Lennox–Gastaut syndrome

Definition

Lennox-Gastaut syndrome (LGS) is one of the most severe forms of epilepsy (a seizure disorder) that develops in children usually between one and eight years old. It is characterized by several types of seizures, developmental delay, and behavioral disturbances such as poor social skills and lack of impulse control.

Description

Lennox-Gastaut syndrome can be the result of any one of many neurological problems of childhood that begins with intractable, or hard to control, seizures. French physician Samuel Auguste A. D. Tissot (1728–1797) first described the syndrome in 1770. He reported an 11-year-old boy with frequent drop attacks, myoclonus (jerking movements), and progressive functional impairment. Seizure types vary among children with LGS. The tonic seizures of LGS include stiffening of the body, upward deviation of the eyes, dilation of the pupils, and altered respiratory patterns. Atonic seizures are also experienced by children with LGS and involve a brief loss of muscle tone and consciousness, which causes abrupt falls. Other seizures common in LGS include the atypical absence seizure type (staring spells) and myoclonic seizures (sudden muscle jerks).

Lennox-Gastaut syndrome frequently affects language development in children, ranging from little or no verbal ability to slowness in ideation and expression. Varying degrees of motor difficulties hinder age-appropriate activities such as walking, skipping, or using a writing instrument. Severe behavioral disorders such as hyperactivity, aggressiveness, and autistic tendencies and personality disorders are nearly always present. There is usually mentalretardation and sometimes a tendency for psychosis that eventually develops with LGS.

In young children, LGS usually begins with episodes of sudden falls. In the school-age group, behavioral disturbances may be the heralding signs, along with sudden falls. This is soon followed by frequent seizures, episodes of status epilepticus (a continuous seizure state that is associated with a change in the child's level of awareness), progressively deteriorating intellectual functions, and personality disturbances. By age six, most children with LGS have some degree of mental retardation.

When children grow older, the types of seizures often change. In most cases, the drop seizures subside. They are replaced by partial, complex partial, and secondarily generalized convulsions. Among teenagers, complex partial seizures are the most common form.

Demographics

In the United States, Lennox-Gastaut syndrome accounts for 1–4% of older children with epilepsy, but 10% of children with epilepsy beginning in the first five years of life. In Europe, studies demonstrated that the proportion of patients with LGS seems similar to that in the US.

No racial differences exist in the occurrence of LGS; however there are differences in respect to sex and age. Males are affected more often than females; the relative risk of occurrence of LGS is significantly higher in boys than in girls (one in 10,000 boys, and one in 50,000 girls). The average age for the onset of seizures is three years.

Causes and symptoms

Causes

Often no specific cause is identifiable, however, some of the known causes include:

• developmental malformations of the brain
• genetic brain diseases such as tuberous sclerosis, and inherited metabolic brain diseases
• brain injury due to problems associated with pregnancy and birth, including prematurity, asphyxia, and/or low birth weight
• severe brain infections, including encephalitis, meningitis, toxoplasmosis, and rubella

In many instances, LGS follows earlier infantile spasms, which are sudden spasms or body bending, either at the trunk or neck. These episodes usually begin between three and eight months of age, and may develop into the mixed seizure pattern that characterizes LGS at two to three years of age.

Symptoms

The main symptom of LGS is the occurrence of seizures. Several different seizure types occur, and a child may experience some or all of these:

• In drop attacks, the child falls suddenly to the ground. This may be because the legs suddenly fold up (atonic seizure) or stiffen (tonic seizures), or because of a violent jerk (myoclonic seizure) that throws the child to the floor.
• During atypical absences, the child appears to be vacant or to stare blankly. Sometimes these seizures are associated with blindness or nodding of the head. Often, children are able to continue their activity to some extent during the seizure. These episodes are usually very brief, but frequent. Sometimes these seizures occur so frequently that they merge into one another. Such a phenomenon can lead to what is called non-convulsive status epilepticus. During these episodes, children may appear to switch off, but can be partly responsive, drool, be unable to speak or eat properly, and be wobbly on their feet.
• Tonic seizures are often difficult to detect as they occur much more frequently at night. During these attacks, there is general stiffening of the arms or legs. This may be associated with the eyes rolling up or the head moving back. Sometimes, breathing is interrupted and the child may turn blue. If the attacks last for more than 10–20 seconds, the arms often start to tremble rapidly while remaining stiff.

