Lennox-Gastaut syndrome 2191954 215291426 2008-05-27T15:43:29Z DOI bot 6652755 Citation maintenance. You can [[WP:DOI|use this bot]] yourself! Please [[User:DOI_bot/bugs|report any bugs]]. {{Infobox_Disease | Name = Lennox-Gastaut syndrome | ICD10 = {{ICD10|G|40|4|g|40}} | ICD9 = {{ICD9|345.0}} | eMedicineSubj = neuro | eMedicineTopic = 186 | DiseasesDB = 29493 | }} '''Lennox-Gastaut syndrome''' (LGS), also known as ''Lennox syndrome'', is a difficult-to-treat form of childhood-onset [[epilepsy]] that most often appears between the second and sixth year of life, and is characterized by frequent seizures and different seizure types; it is often accompanied by [[mental retardation]] and behavior problems. ==Characteristics== As a general rule, the age of seizure onset in LGS patients is between the ages of two and six; however, this does not exclude the possibility that seizures can begin before age two, or after age eight. The syndrome shows clear parallels to [[West syndrome]], enough to suggest a connection. Daily multiple seizures are typical in LGS. Also typical is the broad range of seizures that can occur, larger than that of any other epileptic syndrome. The most frequently occurring seizure types are: [[tonic seizure|tonic]], which are often nocturnal (90%); the second most frequent are [[myoclonic seizure]]s, which often occur when the patient is over-tired.<ref name=tired_bad>{{cite web | title=Childhood seizures - epilepsy and convulsions in children | url=http://hcd2.bupa.co.uk/fact_sheets/html/childhood_seizures.html | accessmonthday= August 16 | accessyear= 2005 }}</ref> [[Atonic seizure|Atonic]], [[atypical absence seizure|atypical absence]], [[complex partial seizure|complex partial]], [[focal seizure|focalized]] and [[tonic-clonic seizure]]s are also common. Additionally, about half of patients will suffer from [[status epilepticus]], usually the nonconvulsive type, which is characterized by dizziness, [[apathy]], and unresponsiveness. <!--Insbesondere die atypischen Absencen können mit statusartiger Häufung vorkommen.--> The seizures can cause sudden falling (or [[spasm]]s in tonic, atonic and myoclonic episodes) and/or loss of balance, which is why patients often wear a helmet to prevent head injury. In addition to daily multiple seizures of various types, children with LGS frequently have arrested/slowed [[psychomotor development]] and behavior disorders. The syndrome is also characterized by an [[Wiktionary:interictal|interictal]] (between-seizures) [[electroencephalogram|EEG]] featuring slow [[spike-wave complexe]]s. ==Incidence and prevalence== Approximately 5% of children with epilepsy have LGS, and is more common in males than females. Whereas some children seem perfectly normal prior to the development of seizures, others already had some form of epilepsy, such as West syndrome, which is seen in 20% of patients before (symptomatic) LGS. West syndrome is characterized by Blitz Nick Salaam seizures, and typically evolves into LGS in the second year of life. ===Finland=== According to a 1997 community-based retrospective study in the Helsinki metropolitan area and the province of Uusimaa, the annual incidence of Lennox-Gastaut was 2 in 100,000 (0.002%) from 1975-1985.<ref name=Finland>{{cite journal | author = Heiskala H. | title = Community-based study of Lennox-Gastaut syndrome | journal = Epilepsia | volume = 38 | issue = 5 | year = 1997 | pages = 526–31 | pmid = 9184597 | url = http://gateway.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=9184597.ui | doi = 10.1111/j.1528-1157.1997.tb01136.x}}</ref> ===United States=== 0.026% of all children in the [[Atlanta, Georgia]] metropolitan area were estimated to have LGS in 1997, which was defined as, "onset of multiple seizure types before age 11 years, with at least one seizure type resulting in falls, and an [[EEG]] demonstrating slow spike-wave complexes (<2.5 Hz)." The study concluded that LGS accounts for 4% of childhood epilepsies.