wistar audiogenic rats. ( Doretto, MC; Drumond, LE; Guidine, PA; Kushmerick, C; Massensini, AR; Moraes, MF, 2011)
"The incidence of constipation as an adverse effect of pregabalin has previously been reported as low, with all cases described as either mild or moderate."	1.36	Severe and disabling constipation: an adverse effect of pregabalin. ( Cook, MJ; D'Souza, WJ; Kamel, JT, 2010)
"Constipation was the most frequent adverse effect that required pregabalin to be withdrawn (6."	1.36	Severe and disabling constipation: an adverse effect of pregabalin. ( Cook, MJ; D'Souza, WJ; Kamel, JT, 2010)
"Oxcarbazepine was consistently less effective than most other AEDs."	1.36	Comparative effectiveness of 10 antiepileptic drugs in older adults with epilepsy. ( Arif, H; Bazil, CW; Buchsbaum, R; Hirsch, LJ; Pierro, J; Resor, SR; Sims, J; Whalen, M, 2010)
"FGF22-deficient mice are resistant to epileptic seizures, and FGF7-deficient mice are prone to them, as expected from the alterations in excitatory/inhibitory balance."	1.36	Distinct FGFs promote differentiation of excitatory and inhibitory synapses. ( Javed, D; Johnson-Venkatesh, EM; Sutton, MA; Terauchi, A; Toth, AB; Umemori, H, 2010)
"Epilepsy is a serious neurological disorder in human beings and the long-term pathological events remain largely obscure."	1.35	Time-course of neuronal death in the mouse pilocarpine model of chronic epilepsy using Fluoro-Jade C staining. ( Chen, LW; Huang, YG; Liu, YH; Wang, L, 2008)
"After 5 days of GBP infusion, seizures were induced by flurothyl dripped onto filter paper."	1.34	Intraventricular administration of gabapentin in the rat increases flurothyl seizure threshold. ( Fisher, RS; Kraus, AC; Oommen, J, 2007)
"First tonic-clonic seizure was at 295."	1.34	Intraventricular administration of gabapentin in the rat increases flurothyl seizure threshold. ( Fisher, RS; Kraus, AC; Oommen, J, 2007)
"Time to first myoclonic or partial seizure was not influenced."	1.34	Intraventricular administration of gabapentin in the rat increases flurothyl seizure threshold. ( Fisher, RS; Kraus, AC; Oommen, J, 2007)
"Both extracts can prevent convulsions as well as convulsion-related GABAergic neuron damage in the brain in the prolonged PTZ kindling model."	1.33	Study of antiepileptic effect of extracts from Acorus tatarinowii Schott. ( Chen, L; Gao, MM; Liao, WP; Su, T; Sun, WW; Yang, SQ; Yi, YH, 2005)
" GBP plasma concentrations in the neonates declined with an estimated half-life of 14 h."	1.33	Pharmacokinetics of gabapentin during delivery, in the neonatal period, and lactation: does a fetal accumulation occur during pregnancy? ( Ohman, I; Tomson, T; Vitols, S, 2005)
"The heightened susceptibility to seizures appears to be due, at least in part, to developmental changes that skew the balance between excitatory and inhibitory neurotransmitter systems in the brain in favor of a state of excitation."	1.33	Rearranging receptors. ( Brooks-Kayal, AR, 2005)
"Patients were stabilised using phenobarbitone and/or potassium bromide to produce tolerable therapeutic serum concentrations and dosed additionally with gabapentin at 35 to 50 mg/kg/d (divided twice or three times daily) for 4 months."	1.33	Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent. ( Govendir, M; Malik, R; Perkins, M, 2005)
"To assess whether there is a change in seizure activity in dogs with refractory epilepsy that are receiving appropriate doses of phenobarbitone and/or potassium bromide, when gabapentin is added to the therapeutic regimen."	1.33	Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent. ( Govendir, M; Malik, R; Perkins, M, 2005)
"Owners recorded seizure activity and side effects during this period in a standardised diary."	1.33	Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent. ( Govendir, M; Malik, R; Perkins, M, 2005)
"In some dogs, seizures were prevented completely, while in others there was an increase in interictal period."	1.33	Improving seizure control in dogs with refractory epilepsy using gabapentin as an adjunctive agent. ( Govendir, M; Malik, R; Perkins, M, 2005)
"In vivo, it potently prevents seizures, pain-related behaviors and has anxiolytic-like activity in rodent models."	1.33	Activity profile of pregabalin in rodent models of epilepsy and ataxia. ( Bertram, E; Kinsora, JJ; Radulovic, LL; Serpa, KA; Taylor, CP; Vartanian, MG; Vergnes, M, 2006)
"In the immature hippocampus, seizures generated with functional GABAergic synapses include fast oscillations that are required to transform a naive network to an epileptic one: blocking GABA receptors prevents the long-lasting sequels of seizures."	1.33	Epileptogenic actions of GABA and fast oscillations in the developing hippocampus. ( Ben-Ari, Y; Gozlan, H; Khalilov, I; Le Van Quyen, M, 2005)
"Dizziness and ataxia are among the most common adverse events associated with antiepileptic medications."	1.33	Measuring the effects of antiepileptic medications on balance in older people. ( Blum, D; Fife, TD; Fisher, RS, 2006)
"The Fregly ataxia battery includes the sum of timed trials in the sharpened Romberg (SR) position, standing on one leg with eyes closed (SOLEC), and when walking in tandem with eyes closed (WITEC)."	1.33	Measuring the effects of antiepileptic medications on balance in older people. ( Blum, D; Fife, TD; Fisher, RS, 2006)
"Kainic acid (KA) solution was injected stereotaxically into medial and lateral sites of the sensori-motor cortex."	1.33	Focal cortical dysplasia: pathophysiological approach. ( Hashizume, K; Hodozuka, A; Tanaka, T; Tsuda, H, 2006)
"Hypoxia of the brain may alter further seizure susceptibility in a different way."	1.32	The epileptogenic effect of seizures induced by hypoxia: the role of NMDA and AMPA/KA antagonists. ( Rubaj, A; Sieklucka-Dziuba, M; Zgodziński, W, 2003)
"The influence of age and administered daily dosage on the plasma concentrations of gabapentin (GBP) at steady state was evaluated in a group of 41 children and young adults (aged 3-30 years) receiving long-term adjunctive treatment with GBP for the management of refractory partial-onset seizures."	1.32	Plasma gabapentin concentrations in children with epilepsy: influence of age, relationship with dosage, and preliminary observations on correlation with clinical response. ( Bonanni, P; Bonomi, I; Ferrari, AR; Gatti, G; Guerrini, R; Perucca, E, 2003)
"We studied 14 patients with juvenile myoclonic epilepsy (JME), 19 patients with refractory localization-related epilepsy (RLE) and 20 healthy volunteers who were matched for age and sex."	1.32	Uptake of GABA and activity of GABA-transaminase in platelets from epileptic patients. ( Keränen, T; Peltola, J; Rainesalo, S; Saransaari, P, 2003)
"Epilepsy is closely related to an altered transmission of GABA, the major inhibitory transmitter in the brain."	1.32	Altered expression of GABAB receptors in the hippocampus after kainic-acid-induced seizures in rats. ( Bettler, B; Furtinger, S; Sperk, G, 2003)
"Epilepsy affects homeostasis and autonomic nervous system functions."	1.32	Extracellular concentrations of catecholamines and amino acids in the dorsomedial hypothalamus of kindled rats. A microdialysis study. ( Aker, R; Gören, MZ; Onat, FY; Yananli, HR, 2003)
"Gabapentin is a clinically effective anticonvulsant with an unclear mechanism of action."	1.32	Gabapentin actions on Kir3 currents and N-type Ca2+ channels via GABAB receptors in hippocampal pyramidal cells. ( Bertrand, S; Lacaille, JC; Morin, F; Nagy, F; Nouel, D, 2003)
"5) Gabapentin actions were linked to activation of pertussis toxin-sensitive G-proteins since N-ethylmaleimide (NEM) blocked K(Gbp) activation and Ca(2+) channel inhibition by gabapentin."	1.32	Gabapentin actions on Kir3 currents and N-type Ca2+ channels via GABAB receptors in hippocampal pyramidal cells. ( Bertrand, S; Lacaille, JC; Morin, F; Nagy, F; Nouel, D, 2003)
"ent/ent mice develop ataxia by postnatal day 13-15, followed by paroxysmal dyskinesia a few days later."	1.32	entla, a novel epileptic and ataxic Cacna2d2 mutant of the mouse. ( Becker, CM; Becker, K; Boison, D; Brill, J; Gouder, N; Hofmann, F; Klocke, R; Klugbauer, N; Paul, D, 2004)
"Vigabatrin was anticonvulsant in all groups for up to 13 days with a maximal effect 24 h after injection."	1.32	The central piriform cortex: anatomical connections and anticonvulsant effect of GABA elevation in the kindling model. ( Ebert, U; Löscher, W; Schwabe, K, 2004)
"It remains unclear whether the seizures result from aberrant neuronal placement, disruption of intrinsic properties of neurons, or both."	1.32	Epileptic-like convulsions associated with LIS-1 in the cytoskeletal control of neurotransmitter signaling in Caenorhabditis elegans. ( Braden, AL; Caldwell, GA; Caldwell, KA; Locke, CJ; Williams, SN, 2004)
"Identical convulsions were obtained using C."	1.32	Epileptic-like convulsions associated with LIS-1 in the cytoskeletal control of neurotransmitter signaling in Caenorhabditis elegans. ( Braden, AL; Caldwell, GA; Caldwell, KA; Locke, CJ; Williams, SN, 2004)
"Electroconvulsions were produced by means of an alternating current (ear-clip electrodes, 0."	1.31	Effect of gabapentin on the anticonvulsant activity of antiepileptic drugs against electroconvulsions in mice: an isobolographic analysis. ( Borowicz, KK; Czuczwar, SJ; Luszczki, J; Swiader, M, 2002)
"To report on the occurrence of myoclonus in patients receiving gabapentin (GBP) for the treatment of epilepsy."	1.31	Myoclonus associated with the use of gabapentin. ( Asconapé, J; DellaBadia, J; Diedrich, A, 2000)
"We found 13 cases of myoclonus."	1.31	Myoclonus associated with the use of gabapentin. ( Asconapé, J; DellaBadia, J; Diedrich, A, 2000)
"GBP-associated myoclonus appears to be relatively frequent."	1.31	Myoclonus associated with the use of gabapentin. ( Asconapé, J; DellaBadia, J; Diedrich, A, 2000)
"p."	1.31	Guanosine and GMP prevent seizures induced by quinolinic acid in mice. ( da Silveira Perla, A; de Faria Maraschin, J; Lara, DR; Onofre Souza, D; Schmidt, AP, 2000)
" The toxic effect of gamma-vinyl-GABA was mimicked by a 24-h treatment with GABA (100 microM) and the GABA(A) receptor agonist, muscimol (10 microM), but not the GABA(B) receptor agonist, baclofen (10 microM)."	1.31	GABA(A)-mediated toxicity of hippocampal neurons in vitro. ( Lukasiuk, K; Pitkänen, A, 2000)
"Bicuculline was used to investigate seizure susceptibility in pre- and peripubertal male and female rats exposed prenatally to morphine."	1.31	Prenatal morphine exposure alters susceptibility to bicuculline seizures in a sex- and age-specific manner. ( Schindler, CJ; Slamberová, R; Vathy, I; Velísková, J, 2000)
"Gabapentin (GBP) was introduced as an antiepileptic drug (AED) and has been used in the management of neuropathic pain."	1.31	Effects of gabapentin on brain GABA, homocarnosine, and pyrrolidinone in epilepsy patients. ( Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 2000)
" We reported that daily dosing increased brain gamma-aminobutyric acid (GABA) in patients with epilepsy."	1.31	Effects of gabapentin on brain GABA, homocarnosine, and pyrrolidinone in epilepsy patients. ( Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 2000)
