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Current and emerging treatments for absence seizures in young patients

Absence seizure

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Absence seizure
Classification and external resources
Specialty Neurology
ICD – 10 G40.3
ICD – 9-CM 345.0
DiseasesDB 32994
MedlinePlus 000696
eMedicine neuro/3
MeSH D004832
[ edit on Wikidata ]

Absence seizures are one of several kinds of generalized seizures . These seizures are sometimes referred to as petit mal seizures (from the French for “little illness”, a term dating from the late 18th century). [1] Absence seizures are characterized by a brief loss and return of consciousness, generally not followed by a period of lethargy (i.e. without a notable postictal state ).

Contents

  • 1 Signs and symptoms
  • 2 Risk factors
  • 3 Diagnosis
    • 3.1 Syndromes
  • 4 Treatment
    • 4.1 Contraindicated drugs
    • 4.2 Data limitations
  • 5 References
  • 6 External links

Signs and symptoms[ edit ]

The clinical manifestations of absence seizures vary significantly among patients. [2] [3] [4] Impairment of consciousness is the essential symptom, and may be the only clinical symptom, but this can be combined with other manifestations. The hallmark of the absence seizures is abrupt and sudden-onset impairment of consciousness, interruption of ongoing activities, a blank stare, possibly a brief upward rotation of the eyes. If the patient is speaking, speech is slowed or interrupted; if walking, they stand transfixed; if eating, the food will stop on its way to the mouth. Usually, the patient will be unresponsive when addressed. In some cases, attacks are aborted when the patient is called. The attack lasts from a few seconds to half a minute, and evaporates as rapidly as it commenced. Absence seizures generally are not followed by a period of disorientation or lethargy (post-ictal state), in contrast to the majority of seizure disorders.[ citation needed ]

  1. Absence with impairment of consciousness only as per the above description.[ citation needed ]
  2. Absence with mild clonic components. Here the onset of the attack is indistinguishable from the above, but clonic components may occur in the eyelids, at the corner of the mouth, or in other muscle groups which may vary in severity from almost imperceptible movements to generalised myoclonic jerks. Objects held in the hand may be dropped.[ citation needed ]
  3. Absence with atonic components. Here there may be a diminution in tone of muscles subserving posture as well as in the limbs leading to dropping of the head, occasionally slumping of the trunk, dropping of the arms, and relaxation of the grip. Rarely tone is sufficiently diminished to cause this person to fall.[ citation needed ]
  4. Absence with tonic components. Here during the attack tonic muscular contraction may occur, leading to increase in muscle tone which may affect the extensor muscles or the flexor muscles symmetrically or asymmetrically. If the patient is standing, the head may be drawn backward and the trunk may arch. This may lead to retropulsion, which may cause eyelids to twitch rapidly, eyes may jerk upwards or the patients head may rock back and forth slowly, as if nodding. [5] [6] [7] The head may tonically draw to one or another side.[ citation needed ]
  5. Absence with automatisms. Purposeful or quasipurposeful movements occurring in the absence of awareness during an absence attack are frequent and may range from lip licking and swallowing to clothes fumbling or aimless walking. If spoken to, the patient may grunt, and when touched or tickled may rub the site. Automatisms are quite elaborate and may consist of combinations of the above described movements or may be so simple as to be missed by casual observation.[ citation needed ]
  6. Absence with autonomic components. These may be pallor, and less frequently flushing, sweating, dilatation of pupils and incontinence of urine.[ citation needed ]

Mixed forms of absence frequently occur.
These seizures can happen a few times a day or in some cases hundreds of times a day, to the point that the person cannot concentrate in school or in other situations requiring sustained, concentrated attention.[ citation needed ]

Risk factors[ edit ]

Typical absences are easily induced by hyperventilation in more than 90% of people with typical absences. This is a reliable test for the diagnosis of absence seizures: a patient suspected of typical absences should be asked to overbreathe for 3 minutes, counting their breaths. Intermittent photic stimulation may precipitate or facilitate absence seizures; eyelid myoclonia is a common clinical feature.[ citation needed ]

A specific mechanism difference exists in absence seizures in that T-type Ca++ channels are believed to be involved. Ethosuximide is specific for these channels and thus it is not effective for treating other types of seizure. Valproate and gabapentin (among others) have multiple mechanisms of action including blockade of T-type Ca++ channels and are useful in treating multiple seizure types.[ citation needed ] Gabapentin can aggravate absence seizures. [8]