<ref name=trevathanetal1997>{{cite journal | author=Trevathan E, Murphy CC, Yeargin-Allsopp M. | title=Prevalence and descriptive epidemiology of Lennox-Gastaut syndrome among Atlanta children | journal=Epilepsia | volume=38 | issue=12 | year=1997 | pages=1283–8 | pmid=9578523 | url = [http://gateway.ut.ovid.com/gw1/ovidweb.cgi?T=JS&PAGE=fulltext&D=ovft&AN=00003606-199712000-00005&NEWS=N&CSC=Y&CHANNEL=PubMed | doi=10.1111/j.1528-1157.1997.tb00065.x}}</ref> ==Mortality and morbidity== The mortality rate ranges from 3% to 7%.<ref name=7percent>{{cite web | author=Glauser, Tracy A. and Morita, Diego A. | year=2002 | title=Introduction | url=http://www.emedicine.com/neuro/topic186.htm | work=Lennox-Gastaut Syndrome | publisher=eMedicine.com, Inc. | accessdaymonth=8 July | accessyear=2005 }}</ref> ==Causes== There is no uniform cause: in 20% of the concerned, the LGS develops from the West syndrome. The medical history frequently includes infantile spasms or focalized and generalized seizures. The most common type of LGS (70-78%). This does not mean that LGS patients in other categories have no symptoms whatsoever; rather, it means that there is an identifiable underlying pathology responsible. This includes [[encephalopathy]] (brain damage) or another disease and/or developmental disorder. Frequent causes include [[tuberous sclerosis]], hereditary metabolic diseases, inflammatory brain disease such as [[encephalitis]], [[meningitis]], and [[toxoplasmosis]]; [[Hypoxia (medical)|hypoxia]]-[[ischemia]] injury and other birth injuries; and [[lesion]]s of the [[frontal lobe]]. These patients tend to have a worse prognosis than the idiopathic ones. In up to one-third of cases no cause can be found. These cases are referred as '''cryptogenic''' and/or '''idiopathic Lennox-Gastaut syndrome'''. Patients are considered to have idiopathic LGS if they were developing normally prior to the seizures, and cryptogenic if a cause is suspected by unknown. Not all investigators mention the second category. Lennox-Gastaut syndrome, drug resistant/drug refractory epilepsy have been recorded with neurovisceral porphyrias including acute intermittent porphyria, hereditary coproporphyria and variegate porphyria. Care must be taken to avoid porphyrinogenic anti-seizure drugs in these cases. Diagnosis may be difficult in children who require enzyme or DNA testing. ==Diagnosis== Generally speaking, LGS can often only be defined as a syndrome and/or distinguished from other syndromes because there are various overlaps with other syndromes. Currently, the fact that there is no uniform cause complicates things. <!--This stays up until someone can better translate it. Allgemein ist zu sagen, dass sich das LGS als Krankheitsbild oft nur schwer eingrenzen bzw. deutlich von anderen Krankheitsbildern abgrenzen lässt, da es diverse und zum teil fließende Übergänge zu ähnlichen [[Syndrom]]en gibt. Wie schon ausgeführt ist beispielsweise keine einheitliche Ursache gegeben, die die<!--duplicate?--> Diagnostik vereinfachen würde. Offen sichtbar ist dieser Form der Epilepsie durch häufige und vielfältige Anfälle. Bei der Messung der Gehirnströme mittels eines [[Elektroenzephalographie|EEG]]s zeigt sich ein in der Regel verlangsamter Grundrhythmus mit stets langsamen Spike-wave-Muster oder multifokalen und generalisierenden Sharp-slow-wave-Entladungen, die mit einer Häufigkeit zwischen 1,5 und 2,5 mal pro Sekunde registriert werden können. Veränderungen der Muster sind dahingehend möglich, dass es zu Seitenunterschieden und herdförmigen Besonderheiten in der Ableitung kommen kann. Im Schlaf können häufig tonische Muster, also Serien rascher Spitzen, registriert werden. Insbesondere die [[Differentialdiagnose]] zum '''Pseudo-Lennox-Syndrom''' muss abgeklärt werden, welches sich dadurch vom LGS unterscheidet, dass keine tonischen Anfälle auftreten. Aufgrund dessen muss