"Gabapentin (GBP) is a novel antiepileptic drug (AED), currently used as add-on therapy in patients with partial seizures."	1.31	Gabapentin-induced modulation of interictal epileptiform activity related to different vigilance levels. ( Bassetti, MA; Marciani, MG; Mattia, D; Placidi, F; Romigi, A; Spanedda, F, 2000)
"A significant decrease in seizure susceptibility could be observed in BCCA treated mice compared with sham-operated controls."	1.31	The influence of MK-801 on bicuculline evoked seizures in adult mice exposed to transient episode of brain ischemia. ( Kleinrok, Z; Rejdak, K; Rejdak, R; Sieklucka-Dziuba, M, 2000)
"Chlormethiazole has sedative, hypnotic, anticonvulsant and neuroprotective properties."	1.31	Chlormethiazole inhibits epileptiform activity by potentiating GABA(A) receptor function. ( Empson, RM; Gee, VJ; Newberry, NR; Sheardown, MJ, 2000)
"However, after kindled seizures, GluRAs block the monosynaptic excitatory postsynaptic potential (EPSP) and isolate a monosynaptic inhibitory postsynaptic potential (IPSP), suggesting that mossy fibers release GABA."	1.31	Seizures induce simultaneous GABAergic and glutamatergic transmission in the dentate gyrus-CA3 system. ( Gutiérrez, R, 2000)
"The purpose of the present investigation was to determine whether the sensitivity to systemic toxic effects of cocaine is altered in genetically epilepsy-prone rats (GEPRs)."	1.31	Phenotypic expression of the systemic toxicity of cocaine in genetically epilepsy-prone rats. ( Heavner, JE; Kao, YJ; Kaye, AD; Reigel, CE; Shi, B, 2000)
"Moderate seizure (GEPR-3) and severe seizure (GEPR-9) rats, and the control strain, Sprague-Dawley rats, 10 weeks of age, were lightly anesthetized with halothane and nitrous oxide."	1.31	Phenotypic expression of the systemic toxicity of cocaine in genetically epilepsy-prone rats. ( Heavner, JE; Kao, YJ; Kaye, AD; Reigel, CE; Shi, B, 2000)
"Chronic seizures were induced by amygdalar injection of kainic acid 60 days before death."	1.31	Collapse of extracellular glutamate regulation during epileptogenesis: down-regulation and functional failure of glutamate transporter function in rats with chronic seizures induced by kainic acid. ( Doi, T; Kamada, H; Mitsuyama, Y; Nakajima, A; Ohya-Nishiguchi, H; Tokumaru, J; Ueda, Y; Willmore, LJ; Yokoyama, H, 2001)
" Serious adverse events were assessed individually."	1.31	Adverse event monitoring in lamotrigine patients: a pharmacoepidemiologic study in the United Kingdom. ( Mawer, GE; Sander, JW; Wong, IC, 2001)
" The adverse events with LTG reported by this study were similar to those reported in the literature."	1.31	Adverse event monitoring in lamotrigine patients: a pharmacoepidemiologic study in the United Kingdom. ( Mawer, GE; Sander, JW; Wong, IC, 2001)
" Life-threatening adverse reactions were rare."	1.31	Adverse event monitoring in lamotrigine patients: a pharmacoepidemiologic study in the United Kingdom. ( Mawer, GE; Sander, JW; Wong, IC, 2001)
"Vigabatrin (VGB) treatment is neuroprotective in various models of status epilepticus (SE) and delays the development of kindling via mechanisms that are assumed to relate to the elevation of GABA levels in the brain."	1.31	Chronic elevation of brain GABA levels beginning two days after status epilepticus does not prevent epileptogenesis in rats. ( Halonen, T; Nissinen, J; Pitkänen, A, 2001)
"A partial but significant inhibition of convulsions was found in these animals."	1.31	Evidence for an involvement of the ammonia-decreasing action of L-arginine in suppressing picrotoxin-induced convulsions in rats and its additive action with diazepam. ( Jayakumar, AR; Vanaja, P, 2001)
"Testosterone's (T) anti-seizure effects may be mediated in part by actions of its 5alpha-reduced metabolites."	1.31	Testosterone reduces pentylenetetrazole-induced ictal activity of wildtype mice but not those deficient in type I 5alpha-reductase. ( Frye, CA; Harney, JP; Rhodes, ME; Walf, AA, 2001)
"gamma-Aminobutyric acid (GABA) is a major neurotransmitter in AMG, and histamine receptor activation is also reported to stimulate GABA release."	1.31	Modulation of audiogenically kindled seizures by gamma-aminobutyric acid-related mechanisms in the amygdala. ( Faingold, CL; Feng, HJ; Naritoku, DK; Randall, ME, 2001)
"Epilepsy is a common condition in people with learning disabilities with many patients continuing to suffer from seizures despite antiepileptic drug (AED) treatment."	1.30	A naturalistic study of the use of vigabatrin, lamotrigine and gabapentin in adults with learning disabilities. ( Bhaumik, S; Branford, D; Duggirala, C; Ismail, IA, 1997)
"Lamotrigine caused increased seizures in 24% of patients, especially when prescribed at a higher dose."	1.30	A naturalistic study of the use of vigabatrin, lamotrigine and gabapentin in adults with learning disabilities. ( Bhaumik, S; Branford, D; Duggirala, C; Ismail, IA, 1997)
"We suggest that, in patients with mental retardation and epilepsy, involuntary movements may either occur as reversible side effects of gabapentin therapy or result from a previously undescribed adverse drug interaction with other antiepileptic agents."	1.30	Choreoathetosis as a side effect of gabapentin therapy in severely neurologically impaired patients. ( Chudnow, RS; Dewey, RB; Lawson, CR, 1997)
"One patient developed recurrent choreiform movements after drug rechallenge."	1.30	Choreoathetosis as a side effect of gabapentin therapy in severely neurologically impaired patients. ( Chudnow, RS; Dewey, RB; Lawson, CR, 1997)
"Lamotrigine was the only drug which antagonized tonic convulsions in the MES test (ED50 = 36 mumol/kg)."	1.30	Comparison of the preclinical anticonvulsant profiles of tiagabine, lamotrigine, gabapentin and vigabatrin. ( Dalby, NO; Nielsen, EB, 1997)
"Tiagabine is a novel antiepileptic drug which has clinical efficacy against complex refractory and myoclonic seizures."	1.30	Comparison of the preclinical anticonvulsant profiles of tiagabine, lamotrigine, gabapentin and vigabatrin. ( Dalby, NO; Nielsen, EB, 1997)
"Tiagabine was the most potent drug in antagonizing tonic convulsions induced by PTZ, DMCM and sound induced seizures in DBA/2 mice with ED50 values of 2, 2 and 1 mumol/kg, respectively, followed by lamotrigine with ED50 values of 9, 43 and 6 mumol/kg, respectively."	1.30	Comparison of the preclinical anticonvulsant profiles of tiagabine, lamotrigine, gabapentin and vigabatrin. ( Dalby, NO; Nielsen, EB, 1997)
" Evoked inhibitory postsynaptic currents (IPSCs) were decreased by kainate by up to 90%, showing a bell-shaped dose-response curve similar to that of native kainate-selective receptors."	1.30	Kainate receptors presynaptically downregulate GABAergic inhibition in the rat hippocampus. ( Herreras, O; Lerma, J; Rodríguez-Moreno, A, 1997)
"The relationship between the ratio of vigabatrin concentration to dosage (VGB C/D) and both patient age and the presence of other antiepileptic drugs (AEDs) was analyzed retrospectively by bivariate and multivariate methods in 179 patients with epilepsy (114 children and 65 adults)."	1.30	Vigabatrin serum concentration to dosage ratio: influence of age and associated antiepileptic drugs. ( Armijo, JA; Arteaga, R; Bravo, J; Cuadrado, A, 1997)
"Gabapentin is a new antiepileptic drug."	1.30	[Gabapentin--a new antiepileptic agent]. ( Johannessen, SI; Nakken, KO; Rytter, E, 1998)
"Gabapentin was well tolerated, and no clinically significant interactions were encountered."	1.30	[Gabapentin--a new antiepileptic agent]. ( Johannessen, SI; Nakken, KO; Rytter, E, 1998)
" However, GBP concentrations were much lower after rectal administration; therefore, we concluded that the aqueous solution was poorly absorbed rectally."	1.30	Failure of absorption of gabapentin after rectal administration. ( Birnbaum, AK; Caruso, KJ; Cloyd, JC; Jones Saete, C; Kriel, RL; Ricker, BJ, 1997)
"Pyridoxine dependency is an uncommon familial cause of intractable seizures in newborns and infants."	1.30	Longitudinal MRI findings in pyridoxine-dependent seizures. ( Gospe, SM; Hecht, ST, 1998)
"Length of seizure disorder, seizure frequency at initiation, the number of previously used failed drugs and the total number of drugs previously used were all significantly lower in the seizure-free group."	1.30	The outcome of prescribing novel anticonvulsants in an outpatient setting: factors affecting response to medication. ( Kerr, MP; Thijs, RD, 1998)
"Gabapentin is a new antiepileptic drug not appreciably metabolized by the liver in humans, and it appears to be safe and effective in the maintenance therapy of epilepsy in these patients."	1.30	Treatment of seizures in acute intermittent porphyria: safety and efficacy of gabapentin. ( Brambilla, A; Erli, LC; Grandi, R; Mirabile, D; Zadra, M, 1998)
" Gabapentin is a new antiepileptic drug not appreciably metabolized by the liver in humans, and it appears to be safe and effective in the maintenance therapy of epilepsy in these patients."	1.30	Treatment of seizures in acute intermittent porphyria: safety and efficacy of gabapentin. ( Brambilla, A; Erli, LC; Grandi, R; Mirabile, D; Zadra, M, 1998)
"Topiramate is a new antiepileptic medication with multiple putative mechanisms of action."	1.30	Topiramate increases brain GABA, homocarnosine, and pyrrolidinone in patients with epilepsy. ( Hyder, F; Mattson, RH; Petroff, OA; Rothman, DL, 1999)
"In 1993, 27% of patients were being treated for epilepsy and in 1995/6, 30."	1.30	The management of epilepsy in a hospital for people with a learning disability. ( Carvill, S; Cassidy, G; Clarke, D, 1999)
"Vigabatrin (VGB) is an antiepileptic drug (AED) that acts by irreversibly inhibiting gamma-aminobutyric acid transaminase (GABA-T)."	1.29	Immunologic aspects of vigabatrin treatment in epileptic children. ( Iannetti, P; Imperato, C; Pacifici, R; Raucci, U; Zuccaro, P, 1995)
"Vigabatrin (VGB) is a safe and effective antiepileptic drug (AED) that irreversibly inhibits neuronal and glial GABA-transaminase."	1.29	Initial observations on effect of vigabatrin on in vivo 1H spectroscopic measurements of gamma-aminobutyric acid, glutamate, and glutamine in human brain. ( Behar, KL; Mattson, RH; Petroff, OA; Rothman, DL, 1995)
"Gabapentin is a new AED not appreciably metabolized by the liver in humans."	1.29	Gabapentin treatment of seizures in acute intermittent porphyria. ( Tatum, WO; Zachariah, SB, 1995)
" In view of the evidence for the role of excitatory amino acids in destruction of CNS nerve cells, the optimal treatment must counteract the raised levels of CSF glutamate and the dosage of vitamin B6 must be adjusted accordingly."	1.29	Glutamate in pyridoxine-dependent epilepsy: neurotoxic glutamate concentration in the cerebrospinal fluid and its normalization by pyridoxine. ( Baumeister, FA; Egger, J; Gsell, W; Shin, YS, 1994)
"The development of mental retardation might theoretically be prevented by adjusting the dose of vitamin B6 to achieve not only remission of epilepsy but also normalization of CSF glutamate."	1.29	Glutamate in pyridoxine-dependent epilepsy: neurotoxic glutamate concentration in the cerebrospinal fluid and its normalization by pyridoxine. ( Baumeister, FA; Egger, J; Gsell, W; Shin, YS, 1994)
