Array ( [0] => {{Short description|Class of medications}} [1] => {{Cs1 config|name-list-style=vanc}} [2] => {{Use dmy dates|date=July 2020}} [3] => {{Infobox drug class [4] => | Name = [5] => | Image = [6] => | Alt = [7] => | Caption = [8] => | Pronounce = [9] => | Synonyms = Antiepileptic drugs, antiseizure drugs [10] => [11] => | Use = Epilepsy [12] => | ATC_prefix = N03 [13] => | Mode_of_action = [14] => | Mechanism_of_action = [15] => | Biological_target = Brain [16] => | Chemical_class = [17] => [18] => | Drugs.com = [19] => | Consumer_Reports = [20] => | medicinenet = [21] => | rxlist = [22] => [23] => | MeshID = [24] => }} [25] => [26] => '''Anticonvulsants''' (also known as '''antiepileptic drugs''', '''antiseizure drugs''', or '''anti-seizure medications''' ('''ASM''')) are a diverse group of [[pharmacological]] agents used in the treatment of [[epilepsy|epileptic]] [[seizure]]s.{{cite journal | last=Al-Otaibi | first=Faisal | title=An overview of structurally diversified anticonvulsant agents | journal=Acta Pharmaceutica (Zagreb, Croatia) | publisher=Walter de Gruyter GmbH | volume=69 | issue=3 | date=2019-09-01 | issn=1846-9558 | pmid=31259739 | doi=10.2478/acph-2019-0023 | pages=321–344| doi-access=free }} Anticonvulsants are also increasingly being used in the treatment of [[bipolar disorder]]{{cite journal | last1=Joshi | first1=A | last2=Bow | first2=A | last3=Agius | first3=M | title=Pharmacological Therapies in Bipolar Disorder: a Review of Current Treatment Options. | journal=Psychiatria Danubina | volume=31 | issue=Suppl 3 | year=2019 | issn=0353-5053 | pmid=31488797 | pages=595–603}}{{cite journal|last1=Keck|first1=Paul E. Jr.|last2=McElroy|first2=Susan L.|author2-link=Susan McElroy|last3=Strakowski|first3=Stephen M.|title=Anticonvulsants and antipsychotics in the treatment of bipolar disorder.|journal=The Journal of Clinical Psychiatry|date=1998|volume=59|issue=Suppl 6|pages=74–82|pmid=9674940}} and [[borderline personality disorder]],American Psychiatric Association, and American Psychiatric Association. Work Group on Borderline Personality Disorder. Practice guideline for the treatment of patients with borderline personality disorder. American Psychiatric Pub, 2001. since many seem to act as [[mood stabilizers]], and for the treatment of [[neuropathic pain]].{{cite journal|last1=Rogawski|first1=Michael A.|last2=Löscher|first2=Wolfgang|title=The neurobiology of antiepileptic drugs|journal=Nature Reviews Neuroscience|date=2004|volume=5|issue=7|pages=553–564|doi=10.1038/nrn1430|pmid=15208697|s2cid=2201038|url=https://zenodo.org/record/1233562}} Anticonvulsants suppress the excessive rapid firing of [[neuron]]s during seizures.{{cite journal|last1=McLean|first1=M J|last2=Macdonald|first2=R L|title=Sodium valproate, but not ethosuximide, produces use- and voltage-dependent limitation of high frequency repetitive firing of action potentials of mouse central neurons in cell culture.|journal=Journal of Pharmacology and Experimental Therapeutics|date=June 1986|volume=237|issue=3|pages=1001–1011|pmid=3086538}} Anticonvulsants also prevent the spread of the seizure within the brain.{{cite journal|last1=Harden|first1=C. L.|title=New antiepileptic drugs|journal=Neurology|date=1 May 1994|volume=44|issue=5|pages=787–95|doi=10.1212/WNL.44.5.787|pmid=8190276|s2cid=75925846}} [27] => [28] => Conventional antiepileptic drugs may block [[sodium channel]]s or enhance γ-aminobutyric acid ([[GABA]]) function. Several antiepileptic drugs have multiple or uncertain mechanisms of action.{{cite web|url=https://www.neurology.wisc.edu/publications/2010%20pubs/stafstrom-4.pdf |title=Archived copy |access-date=2013-01-28 |archive-url=https://web.archive.org/web/20131103055041/https://www.neurology.wisc.edu/publications/2010%20pubs/stafstrom-4.pdf |archive-date=3 November 2013}} Next to the [[Voltage gated sodium channels|voltage-gated sodium channels]] and components of the GABA system, their targets include [[GABAA receptor|GABAA receptor]]s, the [[GABA transporter type 1]], and [[GABA transaminase]].{{cite journal | pmid = 15208697 | doi=10.1038/nrn1430 | volume=5 | issue=7 | title=The neurobiology of antiepileptic drugs |date=July 2004 | vauthors=Rogawski MA, Löscher W | journal=Nature Reviews Neuroscience | pages=553–64 | s2cid=2201038 | url=https://zenodo.org/record/1233562 }} Additional targets include voltage-gated [[calcium channels]], [[SV2A]], and α2δ.{{cite journal |pmid = 18590620 | volume=8 | issue=4 | title=New molecular targets for antiepileptic drugs: alpha(2)delta, SV2A, and K(v)7/KCNQ/M potassium channels | pmc=2587091 |date=July 2008 | vauthors=Rogawski MA, Bazil CW | journal=Curr Neurol Neurosci Rep | pages=345–52 | doi=10.1007/s11910-008-0053-7 }}{{cite journal | pmid = 17199015 | doi=10.1016/j.nurt.2006.11.010 | volume=4 | issue=1 | title=Molecular targets for antiepileptic drug development | pmc=1852436 |date=January 2007 | vauthors=Meldrum BS, Rogawski MA | journal=Neurotherapeutics | pages=18–61 }} By blocking sodium or calcium channels, antiepileptic drugs reduce the release of excitatory [[Glutamate (neurotransmitter)|glutamate]], whose release is considered to be elevated in epilepsy, but also that of GABA.{{cite journal|last=Kammerer|first=M.|author2=Rassner, M. P.|author3= Freiman, T. M.|author4= Feuerstein, T. J.|title=Effects of antiepileptic drugs on GABA release from rat and human neocortical synaptosomes|journal=Naunyn-Schmiedeberg's Archives of Pharmacology|date=2 May 2011|volume=384|issue=1|pages=47–57|doi=10.1007/s00210-011-0636-8|pmid=21533993|s2cid=1388805}} This is probably a side effect or even the actual mechanism of action for some antiepileptic drugs, since GABA can itself, directly or indirectly, act proconvulsively. Another potential target of antiepileptic drugs is the [[peroxisome proliferator-activated receptor alpha]].{{cite journal|vauthors=Puligheddu M, Pillolla G, Melis M, Lecca S, Marrosu F, De Montis MG | title=PPAR-alpha agonists as novel antiepileptic drugs: preclinical findings | journal=PLOS ONE | year= 2013 | volume= 8 | issue= 5 | pages= e64541 | pmid=23724059 | doi=10.1371/journal.pone.0064541 | pmc=3664607 | bibcode=2013PLoSO...864541P | editor1-last=Charpier| editor1-first=Stéphane | display-authors=etal | doi-access=free }}{{cite journal |vauthors=Citraro R, Russo E, Scicchitano F, van Rijn CM, Cosco D, Avagliano C, Russo R, D'Agostino G, Petrosino S, Guida F, Gatta L, van Luijtelaar G, Maione S, Di Marzo V, Calignano A, De Sarro G |title=Antiepileptic action of N-palmitoylethanolamine through CB1 and PPAR-α receptor activation in a genetic model of absence epilepsy |journal=Neuropharmacology |year=2013 |volume=69 |pages=115–26 |doi=10.1016/j.neuropharm.2012.11.017 |pmid=23206503 |s2cid=27701532 |display-authors=1}}{{cite journal |author1=Porta, N. |author2=Vallée, L. |author3=Lecointe, C. |author4=Bouchaert, E. |author5=Staels, B. |author6=Bordet, R. |author7=Auvin, S. | year = 2009 | title = Fenofibrate, a peroxisome proliferator-activated receptor-alpha agonist, exerts anticonvulsive properties. | journal = Epilepsia | volume = 50 | issue = 4 | pages = 943–8 | pmid = 19054409 | doi=10.1111/j.1528-1167.2008.01901.x|s2cid=6796135 |doi-access=free }}{{cite journal| vauthors=Lampen A, Carlberg C, Nau H| title=Peroxisome proliferator-activated receptor delta is a specific sensor for teratogenic valproic acid derivatives | journal=Eur J Pharmacol | year= 2001 | volume= 431 | issue= 1 | pages= 25–33 | doi= 10.1016/S0014-2999(01)01423-6| pmid=11716839 }}{{cite journal| vauthors=Maguire JH, Murthy AR, Hall IH| title=Hypolipidemic activity of antiepileptic 5-phenylhydantoins in mice | journal=Eur J Pharmacol | year= 1985 | volume= 117 | issue= 1 | pages= 135–8 | doi= 10.1016/0014-2999(85)90483-2| pmid=4085542 }}{{cite journal| vauthors=Hall IH, Patrick MA, Maguire JH| title=Hypolipidemic activity in rodents of phenobarbital and related derivatives | journal=Archiv der Pharmazie | year= 1990 | volume= 323 | issue= 9 | pages= 579–86 | doi= 10.1002/ardp.19903230905| pmid=2288480 | s2cid=46002731 }}{{cite journal| vauthors=Frigerio F, Chaffard G, Berwaer M, Maechler P| title=The antiepileptic drug topiramate preserves metabolism-secretion coupling in insulin secreting cells chronically exposed to the fatty acid oleate | journal=Biochem Pharmacol | year= 2006 | volume= 72 | issue= 8 | pages= 965–73 | doi=10.1016/j.bcp.2006.07.013 | pmid=16934763 }} [29] => [30] => Some anticonvulsants have shown antiepileptogenic effects in animal models of epilepsy.{{cite journal | pmid = 24671870| year = 2014| last1 = Kaminski| first1 = R. M.| title = The potential of antiseizure drugs and agents that act on novel molecular targets as antiepileptogenic treatments| journal = Neurotherapeutics| volume = 11| issue = 2| pages = 385–400| last2 = Rogawski| first2 = M. A.| last3 = Klitgaard| first3 = H| doi = 10.1007/s13311-014-0266-1| pmc = 3996125}} That is, they either prevent the development of epilepsy or can halt or reverse the progression of epilepsy. However, no drug has been shown in human trials to prevent [[epileptogenesis]] (the development of epilepsy in an individual at risk, such as after a [[traumatic brain injury|head injury]]).{{cite journal |author=Abou-Khalil BW |title=Comparative Monotherapy Trials and the Clinical Treatment of Epilepsy |journal=Epilepsy Currents |volume=7 |issue=5 |pages=127–9 |year=2007 |pmid=17998971 |doi=10.1111/j.1535-7511.2007.00198.x |pmc=2043140}} [31] => [32] => == Terminology == [33] => Anticonvulsants are more accurately called antiepileptic drugs (AEDs) because not every epileptic seizure involves [[convulsion]], and vice versa, not every convulsion is caused by an epileptic seizure.{{Cite web |title=Antiseizure medication |url=https://my.clevelandclinic.org/health/treatments/24781-antiseizure-medications-anticonvulsants |access-date=2024-03-16 |website=Cleveland Clinic |language=en}} They are also often referred to as antiseizure drugs because they provide symptomatic treatment only and have not been demonstrated to alter the course of epilepsy.{{cite book |last1=Rogawski |first1=Michael|date= 2021 |editor-last=Katzung |editor-first=B |title=Basic and Clinical Pharmacology, 15th Edition |publisher=McGraw-Hill Education| pages=422–455 |chapter=Chapter 24: Antiseizure Drugs}} [34] => [35] => == Approval == [36] => [37] => The usual method of achieving approval for a drug is to show it is effective when compared against [[placebo]], or that it is more effective than an existing drug. In monotherapy (where only one drug is taken) it is considered unethical by most to conduct a trial with placebo on a new drug of uncertain efficacy. This is because untreated epilepsy leaves the patient at significant risk of death. Therefore, almost all new epilepsy drugs are initially approved only as adjunctive (add-on) therapies. Patients whose epilepsy is uncontrolled by their medication (i.e., it is refractory to treatment) are selected to see if supplementing the medication with the new drug leads to an improvement in seizure control. Any reduction in the frequency of seizures is compared against a placebo. The lack of superiority over existing treatment, combined with lacking placebo-controlled trials, means that few modern drugs have earned [[Food and Drug Administration|FDA]] approval as initial monotherapy. In contrast, Europe only requires equivalence to existing treatments and has approved many more. Despite their lack of FDA approval, the [[American Academy of Neurology]] and the [[American Epilepsy Society]] still recommend a number of these new drugs as initial monotherapy. [38] => [39] => == Drugs == [40] => In the following list, the dates in parentheses are the earliest approved use of the drug. [41] => [42] => === Aldehydes === [43] => {{main|Aldehyde}} [44] => * [[Paraldehyde]] (1882). One of the earliest anticonvulsants. It is still used to treat [[status epilepticus]], particularly where there are no [[resuscitation]] facilities.Browne TR. Paraldehyde, chlormethiazole, and lidocaine for treatment of status epilepticus. In: Delgado-Escueta AV, Wasterlain CG, Treiman DM, Porter RJ, eds. Status Epilepticus. Mechanisms of Brain Damage and Treatment (Advances in Neurology, Vol 34). New York, Raven Press 1983: 509–517{{cite journal | author = Ramsay RE | year = 1989 | title = Pharmacokinetics and clinical use of parenteral phenytoin, phenobarbital, and paraldehyde | journal = Epilepsia | volume = 30 | issue = Suppl 2| pages = S1–S3 | doi = 10.1111/j.1528-1157.1989.tb05818.x | pmid = 2767008 | s2cid = 44798815 }} [45] => [46] => === Aromatic allylic alcohols === [47] => * [[Stiripentol]] (2007). Indicated for the treatment of [[severe myoclonic epilepsy of infancy|Dravet syndrome]].{{cite journal|last=Plosker|first=GL|title=Stiripentol: in severe myoclonic epilepsy of infancy (dravet syndrome)|journal=CNS Drugs|date=November 2012|volume=26|issue=11|pages=993–1001|pmid=23018548|doi=10.1007/s40263-012-0004-3|s2cid=42911844 }}{{cite web|title=Public summary of positive opinion for orpphan opinion for orphan designation of stiripentol for the treatment of severe myoclonic epilepsy in infancy|url=http://www.ema.europa.eu/docs/en_GB/document_library/Orphan_designation/2009/10/WC500005711.pdf|publisher=European Medicines Agency|access-date=19 May 2013|date=30 July 2007|quote=Doc.Ref.: EMEA/COMP/269/04|archive-date=17 December 2013|archive-url=https://web.archive.org/web/20131217120247/http://www.ema.europa.eu/docs/en_GB/document_library/Orphan_designation/2009/10/WC500005711.pdf|url-status=dead}}{{cite web | title=Diacomit- stiripentol capsule Diacomit- stiripentol powder, for suspension | website=DailyMed | date=15 May 2020 | url=https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=58304ba8-9779-4658-811e-94ffe08c3f16#section-1 | access-date=8 November 2020}} [48] => [49] => === Barbiturates === [50] => {{main|Barbiturate}} [51] => [[Barbiturate]]s are [[medication|drugs]] that act as [[central nervous system]] (CNS) [[depressant]]s, and by virtue of this they produce a wide spectrum of effects, from mild [[sedation]] to [[anesthesia]]. The following are [[ATC code N03|classified]] as anticonvulsants:Suddock JT, Kent KJ, Cain MD. Barbiturate Toxicity. 