die Diagnose durch [[Elektroenzephalographie|EEG]] im Schlaf (Schlaf-EEG) erfolgen, da die für das LGS typischen tonischen Anfälle meist im Schlaf auftreten Für die Überprüfung des Vorliegens einer hirnorganischen Besonderheit ist eine bildgebende Untersuchung des Gehirns mittels [[Magnetresonanztomographie]] (MRT) oder [[Computertomographie]] (CT) möglich. Treten die Bewegungsmuster bei insbesondere den tonischen Anfälle seitenbetont auf, lässt dies z. B. eine Hirnschädigung der entsprechenden Seite vermuten, der nachgegangen werden sollte. Bei der allgemeinmedizinischen Untersuchung fallen bei den meisten Kindern mit LGS im physischen Bereich Besonderheiten auf, insbesondere ist eine deutliche Entwicklungsverzögerung zu erkennen. Darüber hinaus zeigen sich vielfach kognitive Schwächen, eine entsprechende Einschränkung der Leistungsfähigkeit und Verhaltenauffälligkeiten. Die Besonderheiten können schon vor dem erstmaligen Auftreten der epileptischen Anfälle in Erscheinung getreten sein, aber auch erst nach bis zu zwei Jahren nach der Manifestation des LGS auftreten und sind vielfach auf die Grunderkrankung zurückzuführen, dass zu den Anfällen geführt hat.--> ''A temporary machine translation of the above German text is:'' ::Generally is to be said that the LGS often only heavily can be limited as a syndrome and/or lets delimit clearly of other syndromes because there are various and in part fluent transitions to similar [[Syndrom]]en. How already carried out is no uniform cause for example given, that that<!--duplicate?--> Diagnostics simplify would become. ::Is openly visible this form of the epilepsy through frequent and manifold attacks. In the measurement of the brain waves by means of a [[Elektroenzephalographie|EEG]]s, an as a rule slowed down reason rhythm with of Spike-wave-pattern slow always or multifokalen and generalizing Sharp-slow-wave-discharges, that can be registered with a frequency between 1.5 and 2.5 once per second, appears. Variations of the patterns are indicating possible that it can come to side difference and stove-shaped peculiarities in the derivation. In the sleep, frequently tonic patterns can, therefore series of quick tip, registers become. ::Especially the [[Differentialdiagnose]] to the '' ‚Pseudo-Lennox-Syndrom' '' must be clarified, which differs through it by the LGS, that no tonic attacks appear. Based on whose the diagnosis must result through [[Elektroenzephalographie|EEG]] in the sleep (sleep EEG) because the attacks typical tonic for the LGS appear usually in the sleep ::For the examination of the existence of a brain organic peculiarity, an imaging investigation of the brain is by means of [[Magnetresonanztomographie]] (MRT) or [[Computertomographie]] (CT) possible. If the movement patterns appear side emphasizes in especially the tonic attacks, this lets assume for example a brain damage of the corresponding side, that should investigated become. ::In the general medical investigation, peculiarities be noticeable is to be recognized at most children with LGS in the physical area, especially a clear development delay. In addition multiply cognitive weakness, a corresponding restriction of the efficiency and behavior striking features appear. The peculiarities can have appeared already before the initial appearance of the epileptic attacks, but appear and are also first after up to two years after the manifestation of the LGS to lead back multiply to the reason disease that to the attacks led has. * [[EEG]] * [[MRI]] * [[CT scan]]s, usually in the case of suspected injury resulting from an atonic and/or tonic seizure. ==Treatment== LGS seizures are often treatment resistant, but this does not mean that treatment is futile. Options include anticonvulsants, anesthetics, steroids such as [[prednisone]], [[immunoglobulin]]s, and various other pharmacological agents that have been reported to work in individual