Diagnosis[ edit ]

The primary diagnostic test for absence seizures is EEG. [9] However, brain scans such as by an MRI can help rule out other diseases, such as a stroke or a brain tumor. [10]

During electroencephalography, hyperventilation can be used to provoke these seizures. [9] Ambulatory EEG monitoring over 24 hours can quantify the number of seizures per day and their most likely times of occurrence. [9]

Absence seizures are brief (usually less than 20 seconds) generalized epileptic seizures of sudden onset and termination. When someone experiences an absence seizure they are often unaware of their episode. [11] Those most susceptible to this are children, and the first episode usually occurs between 4–12 years old. It is very rare that someone older will experience their first absence seizure.[ citation needed ] Episodes of absence seizures can often be mistaken for inattentiveness when misdiagnosed, and can occur 50-100 times a day. They can be so difficult to detect that some people may go months or years before being given a proper diagnosis. There are no known before or after effects of absence seizures. [12]

Absence seizures have two essential components: [2] [3] [4]

  • Clinical – the impairment of consciousness (absence)
  • Electroencephalography – an (EEG) shows generalized spike-and-slow wave discharges

Absence seizures are broadly divided into typical and atypical types:

  • Typical absence seizures usually occur in the context of idiopathic generalised epilepsies and an EEG shows fast >2.5 Hz generalised spike-wave discharges. The prefix “typical” is to differentiate them from atypical absences rather than to characterise them as “classical” or characteristic of any particular syndrome.
  • Atypical absence seizures:
    • Occur only in the context of mainly severe symptomatic or cryptogenic epilepsies of children with learning difficulties who also suffer from frequent seizures of other types, such as atonic, tonic and myoclonic.
    • Onset and termination is not so abrupt and changes in tone are more pronounced.
    • Ictal – EEG is of slow (less than 2.5 Hz) spike and slow wave. The discharge is heterogeneous, often asymmetrical and may include irregular spike and slow wave complexes, fast and other paroxysmal activity. Background interictal EEG is usually abnormal.

Syndromes[ edit ]

These syndromes are childhood absence epilepsy , epilepsy with myoclonic absences , juvenile absence epilepsy and juvenile myoclonic epilepsy . Other proposed syndromes are Jeavons syndrome (eyelid myoclonia with absences), and genetic generalised epilepsy with phantom absences .

These types of seizures are also known to occur to patients suffering with porphyria and can be triggered by stress or other porphyrin -inducing factors.

Treatment[ edit ]

Treatment of patients with absence seizures only is mainly with valproic acid or ethosuximide , which are of equal efficacy controlling absences in around 75% of patients. Lamotrigine monotherapy is less effective, with nearly half of the patients becoming seizure free. This view has been recently confirmed by Glauser et al. (2010), [13] who studied the effects of ethosuximide, valproic acid, and lamotrigine in children with newly diagnosed childhood absence epilepsy. Drug dosages were incrementally increased until the child was free of seizures, the maximal allowable dose was reached, or a criterion indicating treatment failure was met. The primary outcome was freedom from treatment failure after 16 weeks of therapy; the secondary outcome was attentional dysfunction. After 16 weeks of therapy, the freedom-from-failure rates for ethosuximide and valproic acid were similar and were higher than the rate for lamotrigine. There were no significant differences between the three drugs with regard to discontinuation because of adverse events. Attentional dysfunction was more common with valproic acid than with ethosuximide.
If monotherapy fails or unacceptable adverse reactions appear, replacement of one by another of the three antiepileptic drugs is the alternative. Adding small doses of lamotrigine to sodium valproate may be the best combination in resistant cases.