Most children with LGS experience some degree of impaired intellectual functioning or mental retardation. In approximately 65% of children with LGS, intellectual disability is evident, either previous to or at the time of diagnosis. Behavioral disturbances are also usually present, including persistent attention-seeking behavior, impulsiveness, lack of regard for personal safety and fearlessness, and, in severe cases, autistic behaviors. These behavior disturbances may be the result of the condition causing LGS, effects of a particular medication, uncontrolled epilepsy, difficulty interpreting information, or even a lower level of concept understanding.

Diagnosis

LGS is diagnosed by some or all of the following symptoms, including:

• presence of a mixed seizure pattern
• some degree of developmental delay or intellectual disability
• distinct, slow, spike-and-wave pattern shown during electroencephalogram (EEG)

Magnetic resonance imaging (MRI) is an important part of the search for an underlying cause in a child with LGS. Abnormalities revealed by MRI associated with LGS include tuberous sclerosis, brain malformations, or evidence of previous brain injury.

Treatment team

Treatment for LGS involves a multidisciplinary team that may include a neurologist, a neuropsychologist, and a neurosurgeon. A dietitian may help with specialized diet regimens.

Treatment

The drug treatment for LGS is based on the use of anti-epileptic drugs that are effective in reducing the number of seizures. However, the improvement often only lasts for a period of months or, rarely, a year or more. Carbamazepine, sodium valproate, vigabatrin, lamotrigine, and the benzodiazepines (clobazam, in particular) are often prescribed.

One alternative treatment involves a ketogenic diet in which 87% of calories come from fat, 6% from carbohydrates, and 7% from protein. The diet is restrictive, difficult to follow, but has shown results in reducing seizures in some affected children. Other less conventional therapies such as intravenous immunoglobulin therapy have also been attempted.

For children with repeated drop attacks, a procedure to cut the corpus collosum (the large group of nerve fibers connecting the two halves of the brain) may be very helpful. However, this procedure involves significant surgery and is not always effective, and seizures may return after several months or years.

An implanted vagus nerve stimulator is effective in reducing seizures in many children with Lennox-Gastaut syndrome. It is a device, similar in size to a heart pacemaker, that is implanted in the chest with a lead wrapped around the vagus nerve in the neck. It is able to stimulate the vagus nerve automatically at adjustable intervals. The device may take months to show maximum benefit, and requires a surgical procedure for insertion as well as for removal. The batteries require replacement approximately every eight to ten years, which entails further surgery.

Recovery and rehabilitation

A very small percentage of children with LGS experience a spontaneous improvement in seizures, usually during adolescence. In these cases, mental function also shows some improvement. In the overwhelming majority of cases, however, emphasis is placed on maximizing quality of life rather than recovery.

Protective devices such as helmets and pads may be necessary during periods of high seizure activity, but many children and parents consider them too burdensome and restrictive for continuous daily use.

Clinical trials

Although as of early 2004 there were no ongoing clinical trials for LGS, the National Institutes of Health (NIH) sponsors research related to many seizure disorders. Information on the numerous current clinical trials for the study and treatment of seizure disorders can be found at the NIH Web site: .

Prognosis

The prognosis for individuals with LGS is unfavorable, but variable. Long-term studies of children with LGS found that a majority of patients continue to have typical LGS characteristics (mental retardation, treatment-resistant seizures) many years after onset. Children with an early onset of seizures, prior history of West syndrome, higher frequency of seizures, or constant slow EEG background activity have a worse prognosis than those with seizures beginning later in childhood. Tonic seizures may persist and be more difficult to control over time, while myoclonic and atypical absences become easier to control.

Special concerns

It is recognized that the frequency of seizures may be associated with the child's level of alertness. The child who is overexcited or lacks sufficient stimulation may experience more seizures. Therefore, a stable but stimulating environment may be important in reducing the number of daily seizures. This may include a strict routine of regular meals, sleep, and medication.