patients. ===Pharmacological=== ====Approved==== =====First-line drugs===== * valproates ([[valproic acid]], [[sodium valproate]] and [[valproate semisodium]]) * [[benzodiazepine]]s, specifically [[clonazepam]], [[nitrazepam]], and [[clobazam]] Nitrazepam and Clobazam are not approved in the USA. =====Second-line drugs===== In 1999, Dr. Sachdeo and colleagues at the University of Medicine and Dentistry of New Jersey and the Robert Wood Johnson Medical School in New Brunswick reported that 33% of the patients in the [[topiramate]] group experienced a minimum 50% reduction in seizures (specifically drop attacks and tonic-clonics), compared with 8% in the [[placebo]] group.<ref name=topiramate>{{cite journal | author=Sachdeo RC, Glauser TA, Ritter F, Reife R, Lim P, Pledger G | title=A double-blind, randomized trial of topiramate in Lennox-Gastaut syndrome. Topiramate YL Study Group | journal=Neurology | volume=10 | issue=52 | year=1999 | pages=1882–7 | pmid=10371538 | url = [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=10371538&dopt=ExternalLink}}</ref> It was also found to be effective as an adjunctive therapy in a review published by Drs. Edith Alva Moncayo and Antonio Ruiz Ruiz<!--duplicate?--> in March of 2003.<ref name=topiramate_adjunct>{{cite journal | author=Alva-Moncayo E, Ruiz-Ruiz A | title=[The value of topiramate used with conventional schemes as an adjunctive therapy in the treatment of Lennox-Gastaut syndrome] | journal= Revista de Neurologia | volume=36 | issue=5 | year=2003 | pages=453–7 | pmid=12640599 | url = http://www.revneurol.com/LinkOut/formMedLine.asp?Refer=2002014&Revista=Revneurol}}</ref> Dr. Motte and colleagues at the American Memorial Hospital at [[Reims]], France reported in 1997 that [[lamotrigine]] was effective in the treatment of LGS, with the most common side effect in the treatment group relative to placebo being colds or viral illnesses.<ref name=lamotrigine>{{cite journal | author=Motte J, Trevathan E, Arvidsson JF, Barrera MN, Mullens EL, Manasco P | title=Lamotrigine for generalized seizures associated with the Lennox-Gastaut syndrome. Lamictal Lennox-Gastaut Study Group | journal=New England Journal of Medicine | volume=337 | issue=25 | year=1997 | pages=1807–12 | pmid=9400037 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=9400037&dopt=ExternalLink | doi=10.1056/NEJM199712183372504}}</ref> Two years later, it was approved by Health Canada for adjunctive therapy in Lennox Gastaut in adults and children.<ref name=epilepsy_ontario>{{cite web | author = Epilepsy Ontario | year = 1999 | url = http://epilepsyontario.org/client/EO/EOWeb.nsf/web/Lamotrigine+Approved+in+Canada+for+Lennox-Gastaut+Syndrome | title = Lamotrigine Approved in Canada for Lennox-Gastaut Syndrome | work = <nowiki>'</nowiki>Sharing<nowiki>'</nowiki> News | accessdaymonth = 13 November | accessyear = 2005}}</ref> The United States [[Food and Drug Administration]] approved it for that in August of 1998.<ref name=US_lamotrigine_approval>{{cite web | author = Glaxo Wellcome Inc | year = 1998 | url = http://www.fda.gov/cder/foi/nda/98/020241s003.htm | title = Final Printed Labeling -- Part 1 | work = Lamictal Tablets & Chewable Dispersible Tablets (Lamotrigine) Drug Approval Page | publisher = United States Food and Drug Administration Center for Drug Evaluation and Research | accessdaymonth = 13 November | accessyear = 2005}}</ref> [[Felbamate]] is indicated in the use of LGS in the event that everything else fails,<ref name=Felbatol_PI_sheet>{{cite web | url = http://www.rxlist.com/cgi/generic/felbamate_ids.htm | title = Felbatol (felbamate) | accessdate = 2007-09-19 | page = 3 }}</ref> and was found to be superior to placebo in controlling treatment resistant [[partial seizure]]s and [[atonic seizure]]s.