While ethosuximide is effective in treating only absence seizures, valproic acid is effective in treating multiple seizure types including tonic-clonic seizure and partial seizure , as such it may be a better choice if a patient is exhibiting multiple types of seizures. [14]
Similarly, lamotrigine treats multiple seizure types including partial seizures and generalized seizures, therefore it is also an option for patients with multiple seizure types. [15] Clonazepam (Klonopin, Rivotril) is effective in the short term but is not generally recommended for treatment of absence seizure because of the rapid development of tolerance and high frequency of side effects. [16]

Contraindicated drugs[ edit ]

Carbamazepine , vigabatrin , and tiagabine are contraindicated in the treatment of absence seizures, irrespective of cause and severity. This is based on clinical and experimental evidence. [4] In particular, the GABA agonists vigabatrin and tiagabine are used to induce, not to treat, absence seizures and absence status epilepticus . [17] Similarly, oxcarbazepine , phenytoin , phenobarbital , gabapentin , and pregabalin should not be used in the treatment of absence seizures because these medications may worsen absence seizures. [15]

Data limitations[ edit ]

In the treatment of absence seizures there is often insufficient evidence for which of the available medications has the best combination of safety and efficacy for a particular patient. [18] Nor is it easily known how long a medication must be continued before an off-medication trial should be conducted to determine whether the patient has outgrown the absence seizures, as is often the case in children.
To date there have been no published results of any large, double-blind, placebo-controlled studies comparing the efficacy and safety of these or any other medications for absence seizures.[ citation needed ] The studies that exist have been small and not produced clear conclusions. [18] [19]

References[ edit ]

  1. ^ Daly, D. D. (1968). “Reflections on the Concept of Petit Mal”. Epilepsia. 9 (3): 175–8. doi : 10.1111/j.1528-1157.1968.tb04618.x . PMID   4975023 .

  2. ^ a b “Proposal for revised clinical and electroencephalographic classification of epileptic seizures. From the Commission on Classification and Terminology of the International League Against Epilepsy”. Epilepsia. 22 (4): 489–501. 1981. doi : 10.1111/j.1528-1157.1981.tb06159.x . PMID   6790275 .
  3. ^ a b Panayiotopoulos, Chrysostomos P. (2008). “Typical absence seizures and related epileptic syndromes: Assessment of current state and directions for future research”. Epilepsia. 49 (12): 2131–9. doi : 10.1111/j.1528-1167.2008.01777.x . PMID   19049569 .
  4. ^ a b c Panayiotopoulos, C. P. (2010). A clinical guide to epileptic syndromes and their treatment (2nd ed.). London: Springer.[ page needed ]
  5. ^ Takahashi S, Yamamoto S, Tanaka R, Okayama A, Araki A, Azuma H (2015). “Focal frontal epileptiform discharges in a patient with eyelid myoclonia and absence seizures” . Epilepsy Behav Case Rep. 4: 35–7. doi : 10.1016/j.ebcr.2015.06.006 . PMC   4491640 . PMID   26155465 .
  6. ^ John S. Duncan (1996). Eyelid Myoclonia with Absences . John Libbey Eurotext. pp. 52–. ISBN   978-0-86196-550-2 .
  7. ^ Antonio V. Delgado-Escueta (2005). Myoclonic Epilepsies . Lippincott Williams & Wilkins. pp. 104–. ISBN   978-0-7817-5248-0 .
  8. ^ Perucca, Gram, Avanzini, and Dulac, 1998, “Antiepileptic drugs as a cause of worsening seizures.”
  9. ^ a b c Medscape > Absence Seizures by Scott Segan. Updated: Apr 27, 2011
  10. ^ Mayo Clinic > Absence seizure (petit mal seizure) June 23, 2011
  11. ^ Carlson, Neil R. (2013). Physiology of Behavior.
  12. ^ Epilepsy Therapy Project. “Absence Seizures” . Epilepsy Foundation. Retrieved 8 May 2013.
  13. ^ Glauser, Tracy A.; Cnaan, Avital; Shinnar, Shlomo; Hirtz, Deborah G.; Dlugos, Dennis; Masur, David; Clark, Peggy O.; Capparelli, Edmund V.; Adamson, Peter C. (2010). “Ethosuximide, Valproic Acid, and Lamotrigine in Childhood Absence Epilepsy” . New England Journal of Medicine. 362 (9): 790–9. doi : 10.1056/NEJMoa0902014 . PMC   2924476 . PMID   20200383 . Lay summary – ScienceDaily (March 12, 2010).
  14. ^ Kahan, Scott; Brillman, Jon (2005). In A Page Neurology. Hagerstwon, MD: Lippincott Williams & Wilkins. p. 47. ISBN   978-1-4051-0432-6 .
  15. ^ a b “NICE Guidelines” . Retrieved 3 November 2014.
  16. ^ Dreifuss, FE (1983). “Treatment of the nonconvulsive epilepsies”. Epilepsia. 24 Suppl 1: S45–54. doi : 10.1111/j.1528-1157.1983.tb04642.x . PMID   6413201 .
  17. ^ Knake, S; Hamer, HM; Schomburg, U (August 8, 1999). “Tiagabine-induced absence status in idiopathic generalized epilepsy” . European Journal of Epilepsy. 8 (5): 314–317. doi : 10.1053/seiz.1999.0303 . Retrieved 3 November 2014.
  18. ^ a b Posner, Ewa B; Mohamed, Khalid K; Marson, Anthony G (2005). Posner, Ewa B, ed. “Ethosuximide, sodium valproate or lamotrigine for absence seizures in children and adolescents”. Cochrane Database of Systematic Reviews. doi : 10.1002/14651858.CD003032.pub2 .
  19. ^ Posner, Ewa B.; Mohamed, Khalid; Marson, Anthony G. (2005). “A systematic review of treatment of typical absence seizures in children and adolescents with ethosuximide, sodium valproate or lamotrigine”. Seizure. 14 (2): 117–22. doi : 10.1016/j.seizure.2004.12.003 . PMID   15694565 .