"Vigabatrin has a definite role to play in the management of persons with intractable complex partial seizures where standard anti-epileptic therapy has failed to achieve control."	1.29	Vigabatrin use in 72 patients with drug-resistant epilepsy. ( Buchanan, N, 1994)
"Dexmedetomidine and the lower dose of atipamezole (0."	1.29	Effect of alpha 2-adrenergic drugs dexmedetomidine and atipamezole on extracellular amino acid levels in vivo. ( Haapalinna, A; Halonen, T; Riekkinen, P; Valtonen, P, 1995)
"Gabapentin is a gamma-aminobutyric acid (GABA) analog which passes the blood-brain barrier."	1.29	[New medical treatment of epilepsy]. ( Loiseau, P, 1996)
"Gabapentin is a novel antiepileptic drug that has recently been introduced in Canada."	1.29	Gabapentin. ( Bruni, J, 1996)
"Gabapentin has a favorable pharmacokinetic profile and is generally well tolerated."	1.29	Gabapentin. ( Bruni, J, 1996)
"Vigabatrin (VGB) is a recently-released antiepileptic drug which works by a clearly-defined mechanism of action: inhibition of GABA transaminase leading to an elevation of brain GABA concentration."	1.29	Vigabatrin. ( Guberman, A, 1996)
"Vigabatrin is a safe and effective antiepileptic medication designed to increase brain GABA by irreversibly inhibiting GABA-transaminase."	1.29	Human brain GABA levels rise rapidly after initiation of vigabatrin therapy. ( Behar, KL; Collins, TL; Mattson, RH; Petroff, OA; Rothman, DL, 1996)
" Once-a-day dosing should be as effective as divided doses."	1.29	Human brain GABA levels rise rapidly after initiation of vigabatrin therapy. ( Behar, KL; Collins, TL; Mattson, RH; Petroff, OA; Rothman, DL, 1996)
"Gabapentin is a novel anti-epileptic drug which enhances GABA (gamma-aminobutyric acid) turnover in certain brain regions, including substantia nigra."	1.29	The anticonvulsant gabapentin decreases firing rates of substantia nigra pars reticulata neurons. ( Bloms-Funke, P; Löscher, W, 1996)
" The results show that whether or not the introduction of vigabatrin results in an increase or a reduction in costs to the healthcare system depends largely on 3 factors: (i) the administered dosage of vigabatrin; (ii) the effect that vigabatrin has on hospital admissions; and (iii) the proportion of epileptic patients who take the drug."	1.29	The economic effects of introducing vigabatrin, a new antiepileptic medication. ( Champagne, F; Contandriopoulos, AP; Kennedy, W; Reinharz, D; Tessier, G, 1995)
"Epilepsy is a common disorder, the prevalence of which is estimated at between 0."	1.29	The economic effects of introducing vigabatrin, a new antiepileptic medication. ( Champagne, F; Contandriopoulos, AP; Kennedy, W; Reinharz, D; Tessier, G, 1995)
"Putrescine has been shown to be catabolized to GABA in brain tissue and astrocytes."	1.28	Characteristics of putrescine uptake and subsequent GABA formation in primary cultured astrocytes from normal C57BL/6J and epileptic DBA/2J mouse brain cortices. ( Bureau, M; Grisar, T; Guillaume, D; Laschet, J, 1992)
"Loreclezole was also shown to inhibit 'low Ca2+' and 'low Mg2+' epileptogenesis at similar concentrations to those active on inhibition."	1.28	In vitro studies on the broad spectrum anticonvulsant loreclezole in the hippocampus. ( Ashton, D; Willems, R, 1992)
"Epilepsy is a state of neuronal hyperactivity which may be caused by an altered relationship between inhibitory and excitatory influences on neurons."	1.28	Sensitivity of cerebellar Purkinje neurons to neurotransmitters in genetically epileptic rats. ( Craig, CR; Fleming, WW; Gould, EM; Taylor, DA, 1991)
"This taurine increase was highly reversible."	1.28	The epileptogenic action of the taurine analogue guanidinoethane sulfonate may be caused by a blockade of GABA receptors. ( Ambrosio, E; Herranz, AS; Herreras, O; Martin del Rio, R; Menéndez, N; Orensanz, LM; Solis, JM, 1990)
"1."	1.28	The effect of different vigabatrin treatment regimens on CSF biochemistry and seizure control in epileptic patients. ( Ben-Menachem, E; Dahlgren, L; Haegele, KD; Hardenberg, J; Huebert, N; Mumford, JP; Persson, LI; Schechter, PJ, 1989)
" Lumbar punctures were carried out prior to treatment and at the end of each dosage regimen and cerebrospinal fluid (CSF) evaluated for concentrations of free and total GABA, homocarnosine (GABA-histidine dipeptide), homovanillic acid (HVA), 5-hydroxyindole acetic acid (5-HIAA) and vigabatrin."	1.28	The effect of different vigabatrin treatment regimens on CSF biochemistry and seizure control in epileptic patients. ( Ben-Menachem, E; Dahlgren, L; Haegele, KD; Hardenberg, J; Huebert, N; Mumford, JP; Persson, LI; Schechter, PJ, 1989)
"Their convulsion properties are apparently related to the specific levels, locations and convulsive potential of the individual substances."	1.27	[Neuroendocrinologic aspects of epilepsy]. ( Bergamasco, B; Bianco, C; Cavallo, G; Pinessi, L, 1984)
"Bicuculline has been applied electrophoretically from a fluid filled microelectrode at different depths within the primary somatosensory area of the cerebral cortex of rats anaesthetized with urethane."	1.27	Bicuculline epileptogenesis in the rat. ( Campbell, AM; Holmes, O, 1984)
"In audiogenic seizure-susceptible (AGS) mice, evidence suggests a role for dopamine as well as GABA and possibly serotonin."	1.27	Neurotransmitter abnormalities in genetically epileptic rodents. ( Dailey, JW; Jobe, PC; Laird, HE, 1984)
"In 14 children with epilepsy, 51 with febrile convulsions and 22 with meningitis gamma-aminobutyric acid (GABA) concentrations in lumbar CSF were determined."	1.27	Low CSF GABA concentration in children with febrile convulsions, untreated epilepsy, and meningitis. ( Löscher, W; Rating, D; Siemes, H, 1983)
"gamma-Aminobutyric acid (GABA) was measured in CSF as such and following acid hydrolysis by the ion-exchange/fluorometric method."	1.27	Free and conjugated GABA in human cerebrospinal fluid: effect of degenerative neurologic diseases and isoniazid. ( Manyam, BV; Tremblay, RD, 1984)
"In patients with Huntington's disease, on administration of isoniazid at 900 mg/day, along with pyridoxine at 100 mg/day, a 4-fold increase of both free (P less than 0."	1.27	Free and conjugated GABA in human cerebrospinal fluid: effect of degenerative neurologic diseases and isoniazid. ( Manyam, BV; Tremblay, RD, 1984)
"L-Allylglycine treatment led to a substantial decrease in the concentration of detectable GABA-immunoreactive bouton-like dots in the stratum oriens, radiatum and lacunosum-moleculare and in the deep hilar region, but did not produce statistically significant changes in this parameter in the outer and intermediate zones of the dentate molecular layer."	1.27	Redistribution of transmitter amino acids in rat hippocampus and cerebellum during seizures induced by L-allylglycine and bicuculline: an immunocytochemical study with antisera against conjugated GABA, glutamate and aspartate. ( Meldrum, BS; Ottersen, OP; Storm-Mathisen, J; Swan, JH, 1987)
"Bicuculline-induced PDSs were reversibly reduced in amplitude and duration, but not abolished by the EAA receptor antagonists kynurenic acid (1 mM), cis-2,3-piperidine dicarboxylic acid (cis-2,3-PDA) (1 mM), or DL-2-amino-5-phosphonovalerate (DL-AP-5) (100 microM), revealing a long-lasting hyperpolarizing afterpotential."	1.27	GABAergic inhibition and epileptiform discharges in the turtle hippocampus in vitro. ( Larson-Prior, LJ; Slater, NT, 1988)
"Stiff-man syndrome is a rare disorder of the central nervous system consisting of progressive, fluctuating muscle rigidity with painful spasms."	1.27	Autoantibodies to glutamic acid decarboxylase in a patient with stiff-man syndrome, epilepsy, and type I diabetes mellitus. ( Comi, GC; De Camilli, P; Denis-Donini, S; Folli, F; Pozza, G; Solimena, M; Vicari, AM, 1988)
"Autonomic dysfunction, including arrhythmias, has been shown to be associated with epileptogenic activity."	1.27	The role of enkephalins in the production of epileptogenic activity and autonomic dysfunction: origin of arrhythmia and sudden death in the epileptic patient? ( Kraras, CM; Lathers, CM; Tumer, N, 1987)
"gamma-Vinyl GABA (GVG), an irreversible inhibitor of GABA degradation, was administered to seizure-susceptible gerbils at different dosage regimens."	1.27	One to three day dose intervals during subchronic treatment of epileptic gerbils with gamma-vinyl GABA: anticonvulsant efficacy and alterations in regional brain GABA levels. ( Frey, HH; Löscher, W, 1987)
"A form of endogenous (binaural) inhibition in inferior colliculus neurons, which is proposed to be GABA-mediated, was also significantly reduced in the epilepsy-prone rat as compared with the normal rat."	1.27	Decreased effectiveness of GABA-mediated inhibition in the inferior colliculus of the genetically epilepsy-prone rat. ( Caspary, DM; Faingold, CL; Gehlbach, G, 1986)
"Progabide was administered at a mean daily dose of 30."	1.27	Long-term treatment of epilepsy: open multicenter trial with progabide in epileptic patients. ( Beaussart, M; Benoit, C; Broglin, D; Cambier, J; Cenraud, M; Chatel, M; Deville, MC; Fournier, V; Loiseau, P; Musch, B, 1987)
"In this study the pentetrazole seizure threshold of dogs was compared with the concentration of GABA in the CSF and blood plasma."	1.26	Relationship between GABA concentrations in cerebrospinal fluid and seizure excitability. ( Löscher, W, 1982)
"Progabide is a GABA agonist which is nontoxic and crosses the blood-brain barrier."	1.26	Action of progabide in the photosensitive baboon, Papio papio. ( Cepeda, C; Lloyd, KG; Naquet, R; Worms, P, 1982)
"Progabide was tested in naturally and allylglycine-induced photosensitive baboons (Papio papio)."	1.26	Action of progabide in the photosensitive baboon, Papio papio. ( Cepeda, C; Lloyd, KG; Naquet, R; Worms, P, 1982)
"In 49 patients with various neurological disorders plasma and CSF gamma-aminobutyric acid (GABA) concentrations were determined by radioreceptor assay."	1.26	Plasma and cerebrospinal fluid gamma-aminobutyric acid in neurological disorders. ( Löscher, W; Schmidt, D, 1982)
"Behavioral seizures reappeared 2 to 3 days after termination of GAG treatment."	1.26	Amygdaloid kindling and the GABA system. ( Myslobodsky, MS; Valenstein, ES, 1980)
"Gamma-Aminobutyric acid (GABA) has been implicated in the neurochemistry of epilepsy."	1.26	Low cerebrospinal fluid gamma-aminobutyric acid content in seizure patients. ( Ballenger, JC; Glaeser, BS; Hare, TA; Post, RM; Wood, JH, 1979)
"Although lumbar CSF GABA levels in our seizure patients did not significantly correlate with serum concentrations of phenytoin, phenobarbital, or primidone, additional study of medication-free epileptic patients may be required to evaluate the possibility of anticonvulsant-drug-induced CSF GABA alterations."	1.26	Low cerebrospinal fluid gamma-aminobutyric acid content in seizure patients. ( Ballenger, JC; Glaeser, BS; Hare, TA; Post, RM; Wood, JH, 1979)
"The types of seizure patterns were classed as major (including focal) and minor (akinetic, myoclonic and hypsarrhythmic) and the patients were followed for up to one year."	1.24	Trial of amino-oxyacetic acid, an anticonvulsant. ( McGREAL, DA; TIBBLES, JA, 1963)