Providing for the safety of a child with Lennox-Gastaut syndrome is a 24-hour concern for parents. Coupled with safety concerns, children with LGS are often dependent for personal care such as toileting, management of behavioral impulses, and interpretation of attempts at communication. Often, respite care can provide parents with a chance to reenergize. As the child matures into adulthood, an assisted living center or group home may help provide maximum independence and social integration, along with continued medical supervision.

Resources

BOOKS

The Official Parent's Sourcebook on Lennox-Gastaut Syndrome: A Revised and Updated Directory for the Internet Age. San Diego: Icon Group International, 2002.

PERIODICALS

Frost, M., et al. "Vagus Nerve Stimulation in Children with Refractory Seizures Associated with Lennox-Gastaut Syndrome." Epilepsia 42 (2001): 1148–1152.

OTHER

NINDS Lennox-Gastaut Syndrome Information Page. National Institute of Neurological Disorders and Stroke. March 10, 2004 (May 23, 2004). http://www.ninds.nih.gov/health_and_medical/disorders/lennoxgastautsyndrome_doc.htm.

ORGANIZATIONS

Lennox-Gastaut Syndrome Group. 3872 Lyceum Avenue, Los Angeles, CA 90066. (310) 391-0335; Fax: (310) 397-2687. CandaceLGS@aol.com.

Epilepsy Foundation. 4351 Garden City Drive, Suite 500, Landover, MD 20785-7223. (301) 459-3700 or (800) EFA-1000 (332-1000); Fax: (301) 577-2684. postmaster@efa.org. http://www.epilepsyfoundation.org/.

NIH/NINDS Brain Resources and Information Network. PO Box 5801, Bethesda, MD 20824. (301) 496-5751 or (800) 352-9424; Fax: (301) 402-2186. http://www.ninds.nih.gov/.

Greiciane Gaburro Paneto

Iuri Drumond Louro, MD, PhD

A generalized myoclonic astatic epilepsy that occurs in children as a result of various cerebral afflictions such as perinatal hypoxia, cerebral hemorrhage, encephalitis, and maldevelopment or metabolic disorders of the brain; it is characterized by mental retardation and generalized tonic seizures or akinetic attacks. Also called Lennox syndrome.

Lennox–Gastaut syndrome
Classification and external resources
ICD-10	G40.4
ICD-9	345.0
DiseasesDB	29493
eMedicine	neuro/186

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.

Contents 1 Characteristics 2 Incidence and prevalence 2.1 Finland 2.2 United States 3 Mortality and morbidity 4 Causes 5 Diagnosis 6 Treatment 6.1 Pharmacological 6.1.1 Approved 6.1.1.1 First-line drugs 6.1.1.2 Second-line drugs 6.1.2 Unapproved, off-label, and investigational drugs 6.2 Surgical 6.3 Other 6.3.1 Ketogenic diet 6.3.2 Intravenous immunoglobulin therapy 7 History 8 References 9 See also

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 six. 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, which are often nocturnal (90%); the second most frequent are myoclonic seizures, which often occur when the patient is over-tired.^[1]

Atonic, atypical absence, complex partial, focalized and tonic–clonic seizures 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. The seizures can cause sudden falling (or spasms 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 interictal (between-seizures) EEG featuring slow spike-wave complexes.

Incidence and prevalence

Approximately 5% of children with epilepsy have LGS, and it 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.^[2]

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.^[3]

Mortality and morbidity

The mortality rate ranges from 3% to 7%.^[4]

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–ischemia injury and other birth injuries; and lesions 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

This section is a rough translation from German. It may have been generated by a computer or by a translator without dual proficiency. Please help to enhance the translation. The original article is under "German" in the "languages" sidebar.

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.

The diagnosis or suspicion of LGS is often a question of probability rather than certainty. This is because the varied presentations of LGS share features with other disorders, many of which may be said to have overlapping characteristics.

The diagnosis is more obvious when the epilepsy has frequent and manifold attacks, with the classic pattern on the electro-encephalogram (EEG); the latter is a slowed rhythm with Spike-wave-pattern, or with a multifocal and generalizing Sharp-slow-wave-discharges at 1.5–2.5 Hz. During sleep, frequently, tonic patterns can be seen. But variations of these patterns are known in patients with no diagnosis other than LGS, and they can differ bilaterally, and from time to time, within the same patient.