2023 Apr 12. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID 29763050.( 26 / August / 2023 ) [52] => * [[Phenobarbital]] (1912). See also the related drug [[primidone]]. [53] => * [[Methylphenobarbital]] (1935). Known as mephobarbital in the US. No longer marketed in the UK. [54] => * [[Barbexaclone]] (1982). Only available in some European countries. [55] => [56] => Phenobarbital was the main anticonvulsant from 1912 until the development of phenytoin in 1938. Today, phenobarbital is rarely used to treat epilepsy in new patients since there are other effective drugs that are less sedating. Phenobarbital sodium injection can be used to stop acute convulsions or [[status epilepticus]], but a benzodiazepine such as [[lorazepam]], [[diazepam]] or [[midazolam]] is usually tried first. Other barbiturates only have an anticonvulsant effect at [[Anesthetic|anaesthetic]] doses.{{citation needed|date=July 2021}} [57] => [58] => === Benzodiazepines === [59] => {{main|Benzodiazepine}} [60] => The benzodiazepines are a class of [[medication|drugs]] with [[hypnotic]], [[anxiolytic]], anticonvulsive, [[amnesia|amnestic]] and [[muscle relaxant]] properties. Benzodiazepines act as a central nervous system depressant. The relative strength of each of these properties in any given benzodiazepine varies greatly and influences the indications for which it is prescribed. Long-term use can be problematic due to the development of [[drug tolerance|tolerance]] to the anticonvulsant effects and [[Substance use disorder|dependency]].{{cite journal |author=Browne TR |date=May 1976 |title=Clonazepam. A review of a new anticonvulsant drug |volume=33 |issue=5 |pages=326–32 |pmid=817697 |journal=Arch Neurol |doi=10.1001/archneur.1976.00500050012003}}{{cite journal |last=Isojärvi |first=JI |author2=Tokola RA |date=December 1998 |title=Benzodiazepines in the treatment of epilepsy in people with intellectual disability |journal=J Intellect Disabil Res |volume=42 |issue=1 |pages=80–92 |pmid=10030438}}{{cite journal |journal=Epilepsia |date=May–Jun 1986 |volume=27 |issue=3 |pages=276–85 |title=Nonconvulsive status epilepticus|last2=Svanborg |first2=E |last3=Wedlund |first3=JE |pmid=3698940 |last1=Tomson |first1=T |doi=10.1111/j.1528-1157.1986.tb03540.x|s2cid=26694857 }}{{cite journal |last=Djurić |first=M |author2=Marjanović B |author3=Zamurović D |date=May–Jun 2001 |title=[West syndrome--new therapeutic approach] |journal=Srp Arh Celok Lek |volume=129 |issue=1 |pages=72–7 |pmid=15637997}} Of many drugs in this class, only a few are used to treat epilepsy: [61] => * [[Clobazam]] (1979). Notably, used on a short-term basis around menstruation in women with [[catamenial epilepsy]]. [62] => * [[Clonazepam]] (1974). [63] => * [[Clorazepate]] (1972). [64] => [65] => The following benzodiazepines are used to treat [[status epilepticus]]: [66] => * [[Diazepam]] (1963). Can be given rectally by trained care-givers. [67] => * [[Midazolam]] (N/A). Increasingly being used as an alternative to diazepam. This water-soluble drug is squirted into the side of the mouth but not swallowed. It is rapidly absorbed by the [[buccal mucosa]]. [68] => * [[Lorazepam]] (1972). Given by injection in hospital. [69] => [70] => [[Nitrazepam]], [[temazepam]], and especially [[nimetazepam]] are powerful anticonvulsant agents, however their use is rare due to an increased incidence of side effects and strong sedative and motor-impairing properties. [71] => [72] => === Bromides === [73] => {{main|Bromide}} [74] => * [[Potassium bromide]] (1857). The earliest effective treatment for epilepsy. There would not be a better drug until phenobarbital in 1912. It is still used as an anticonvulsant for dogs and cats but is no longer used in humans. [75] => [76] => === Carbamates === [77] => {{main|Carbamate}} [78] => * [[Felbamate]] (1993). This effective anticonvulsant has had its usage severely restricted due to rare but life-threatening side effects.{{cite book |last= |first= |url=https://books.google.com/books?id=47fckyBY2XwC&q=felbamate+side+effects+restrictions&pg=RA1-PA100 |title=Pediatric epilepsy: diagnosis and therapy |publisher=Demos Medical Publishing |isbn=978-1-933864-16-7 |editor-last=Bourgeois |editor-first=Blaise F. |edition=3rd |location=New York |publication-date=2007-12-16 |editor-last2=Dodson |editor-first2=Edwin |editor-last3=Nordli |editor-first3=Douglas R. Jr |editor-last4=Pellock |editor-first4=John M. |editor-last5=Sankar |editor-first5=Raman}}{{cite journal|last=French|first=J|author2=Smith, M|author3=Faught, E|author4=Brown, L|title=Practice advisory: The use of felbamate in the treatment of patients with intractable epilepsy: report of the Quality Standards Subcommittee of the American Academy of Neurology and the American Epilepsy Society|journal=Neurology|date=12 May 1999|volume=52|issue=8|pages=1540–5|pmid=10331676|doi=10.1212/WNL.52.8.1540|doi-access=free}}{{cite web|title=Felbamate|url=https://www.nlm.nih.gov/medlineplus/druginfo/meds/a606011.html|publisher=MedlinePlus : U.S. National Library of Medicine|access-date=19 May 2013}} [79] => * [[Cenobamate]] (2019). [80] => [81] => === Carboxamides === [82] => [[File:Carbamazepine 3D.png|thumb|right|Carbamazepine]] [83] => {{main|Carboxamide}} [84] => The following are carboxamides: [85] => * [[Carbamazepine]] (1963). A popular anticonvulsant that is available in generic formulations. [86] => * [[Oxcarbazepine]] (1990). A derivative of carbamazepine that has similar efficacy and is better tolerated and is also available generically. [87] => * [[Eslicarbazepine acetate]] (2009). [88] => [89] => === Fatty acids === [90] => {{main|Fatty acid}} [91] => The following are fatty-acids: [92] => * The [[valproic acid|valproates]] — [[valproic acid]], [[sodium valproate]], and [[divalproex sodium]] (1967). [93] => * [[Vigabatrin]] (1989). [94] => * [[Progabide]] (1987). [95] => * [[Tiagabine]] (1996). [96] => [97] => ''Vigabatrin and progabide are also analogs of GABA.'' [98] => [99] => === Fructose derivatives === [100] => {{main|Fructose}} [101] => * [[Topiramate]] (1995). [102] => [103] => === Gabapentinoids === [104] => {{main|Gabapentinoid}} [105] => [106] => {{multiple image [107] => | align = right [108] => | total_width = 320 [109] => | image1 = Phenibut and analogues.png [110] => | alt1 = GABA analogues [111] => | caption1 = [[GABA]] analogues [112] => | image2 = Voltage gated calcium channel.jpg [113] => | alt2 = Binding sites of [[pregabalin]] and the non-gabapentenoid [[ziconotide]] to the voltage-gated calcium channel complex. [114] => | caption2 = [[Voltage-gated calcium channel]] [115] => }} [116] => Gabapentinoids are used in [[epilepsy]], [[neuropathic pain]], [[fibromyalgia]], [[restless leg syndrome]], [[opioid withdrawal]] and [[generalized anxiety disorder]] (GAD). Gabapentinoids block [[voltage-gated calcium channel]]s, mainly the [[N-type calcium channel|N-Type]], and [[P-type calcium channel|P/Q]]-type calcium channels. The following are gabapentinoids: [117] => * [[Pregabalin]] (2004) [118] => * [[Mirogabalin]] (2019) (Japan