Research

Studies (1,294)

Authors

Clinical Trials (31)

Trial Overview

Trial Outcomes

Prefrontal GABA+ Concentrations

Timeframe	Studies, this research(%)	All Research%
pre-1990	249 (19.24)	18.7374
1990's	383 (29.60)	18.2507
2000's	363 (28.05)	29.6817
2010's	240 (18.55)	24.3611
2020's	59 (4.56)	2.80

Authors	Studies
Hawker, DD	1
Silverman, RB	2
Waszkielewicz, AM	1
Gunia-Krzyżak, A	1
Powroźnik, B	1
Słoczyńska, K	1
Pękala, E	1
Walczak, M	1
Bednarski, M	1
Żesławska, E	1
Nitek, W	1
Marona, H	1
Feja, M	1
Meller, S	1
Deking, LS	1
Kaczmarek, E	1
During, MJ	1
Gernert, M	5
Ahring, PK	2
Liao, VWY	1
Gardella, E	2
Johannesen, KM	1
Krey, I	1
Selmer, KK	1
Stadheim, BF	1
Davis, H	1
Peinhardt, C	1
Koko, M	1
Coorg, RK	1
Syrbe, S	1
Bertsche, A	1
Santiago-Sim, T	1
Diemer, T	1
Fenger, CD	1
Platzer, K	3
Eichler, EE	1
Lerche, H	3
Lemke, JR	3
Chebib, M	2
Møller, RS	2
Frazzini, V	1
Mathon, B	1
Donneger, F	1
Cousyn, L	1
Hanin, A	1
Nguyen-Michel, VH	1
Adam, C	1
Lambrecq, V	1
Dupont, S	1
Poncer, JC	1
Bielle, F	2
Navarro, V	3
Chen, W	1
Ge, Y	2
Lu, J	1
Melo, J	1
So, YW	1
Juneja, R	1
Liu, L	2
Wang, YT	1
Li, X	3
Liu, Y	8
Wang, S	3
Jiang, Y	4
Algradi, AM	1
Zhou, Y	1
Pan, J	1
Guan, W	1
Kuang, H	1
Yang, B	1
Jiang, YL	1
Song, CG	1
Zhou, HM	1
Feng, B	1
Zhao, JJ	1
Man, YL	1
Han, J	1
Liu, SB	1
Jiang, W	1
Wen, Y	1
Zhang, G	1
Zhang, P	3
Lin, L	4
Mei, R	3
Zhang, F	2
Chen, Y	4
Li, R	3
Feng, Y	1
Wei, ZH	1
Liu, C	2
Li, GY	1
Qiao, XZ	1
Gan, YJ	1
Zhang, CC	1
Deng, YC	1
Sun, Y	2
Peng, Z	1
Wei, X	1
Zhang, N	1
Huang, CS	1
Wallner, M	1
Mody, I	5
Houser, CR	3
Desai, D	1
Shende, P	1
Sticht, H	1
Bupp, C	1
Ganapathi, M	1
Pereira, EM	1
Le Guyader, G	1
Bilan, F	1
Henderson, LB	1
Taschenberger, H	1
Brose, N	1
Abou Jamra, R	1
Wojcik, SM	1
Cediel, ML	1
Stawarski, M	1
Blanc, X	1
Nosková, L	1
Magner, M	1
Gburek-Augustat, J	1
Baldridge, D	1
Constantino, JN	1
Ranza, E	1
Bettler, B	2
Antonarakis, SE	1
Rodrigues, TCML	1
de Moura, JP	1
Dos Santos, AMF	1
Monteiro, AFM	1
Lopes, SM	1
Scotti, MT	1
Scotti, L	1
Plumereau, Q	1
Ebdalla, A	1
Poulin, H	1
Appendino, JP	1
Scantlebury, MH	1
Au, PYB	1
Chahine, M	1
Kuanyshbek, A	1
Wang, M	2
Andersson, Å	1
Tuifua, M	1
Palmer, EE	1
Sachdev, RK	1
Mu, TW	2
Vetter, I	1
Keramidas, A	1
Avoli, M	18
de Curtis, M	3
Lévesque, M	1
Librizzi, L	1
Uva, L	1
Gao, M	3
Wang, K	4
Zhao, H	3
Zhang, XL	2
Zhou, JY	2
Zhang, FL	2
Chen, YM	2
Josiah, SS	1
Meor Azlan, NF	1
Oguro-Ando, A	1
Zhang, J	5
Chan, CK	1
Lim, KS	1
Low, SK	1
Tan, CT	1
Ng, CC	1
Bryson, A	1
Reid, C	1
Petrou, S	5
Stieve, BJ	1
Smith, MM	1
Krook-Magnuson, E	1
Zayed, AA	1
Seleem, MM	1
Darwish, HA	1
Shaheen, AA	1
Salaria, P	1
Akshinthala, P	1
Kapavarapu, R	1
M, AR	1
Tokatly Latzer, I	1
Bertoldi, M	1
DiBacco, ML	1
Arning, E	1
Tsuboyama, M	1
MacMullin, P	1
Sachee, D	1
Rotenberg, A	2
Lee, HHC	1
Aygun, D	1
Opladen, T	1
Jeltsch, K	1
García-Cazorla, À	2
Roullet, JB	2
Gibson, KM	4
Pearl, PL	4
Hajipour, S	1
Khombi Shooshtari, M	1
Farbood, Y	1
Ali Mard, S	1
Sarkaki, A	1
Moradi Chameh, H	1
Sistani Karampour, N	1
Ghafouri, S	1
Xie, J	1
Dai, Y	1
Xing, Y	1
Wang, Y	7
Yang, G	1
He, E	1
Xu, Z	2
Fan, P	1
Mo, F	1
Wu, Y	4
Song, Y	2
Cai, X	2
Khorram, E	1
Amini, M	1
Khorrami, M	1
Fukushima, K	2
Higashiyama, H	1
Kazuta, Y	1
Hashimoto, K	2
Watanabe, N	1
Furuya, Y	1
Ito, Y	1
Wu, T	1
Kosasa, T	1
Talos, DM	1
Roberts, NS	1
Jensen, FE	1
Hanada, T	1
Ido, K	1
van van Hugte, EJH	1
Schubert, D	1
Nadif Kasri, N	1
Nkwingwa, BK	1
Wado, EK	1
Foyet, HS	1
Bouvourne, P	1
Jugha, VT	1
Mambou, AHMY	1
Bila, RB	1
Taiwe, GS	1
Rajput, A	1
Sharma, P	1
Kumar, N	1
Singh, H	1
Singh, T	1
Singh, S	1
Singh Bedi, PM	1
Singh, B	1
Arora, S	1
Kaur, S	1
Foutsop, AF	1
Ateufack, G	1
Adassi, BM	1
Yassi, FB	1
Kom, TD	1
Noungoua, CM	1
Petsou, A	1
Ngoupaye, GT	1
Yakovlev, AV	1
Kurmashova, E	1
Gataulina, E	1
Gerasimova, E	1
Khalilov, I	8
Sitdikova, GF	1
Ciltas, AC	1
Toy, CE	1
Güneş, H	1
Yaprak, M	1
Xie, Y	2
Yang, Y	2
Yuan, X	1
He, X	3
Ali, I	2
Silva, J	1
Casillas-Espinosa, PM	1
Braine, E	1
Yamakawa, GR	1
Hudson, MR	1
Brady, RD	1
Major, B	1
Thergarajan, P	1
Haskali, MB	1
Wright, DK	1
Jupp, B	1
Vivash, L	1
Shultz, SR	1
Mychasiuk, R	1
Kwan, P	3
Jones, NC	1
Sachdev, P	1
Cheng, JY	1
O'Brien, TJ	2
Liu, N	2
Li, J	1
Gao, K	1
Perszyk, RE	1
Wang, J	7
Jenkins, A	2
Yuan, H	1
Traynelis, SF	1
Serrano-Castro, PJ	1
Rodríguez-Uranga, JJ	1
Cabezudo-García, P	1
García-Martín, G	1
Romero-Godoy, J	1
Estivill-Torrús, G	1
Ciano-Petersen, NL	1
Oliver, B	1
Ortega-Pinazo, J	1
López-Moreno, Y	1
Aguilar-Castillo, MJ	1
Gutierrez-Cardo, AL	1
Ramírez-García, T	1
Sanchez-Godoy, L	1
Carreño, M	1
Burman, RJ	1
Selfe, JS	1
Lee, JH	1
van den Berg, M	1
Calin, A	1
Codadu, NK	1
Wright, R	1
Newey, SE	1
Parrish, RR	1
Katz, AA	1
Wilmshurst, JM	1
Akerman, CJ	1
Trevelyan, AJ	3
Raimondo, JV	1
Cepeda, C	4
Levinson, S	1
Nariai, H	1
Yazon, VW	1
Tran, C	1
Barry, J	1
Oikonomou, KD	1
Vinters, HV	2
Fallah, A	1
Mathern, GW	3
Wu, JY	1
Cheng, A	1
Ghena, N	1
Zhao, Q	1
Perone, I	1
King, TM	1
Veech, RL	1
Gorospe, M	1
Wan, R	1
Mattson, MP	1
Righes Marafiga, J	1
Vendramin Pasquetti, M	2
Calcagnotto, ME	4
Steudle, F	1
Rehman, S	1
Bampali, K	1
Simeone, X	1
Rona, Z	1
Hauser, E	1
Schmidt, WM	1
Scholze, P	1
Ernst, M	1
Fukuyama, K	2
Fukuzawa, M	1
Shiroyama, T	1
Okada, M	4
Denoyer, Y	1
Merlet, I	1
Wendling, F	3
Benquet, P	2
Poliquin, S	2
Mermer, F	2
Eissman, J	1
Delpire, E	1
Shen, W	4
Cai, K	1
Li, BM	1
Li, ZY	1
Xu, D	1
Nwosu, G	2
Flamm, C	1
Liao, WP	3
Shi, YW	1
Kang, JQ	3
Colangeli, R	1
Morena, M	1
Pittman, QJ	2
Hill, MN	1
Teskey, GC	1
Viswanatha, GL	3
Shylaja, H	1
Kishore, DV	1
Venkataranganna, MV	3
Prasad, NBL	3
Gonen, OM	1
Moffat, BA	1
Desmond, PM	1
Lui, E	1
Colijn, MA	1
Akyuz, E	1
Polat, AK	1
Eroglu, E	1
Kullu, I	1
Angelopoulou, E	1
Paudel, YN	1
Virtanen, MA	1
Uvarov, P	1
Hübner, CA	2
Kaila, K	6
Deidda, G	1
Crunelli, V	2
Di Giovanni, G	1
Lybrand, ZR	1
Goswami, S	1
Zhu, J	2
Jarzabek, V	1
Merlock, N	1
Aktar, M	1
Smith, C	1
Zhang, L	3
Varma, P	1
Cho, KO	1
Ge, S	1
Hsieh, J	1
Kim, HY	1
Suh, PG	1
Kim, JI	1
Rigsby, K	1
Rastogi, A	1
Romero-Morales, A	1
McGrath, P	1
Demerast, S	1
Aoto, J	1
Bilousova, G	1
Lal, D	1
Gama, V	1
Sarlo, GL	1
Holton, KF	1
Gong, T	1
Lin, Y	1
Wang, G	1
Smith, AK	1
Wade, AR	1
Penkman, KEH	1
Baker, DH	1
Liu, W	1
Ge, T	1
Pan, Z	1
Leng, Y	1
Lv, J	1
Li, B	1
Bozzi, Y	1
Provenzano, G	1
Casarosa, S	1
Uchida, T	1
Lossin, C	1
Ihara, Y	1
Deshimaru, M	1
Yanagawa, Y	1
Koyama, S	1
Hirose, S	1
Jacob, L	1
Hamer, HM	1
Kostev, K	1
Nevitt, SJ	2
Sudell, M	2
Weston, J	2
Tudur Smith, C	2
Marson, AG	7
Zhang, HJ	1
Wang, Q	3
Zhang, DW	1
Wu, D	2
Li, W	2
Quan, ZS	1
Meier, L	1
Loureiro, S	1
Ganzella, M	1
Junges, B	1
Barbieri Caus, L	1
Umpierrez Amaral, A	1
Koeller, DM	1
Goodman, S	1
Woontner, M	1
Gomes de Souza, DO	1
Wajner, M	1
Conway, JM	1
Eberly, LE	1
Collins, JF	2
Macias, FM	1
Ramsay, RE	6
Leppik, IE	7