General medical investigation usually reveals developmental delay and cognitive deficiencies in children with true LGS. These may precede development of seizures, or require up to two years after the seizures begin, in order to become apparent.

Exclusion of organic or structural brain lesions is also important in establishing a correct diagnosis of LGS; this may require magnetic resonance imaging (MRI) or computerized tomography (CT). An important differential diagnosis is 'Pseudo-Lennox-Syndrome', which differs from LGS, in that there are no tonic seizures; sleeping EEG provides the best basis for distinguishing between the two.

Treatment

LGS seizures are often treatment resistant, but this does not mean that treatment is futile. Options include anticonvulsants, anesthetics, steroids such as prednisone, immunoglobulins, and various other pharmacological agents that have been reported to work in individual patients.

Pharmacological

No scientific study has shown any drug to be highly efficacious for treatment of LGS, and its best treatment remains uncertain. Rufinamide(Banzel), lamotrigine, topiramate and felbamate may help as add-on therapy.^[5]

Approved

First-line drugs

• valproates (valproic acid, sodium valproate and valproate semisodium)
• benzodiazepines, 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.^[6] It was also found to be effective as an adjunctive therapy in a review published by Drs. Edith Alva Moncayo and Antonio Ruiz Ruiz in March 2003.^[7]

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.^[8] Two years later, it was approved by Health Canada for adjunctive therapy in Lennox Gastaut in adults and children.^[9] The United States Food and Drug Administration approved it for that in August 1998.^[10]

Felbamate is indicated in the use of LGS in the event that everything else fails,^[11] and was found to be superior to placebo in controlling treatment resistant partial seizures and atonic seizures.^[12][13] However, it has been known to cause aplastic anemia and liver toxicity.^[14]

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).^[15]

Zonisamide showed promise in an overview of controlled and uncontrolled trials conducted in Japan.^[16] However, in a physician survey conducted December 2004, only 28% of Lennox–Gastaut and West syndrome patients improved on zonisamide.^[17]

Surgical

• vagus nerve stimulation
• corpus callosotomy

Other

Ketogenic diet

Main article: Ketogenic diet

A ketogenic diet is a diet that causes ketosis, a state in which there is an excessive amount of ketones 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.^[18]

History

LGS was named for neurologists William G. Lennox (Boston, USA) and Henri Gastaut (Marseille, France).