only) [119] => * [[Gabapentin]] (1993) [120] => * [[Gabapentin enacarbil]] (Horizant) (2011) [121] => * [[Gabapentin extended release]] (Gralise) (1996) [122] => [123] => Gabapentinoids are analogs of GABA, but they do not act on GABA receptors. They have analgesic, anticonvulsant, and anxiolytic effects. [124] => [125] => === Hydantoins === [126] => {{main|Hydantoin}} [127] => The following are hydantoins: [128] => * [[Ethotoin]] (1957). [129] => * [[Phenytoin]] (1938). [130] => * [[Mephenytoin]]. [131] => * [[Fosphenytoin]] (1996). [132] => [133] => === Oxazolidinediones === [134] => {{main|2,4-Oxazolidinedione}} [135] => The following are oxazolidinediones: [136] => * [[Paramethadione]]. [137] => * [[Trimethadione]] (1946). [138] => * [[Ethadione]]. [139] => [140] => === Propionates === [141] => {{main|Propionate}} [142] => * [[Beclamide]]. [143] => [144] => === Pyrimidinediones === [145] => {{main|Pyrimidinedione}} [146] => * [[Primidone]] (1952). [147] => [148] => === Pyrrolidines === [149] => {{main|Pyrrolidine}} [150] => * [[Brivaracetam]] (2016). [151] => * [[Etiracetam]]. [152] => * [[Levetiracetam]] (1999). [153] => * [[Seletracetam]]. [154] => [155] => === Succinimides === [156] => {{main|Succinimide}} [157] => The following are succinimides: [158] => * [[Ethosuximide]] (1955). [159] => * [[Phensuximide]]. [160] => * [[Mesuximide]]. [161] => [162] => === Sulfonamides === [163] => {{main|Sulfonamide (medicine)}} [164] => * [[Acetazolamide]] (1953). [165] => * [[Sultiame]]. [166] => * [[Methazolamide]]. [167] => * [[Zonisamide]] (2000). [168] => [169] => === Triazines === [170] => {{main|Triazine}} [171] => * [[Lamotrigine]] (1990). [172] => [173] => === Ureas === [174] => {{main|Urea}} [175] => * [[Pheneturide]]. [176] => * [[Phenacemide]]. [177] => [178] => === Valproylamides === [179] => {{main|Amide}} [180] => * [[Valpromide]]. [181] => * [[Valnoctamide]]. [182] => [183] => === Other === [184] => * [[Perampanel]]. [185] => * [[Stiripentol]].{{cite web | title=Diacomit EPAR | website=European Medicines Agency | url=https://www.ema.europa.eu/en/medicines/human/EPAR/diacomit | access-date=8 November 2020}} [186] => * [[Pyridoxine]] (1939). [187] => [188] => == Non-pharmaceutical anticonvulsants == [189] => {{Further information|Epilepsy#Management}} [190] => [191] => The [[ketogenic diet]] and [[vagus nerve stimulation]] are alternative treatments for epilepsy without the involvement of pharmaceuticals. The ketogenic diet consists of a high-fat, low-carbohydrate diet, and has shown good results in patients whose epilepsy has not responded to medications and who cannot receive surgery. The vagus nerve stimulator is a device that can be implanted into patients with epilepsy, especially that which [[Focal seizure|originates from a specific part of the brain]]. However, both of these treatment options can cause severe adverse effects. Additionally, while seizure frequency typically decreases, they often do not stop entirely.{{cite journal |last1=D'Andrea Meira |first1=Isabella |title=Ketogenic Diet and Epilepsy: What We Know So Far |date=2019 |volume=13 |page=5 |journal=Frontiers in Neuroscience |doi=10.3389/fnins.2019.00005 |pmid=30760973 |pmc=6361831 |ref=ketogenic |doi-access=free }}{{cite web |last1=Pruthi |first1=Sandhya |title=Vagus nerve stimulation |url=https://www.mayoclinic.org/tests-procedures/vagus-nerve-stimulation/about/pac-20384565 |website=Mayo Clinic |access-date=20 July 2023 |ref=vagus}} [192] => [193] => == Treatment guidelines == [194] => According to guidelines by the [[American Academy of Neurology]] and [[American Epilepsy Society]],[http://aan.com/professionals/practice/pdfs/clinician_ep_onset_e.pdf AAN Guideline Summary for Clinicians – Efficacy and Tolerability of the New Antiepileptic Drugs, I: Treatment of New Onset Epilepsy] {{webarchive |url=https://web.archive.org/web/20110224155853/http://aan.com/professionals/practice/pdfs/clinician_ep_onset_e.pdf |date=24 February 2011 }} Retrieved on 29 June 2010 mainly based on a major [[article review]] in 2004,{{cite journal |vauthors=French JA, Kanner AM, Bautista J |title=Efficacy and tolerability of the new antiepileptic drugs, I: Treatment of new-onset epilepsy: report of the TTA and QSS Subcommittees of the American Academy of Neurology and the American Epilepsy Society |journal=Epilepsia |volume=45 |issue=5 |pages=401–9 |date=May 2004 |pmid=15101821 |doi=10.1111/j.0013-9580.2004.06204.x |url=https://deepblue.lib.umich.edu/bitstream/2027.42/65231/1/j.0013-9580.2004.06204.x.pdf|display-authors=etal|hdl=2027.42/65231 |s2cid=12259676 |hdl-access=free }} patients with newly diagnosed epilepsy who require treatment can be initiated on standard anticonvulsants such as [[carbamazepine]], [[phenytoin]], [[valproic acid]]/[[valproate semisodium]], [[phenobarbital]], or on the newer anticonvulsants [[gabapentin]], [[lamotrigine]], [[oxcarbazepine]] or [[topiramate]]. The choice of anticonvulsants depends on individual patient characteristics. Both newer and older drugs are generally equally effective in new onset epilepsy. The newer drugs tend to have fewer side effects. For newly diagnosed [[partial seizures|partial]] or [[mixed seizures]], there is evidence for using gabapentin, lamotrigine, oxcarbazepine or topiramate as [[monotherapy]]. [[Lamotrigine]] can be included in the options for children with newly diagnosed [[absence seizures]]. [195] => [196] => == History == [197] => The first anticonvulsant was [[bromide]], suggested in 1857 by the British gynecologist [[Charles Locock]] who used it to treat women with "hysterical epilepsy" (probably ''[[catamenial epilepsy]]''). Bromides are effective against epilepsy, and also cause [[Erectile dysfunction|impotence]], which is not related to its anti-epileptic effects. Bromide also suffered from the way it affected behaviour, introducing the idea of the "epileptic personality" which was actually a result of medication. [[Phenobarbital]] was first used in 1912 for both its sedative and antiepileptic properties. By the 1930s, the development of animal models in epilepsy research led to the development of [[phenytoin]] by Tracy Putnam and [[H. Houston Merritt]], which had the distinct advantage of treating epileptic seizures with less sedation.