Trial	Phase	Enrollment	Study Type	Start Date	Status
Phenylbutyrate for Monogenetic Developmental and Epileptic Encephalopathy[NCT04937062]	Early Phase 1	50 participants (Anticipated)	Interventional	2021-03-01	Enrolling by invitation
Biperiden for Prevention of Epilepsy in Patients With Traumatic Brain Injury[NCT04945213]	Phase 3	312 participants (Anticipated)	Interventional	2023-01-10	Recruiting
The BrainDrugs-Epilepsy Study: A Prospective Open-label Cohort Precision Medicine Study in Epilepsy[NCT05450822]		550 participants (Anticipated)	Observational	2022-02-18	Recruiting
The Effect of Probiotic Supplementation in Drug-resistant Epilepsy Patients[NCT03403907]		45 participants (Actual)	Interventional	2014-10-01	Completed
A Retrospective Study to Evaluate Retention Rate of Topiramate With That of Levetiracetam and Oxcarbazepine in a Long-term Epilepsy Treatment[NCT02098941]		2,500 participants (Anticipated)	Observational	2014-03-31	Recruiting
Evaluation of Valproic Acid (VPA) as Adjunctive Therapy for Liver Transplant Patients With Moderate to Severe Hemorrhage at Risk of Ischemia Reperfusion (I/R) Injury[NCT04531592]	Phase 2	0 participants (Actual)	Interventional	2022-01-31	Withdrawn (stopped due to Study terminated by the Sponsor)
Phase I Study of Cytolytic Viral Activation Therapy (CVAT) for Recurrent/Metastatic Nasopharyngeal Carcinoma[NCT02761291]	Phase 1	18 participants (Anticipated)	Interventional	2016-05-31	Recruiting
Evaluation of Valproic Acid (VPA) as Adjunctive Therapy for Trauma Patients With Moderate to Severe Hemorrhage at Risk of Ischemia Reperfusion (I/R) Injury[NCT04531579]	Phase 2	0 participants (Actual)	Interventional	2022-01-31	Withdrawn (stopped due to Study terminated by the Sponsor.)
Imaging Framework for Testing GABAergic/Glutamatergic Drugs in Bipolar Alcoholics[NCT03220776]	Phase 2	54 participants (Actual)	Interventional	2017-08-07	Completed
Application of Vagal Stimulation by Cold Face Mask in Exposure and Response Prevention for Obsessive Compulsive Disorder[NCT02196090]		10 participants (Anticipated)	Interventional	2014-07-31	Recruiting
Efficacy of Pregabalin and Duloxetine in Patients With Painful Diabetic Peripheral Neuropathy (PDPN): the Effect of Pain on Cognitive Function, Sleep and Quality of Life (BLOSSOM)[NCT04246619]	Phase 4	254 participants (Actual)	Interventional	2019-11-12	Terminated (stopped due to The statistical analysis will still provide relevant results with the same statistical power as initially planned.COVID-19 pandemic prolonged the recruiting period and consequently affected the costs of the clinical trial.)
A Multicentre, Double-blind, Randomized, Phase IV Clinical Trial Comparing the Safety, Tolerability and Efficacy of Levetiracetam Versus Lamotrigine and Carbamazepine in the Oral Antiepileptic Therapy of Newly Diagnosed Elderly Patients With Focal Epileps[NCT00438451]	Phase 4	361 participants (Actual)	Interventional	2007-01-31	Completed
Remote Effects of Stroke on Cerebral Metabolism. Evaluation With Positron Emission Tomography and Proton Magnetic Resonance Spectroscopy[NCT00063180]		70 participants	Observational	2003-06-19	Completed
A Double-Blind, Placebo-Controlled Study of Dronabinol in Trichotillomania and Other Body Focused Repetitive Behaviors[NCT03530800]	Phase 2/Phase 3	50 participants (Actual)	Interventional	2018-10-01	Completed
Opioid-Induced Hyperalgesia in Prescription Opioid Abusers: Effects of Pregabalin[NCT01821430]	Phase 2	4 participants (Actual)	Interventional	2013-03-31	Terminated (stopped due to poor recruitment)
Use of Single Dose Pre-Operative Pregabalin for Post-Operative Analgesia in Bilateral Head and Neck Cancer Surgery: A Randomized, Double-Blinded, Placebo-Controlled Trial[NCT03714867]	Phase 4	0 participants (Actual)	Interventional	2019-03-22	Withdrawn (stopped due to Inability to recruit patients)
Pharmacokinetic Non-interaction Study Between Pregabalin 150 mg and Tramadol 50 mg, Administered Individually or in Combination, Single Dose in Healthy Subjects of Both Genders Under Fasting Conditions[NCT05389150]	Phase 1	30 participants (Actual)	Interventional	2019-01-17	Completed
The Effect of Pregabalin on Post-operative Pain and Opioid Consumption in Spine Surgery, a Prospective, Randomized, Controlled Study[NCT05083793]	Phase 2	90 participants (Anticipated)	Interventional	2020-04-01	Enrolling by invitation
A Prospective Study on Long-term Outcome and Potential Usefulness fo an Intervention Aimed at Reducing Adverse Effects in Patients With Refractory Epilepsy[NCT03939507]		1,000 participants (Actual)	Interventional	2006-11-06	Completed
Bridging Cognitive Aging in Rodents to Man Using fMRI in Amnestic MCI[NCT01044758]	Phase 2	96 participants (Actual)	Interventional	2009-12-31	Completed
Network-Level Mechanisms for Preclinical Alzheimer's Disease Development[NCT03461861]	Phase 2	26 participants (Actual)	Interventional	2019-04-11	Completed
Levetiracetam for Alzheimer's Disease Neuropsychiatric Symptoms Related to Epilepsy Trial (LAPSE) - A Phase II Exploratory Study[NCT04004702]	Phase 2	65 participants (Anticipated)	Interventional	2020-01-31	Not yet recruiting
Efficacy, Tolerability and Adherence of the Modified Atkins Diet on Drug-resistant Epilepsy in Adults Patients[NCT03183076]		14 participants (Actual)	Interventional	2015-09-01	Completed
Measurement of GABA and Neurosteroid Levels in Women With Menopausal Major Depression Before and After Treatment With Estrogen Alone, Fluoxetine Alone, or Estrogen and Fluoxetine and Normal Controls Before and After Treatment With Estrogen[NCT00626340]	Phase 4	18 participants (Actual)	Interventional	1999-07-31	Completed
Open Labeled, Non-randomized, Study of Efficacy and Safety of Gralise in Fibromyalgia Patients.[NCT02052414]		34 participants (Actual)	Interventional	2012-07-31	Completed
The Effect of Gabapentin on Prefrontal GABA Concentration and Emotional Processing in Healthy Humans[NCT00094510]		30 participants (Actual)	Observational	2004-10-14	Completed
The Efficacy of Gabapentine and Splint Therapy in Bruxers: a Randomized Clinical Trial[NCT01255878]		20 participants (Actual)	Interventional	2010-03-31	Completed
An Open Prospective Randomised Long-Term Effectiveness Study, Comparing Best Medical Practice With or Without Adjunctive VNS Therapy in Patients 16 Years and Older With Pharmaco-resistant Partial Epilepsy[NCT00522418]	Phase 4	122 participants (Actual)	Interventional	2006-02-28	Terminated (stopped due to Insufficient enrollment)
Trial of Intracerebral Infusion in Patients With Medically Intractable Epilepsy[NCT00005925]	Phase 1	3 participants (Actual)	Interventional	2000-06-23	Terminated
The Effect of Vigabatrin on Cerebral Blood Flow and Glucose Metabolism[NCT00001489]		20 participants	Observational	1994-10-31	Completed
The Efficacy of High-Dose Intravenous Immunoglobulin Therapy in Patients With Stiff-Man Syndrome: A Double-Blind, Placebo-Controlled Trial[NCT00001550]	Phase 1	20 participants	Interventional	1996-04-30	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Concentrations of GABA+, referenced to unsuppressed water and corrected for within-voxel CSF proportion, in dorsal anterior cingulate cortex measured via Proton Magnetic Resonance Spectroscopy (i.e., MEGA-PRESS). (NCT03220776)
Timeframe: Day 5 of each experimental condition

Prefrontal Glx Concentrations

Intervention	mmol/kg (Mean)
N-Acetylcysteine	3.90
Gabapentin	3.93
Placebo Oral Tablet	3.73

Concentrations of Glx (i.e., glutamate + glutamine), referenced to unsuppressed water and corrected for within-voxel CSF proportion, in dorsal anterior cingulate cortex measured via Proton Magnetic Resonance Spectroscopy. (NCT03220776)
Timeframe: Day 5 of each experimental condition

58-week Retention Rate Measured by the Number of Drop Outs Due to Adverse Events or Seizures From Day 1 of Treatment

Percentage of Patients Remaining Seizure Free at Week 58 (Visit 6)

Intervention	mmol/kg (Mean)
N-Acetylcysteine	21.59
Gabapentin	21.69
Placebo Oral Tablet	22.25

Intervention	proportion of participants (Mean)
Levetiracetam	0.61
Carbamazepine	0.46
Lamotrigine	0.56

Percentage of patients experiencing no seizures until week 58 (Visit 6) and did not discontinue the study until week 58. (NCT00438451)
Timeframe: week 58

Percentage of Patients Remaining Seizure-free at Week 30 (Visit 4)

Intervention	percentage of participants (Number)
Levetiracetam	43
Carbamazepine	33
Lamotrigine	38

Percentage of patients experiencing no seizures until week 30 (Visit 4) and did not discontinue the study until week 30. (NCT00438451)
Timeframe: Week 30

Proportion of Seizure-free Days During the Maintenance Phase for Subjects Who Enter the Maintenance Phase

Results of Cognitive Testing (EpiTrack© by UCB) - Score at V6

Intervention	percentage of participants (Number)
Levetiracetam	48
Carbamazepine	39
Lamotrigine	49

Intervention	proportion of seizure-free days (Number)
Levetiracetam	0.99
Carbamazepine	0.99
Lamotrigine	0.99

EPITrack-Score shows the performance of attention and executive functions. Higher values indicate a better performance. The results of EPITrack Score ranges between 7 and 45. (NCT00438451)
Timeframe: week 58

The Absolute Seizure Frequency During the Maintenance Phase (Weeks 7 - 58)

Intervention	units on a scale (Mean)
Levetiracetam	26.0
Carbamazepine	26.0
Lamotrigine	25.4

"Seizure frequency was assessed by investigators in the CRF at the Visits V3, V4, V5 and V6.~The absolute seizure frequency during the maintenance phase was defined as the sum of those entries." (NCT00438451)
Timeframe: over 52 weeks

The Time (in Days) to First Break-through Seizure (From Day 1 of Treatment)