<ref name=felbamate>{{cite journal | first = Frank J. | last = Ritter | coauthors = Ilo E. Leppik, Fritz E. Dreifuss, Ihor Rak, Nancy Santilli, Roberta Homzie, W. Edwin Dodson, Tracy A. Glauser, J. Chris Sackellares, Larry Olson, Elizabeth A. Garafolo, W. Donald Shields, Jacqueline French, Michael Sperling, Lynn D. Kramer, Marc Kamin, Alberto Rosenberg, Robert Shumaker, James L. Perhach, and Robert Dix | title=Efficacy of Felbamate in Childhood Epileptic Encephalopathy (Lennox-Gastaut Syndrome) | journal=New England Journal of Medicine | volume=328 | issue=1 | year=1993 | pages=29–33 | pmid=8347179 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=8347179&dopt=ExternalLink | doi=10.1056/NEJM199301073280105}}</ref><ref name=felbamate2>{{cite journal | first = Orrin | last = Devinsky | coauthors = R. Edward Faught, B. Joseph Wilder, Andres M. Kanner, Marc Kamin, L. D. Kramer and A. Rosenberg | title=Efficacy of felbamate monotherapy in patients undergoing presurgical evaluation of partial seizures | journal=Epilepsy Research | volume=20 | issue=3 | year=1995 | pages=241–6 | pmid=7796796 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=7796796&dopt=ExternalLink | doi=10.1016/0920-1211(94)00084-A}}</ref> However, it has been known to cause [[aplastic anemia]] and liver toxicity.<ref name=felbamateliver>{{cite journal | author=O'Neil MG, Perdun CS, Wilson MB, McGown ST, Patel S | title=Felbamate-associated fatal acute hepatic necrosis | journal=Neurology | volume=46 | issue=5 | year=1996 | pages=1457–1459 | pmid=8628501 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=8628501&dopt=ExternalLink}}</ref> ====Unapproved, off-label, and investigational drugs==== [[Vigabatrin]] was found by Feucht et al to be an effective add-on in patients whose seizures were not satisfactorily controlled by valproate. Out of 20 children, only 1 experienced a serious side effect ([[dyskinesia]]).<ref name=feuchtetal>{{cite journal | author=Feucht M, Brantner-Inthaler S | title=Gamma-vinyl-GABA (vigabatrin) in the therapy of Lennox-Gastaut syndrome: an open study | journal=Epilepsia | volume=35 | issue=5 | year=1994 | pages=993–8 | pmid=7925171 | doi=10.1111/j.1528-1157.1994.tb02544.x}}</ref> [[Zonisamide]] showed promise in an overview of controlled and uncontrolled trials conducted in Japan.<ref name=zonisamideoverview>{{cite journal | author=Yagi K | title=Overview of Japanese experience-controlled and uncontrolled trials | journal=Seizure | volume=13 | issue=Supplement 1 | year=2004 | pages=S11–5; discussion S16 | id=[[PMID]] [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15511680&query_hl=14&itool=pubmed_docsum 15511680] | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=15511680&dopt=ExternalLink | doi=10.1016/j.seizure.2004.04.018}}</ref> However, in a physician survey conducted December of 2004, only 28% of Lennox-Gastaut and [[West syndrome]] patients improved on zonisamide.<ref name=zonisamidesurvey>{{cite journal | first = Toshio | last = Yamauchi | coauthors = Aikawa Hiroshi | year = 2004 | month = December | title = Efficacy of zonisamide: our experience | journal = Seizure | volume = 13 | issue = Suppl 1 | pages = S41–8 discussion S49 | doi = 10.1016/j.seizure.2004.04.021 | url = http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&list_uids=15511689&dopt=ExternalLink}}</ref> ===Surgical=== * [[vagus nerve stimulation]] * [[corpus callosotomy]] ===Other=== ====Ketogenic diet==== {{main|Ketogenic diet}} A [[ketogenic diet]] is a diet that causes [[ketosis]], a state in which there is an excessive amount of [[ketone]]s in the body. It is becoming increasingly popular for treating intractable epilepsy. ====Intravenous immunoglobulin therapy==== Intravenous immunoglobulin therapy has been used in Lennox-Gastaut syndrome as early as 1986, when van Rijckevorsel-Harmant and colleagues used it in seven patients with ostensibly idiopathic LGS and saw EEG improvement and decreased seizure frequency in six of them.