{{cite journal |vauthors=Eadie MJ, Bladin PF |year=2001 |title=A Disease Once Sacred: a History of the Medical Understanding of Epilepsy}} By the 1970s, a [[National Institutes of Health]] initiative, the Anticonvulsant Screening Program, headed by J. Kiffin Penry, served as a mechanism for drawing the interest and abilities of pharmaceutical companies in the development of new anticonvulsant medications. [198] => [199] => === Marketing approval history === [200] => [201] => The following table lists anticonvulsant drugs together with the date their marketing was approved in the US, UK and France. Data for the UK and France are incomplete. The [[European Medicines Agency]] approves drugs throughout the European Union. Some of the drugs are no longer marketed. [202] => [203] => {| class="wikitable sortable" [204] => |- [205] => !Drug!!Brand!!US!!UK!!France [206] => |- [207] => |[[acetazolamide]] [208] => |Diamox [209] => |1953-07-2727 July 1953{{cite web | title=New Drug Application (NDA) 008943 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=008943 | access-date=21 November 2019}} [210] => |1988[http://www.epilepsy.org.uk/info/drugslist.html Epilepsy Action: Druglist.] {{Webarchive|url=https://web.archive.org/web/20110301212357/http://www.epilepsy.org.uk/info/drugslist.html |date=1 March 2011 }} Retrieved on 1 November 2007. [211] => | [212] => |- [213] => |[[brivaracetam]] [214] => |Briviact [215] => |2016-02-1818 February 2016{{cite web | title=New Drug Application (NDA) 205836 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=205836 | access-date=21 November 2019}}{{cite web | title=Drug Approval Package: Briviact (brivaracetam) | website=U.S. [[Food and Drug Administration]] (FDA) | date=30 March 2016 | url=https://www.accessdata.fda.gov/drugsatfda_docs/nda/2016/205836-205837-205838-Briviact-TOC.cfm | archive-url=https://web.archive.org/web/20191122035432/https://www.accessdata.fda.gov/drugsatfda_docs/nda/2016/205836-205837-205838-Briviact-TOC.cfm | archive-date=22 November 2019 | url-status=live | access-date=21 November 2019}} [216] => | [217] => | [218] => |- [219] => |[[carbamazepine]] [220] => |Tegretol [221] => |1974-07-1515 July 1974{{cite web | title=New Drug Application (NDA) 016608 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=016608 | access-date=21 November 2019}} (Initial approval on 11 March 1968 was for trigeminal neuralgia.){{cite journal | last = Schain | first = Richard J. |date=1 March 1978| title = Pediatrics—Epitomes of Progress: Carbamazepine (Tegretol) in the Treatment of Epilepsy | journal = Western Journal of Medicine | volume = 128 | issue = 3 | pages = 231–232 | pmid = 18748164 | pmc = 1238063 }} [222] => |1965 [223] => |1963{{cite journal | last = Loiseau | first = Pierre Jean-Marie |date=June 1999 | title = Clinical Experience with New Antiepileptic Drugs: Antiepileptic Drugs in Europe |journal = [[Epilepsia (journal)|Epilepsia]] | volume = 40 | issue = Suppl 6 | pages = S3–8 | doi = 10.1111/j.1528-1157.1999.tb00925.x | pmid = 10530675 | s2cid = 29638422 | doi-access = free }} [224] => |- [225] => |[[cenobamate]] [226] => |Xcopri [227] => ||2019-11-2121 November 2019 [228] => | [229] => | [230] => |- [231] => |[[clobazam]] [232] => |Onfi/Frisium [233] => |2011-10-2121 October 2011{{cite web | title=New Drug Application (NDA) 202067 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=202067 | access-date=21 November 2019}}{{cite web | title=Drug Approval Package: Onfi NDA #202067 | website=U.S. [[Food and Drug Administration]] (FDA) | date=20 August 2013 | url=https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/202067Orig1s000TOC.cfm | archive-url=https://web.archive.org/web/20191122035714/https://www.accessdata.fda.gov/drugsatfda_docs/nda/2011/202067Orig1s000TOC.cfm | archive-date=22 November 2019 | url-status=live | access-date=21 November 2019}} [234] => |1979 [235] => | [236] => |- [237] => |[[clonazepam]] [238] => |Klonopin/Rivotril [239] => |1975-06-044 June 1975{{cite web | title=New Drug Application (NDA) 017533 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=017533 | access-date=21 November 2019}} [240] => |1974 [241] => | [242] => |- [243] => |[[diazepam]] [244] => |Valium [245] => |1963-11-1515 November 1963{{cite web | title=New Drug Application (NDA) 013263 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=013263 | access-date=21 November 2019}} [246] => | [247] => | [248] => |- [249] => |[[divalproex sodium]] [250] => |Depakote [251] => |1983-03-1010 March 1983{{cite web | title=New Drug Application (NDA) 018723 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=018723 | access-date=21 November 2019}} [252] => | [253] => | [254] => |- [255] => |[[eslicarbazepine]] [256] => |Aptiom [257] => |2013-08-1111 August 2013{{cite web | title=New Drug Application (NDA) 022416 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=022416 | access-date=21 November 2019}}{{cite web | title=Drug Approval Package: Brand Name (Generic Name) NDA # | website=U.S. [[Food and Drug Administration]] (FDA) | date=20 December 2013 | url=https://www.accessdata.fda.gov/drugsatfda_docs/nda/2013/022416Orig1s000TOC.cfm | archive-url=https://web.archive.org/web/20191122040059/https://www.accessdata.fda.gov/drugsatfda_docs/nda/2013/022416Orig1s000TOC.cfm | archive-date=22 November 2019 | url-status=live | access-date=21 November 2019}} [258] => | [259] => | [260] => |- [261] => |[[ethosuximide]] [262] => |Zarontin [263] => |1960-11-022 November 1960{{cite web | title=New Drug Application (NDA) 012380 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=012380 | access-date=21 November 2019}} [264] => |1955 [265] => |1962 [266] => |- [267] => |[[ethotoin]] [268] => |Peganone [269] => |1957-04-2222 April 1957{{cite web | title=New Drug Application (NDA) 010841 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=010841 | access-date=21 November 2019}} [270] => | [271] => | [272] => |- [273] => |[[everolimus]] [274] => |Afinitor/Votubia [275] => |2009-03-3030 January 2009{{cite web | title=New Drug Application (NDA) 022334 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=022334 | access-date=21 November 2019}} [276] => | [277] => | [278] => |- [279] => |[[felbamate]] [280] => |Felbatol [281] => |1993-07-2929 July 1993{{cite web | title=New Drug Application (NDA) 020189 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=020189 | access-date=21 November 2019}} [282] => | [283] => | [284] => |- [285] => |[[fosphenytoin]] [286] => |Cerebyx [287] => |1996-08-055 August 1996{{cite web | title=New Drug Application (NDA) 020450 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=020450 | access-date=21 November 2019}} [288] => | [289] => | [290] => |- [291] => |[[gabapentin]] [292] => |Neurontin [293] => |1993-12-3030 December 1993{{cite web | title=New Drug Application (NDA) 020235 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=020235 | access-date=21 November 2019}} [294] => |1993-05May 1993 [295] => |1994-10October 1994 [296] => |- [297] => |[[lacosamide]] [298] => |Vimpat [299] => |2008-10-2828 October 2008{{cite web | title=New Drug Application (NDA) 022253 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=022253 | access-date=21 November 2019}} [300] => | [301] => | [302] => |- [303] => |[[lamotrigine]] [304] => |Lamictal [305] => |1994-12-2727 December 1994{{cite web | title=New Drug Application (NDA) 020241 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=020241 | access-date=21 November 2019}} [306] => |1991-10October 1991 [307] => |1995-05May 1995 [308] => |- [309] => |[[levetiracetam]] [310] => |Keppra [311] => |1999-11-3030 November 1999{{cite web | title=New Drug Application (NDA) 021035 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=021035 | access-date=21 November 2019}} [312] => |2000-09-2929 September 2000[http://www.emea.europa.eu/humandocs/Humans/EPAR/keppra/keppra.htm EPAR: Keppra.] {{webarchive |url=https://web.archive.org/web/20090619081026/http://www.emea.europa.eu/humandocs/Humans/EPAR/keppra/keppra.htm |date=19 June 2009 }} Retrieved on 1 November 2007. [313] => |2000-09-2929 September 2000 [314] => |- [315] => |[[mephenytoin]] [316] => |Mesantoin [317] => |1946-10-2323 October 1946{{cite web | title=New Drug Application (NDA) 006008 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=006008 | access-date=21 November 2019}} [318] => | [319] => | [320] => |- [321] => |[[metharbital]] [322] => |Gemonil [323] => |1952{{cite web | title=New Drug Application (NDA) 008322 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=008322 | access-date=21 November 2019}}{{cite book |author1=Dodson, W. Edwin |author2=Giuliano Avanzini |author3=Shorvon, Simon D. |author4=Fish, David R. |author5=Emilio Perucca |title=The treatment of epilepsy |publisher=Blackwell Science |location=Oxford |year=2004 |page=xxviii |isbn=978-0-632-06046-7 |no-pp=true}} [324] => | [325] => | [326] => |- [327] => |[[methsuximide]] [328] => |Celontin [329] => |1957-02-088 February 1957{{cite web | title=New Drug Application (NDA) 010596 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=010596 | access-date=21 November 2019}} [330] => | [331] => | [332] => |- [333] => |[[methazolamide]] [334] => |Neptazane [335] => |1959-01-2626 January 1959{{cite web | title=New Drug Application (NDA) 011721 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=011721 | access-date=21 November 2019}} [336] => | [337] => | [338] => |- [339] => |[[oxcarbazepine]] [340] => |Trileptal [341] => |2000-01-1414 January 2000{{cite web | title=New Drug Application (NDA) 021014 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=021014 | access-date=21 November 2019}} [342] => |2000 [343] => | [344] => |- [345] => |[[phenobarbital]] [346] => |Luminal [347] => |Unknown [348] => |1912 [349] => |1920 [350] => |- [351] => |[[phenytoin]] [352] => |Dilantin/Epanutin [353] => |1938{{cite web | title=New Drug Application (NDA) 008762 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=008762 | access-date=21 November 2019}} (Marketed in 1938, approved 1953) [354] => |1938 [355] => |1941 [356] => |- [357] => |[[piracetam]] [358] => |Nootropil [359] => |never approved [360] => | [361] => | [362] => |- [363] => |[[phensuximide]] [364] => |Milontin [365] => |1953{{cite web | title=New Drug Application (NDA) 008855 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=008855 | access-date=21 November 2019}}{{cite book |author1=Kutt, Henn |author2=Resor, Stanley R. |title=The Medical treatment of epilepsy |publisher=Dekker |location=New York |year=1992 |page=385 |isbn=978-0-8247-8549-9}} (first usage) [366] => | [367] => | [368] => |- [369] => |[[pregabalin]] [370] => |Lyrica [371] => |2004-12-3030 December 2004{{cite web | title=New Drug Application (NDA) 021446 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=021446 | access-date=21 November 2019}} [372] => |2004-07-066 July 2004[http://www.emea.europa.eu/humandocs/Humans/EPAR/lyrica/lyrica.htm EPAR: Lyrica] {{webarchive |url=https://web.archive.org/web/20090621214027/http://www.emea.europa.eu/humandocs/Humans/EPAR/lyrica/lyrica.htm |date=21 June 2009 }} Retrieved on 1 November 2007. [373] => |2004-07-066 July 2004 [374] => |- [375] => |[[primidone]] [376] => |Mysoline [377] => |1954-03-088 March 1954{{cite web | title=New Drug Application (NDA) 009170 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=009170 | access-date=21 November 2019}} [378] => |1952 [379] => |1953 [380] => |- [381] => |[[rufinamide]] [382] => |Banzel/Inovelon [383] => |2008-11-1414 November 2008{{cite web | title=New Drug Application (NDA) 021911 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=021911 | access-date=21 November 2019}}{{cite web | title=Drug Approval Package: Banzel (Rufinamide) NDA #021911 | website=U.S. [[Food and Drug Administration]] (FDA) | date=30 May 2012 | url=https://www.accessdata.fda.gov/drugsatfda_docs/nda/2008/021911s000_TOC.cfm | archive-url=https://web.archive.org/web/20191122035150/https://www.accessdata.fda.gov/drugsatfda_docs/nda/2008/021911s000_TOC.cfm | archive-date=22 November 2019 | url-status=live | access-date=21 November 2019}} [384] => | [385] => | [386] => |- [387] => |[[sodium valproate]] [388] => |Epilim [389] => |Unknown [390] => |1977-12December 1977 [391] => |1967-06June 1967 [392] => |- [393] => |[[stiripentol]] [394] => |Diacomit [395] => |2018-08-2020 August 2018{{cite web | title=New Drug Application (NDA) 206709 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=206709 | access-date=21 November 2019}}{{cite web | title=Drug Approval Package: Diacomit (stiripentol) | website=U.S. [[Food and Drug Administration]] (FDA) | date=7 September 2018 | url=https://www.accessdata.fda.gov/drugsatfda_docs/nda/2018/206709Orig1s000,207223Orig1s000TOC.cfm | archive-url=https://web.archive.org/web/20191122034549/https://www.accessdata.fda.gov/drugsatfda_docs/nda/2018/206709Orig1s000,207223Orig1s000TOC.cfm | archive-date=22 November 2019 | url-status=live | access-date=21 November 2019}} [396] => |2007-01January 2007 [397] => |2007-01January 2007 [398] => |- [399] => |[[tiagabine]] [400] => |Gabitril [401] => |1997-09-3030 September 1997{{cite web | title=New Drug Application (NDA) 020646 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=020646 | access-date=21 November 2019}}{{cite web|title=NDA: 020646|url=http://www.drugpatentwatch.com/p/NDA/020646|publisher=DrugPatentWatch|access-date=19 May 2013}} [402] => |1998 [403] => |1997-11November 1997 [404] => |- [405] => |[[topiramate]] [406] => |Topamax [407] => |1996-12-2424 December 1996{{cite web | title=New Drug Application (NDA) 020505 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=020505 | access-date=21 November 2019}} [408] => |1995 [409] => | [410] => |- [411] => |[[trimethadione]] [412] => |Tridione [413] => |1946-01-2525 January 1946{{cite web | title=New Drug Application (NDA) 005856 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=005856 | access-date=21 November 2019}} [414] => | [415] => | [416] => |- [417] => |[[valproic acid]] [418] => |Depakene/Convulex [419] => |1978-02-2828 February 1978{{cite web | title=New Drug Application (NDA) 018081 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=018081 | access-date=21 November 2019}} [420] => |1993 [421] => | [422] => |- [423] => |[[vigabatrin]] [424] => |Sabril [425] => |2009-08-2121 August 2009{{cite web | title=New Drug Application (NDA) 020427 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=020427 | access-date=21 November 2019}} [426] => |1989 [427] => | [428] => |- [429] => |[[zonisamide]] [430] => |Zonegran [431] => |2000-03-2727 March 2000{{cite web | title=New Drug Application (NDA) 020789 | publisher=U.S. [[Food and Drug Administration]] (FDA) | work=Drugs@FDA | url=https://www.accessdata.fda.gov/scripts/cder/daf/index.cfm?event=overview.process&ApplNo=020789 | access-date=21 November 2019}} [432] => |2005-03-1010 March 2005[http://www.emea.europa.eu/humandocs/Humans/EPAR/zonegran/zonegran.htm EPAR: Zonegran.] {{webarchive |url=https://web.archive.org/web/20090713160256/http://www.emea.europa.eu/humandocs/Humans/EPAR/zonegran/zonegran.htm |date=13 July 2009 }} Retrieved on 1 November 2007 [433] => |2005-03-1010 March 2005 [434] => |} [435] => [436] => == Pregnancy == [437] => {{See also|Epilepsy and pregnancy}} [438] => [439] => Many of the commonly used '''anticonvulsant/anti-seizure''' medications (ASMs), such as valproate, phenytoin, carbamazepine, phenobarbitol, gabapentin have been reported to cause an increased risk of [[birth defect]]s including major congenital malformations such as neural tube defects.