Time to Drop Out

Intervention	number of seizures (Number)
Levetiracetam	168
Carbamazepine	131
Lamotrigine	130

Intervention	days (Median)
Levetiracetam	NA
Carbamazepine	NA
Lamotrigine	NA

number of days between randomization and premature discontinuation of the study (NCT00438451)
Timeframe: 58 weeks

Portland Neurotoxicity Scale (PNS) at V6

Intervention	days (Median)
Levetiracetam	NA
Carbamazepine	265
Lamotrigine	NA

"The PNS is a 15-item scale. Each item can be scored from 1 to 9. There are a total score (includes all items, range:15 to 135) and two subscores: The cognitive toxicity subscore (10 items: Energy Level, Memory, Interest, Concentration, Forgetfulness, Sleepliness, Moodiness, Alertness, Attention Span, Motivation, range:10 to 90) and the somatomoto subscore (5 items: Vision, Walking, Coordination, Tremor, Speech, range:5-45). The score is calculated by taking the mean of all non-missing values times the number of items.~Lower values indicate better quality of life." (NCT00438451)
Timeframe: at week 58

QOLIE-31 (Quality Of Life In Epilepsy) Results at V6

Intervention	units on a scale (Mean)
	Cognitive toxicity subscore	Somatomotor subscore	Total Score
Carbamazepine	27.3	11.4	38.7
Lamotrigine	23.7	10.8	34.5
Levetiracetam	22.2	10.5	32.7

The QOLIE-31 is a 31 item score that measures the quality of life in epilepsy (each item with a range of 0 to 100). There are 7 sub-scores seizure worry (items 11,21,22,23,25), overall quality of life (items 1,14), emotional well-being (items 3,4,5,7,9), energy/fatigue (items 2,6,8,10), cognitive functioning (items 12,15,16,17,18,26), medication effects (items 24,29,30) and social functioning (13,19,20,27,28). These scores were combined to a total score by Total score = seizure worry*0.08 + overall quality of life*0.14 + emotional well-being*0.15 + energy/fatigue*0.12 + cognitive functioning*0.27 + medication effects*0.03 + social functioning*0.21 For all scores, higher values indicate better quality of life. Each score has a possible range from 0 to 100. (NCT00438451)
Timeframe: 58 weeks, final visit

Results of Cognitive Testing (EpiTrack© by UCB) - Categories at V6

Intervention	units on a scale (Mean)
	Seizure worry	Overall quality of life	Emotional well-being	Energy/fatigue	Cognitive functioning	Medication effects	Social functioning	Total Score	Health Scale
Carbamazepine	75.4	65.0	69.8	54.5	68.9	70.6	76.3	68.9	65.7
Lamotrigine	75.0	67.1	67.4	59.8	68.0	72.6	76.7	69.1	67.5
Levetiracetam	85.1	67.2	72.0	60.8	75.1	77.6	81.1	73.9	69.5

"Evaluation of current testing at V6:~≥29 score points: Inconspicuous; 26 to 28 score points: Borderline;~≤25 score points: Impaired" (NCT00438451)
Timeframe: 58 weeks

Results of Cognitive Testing (EpiTrack© by UCB) - Changes to Baseline (V0) at Week 58 (V6)

Intervention	participants (Number)
	Without pathological findings	Borderline	Impaired
Carbamazepine	34	17	33
Lamotrigine	31	15	39
Levetiracetam	38	10	36

"Evaluation of Changes~Changes in the EpiTrack® Score were categorized as follows:~≥5 score points: Improved;~-3 to 4 score points: Unchanged;~≤-4 score points: Worsened" (NCT00438451)
Timeframe: week 58

NIMH Trichotillomania Symptom Severity Scale (NIMH-TSS)

Intervention	participants (Number)
	Improved	Unchanged	Worsened
Carbamazepine	16	56	8
Lamotrigine	15	53	13
Levetiracetam	15	61	6

The entire study lasts 10 weeks. Every two weeks subjects will take the NIMH-TSS. The change in scores from baseline to after 10 weeks will be assessed. The scale itself assesses severity of trichotillomania symptoms. The NIMH-TSS score ranges from 0 to 20, with 0 being no symptoms and 20 being the most severe. (NCT03530800)
Timeframe: Assessed every two weeks up to 10 weeks, baseline data reported

Skin Picking Symptom Assessment Scale (SP-SAS)

Intervention	score on a scale (Mean)
Dronabinol	12.38
Placebo	10.63

The entire study lasts 10 weeks. Every two weeks subjects will take the SP-SAS. The change in scores from baseline to after 10 weeks will be assessed. The scale itself assesses severity of skin-picking symptoms. The SP-SAS score ranges from 0 to 48, with 0 being no symptoms and 48 being the most severe. (NCT03530800)
Timeframe: Assessed every two weeks up to 10 weeks, baseline reported

Behavioral Performance as Assessed in the Functional Magnetic Resonance Imaging (fMRI) Memory Task

Intervention	score on a scale (Mean)
Dronabinol	24.44
Placebo	28.5

Mnemonic similarity task which assesses long term memory function. Scale ranges from 0-100 with higher scores indicating better memory performance. (NCT01044758)
Timeframe: 2 weeks

Brain Activity in the Dentate Gyrus / CA3 Subregion of the Hippocampus Measured With Blood Oxygenation Level Dependent (BOLD) Functional MRI

Intervention	percent correct recalled (Mean)
aMCI_62.5	38
aMCI_62.5 Placebo	33
aMCI_125	33
aMCI_125 Placebo	28
aMCI_250	34
aMCI_250 Placebo	31
Age Matched Control	44

Measurement of average brain activity in the dentate gyrus / CA3 subregion of the hippocampus measured with BOLD functional MRI in patients with mild cognitive impairment on placebo and on drug compared to average brain activity in this brain area in control subjects. (NCT01044758)
Timeframe: 2 weeks

Functional Connectivity Strengths of Neural Networks

Intervention	mean beta coefficient (Mean)
aMCI_62.5	-0.1203
aMCI_62.5 Placebo	0.4353
aMCI_125	-0.2238
aMCI_125 Placebo	0.8814
aMCI_250	0.3928
aMCI_250 Placebo	0.4825
Age Matched Control	-.02507

The seed-based functional connectivity strengths of the hippocampus network and the default mode network will be employed to measure the changes between AGB101 and Placebo perturbation. The functional connectivity strengths will be measured with the median of the Pearson cross-correlation coefficients over entire brain regions. (NCT03461861)
Timeframe: 2 weeks after treatment between AGB101 and Placebo

Rey Auditory Verbal Learning Test (AVLT), Delayed Recall Scaled Integer. The Higher is the Better

Intervention	Pearson coefficient (Median)
AGB101 220 mg	0.233
Placebo	0.318

Rey Auditory Verbal Learning Test (AVLT), delayed recall Scaled integer will be employed to measure the episodic memory changes before and after AGB101 treatment. The AVLT score will be recorded as a standard score. The theoretical range: min 50, max 155, the higher the better. The higher the number is, the better the memory. It is an integer number. (NCT03461861)
Timeframe: Placebo vs AGB101 2 weeks after treatment paired t-test

Comparison of Cortical GABA Levels in 4 Groups of Subjects Using Estrogen Alone, Fluoxetine Alone, Estrogen and Fluoxetine Combined in Pre and Post 4.0T Magnetic Resonance Spectroscopy Sessions.

Intervention	score on a scale (Mean)
AGB101 220 mg	108
Placebo	105

"This study was conducted at Yale University almost two decades ago. Our group at the University of Pennsylvania only has very basic information about this study. This includes the number of participants, which was 18, and the fact that no adverse events occurred. Staff members at the University of Pennsylvania do not have access to any additional study data. The contact person who initially entered this study protocol information is no longer at the University of Pennsylvania and we are unable to contact for additional information.~We only know that 18 participants completed, but as far as we know data was never analyzed for these 18 participants." (NCT00626340)
Timeframe: Healthy controls will undergo scans pre and post 3 weeks of estrogen treatment. Women with depression will undergo scans pre and post 6 weeks of treatment with estrogen alone, estrogen and fluoxetine, or fluoxetine alone

Fibromyalgia Impact Questionnaire (FIQ)

Intervention	()
All Participants	0

The Fibromyalgia Impact Questionnaire (FIQ) is an instrument designed to quantitate the overall impact of fibromyalgia over many dimensions (e.g. function, pain level, fatigue, sleep disturbance, psychological distress etc.). It is scored from 0 to 100 with the latter number being the worst case. The average score for patients seen in tertiary care settings is about 50. The FIQ is widely used to assess change in fibromyalgia status. (NCT02052414)
Timeframe: 15 weeks.

Medical Outcome Study (MOS) Sleep Questionnaires

Intervention	units on a scale (Mean)
	FIQ Baseline	FIQ Week 4	FIQ Week 8	FIQ Week 12	FIQ Week 15
Gralise (Gabapentin ER)	71.04	41.82	40.79	39.27	61.86

"Medical Outcomes Study (MOS) sleep questionnaires to assess how Fibromyalgia impacts patients' sleep in various areas.~Specifically, Data reported below measured number of hours subjects spent per night sleeping. MOS sleep questionnaires were assessed at each follow up visits. (visits 1, 2, 3, 4, and 5)." (NCT02052414)
Timeframe: 15 weeks

Numeric Pain Rating System (NPRS)

Intervention	Hours (Mean)
	Sleep Quantity Baseline	Sleep Quantity week 4	Sleep quantity week 8	Sleep quantity week 12	Sleep quantity week 15
Gralise (Gabapentin ER)	5.86	7.17	6.81	7.04	6.23

Fibromyalgia pain experienced by study subjects will be captured using NPRS at baseline visit, at each follow visits that are scheduled to occur every 4 weeks over 12 weeks of treatment period, and at the end of treatment visit that will occur 3 weeks after treatment period (12 weeks treatment period + 3 weeks = 15 weeks). Any difference in NPRS scores between baseline and any subsequent visits will indicate the magnitude of pain relief as reflected in digital scale of 0-10 (0=no pain, 10=worst pain imaginable). (NCT02052414)
Timeframe: 15 weeks

Patient Global Impression of Change (PGIC)

Intervention	units on a scale (Mean)
	NPRS Baseline (Visit 1)	NPRS on Week 4 (Visit 2)	NPRS on week 8 (Visit 3)	NPRS on Week 12 (Visit 4)	NPRS on week 15 (Visit 5)
Gralise (Gabapentin ER)	7.29	4.72	3.95	3.83	6.94

Patient Global impression of Change (PGIC) is an outcome commonly used measure of the efficacy of treatments. PGIC is a 7 point scale that requires the subjects to assess how much the patient's illness has improved or worsened relative to a baseline state at the beginning of the intervention. and rated as: 1, very much improved; 2, much improved; 3, minimally improved; 4, no change; 5, minimally worse; 6, much worse; or 7, very much worse. (NCT02052414)
Timeframe: 15 Weeks.

Self Reported Side Effects.