External links[ edit ]

  • (Video of Absence Seizure)
  • Mechanisms of absence seizures (Scholarpedia)
  • Thalamocortical oscillations (Scholarpedia)
  • Absence (a comic about a sufferer’s experiences)
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      Neurology

      Absence Seizures

      Updated: Sep 25, 2018
      • Author: Scott Segan, MD; Chief Editor: Selim R Benbadis, MD  more…
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      Sections
      Absence Seizures
      • Sections
        Absence Seizures
      • Overview
      • Etiology
      • Epidemiology
      • Presentation
      • Differential Diagnosis
      • Laboratory Studies
      • Neuroimaging Studies
      • Electroencephalography
      • Pharmacologic Treatment
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      Overview

      Overview

      Absence seizures are a type of generalized non-motor seizures.
      [ 1 ]
      They were first described by Poupart in 1705, and later by Tissot in 1770, who used the term petit access. In 1824, Calmeil used the term absence.
      [ 2 ]
      In 1935, Gibbs, Davis, and Lennox described the association of impaired consciousness and 3-Hz spike-and-slow-wave complexes on electroencephalograms ( EEGs ).
      [ 3 ]

      Absence seizures occur in idiopathic and symptomatic generalized epilepsies.
      [ 4 ]
      Among the idiopathic generalized epilepsies, absence seizures are seen in childhood absence epilepsy (pyknolepsy), juvenile absence epilepsy, and juvenile myoclonic epilepsy (impulsive petit mal).
      [ 5 ]
      The seizures in these conditions are called typical absence seizures and are usually associated with generalized 3-4 Hz spike-and-slow-wave complexes on EEG.
      [ 6 ]

      In childhood absence epilepsy, seizures are frequent and brief, lasting just a few seconds (pyknoleptic). Some children can have many such seizures per day. In other epilepsies, particularly those with an older age of onset, the seizures can last several seconds to minutes and may occur only a few times a day; these are called nonpyknoleptic or spanioleptic absence seizures.

      Myoclonic and tonic-clonic seizures may also be present, especially in syndromes with an older age of onset.

      In the cryptogenic or symptomatic generalized epilepsies, absence seizures are often associated with slow spike-wave complexes of 1.5-2.5 Hz
      [ 5 ]
      ; these are also called sharp-and-slow-wave complexes. These seizures may be associated with loss of axial tone and head nodding; a fall may occur. Increased tone, autonomic features, and automatisms may also be seen. Absence seizures associated with slow spike-wave complexes are called atypical absence seizures.
      [ 7 ]

      See Epilepsy and Seizures for a general overview of these topics.

      Classification

      The International League Against Epilepsy (ILAE) Commission on Classification and Terminology revised the concepts, terminology, and approaches for classifying seizures and epilepsy.
      [ 8 ]

      The classification of absence seizures has been simplified as follows:

      • Typical absence
      • Atypical absence
      • Myoclonic absence
      • Eyelid myoclonia

      Patient education

      Patients who are old enough to drive should be warned about driving and operating heavy machinery. Physicians should be familiar with state laws concerning driving with epilepsy; inform patients concerning these legal matters.