{{cite journal |last1=Bromley |first1=Rebecca |last2=Adab |first2=Naghme |last3=Bluett-Duncan |first3=Matt |last4=Clayton-Smith |first4=Jill |last5=Christensen |first5=Jakob |last6=Edwards |first6=Katherine |last7=Greenhalgh |first7=Janette |last8=Hill |first8=Ruaraidh A. |last9=Jackson |first9=Cerian F. |last10=Khanom |first10=Sonia |last11=McGinty |first11=Ronan N. |last12=Tudur Smith |first12=Catrin |last13=Pulman |first13=Jennifer |last14=Marson |first14=Anthony G. |date=2023-08-29 |title=Monotherapy treatment of epilepsy in pregnancy: congenital malformation outcomes in the child |journal=The Cochrane Database of Systematic Reviews |volume=2023 |issue=8 |pages=CD010224 |doi=10.1002/14651858.CD010224.pub3 |issn=1469-493X |pmc=10463554 |pmid=37647086}} The risk of birth defects associated with taking these medications while pregnant may be dependent on the dose and on the timing of gestation (how well developed the baby is). While trying to conceive a child and during pregnancy, medical advice should be followed to optimize the management of the person's epilepsy in order to keep the person and the unborn baby safe from epileptic seizures and also ensure that the risk of birth defects due to ''in utero'' exposure of anticonvulsants is as low as possible. Use of anticonvulsant medications should be carefully monitored during use in pregnancy.{{cite journal |display-authors=etal |vauthors=Harden CL, Pennell PB, Koppel BS |date=May 2009 |title=Management issues for women with epilepsy—focus on pregnancy (an evidence-based review): III. Vitamin K, folic acid, blood levels, and breast-feeding: Report of the Quality Standards Subcommittee and Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology and the American Epilepsy Society |journal=Epilepsia |volume=50 |issue=5 |pages=1247–55 |doi=10.1111/j.1528-1167.2009.02130.x |pmid=19507305 |s2cid=221731995 |doi-access=free}} For example, since the first trimester is the most susceptible period for fetal development, planning a routine antiepileptic drug dose that is safer for the first trimester could be beneficial to prevent pregnancy complications.{{cite journal |last=George |first=Ilena C. |date=2017 |title=Practice Current: How do you treat epilepsy in pregnancy? |journal=Neurology: Clinical Practice |volume=7 |issue=4 |pages=363–371 |doi=10.1212/cpj.0000000000000387 |issn=2163-0402 |pmc=5648199 |pmid=29185530}} [440] => [441] => [[Valproic acid]], and its derivatives such as [[sodium valproate]] and [[divalproex sodium]], causes [[cognitive deficit]] in the child, with an increased dose causing decreased [[intelligence quotient]] and use is associated with adverse neurodevelopmental outcomes (cognitive and behavioral)  in children.{{cite journal|last1=Bromley|first1=Rebecca|last2=Weston|first2=Jennifer|last3=Adab|first3=Naghme|last4=Greenhalgh|first4=Janette|last5=Sanniti|first5=Anna|last6=McKay|first6=Andrew J|last7=Tudur Smith|first7=Catrin|last8=Marson|first8=Anthony G|title=Treatment for epilepsy in pregnancy: neurodevelopmental outcomes in the child|year=2014|doi=10.1002/14651858.CD010236.pub2|pmid=25354543|journal=Reviews|volume=2020|issue=10|pages=CD010236|pmc=7390020}}{{cite journal |last1=Tomson |first1=Torbjörn |last2=Marson |first2=Anthony |last3=Boon |first3=Paul |last4=Canevini |first4=Maria Paola |last5=Covanis |first5=Athanasios |last6=Gaily |first6=Eija |last7=Kälviäinen |first7=Reetta |last8=Trinka |first8=Eugen |date=July 2015 |title=Valproate in the treatment of epilepsy in girls and women of childbearing potential|journal=Epilepsia |language=en |volume=56 |issue=7 |pages=1006–1019 |doi=10.1111/epi.13021 |issn=0013-9580|doi-access=free |pmid=25851171 |url=https://biblio.ugent.be/publication/6985189/file/7011646 }} On the other hand, evidence is conflicting for [[carbamazepine]] regarding any increased risk of [[congenital physical anomalies]] or [[neurodevelopmental disorder]]s by intrauterine exposure. Similarly, children exposed [[lamotrigine]] or [[phenytoin]] in the womb do not seem to differ in their skills compared to those who were exposed to carbamazepine. [442] => [443] => There is inadequate evidence to determine if newborns of women with epilepsy taking anticonvulsants have a substantially increased risk of [[hemorrhagic disease of the newborn]]. [444] => [445] => There is little evidence to suggest that anticonvulsant/ASM exposure through breastmilk has clinical effects on newborns. The [https://www.clinicaltrials.gov/study/NCT01730170 Maternal Outcomes and Neurodevelopmental Effects of Antiepileptic Drugs (MONEAD)] study showed that most blood concentrations in breastfed infants of mothers taking carbamazepine, oxcarbazepine, valproate, levetiracetam, and topiramate were quite low, especially in relationship to the mother's level and what the fetal level would have been during pregnancy. (Note: valproic acid is NOT a recommended ASM for people with epilepsy who are considering having children.) {{cite journal |last1=Birnbaum |first1=Angela K. |last2=Meador |first2=Kimford J. |last3=Karanam |first3=Ashwin |last4=Brown |first4=Carrie |last5=May |first5=Ryan C. |last6=Gerard |first6=Elizabeth E. |last7=Gedzelman |first7=Evan R. |last8=Penovich |first8=Patricia E. |last9=Kalayjian |first9=Laura A. |last10=Cavitt |first10=Jennifer |last11=Pack |first11=Alison M. |last12=Miller |first12=John W. |last13=Stowe |first13=Zachary N. |last14=Pennell |first14=Page B. |last15=for the MONEAD Investigator Group |date=2020-04-01 |title=Antiepileptic Drug Exposure in Infants of Breastfeeding Mothers With Epilepsy |journal=JAMA Neurology |volume=77 |issue=4 |pages=441–450 |doi=10.1001/jamaneurol.2019.4443 |issn=2168-6149|doi-access=free |pmid=31886825 |pmc=6990802 }} [446] => [447] => Infant exposure to newer ASMs (cenobamate, perampanel, brivaracetam, eslicarbazepine, rufinamide, levetiracetam, topiramate, gabapentin, oxcarbazepine, lamotrigine, and vigabatrin) via breastmilk was not associated with negative neurodevelopment (such as lower IQ and autism spectrum disorder) at 36 months.