References

1. ^ "Childhood seizures – epilepsy and convulsions in children". http://hcd2.bupa.co.uk/fact_sheets/html/childhood_seizures.html. Retrieved August 16, 2005. 
2. ^ Heiskala, H (1997). "Community-based study of Lennox-Gastaut syndrome". Epilepsia 38 (5): 526–31. doi:10.1111/j.1528-1157.1997.tb01136.x. PMID 9184597. 
3. ^ Trevathan, E; Murphy, CC; Yeargin-Allsopp, M (1997). "Prevalence and descriptive epidemiology of Lennox-Gastaut syndrome among Atlanta children". Epilepsia 38 (12): 1283–8. doi:10.1111/j.1528-1157.1997.tb00065.x. PMID 9578523. 
4. ^ Glauser, Tracy A. and Morita, Diego A. (2002). "Introduction". Lennox–Gastaut Syndrome. eMedicine.com, Inc.. http://www.emedicine.com/neuro/topic186.htm. Retrieved 8 July 2005. 
5. ^ Hancock, EC; Cross, HH (2009). "Treatment of Lennox-Gastaut syndrome". Cochrane database of systematic reviews (Online) (3): CD003277. doi:10.1002/14651858.CD003277.pub2. PMID 19588340. 
6. ^ Sachdeo, R. C. (1999). "A double-blind, randomized trial of topiramate in Lennox-Gastaut syndrome". Neurology 52 (9): 1882. PMID 10371538. http://www.neurology.org/cgi/content/abstract/52/9/1882. 
7. ^ Alva-Moncayo, E; Ruiz-Ruiz, A (2003). "Utilidad del topiramato como terapia añadida a esquemas convencionales para el síndrome de Lennox-Gastaut [The value of topiramate used with conventional schemes as an adjunctive therapy in the treatment of Lennox-Gastaut syndrome]" (in Spanish). Revista de neurologia 36 (5): 453–7. PMID 12640599. http://www.revneurol.com/sec/resumen.php?or=pubmed&id=2002014. 
8. ^ Motte, J; Trevathan, E; Arvidsson, JF; Barrera, MN; Mullens, EL; Manasco, P (1997). "Lamotrigine for generalized seizures associated with the Lennox-Gastaut syndrome. Lamictal Lennox-Gastaut Study Group". The New England journal of medicine 337 (25): 1807–12. doi:10.1056/NEJM199712183372504. PMID 9400037. 
9. ^ Epilepsy Ontario (1999). "Lamotrigine Approved in Canada for Lennox–Gastaut Syndrome". 'Sharing' News. http://epilepsyontario.org/client/EO/EOWeb.nsf/web/Lamotrigine+Approved+in+Canada+for+Lennox-Gastaut+Syndrome. Retrieved 13 November 2005. 
10. ^ Glaxo Wellcome Inc (1998). "Final Printed Labeling—Part 1". Lamictal Tablets & Chewable Dispersible Tablets (Lamotrigine) Drug Approval Page. United States Food and Drug Administration Center for Drug Evaluation and Research. http://www.fda.gov/cder/foi/nda/98/020241s003.htm. Retrieved 13 November 2005. 
11. ^ "Felbatol (felbamate)". p. 3. http://www.rxlist.com/cgi/generic/felbamate_ids.htm. Retrieved 2007-09-19. 
12. ^ The Felbamate Study Group In Lennox-gastaut Syndrome (1993). "Efficacy of felbamate in childhood epileptic encephalopathy (Lennox-Gastaut syndrome). The Felbamate Study Group in Lennox-Gastaut Syndrome". The New England journal of medicine 328 (1): 29–33. doi:10.1056/NEJM199301073280105. PMID 8347179. 
13. ^ Devinsky, O; Faught, RE; Wilder, BJ; Kanner, AM; Kamin, M; Kramer, LD; Rosenberg, A (1995). "Efficacy of felbamate monotherapy in patients undergoing presurgical evaluation of partial seizures". Epilepsy research 20 (3): 241–6. doi:10.1016/0920-1211(94)00084-A. PMID 7796796. 
14. ^ O'neil, MG; Perdun, CS; Wilson, MB; Mcgown, ST; Patel, S (1996). "Felbamate-associated fatal acute hepatic necrosis". Neurology 46 (5): 1457–9. PMID 8628501. 
15. ^ Feucht, M; Brantner-Inthaler, S (1994). "Gamma-vinyl-GABA (vigabatrin) in the therapy of Lennox-Gastaut syndrome: an open study". Epilepsia 35 (5): 993–8. doi:10.1111/j.1528-1157.1994.tb02544.x. PMID 7925171. 
16. ^ Yagi, K (2004). "Overview of Japanese experience-controlled and uncontrolled trials". Seizure : the journal of the British Epilepsy Association 13 Suppl 1: S11–5; discussion S16. doi:10.1016/j.seizure.2004.04.018. PMID 15511680. 
17. ^ Yamauchi, T; Aikawa, H (2004). "Efficacy of zonisamide: our experience". Seizure : the journal of the British Epilepsy Association 13 Suppl 1: S41–8; discussion S49. doi:10.1016/j.seizure.2004.04.021. PMID 15511689. 
18. ^ Van Rijckevorsel-Harmant, K; Delire, M; Rucquoy-Ponsar, M (1986). "Treatment of idiopathic West and Lennox-Gastaut syndromes by intravenous administration of human polyvalent immunoglobulins". European archives of psychiatry and neurological sciences 236 (2): 119–22. doi:10.1007/BF00454021. PMID 3792407. 

See also

• Epilepsy
• West syndrome
• Ohtahara syndrome
• Syndromes
• Epilepsy Phenome/Genome Project

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