Intervention	units on a scale (Mean)
	PGIC After 4 weeks	PGIC After 8 weeks	PGIC After 12 weeks	PGIC After 15 weeks
Gralise (Gabapentin ER)	4.96	5.40	5.37	4.44

Side / adverse effects were assessed at each follow up visits and resulted are as follows. (NCT02052414)
Timeframe: 15 Weeks

Change From Baseline in Adverse Event Profile (AEP) Score

Intervention	participants (Number)
	Extremity Swelling	Weight Gain	Drowsy	Dizzy	Irritability	Dry Eyes	Pain	Mood Changes	Difficulty Concentrating	Dry Mouth	Suspected Drug interaction	Acute Delerium	Adhesion	None
Gralise (Gabapentin ER)	2	2	8	3	3	2	1	2	2	1	1	1	1	12

Adverse Events Profile (AEP) is a 19-item scale used as a systematic measure of adverse effects from antiepileptic drugs (AEDs). Scores range from 19-76; higher scores indicate high prevelance and severity of adverse events. (NCT00522418)
Timeframe: Mean change from baseline AEP Score at 12 months

Change From Baseline in Center for Epidemiologic Studies Depression Scale (CES-D) Score

Intervention	Units on a scale (Mean)
VNS Therapy	-6.0
Best Medical Practice	-3.2

The Center for Epidemiologic Studies Depression Scale (CES-D) includes 20 items comprising six scales reflecting major dimensions of depression: depressed mood, feelings of guilt and worthlessness, feelings of helplessness and hopelessness, psychomotor retardation, loss of appetite, and sleep disturbance. Possible range of scores is 0 to 60, higher scores indicate more depressive symptoms. (NCT00522418)
Timeframe: Mean change from baseline CES-D Score at 12 months

Change From Baseline in Neurological Disorders Depression Inventory for Epilepsy (NDDI-E) Score

Intervention	Units on a Scale (Mean)
VNS Therapy	-2.2
Best Medical Practice	0.5

The Neurological Disorders Depression Inventory for Epilepsy (NDDI-E) is a 6-item questionnaire validated to screen for depression in people with epilepsy. Scores range from 6 to 24, with higher scores indicating more depressive symptoms. (NCT00522418)
Timeframe: Mean change from baseline NDDI-E Score at 12 months

Changes in Anti-epileptic Drugs (AEDs)

Intervention	Units on a Scale (Mean)
VNS Therapy	-1.0
Best Medical Practice	-0.2

Change from baseline in number of AED medications by visit (NCT00522418)
Timeframe: Change from baseline in number of AEDs at 12 months

Mean Change From Beginning of Intervention Clinical Global Impression-Improvement Scale (CGI-I) Score at 12 Months

Intervention	Number of AEDs Taken (Median)
VNS Therapy	0
Best Medical Practice	0

The Clinical Global Impression scale (CGI-I) is a 7 point scale that requires the clinician to assess how much the patient's illness has improved or worsened relative to a baseline state at the beginning of the intervention Scores range from 1-7: 1, very much improved; 2, much improved; 3, minimally improved; 4, no change; 5, minimally worse; 6, much worse; or 7, very much worse. (NCT00522418)
Timeframe: Mean change from baseline CGI-I Score at 12 months

Mean Percent Change in Seizure Frequency

Intervention	Units on a Scale (Mean)
VNS Therapy	-0.8
Best Medical Practice	-0.3

Percent change in total seizuires per week from baseline at 12 months (NCT00522418)
Timeframe: Mean percent change from baseline in seizure frequency at 12 months

Overall Quality of Life in Epilepsy-89 (QOLIE-89) Score in Patients With Baseline & at Least One Post-baseline QOLIE Assessment

Intervention	Percent Change (Mean)
VNS Therapy	-19.1
Best Medical Practice	-1.0

QOLIE-89 contains 17 multi-item measures of overall quality of life, emotional well-being, role limitations due to emotional problems, social support, social isolation, energy/fatigue, worry about seizure, medication effects, health discouragement, work/driving/social function, attention/concentration, language, memory, physical function, pain, role limitations due to physical problems, and health perceptions. Range of values 0-100. Higher scores reflect better quality of life; lower ones, worse quality of life. (NCT00522418)
Timeframe: Mean change from baseline QOLIE-89 Overall Score at 12 months

Response Rate

Intervention	units on a scale (Mean)
VNS Therapy	5.5
Best Medical Practice	1.2

Response Rate is defined as the percent of participants who are responders. A Responder is defined as participants with a reduction of at least 50% or 75% in seizure frequency from baseline to the seizure count evaluation period. (NCT00522418)
Timeframe: Number of Responders at 12 Months

Change From Baseline in QOLIE-89 Measures: Subgroup Analysis of Population With Baseline Adverse Event Profile Score < 40

Intervention	participants (Number)
VNS Therapy	10
Best Medical Practice	7

QOLIE-89 contains 17 multi-item measures of overall quality of life. Range of values 0-100. Higher scores reflect better quality of life; lower ones, worse quality of life. Adverse Events Profile (AEP) is a 19-item scale used as a systematic measure of adverse effects from antiepileptic drugs (AEDs). Scores range from 19-76; higher scores indicate high prevelance and severity of adverse events. (NCT00522418)
Timeframe: Change from baseline up to 12 months

Change From Baseline in QOLIE-89 Measures: Subgroup Analysis of Population With Baseline Adverse Event Profile Score >= 40