      For patient education information, see the Brain and Nervous System Center , as well as Epilepsy .

      Next:

      Etiology

      The etiology of idiopathic epilepsies with age-related onset is genetic. About 15-40% of patients with these epilepsies have a family history of epilepsy; overall concordance in monozygotic twins is 74%, with a 100% concordance during the peak age of phenotypic expression.
      [ 9 ]
      Family members may have other forms of idiopathic or genetic epilepsy (eg, febrile convulsions, generalized tonic-clonic seizures).

      The idiopathic generalized epilepsies are a group of primary generalized epilepsies with absence, myoclonic, and tonic-clonic seizures. Based on age of onset and seizure types, some can be grouped into well-recognized syndromes, such as childhood absence epilepsy, juvenile absence epilepsy, and juvenile myoclonic epilepsy.

      However, patients with other syndromes, such as generalized epilepsy with febrile seizures plus (GEFS+), as well as patients who have childhood absence epilepsy that leads into juvenile myoclonic epilepsy, illustrate that these syndromes represent a genetically determined lower threshold to have seizures.

      The idiopathic generalized epilepsies are best viewed as a spectrum of clinical syndromes
      [ 10 ]
      with varied genetic causes that affect the function of ion channels.

      Genetic studies have shown that these syndromes are channelopathies, but different gene mutations have been found in the same syndromes. Juvenile myoclonic epilepsy has been linked to chromosome 6,
      [ 11 , 12 ]
      with linkage to chromosome 6p12 in Mexican families.
      [ 13 ]
      Mutations in the EFHC1 gene have been found in Mexican
      [ 14 , 15 ]
      and Italian families
      [ 16 ]
      with juvenile myoclonic epilepsy, but not in a group of Dutch families.
      [ 17 ]

      Childhood absence epilepsy with generalized tonic-clonic seizure has been linked to chromosome 8q24 in a 5-generation family from Bombay, India.
      [ 18 ]
      Childhood absence epilepsy with febrile seizures has been linked to the GABA(A) receptor γ2 subunit (GABRG2) on chromosome 5q3.1-33.1.
      [ 19 ]

      A mutation in the GABA(A) receptor gene GABRB3 was found in Mexican families with childhood absence epilepsy. Mutations showed hyperglycosylation in vitro, with reduced GABA-evoked current density from whole cells. Expression of this gene in the developing brain may help explain an age-related onset and remission in childhood absence epilepsy.
      [ 20 ]

      Pathophysiology

      The pathophysiology of absence seizures is not fully understood. In 1947, Jasper and Droogleever-Fortuyn electrically stimulated nuclei in the thalami of cats at 3 Hz and produced bilaterally synchronous spike-and-wave discharges on EEG.
      [ 21 ]
      In 1953, bilaterally synchronous spike-and-wave discharges were recorded by placing depth electrodes in the thalamus of a child with absence seizures.
      [ 22 ]

      In 1977, Gloor et al demonstrated that the bilaterally synchronous, 3-Hz spike-wave discharges in the feline penicillin model of absence seizures were generated in the cortex. This led to the corticoreticular theory of primarily generalized seizures.

      Abnormal oscillatory rhythms are believed to develop in thalamocortical pathways. This involves gamma-aminobutyric acid (GABA)-B–mediated inhibition alternating with glutamate-mediated excitation.

      The cellular mechanism is believed to involve T-type calcium currents. T channels of the GABAergic reticular thalamic nucleus neurons appear to play a major role in the spike-wave discharges of the GABAergic thalamic neurons.
      [ 23 ]

      GABA-B inhibition appears to be altered in absence seizures, and potentiation of GABA-B inhibition with tiagabine (Gabitril), vigabatrin (Sabril),
      [ 24 ]
      and, possibly, gabapentin (Neurontin), results in exacerbation of absence seizures. Enhanced burst firing in selected corticothalamic networks may increase GABA-B receptor activation in the thalamus, leading to generalized spike-wave activity.