<ref name=van_Rijckevorsel-Harmant_et_al_1986>{{cite journal | first = K. | last = van Rijckevorsel-Harmant | coauthors = M. Delire and M. Rucquoy-Ponsar | year = 1986 | title = Treatment of idiopathic West and Lennox-Gastaut syndromes by intravenous administration of human polyvalent immunoglobulins | journal = European Archives of Psychiatry and Neurological Sciences | volume = 236 | issue = 2 | pages = 119–22 | pmid = 3792407 | doi = 10.1007/BF00454021}}</ref> <!-- ==Prognosis== Allgemein ist das LGS (bzw. die dem Epilepsie-Syndrom häufig zugrunde liegende Schädigung des Gehirns) durch eine vergleichsweise ungünstige Prognose, sowohl in Bezug auf die medizinische Behandelbarkeit als auch auf die Lebensqualität und die Kindesentwicklung sowie in manchen Fällen auch auf die Lebensdauer, gekennzeichnet. Unabhängig von Ausmaß und Auswirkung der Grunderkrankung werden ein früher Beginn des LGS und häufige tonische Anfälle als Merkmal einer ungünstigen Gesamtprognose gesehen. Zum Teil werden im Verlauf des LGS die epileptischen Anfälle zweitrangig, während oftmals fortschreitende kognitive und körperliche Beeinträchtigungen sowie Verhaltensstörungen in den Vordergrund treten. Statistisch gesehen überleben fünf von 100 Kindern die ersten fünf Jahre ihres Lebens nicht, wobei sie nicht an den epileptischen Anfällen, sondern an der die Anfälle auslösenden Grunderkrankung oder daraus resultierenden Komplikationen sterben. Bei etwa zwei Drittel der Kinder können die Anfälle nicht eingestellt werden, sodass keine Anfallsfreiheit erreicht wird. Statistisch gesehen können wenig mehr als die Hälfte der Kindern mit LGS durch Medikamente vergleichsweise befriedigend behandelt werden, wobei nur 5 bis 10 Kindern langfristig anfallsfrei bleiben und sich lediglich 15 von 100 Kindern kognitiv und motorisch regelgerecht entwickeln und im Erwachsenenalter ein selbständiges und weitgehend beschwerdefreies Leben führen. Letztere sind in aller Regel diejenigen, bei denen auch vor dem erstmaligen Auftreten des LGS keine Auffälligkeiten bestanden und keine Grunderkrankung (Hirnschädigung) als Ursache der Anfälle vorliegt. Eine Zunahme von Entwicklungsauffälligkeiten ist in der Regel bei solchen Kindern zu beobachten, bei denen schon vor der Erstmanifestation des LGS Störungen der kognitiven und psycho-motorischen Entwicklung bestanden. Dieser Verlauf ist jedoch häufig nicht auf die epileptischen Anfälle sondern auf die Grunderkrankung zurückzuführen, z. B. auf eine fortschreitende Fehlentwicklung des Gehirns. Aber auch ein ungünstiger Verlauf der epileptischen Anfälle, insbesondere bei statusartigem Auftreten der Krämpfe, kann (weitere) bleibende Schädigungen verursachen. Viele Betroffene sind auch nach erfolgreicher Einstellung der Anfälle körperlich und kognitiv deutlich beeinträchtigt, wobei dies in der Regel nicht in erster Linie auf die epileptischen Anfälle sondern auf deren Ursache (hirnorganische Besonderheit bzw. dessen Schweregrad) zurückgeführt werden kann. Häufig zeigen sich auch im Erwachsenenalter Lernstörungen, Sprachstörungen und Bewegungsstörungen sowie eine Einschränkung der kognitiven Leistungsfähigkeit und [[Cerebralparese]]n.--> ==History== LGS was named for [[neurology|neurologist]] [[William G. Lennox]] (Boston, USA) and [[Henri Gastaut]] (Marseille, France).<!-- die diese Form der Epilepsie in den 1950er Jahren (ab [[1945]]) erstmals eingehend unter wissenschaftlichen Gesichtspunkten beschrieben und sich intensiv mit ihrer Erforschung und Abgrenzung zu anderen Formen der Epilepsie befassten.--> ==References== {{Reflist|2}} ==See also== * [[Epilepsy]] * [[West syndrome]] * [[Ohtahara syndrome]] * [[Syndromes]] <!--This article is heavily based on [[:de:Lennox-Gastaut-Syndrom]] from [de:Wikipedia] on [[August 14]], [[2005]]--> {{Diseases of the nervous system}} [[Category:Neurology]] [[Category:Epilepsy]] [[de:Lennox-Gastaut-Syndrom]] [[fi:Lennox-Gastaut'n oireyhtymä]] [[fr:Syndrome de Lennox-Gastaut]] [[nl:Lennox-syndroom]] [[pl:Zespół Lennoxa-Gastauta]] [[pt:Síndrome de Lennox-Gastaut]]