Article	Year
The beneficial effect of probiotics as a supplementary treatment in drug-resistant epilepsy: a pilot study. Beneficial microbes, 2018, Dec-07, Volume: 9, Issue:6 Topics: Adolescent; Adult; Dietary Supplements; Drug Resistance; Epilepsy; Female; gamma-Aminobutyric Acid;	2018
The beneficial effect of probiotics as a supplementary treatment in drug-resistant epilepsy: a pilot study. Beneficial microbes, 2018, Dec-07, Volume: 9, Issue:6 Topics: Adolescent; Adult; Dietary Supplements; Drug Resistance; Epilepsy; Female; gamma-Aminobutyric Acid;	2018
The beneficial effect of probiotics as a supplementary treatment in drug-resistant epilepsy: a pilot study. Beneficial microbes, 2018, Dec-07, Volume: 9, Issue:6 Topics: Adolescent; Adult; Dietary Supplements; Drug Resistance; Epilepsy; Female; gamma-Aminobutyric Acid;	2018
The beneficial effect of probiotics as a supplementary treatment in drug-resistant epilepsy: a pilot study. Beneficial microbes, 2018, Dec-07, Volume: 9, Issue:6 Topics: Adolescent; Adult; Dietary Supplements; Drug Resistance; Epilepsy; Female; gamma-Aminobutyric Acid;	2018
Levetiracetam and pregabalin for antiepileptic monotherapy in patients with primary brain tumors. A phase II randomized study. Neuro-oncology, 2014, Volume: 16, Issue:4 Topics: Anticonvulsants; Brain Neoplasms; Epilepsy; Female; Follow-Up Studies; gamma-Aminobutyric Acid; Huma	2014
[Diagnosis and correction of cognitive impairment in preschool age children with epilepsy]. Zhurnal nevrologii i psikhiatrii imeni S.S. Korsakova, 2015, Volume: 115, Issue:10 Topics: Child; Child, Preschool; Cognition Disorders; Electroencephalography; Epilepsy; Female; gamma-Aminob	2015
Adjunctive pregabalin therapy in mentally retarded, developmentally delayed patients with epilepsy. Epilepsy & behavior : E&B, 2008, Volume: 13, Issue:3 Topics: Adult; Anticonvulsants; Epilepsy; Female; Follow-Up Studies; gamma-Aminobutyric Acid; Humans; Intell	2008
Pregabalin: preliminary experience in intractable childhood epilepsy. Pediatric neurology, 2009, Volume: 40, Issue:5 Topics: Adolescent; Anticonvulsants; Child; Child, Preschool; Cognition Disorders; Drug Therapy, Combination	2009
Pregabalin as an adjunct to phenobarbital, potassium bromide, or a combination of phenobarbital and potassium bromide for treatment of dogs with suspected idiopathic epilepsy. Journal of the American Veterinary Medical Association, 2009, Dec-15, Volume: 235, Issue:12 Topics: Animals; Anticonvulsants; Bromides; Dog Diseases; Dogs; Drug Therapy, Combination; Epilepsy; Female;	2009
Pregabalin effect on steady-state pharmacokinetics of carbamazepine, lamotrigine, phenobarbital, phenytoin, topiramate, valproate, and tiagabine. Epilepsia, 2011, Volume: 52, Issue:2 Topics: Anticonvulsants; Dose-Response Relationship, Drug; Double-Blind Method; Drug Interactions; Drug Ther	2011
Modeling longitudinal daily seizure frequency data from pregabalin add-on treatment. Journal of clinical pharmacology, 2012, Volume: 52, Issue:6 Topics: Adolescent; Adult; Aged; Aged, 80 and over; Anticonvulsants; Child; Dose-Response Relationship, Drug	2012
Analysis of exposure-response of CI-945 in patients with epilepsy: application of novel mixed hidden Markov modeling methodology. Journal of pharmacokinetics and pharmacodynamics, 2012, Volume: 39, Issue:3 Topics: Adolescent; Adult; Amines; Anticonvulsants; Child; Cyclohexanecarboxylic Acids; Dose-Response Relati	2012
Gabapentin versus lamotrigine monotherapy: a double-blind comparison in newly diagnosed epilepsy. Epilepsia, 2002, Volume: 43, Issue:9 Topics: Acetates; Adolescent; Adult; Aged; Amines; Anticonvulsants; Asthenia; Clinical Protocols; Cyclohexan	2002
The absorption of gabapentin following high dose escalation. Seizure, 2003, Volume: 12, Issue:1 Topics: Absorption; Acetates; Amines; Anticonvulsants; Biological Availability; Cyclohexanecarboxylic Acids;	2003
Treating refractory epilepsy with tiagabine: clinical experience. Seizure, 2004, Volume: 13, Issue:7 Topics: Adult; Anticonvulsants; Carbamazepine; Dose-Response Relationship, Drug; Drug Administration Schedul	2004
Ketter's hypothesis of the mood effects of antiepileptic drugs coupled to the mechanism of action of topiramate and levetiracetam. Epilepsy & behavior : E&B, 2005, Volume: 6, Issue:3 Topics: Adult; Anticonvulsants; Chi-Square Distribution; Demography; Drug Therapy, Combination; Epilepsy; Fe	2005
New onset geriatric epilepsy: a randomized study of gabapentin, lamotrigine, and carbamazepine. Neurology, 2005, Jun-14, Volume: 64, Issue:11 Topics: Aged; Aging; Amines; Anticonvulsants; Carbamazepine; Cerebral Infarction; Cyclohexanecarboxylic Acid	2005
Analysis of pregabalin at therapeutic concentrations in human plasma/serum by reversed-phase HPLC. Therapeutic drug monitoring, 2005, Volume: 27, Issue:4 Topics: Anticonvulsants; Calibration; Carbamazepine; Chromatography, High Pressure Liquid; Dose-Response Rel	2005
[Efficacy, safety and effect on the quality of life of gabapentin in adult epilepsy--results of a prospective open-label quasi naturalistic Hungarian multicenter study (phase human-IV)]. Ideggyogyaszati szemle, 2006, Sep-20, Volume: 59, Issue:9-10 Topics: Adult; Aged; Ambulatory Care Facilities; Amines; Anticonvulsants; Cyclohexanecarboxylic Acids; Epile	2006
A randomised controlled trial examining the longer-term outcomes of standard versus new antiepileptic drugs. The SANAD trial. Health technology assessment (Winchester, England), 2007, Volume: 11, Issue:37 Topics: Adult; Amines; Anticonvulsants; Carbamazepine; Cyclohexanecarboxylic Acids; Epilepsy; Female; Fructo	2007
Serum concentrations of pregabalin in patients with epilepsy: the influence of dose, age, and comedication. Therapeutic drug monitoring, 2007, Volume: 29, Issue:6 Topics: Adult; Aged; Aging; Anticonvulsants; Dose-Response Relationship, Drug; Drug Interactions; Drug Monit	2007
Bodyweight gain under pregabalin therapy in epilepsy: mitigation by counseling patients? Seizure, 2008, Volume: 17, Issue:4 Topics: Adult; Anticonvulsants; Body Mass Index; Counseling; Diet; Epilepsy; Exercise; Female; Follow-Up Stu	2008
Double-blind crossover trial of progabide versus placebo in severe epilepsies. Epilepsia, 1983, Volume: 24, Issue:6 Topics: Adolescent; Adult; Child; Clinical Trials as Topic; Double-Blind Method; Epilepsy; Female; gamma-Ami	1983
Progabide as an add-on drug for epilepsy refractory to high dose antiepileptic drug therapy. Neuroscience letters, 1984, Jun-29, Volume: 47, Issue:3 Topics: Adult; Aged; Anticonvulsants; Clinical Trials as Topic; Double-Blind Method; Drug Therapy, Combinati	1984
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Biochemical and clinical effects of gamma-vinyl GABA in patients with epilepsy. Neurology, 1984, Volume: 34, Issue:2 Topics: Adult; Aminocaproates; Central Nervous System; Epilepsy; Female; gamma-Aminobutyric Acid; Humans; Ma	1984
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Effects of differing dosages of vigabatrin (Sabril) on cognitive abilities and quality of life in epilepsy. Epilepsia, 1995, Volume: 36, Issue:2 Topics: Adolescent; Adult; Affect; Anticonvulsants; Cognition; Dose-Response Relationship, Drug; Double-Blin	1995
Vigabatrin treatment in children. Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery, 1994, Volume: 10, Issue:4 Topics: Adolescent; Anticonvulsants; Child; Child, Preschool; Dose-Response Relationship, Drug; Drug Therapy	1994
[Vigabatrin: results with a new antiepileptic agents in 57 patients in a general neurological practice]. Nederlands tijdschrift voor geneeskunde, 1994, Sep-10, Volume: 138, Issue:37 Topics: 4-Aminobutyrate Transaminase; Adolescent; Adult; Aged; Anticonvulsants; Child; Child, Preschool; Dru	1994
Long-term study with gabapentin in patients with drug-resistant epileptic seizures. Archives of neurology, 1994, Volume: 51, Issue:10 Topics: Acetates; Adult; Amines; Anticonvulsants; Cyclohexanecarboxylic Acids; Double-Blind Method; Epilepsy	1994
Quantitative MR relaxometry study of effects of vigabatrin on the brains of patients with epilepsy. Epilepsy research, 1994, Volume: 18, Issue:2 Topics: Adolescent; Adult; Anticonvulsants; Brain; Double-Blind Method; Electroencephalography; Epilepsy; Fe	1994
Retrospective study of vigabatrin and psychiatric behavioural disturbances. Epilepsy research, 1995, Volume: 21, Issue:3 Topics: Adolescent; Adult; Aged; Anticonvulsants; Child; Epilepsy; Female; Follow-Up Studies; gamma-Aminobut	1995
Tiagabine: the safety landscape. Epilepsia, 1995, Volume: 36 Suppl 6 Topics: Adolescent; Aged; Anticonvulsants; Child; Dose-Response Relationship, Drug; Double-Blind Method; Dru	1995
Effect of gabapentin (Neurontin) [corrected] on mood and well-being in patients with epilepsy. Progress in neuro-psychopharmacology & biological psychiatry, 1996, Volume: 20, Issue:3 Topics: Acetates; Adult; Affect; Amines; Anticonvulsants; Cyclohexanecarboxylic Acids; Epilepsy; Female; Gab	1996
Vigabatrin causes profound reduction in serum alanine transaminase activity. Annals of clinical biochemistry, 1996, Volume: 33 ( Pt 3) Topics: Alanine Transaminase; Anticonvulsants; Child; Enzyme Inhibitors; Epilepsy; gamma-Aminobutyric Acid;	1996
Influence of vigabatrin on cognitive performances and behaviour in patients with drug-resistant epilepsy. Acta neurologica Scandinavica, 1996, Volume: 94, Issue:1 Topics: Adolescent; Adult; Aged; Anticonvulsants; Cognition; Epilepsy; Female; gamma-Aminobutyric Acid; Huma	1996
Vigabatrin withdrawal randomized study in children. Epilepsy research, 1996, Volume: 25, Issue:3 Topics: Adolescent; Anticonvulsants; Child; Child, Preschool; Double-Blind Method; Epilepsies, Partial; Epil	1996
Pharmacokinetics of tiagabine as add-on therapy in patients taking enzyme-inducing antiepilepsy drugs. Epilepsy research, 1995, Volume: 22, Issue:3 Topics: Adolescent; Adult; Analysis of Variance; Anticonvulsants; Circadian Rhythm; Enzyme Induction; Epilep	1995
No effect of long-term vigabatrin treatment on central nervous system conduction in patients with refractory epilepsy: results of a multicenter study of somatosensory and visual evoked potentials. PMS Study Multicenter Group. Epilepsia, 1997, Volume: 38, Issue:3 Topics: Adolescent; Adult; Aged; Anticonvulsants; Drug Administration Schedule; Epilepsy; Evoked Potentials,	1997
A quantitative study of daytime sleepiness induced by carbamazepine and add-on vigabatrin in epileptic patients. Acta neurologica Scandinavica, 1997, Volume: 95, Issue:4 Topics: Adolescent; Adult; Anticonvulsants; Carbamazepine; Drug Therapy, Combination; Epilepsy; Female; gamm	1997
Vigabatrin as add-on therapy in children and adolescents with refractory epilepsy: an open trial. Brain & development, 1997, Volume: 19, Issue:7 Topics: Adolescent; Adult; Anticonvulsants; Child; Child, Preschool; Drug Resistance; Drug Therapy, Combinat	1997
[Tiagabine: a GABA-ergic anti-epileptic drug]. Revista de neurologia, 1997, Volume: 25, Issue:146 Topics: Adolescent; Adult; Aged; Anticonvulsants; Child; Double-Blind Method; Drug Tolerance; Epilepsy; gamm	1997
A comparison of the neuropathological effects of vigabatrin and carbamazepine in patients with newly diagnosed localization-related epilepsy using MR-based cerebral T2 relaxation time measurements. Epilepsy research, 1998, Volume: 29, Issue:2 Topics: Adolescent; Adult; Anticonvulsants; Brain; Brain Mapping; Carbamazepine; Cerebellum; Epilepsy; Femal	1998
Is ACTH a key to understanding anticonvulsant action? Developmental medicine and child neurology, 1998, Volume: 40, Issue:2 Topics: Adenosine; Adrenocorticotropic Hormone; Anticonvulsants; Benzodiazepines; Binding Sites; Child; Chil	1998
Oral gabapentin disposition in patients with epilepsy after a high-protein meal. Epilepsia, 1997, Volume: 38, Issue:10 Topics: Acetates; Adult; Amines; Anticonvulsants; Cyclohexanecarboxylic Acids; Dietary Proteins; Epilepsy; F	1997
Gabapentin bioavailability: effect of dose and frequency of administration in adult patients with epilepsy. Epilepsy research, 1998, Volume: 31, Issue:2 Topics: Acetates; Adult; Amines; Anticonvulsants; Biological Availability; Cyclohexanecarboxylic Acids; Epil	1998
[Therapeutic failure, treatment and non-treatment of childhood epilepsy]. Revista de neurologia, 1998, Volume: 27, Issue:157 Topics: Adolescent; Anticonvulsants; Carbamazepine; Child; Child, Preschool; Electroencephalography; Epileps	1998
Effects of gabapentin on cognition and quality of life in patients with epilepsy. Seizure, 1998, Volume: 7, Issue:5 Topics: Acetates; Adult; Affect; Aged; Amines; Anticonvulsants; Cognition; Cyclohexanecarboxylic Acids; Epil	1998
Adjunctive therapy in epilepsy with new antiepileptic drugs: is it of any value? Seizure, 1998, Volume: 7, Issue:5 Topics: Acetates; Amines; Anti-Anxiety Agents; Anticonvulsants; Benzodiazepines; Clobazam; Cyclohexanecarbox	1998
Gabapentin add-on treatment: how many patients become seizure-free? An open-label multicenter study. Acta neurologica Scandinavica, 1999, Volume: 99, Issue:1 Topics: Acetates; Adolescent; Adult; Aged; Amines; Anticonvulsants; Cyclohexanecarboxylic Acids; Epilepsy; F	1999
An audit of the perceived efficacy and tolerability of gabapentin therapy in an out-patient cohort with chronic epilepsy. European neurology, 1999, Volume: 41, Issue:2 Topics: Acetates; Adult; Ambulatory Care; Amines; Anticonvulsants; Chronic Disease; Cohort Studies; Cyclohex	1999
Antiepileptic efficacy of vigabatrin in people with severe epilepsy and intellectual disability. Journal of intellectual disability research : JIDR, 1998, Volume: 42 Suppl 1 Topics: Anticonvulsants; Dose-Response Relationship, Drug; Double-Blind Method; Epilepsy; Follow-Up Studies;	1998
Once-daily versus twice-daily vigabatrin: is there a difference? The results of a double-blind pilot study. Epilepsia, 1999, Volume: 40, Issue:3 Topics: Adult; Anticonvulsants; Dose-Response Relationship, Drug; Double-Blind Method; Drug Administration S	1999
Vigabatrin use in psychotic epileptic patients: report of a prospective pilot study. Acta neurologica Scandinavica, 1999, Volume: 99, Issue:3 Topics: Adolescent; Adult; Anticonvulsants; Behavioral Symptoms; Child; Child, Preschool; Drug Administratio	1999
Changes in plasma GABA concentration during vigabatrin treatment of epilepsy: a prospective study. Epilepsy research, 1999, Volume: 34, Issue:2-3 Topics: Adult; Anticonvulsants; Chromatography, High Pressure Liquid; Epilepsy; Female; gamma-Aminobutyric A	1999
Safety and tolerability of gabapentin as adjunctive therapy in a large, multicenter study. Epilepsia, 1999, Volume: 40, Issue:7 Topics: Acetates; Adolescent; Adult; Ambulatory Care; Amines; Anticonvulsants; Asthenia; Carbamazepine; Cycl	1999
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Aminoaciduria resulting from vigabatrin administration in children with epilepsy. Pediatric neurology, 1999, Volume: 21, Issue:1 Topics: Adolescent; Amino Acids; Aminoisobutyric Acids; Anticonvulsants; beta-Alanine; Child; Child, Prescho	1999
Gabapentin in childhood epilepsy: a prospective evaluation of efficacy and safety. Epilepsy research, 2000, Volume: 38, Issue:1 Topics: Acetates; Adolescent; Amines; Anticonvulsants; Child; Child, Preschool; Cyclohexanecarboxylic Acids;	2000
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A randomized open-label study of gabapentin and lamotrigine in adults with learning disability and resistant epilepsy. Seizure, 2001, Volume: 10, Issue:2 Topics: Acetates; Adolescent; Adult; Amines; Anticonvulsants; Cyclohexanecarboxylic Acids; Drug Administrati	2001
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Intervention	units on a scale (Least Squares Mean)
	VNS Therapy	Best Medical Practice
Baseline Adverse Event Profile Score < 40	3.3	0.5

Intervention	Units on a Scale (Least Squares Mean)
	VNS Therapy	Best Medical Practice
Baseline Adverse Event Profile Score >= 40	3.3	0.7

Authors	Studies
Hawker, DD	1
Silverman, RB	2
Waszkielewicz, AM	1
Gunia-Krzyżak, A	1
Powroźnik, B	1
Słoczyńska, K	1
Pękala, E	1
Walczak, M	1
Bednarski, M	1
Żesławska, E	1
Nitek, W	1
Marona, H	1
Feja, M	1
Meller, S	1
Deking, LS	1
Kaczmarek, E	1
During, MJ	1
Gernert, M	5
Ahring, PK	2
Liao, VWY	1
Gardella, E	2
Johannesen, KM	1
Krey, I	1
Selmer, KK	1
Stadheim, BF	1
Davis, H	1
Peinhardt, C	1
Koko, M	1
Coorg, RK	1
Syrbe, S	1
Bertsche, A	1
Santiago-Sim, T	1
Diemer, T	1
Fenger, CD	1
Platzer, K	3
Eichler, EE	1
Lerche, H	3
Lemke, JR	3
Chebib, M	2
Møller, RS	2

gamma-aminobutyric acid and Aura