      These data suggest that activity of thalamic networks is necessary for spike-wave discharge rhythmogenesis, and cortical hyperexcitability is necessary for their generation.
      [ 25 ]

      In symptomatic generalized epilepsies, absence seizures are due to a wide variety of causes that at an early stage of neural development, result in diffuse or multifocal brain damage. The causes and management of secondary generalized epilepsies, and the other seizure types that accompany them, are not discussed in this article.

      Risk factors

      After noncompliance with treatment, lack of sleep is the most frequent cause of seizure exacerbations. Drugs that lower the seizure threshold (eg, alcohol, cocaine, high-dose penicillin, isoniazid [INH] overdose, neuroleptics) are most likely to cause seizures in patients with epilepsy. Withdrawal of alcohol, benzodiazepines, and other sedatives are also common causes.

      Previous
      Next:

      Epidemiology

      Incidence in the United States

      The incidence of absence seizures in the United States is 1.9-8 cases per 100,000 population.

      Morbidity and mortality

      The morbidity from typical absence seizures is related to the frequency and duration of the seizures, as well as to the patient’s activities; effective treatment ameliorates these factors.

      Educational and behavioral problems are sequelae of frequent, unrecognized seizures.

      No deaths result directly from absence seizures. However, if an individual suffers an absence seizure while driving or operating dangerous machinery, a fatal accident may occur.

      In children with absence seizures due to secondary generalized epilepsies, death is related to the underlying disease.

      Sex predilection

      Absence seizures are generally believed to be more common in females than in males. Up to two thirds of children with childhood absence epilepsy are girls.
      [ 9 , 26 ]

      Absence epilepsy with myoclonus has a male predominance.
      [ 27 ]

      Age of onset

      The generalized idiopathic epilepsies have age-related onset.

      Onset of absence seizures in children with symptomatic generalized epilepsies depends on the underlying disorder. While many of these disorders may have their onset at an early (prenatal, perinatal, or postnatal) age, absence seizures do not appear until later in childhood. An example is the Lennox-Gastaut syndrome . The cause may be a genetic disorder or a perinatal insult, but the absence seizures do not present until age 1-8 years.
      [ 28 ]

      Childhood absence epilepsy onset is at age 4-8 years, with peak onset at age 6-7 years.
      [ 26 ]

      Juvenile absence epilepsy onset is generally around puberty. Actual age of onset may vary, depending on whether pyknoleptic (8.3 ± 4.5 y) or nonpyknoleptic seizures occur (14.8 ± 8.3 y).
      [ 29 ]

      Juvenile myoclonic epilepsy has a more varied age of onset (8-26 y), but 79% of patients have an onset between the ages of 12 and 18 years.
      [ 30 ]
      Because the absence and myoclonic seizures are brief, they often go unrecognized, and many patients do not present until they experience a tonic-clonic seizure.

      Previous
      Next:

      Clinical Presentation

      Patient history

      Children with idiopathic generalized epilepsies may present with a history of staring spells, but infrequent absence seizures may not be diagnosed until a generalized tonic-clonic seizure has occurred.

      Other symptoms, such as behavioral problems, may be the presenting complaint.
      [ 31 ]
      Whether this is a comorbid condition or a result of brief, unrecognized attacks that cause lapses of awareness and interferes with attention is unknown.

      Decline in school performance may be an indication of the onset or breakthrough of absence seizures.

      In symptomatic generalized epilepsies, atypical absence seizures often occur in the setting of developmental delay or mental retardation. (See Table 1, below, for features of typical and atypical absence seizures.)

      Other seizure types can be present in the patient, such as myoclonic, tonic, atonic, tonic-clonic, and even partial seizures .

      Physical examination

      Physical and neurologic findings are normal in children with idiopathic generalized epilepsies. Having the child hyperventilate for 3-5 minutes can often provoke absence seizures. This procedure can easily be performed in the clinic or office, and the result is diagnostic.

      On clinical examination, typical absence seizures appear as brief staring spells. Patients have no warning or postictal phase, and if engaged in gross motor activity, such as walking, they may stop and stand motionless or they may continue to walk. Children are not responsive during the seizure and have no memory of what happened during the attack; they are generally unaware that a seizure has occurred. (See Table 1, below.)

      Atypical absence seizures, which occur in patients with symptomatic generalized epilepsies, are usually longer than typical absences and often have more gradual onset and resolution.