{{cite web |title=Norwegian Mother, Father and Child Cohort Study (MoBa) |url=https://www.fhi.no/en/ch/studies/moba/ |access-date=2023-10-11 |website=Norwegian Institute of Public Health |language=en}} [448] => [449] => Several studies that followed children exposed to ASMs during pregnancy showed that a number of widely used ones (including lamotrigine and levetiracetam) carried a low risk of adverse neurodevelopmental outcomes (cognitive and behavioral) in children when compared to children born to mothers without epilepsy and children born to mothers taking other anti-seizure medications. Data from several pregnancy registries showed that children exposed to levetiracetam or lamotrigine during pregnancy had the lowest risk of developing major congenital malformations compared to those exposed to other ASMs. The risk of major congenital malformations for children exposed to these ASMs were within the range for children who were not exposed to any ASMs during pregnancy.{{cite journal |last1=Tomson |first1=Torbjörn |last2=Battino |first2=Dina |last3=Perucca |first3=Emilio |date=April 2019 |title=Teratogenicity of antiepileptic drugs |journal=Current Opinion in Neurology |volume=32 |issue=2 |pages=246–252 |doi=10.1097/WCO.0000000000000659 |issn=1473-6551 |pmid=30664067|s2cid=58608931 |url=https://cdm21054.contentdm.oclc.org/digital/api/collection/IR/id/2527/download }} [450] => [451] => People with epilepsy '''can''' have healthy pregnancies and healthy babies. However, proper planning and care is essential to minimize the risk of congenital malformations or adverse neurocognitive outcomes for the fetus while maintaining seizure control for the pregnant person with epilepsy. If possible, when planning pregnancy, people with epilepsy should switch to ASMs with the lowest teratogenic risk for major congenital malformations as well as the least risk of adverse neurodevelopmental outcomes (e.g., lower IQ or autism spectrum disorder). They should also work with their healthcare providers to identify the lowest effective ASM dosage that will maintain their seizure control while regularly checking medication levels throughout pregnancy.{{cite journal |last1=Pennell |first1=Page B. |last2=Karanam |first2=Ashwin |last3=Meador |first3=Kimford J. |last4=Gerard |first4=Elizabeth |last5=Kalayjian |first5=Laura |last6=Penovich |first6=Patricia |last7=Matthews |first7=Abigail |last8=McElrath |first8=Thomas M. |last9=Birnbaum |first9=Angela K. |last10=MONEAD Study Group |date=2022-04-01 |title=Antiseizure Medication Concentrations During Pregnancy: Results From the Maternal Outcomes and Neurodevelopmental Effects of Antiepileptic Drugs (MONEAD) Study |journal=JAMA Neurology |volume=79 |issue=4 |pages=370–379 |doi=10.1001/jamaneurol.2021.5487 |pmid=35157004 |issn=2168-6149|pmc=8845026 }} [452] => [453] => Data from studies conducted on women taking antiepileptic drugs for non-epileptic reasons, including depression and bipolar disorder, show that if high doses of the drugs are taken during the first trimester of pregnancy then there is the potential of an increased risk of congenital malformations.{{cite journal |last1=Jazayeri |first1=Dana |last2=Graham |first2=Janet |last3=Hitchcock |first3=Alison |last4=O'Brien |first4=Terence J. |last5=Vajda |first5=Frank J.E. |date=2018 |title=Outcomes of pregnancies in women taking antiepileptic drugs for non-epilepsy indications |journal=Seizure |volume=56 |pages=111–114 |doi=10.1016/j.seizure.2018.02.009 |issn=1059-1311 |pmid=29471258 |doi-access=free}} [454] => [455] => == Research == [456] => The mechanism of how anticonvulsants cause birth defects is not entirely clear. During [[pregnancy]], the metabolism of many anticonvulsants is affected. There may be an increase in the clearance and resultant decrease in the blood concentration of lamotrigine, phenytoin, and to a lesser extent carbamazepine, and possibly decreases the level of levetiracetam and the active oxcarbazepine metabolite, the monohydroxy derivative. In animal models, several anticonvulsant drugs have been demonstrated to induce neuronal [[apoptosis]] in the developing brain.{{cite journal |vauthors=Bittigau P, Sifringer M, Genz K |title=Antiepileptic drugs and apoptotic neurodegenereation in the developing brain|journal=Proceedings of the National Academy of Sciences of the United States of America |volume=99 |issue=23 |pages=15089–94 |date=May 2002 |pmid=12417760 |doi= 10.1073/pnas.222550499|pmc=137548|bibcode=2002PNAS...9915089B|display-authors=etal|doi-access=free}}{{cite journal |vauthors=Manthey D, Asimiadou S |title=Sulthiame but not levetiracetam exerts neurotoxic effect in the developing rat brain|journal=Exp Neurol|volume=193 |issue=2 |pages=497–503 |date=Jun 2005 |pmid=15869952 |doi= 10.1016/j.expneurol.2005.01.006|s2cid=1493015|display-authors=etal}}{{cite journal |vauthors=Katz I, Kim J |title=Effects of lamotrigine alone and in combination with MK-801, phenobarbital, or phenytoin on cell death in the neonatal rat brain|journal=J Pharmacol Exp Ther |volume=322 |issue=2 |pages=494–500|date=Aug 2007 |pmid=17483293 |doi= 10.1124/jpet.107.123133|s2cid=12741109|display-authors=etal}}{{cite journal |vauthors=Kim J, Kondratyev A, Gale K |title=Antiepileptic drug-induced neuronal cell death in the immature brain: effects of carbamazepine, topiramate, and levetiracetam as monotherapy versus polytherapy|journal=J Pharmacol Exp Ther |volume=323 |issue=1 |pages=165–73|date=Oct 2007 |pmid=17636003 |doi= 10.1124/jpet.107.126250|pmc=2789311}}{{cite journal |vauthors=Forcelli PA, Kim J, etal |title=Pattern of antiepileptic drug-induced cell death in limbic regions of the neonatal rat brain|journal=Epilepsia |volume=52 |issue=12 |pages=e207–11 |date=Dec 2011 |pmid=22050285 |doi= 10.1111/j.1528-1167.2011.03297.x |pmc=3230752 }} [457] => [458] => == References == [459] => [460] => [461] => {{reflist}} [462] => [463] => == Further reading == [464] => * Anti epileptic activity of novel substituted fluorothiazole derivatives by Devid Chutia, RGUHS [465] => [466] => == External links == [467] => * [https://www.neurotransmitter.net/epilepsy_drug_reference.html Drug Reference for FDA Approved Epilepsy Drugs] [468] => [469] => {{Anticonvulsants}} [470] => {{Major Drug Groups}} [471] => {{Authority control}} [472] => [473] => [[Category:Anticonvulsants]] [474] => [[Category:Epilepsy]] [] => )
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Anticonvulsant

An anticonvulsant is a type of medication that is used to prevent or control seizures in people with epilepsy. It works by calming the excessive electrical activity in the brain, which can cause seizures.

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It works by calming the excessive electrical activity in the brain, which can cause seizures. Anticonvulsants are also used to treat other conditions, such as bipolar disorder, neuropathic pain, and migraine headaches. There are several different types of anticonvulsant medications, and the choice of which one to use depends on the individual's specific condition and needs. Some common anticonvulsant medications include phenytoin, valproate, and carbamazepine. While anticonvulsants can be effective in reducing or eliminating seizures, they may also have potential side effects, such as drowsiness, dizziness, and mood changes. Therefore, it is important for individuals to work closely with their healthcare provider to find the most appropriate anticonvulsant medication and dosage for their specific needs.

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