      In symptomatic generalized epilepsies, physical and neurologic findings may be abnormal, reflecting the underlying disorder. Physical examination may reveal stigmata of a genetic disease, such as a neurocutaneous disorder (eg, tuberous sclerosis) or an inborn error of metabolism. Neurologic examination may show signs of developmental delay or more specific signs, such as spastic paresis in cerebral palsy.

      Table 1. Clinical and EEG Findings in Typical and Atypical Absence Seizures* (Open Table in a new window)

      Type of Clinical Seizure

      EEG Findings

      Typical absence

      Impairment of consciousness only

      Usually regular and symmetrical 3 Hz, possible 2- to 4-Hz spike-and-slow-wave complexes, and possible multiple spike-and-slow-wave complexes

      Mild clonic components

      Atonic components

      Tonic component

      Automatisms

      Autonomic components

      Atypical absence

      Changes in tone more pronounced than those of typical absence seizure

      EEG more heterogeneous than in typical absence; may include irregular spike-and-slow-wave complexes, fast activity, or other paroxysmal activity; abnormalities bilateral but often irregular and asymmetrical

      Nonabrupt onset or cessation abrupt

      *May be seen alone or in combination.

      Adapted from Dreifuss FE. Classification of epileptic seizures. In: Engel J Jr, Pedley TA, eds. Epilepsy: A Comprehensive Textbook. Philadelphia, PA: Lippincott-Raven;1997.

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      Differential Diagnosis

      Attention Deficit Hyperactivity Disorder ( ADHD )

      Complex Partial Seizures

      Confusional States and Acute Memory Disorders

      Febrile Seizures

      First Pediatric Seizure

      Migraine Variants

      Psychogenic Nonepileptic Seizures

      Reflex Epilepsy

      Shuddering Attacks

      Status Epilepticus

      Breath-holding spells are another differential.

      Staring spells, daydreaming, migraine equivalents, and panic and/or anxiety attacks all may be confused with nonconvulsive seizures.

      Absence versus complex partial seizures

      Absence seizures may be confused with complex partial seizures, especially in cases of prolonged seizures with automatisms (see Table 2, below).

      Table 2. Differentiating Features of Complex Partial and Absence Seizures (Open Table in a new window)

      Feature

      Complex Partial

      Absence

      Onset

      May have simple partial onset

      Abrupt

      Duration

      Usually >30 s

      Usually < 30 s

      Automatisms

      Present

      Duration dependent

      Awareness

      No

      No

      Ending

      Gradual postictal

      Abrupt

      The occurrence of automatisms is dependent on duration of the seizure; the longer the seizure, the more likely automatisms are to occur (see image below).
      [ 32 ]

      Percentage of absence seizures with automatisms as

      Percentage of absence seizures with automatisms as a function of duration in seconds. (Data gathered from Penry et al, 1975.)

      View Media Gallery

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      Laboratory Studies

      When evaluating a child for staring spells, laboratory tests for metabolic abnormalities or toxic or drug ingestion (especially in older children) may be indicated. If a clear history of the episodic nature of the attacks is obtained, then the EEG can be diagnostic and laboratory tests may not be necessary.

      When evaluating a child with a developmental delay, or if the EEG reveals atypical absences, then a full work-up for the underlying cause of a symptomatic generalized epilepsy is indicated.

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      Neuroimaging Studies

      Neuroimaging findings are normal in idiopathic epilepsies by definition, and therefore, neuroimaging is not indicated if the typical clinical pattern is present.

      However, neuroimaging is often ordered by primary care providers and the emergency department, especially if a child presents with a generalized tonic-clonic seizure, to rule out significant structural causes of seizures. A normal result helps to support the diagnosis of idiopathic epilepsy. For cryptogenic and symptomatic generalized epilepsies, neuroimaging can help in the diagnosis of any underlying structural abnormality.

      If imaging is performed, magnetic resonance imaging (MRI) is preferred to computed tomography (CT) scanning. MRI is more sensitive for certain anatomic abnormalities.

      A review of 134 MRI scans in patients with idiopathic generalized epilepsies found nonspecific abnormalities in 24%.
      [ 33 ]

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      Electroencephalography

      The only diagnostic test for absence seizures is the EEG.

      Background activity is normal. In syndromes with frequent absence seizures, such as childhood absence epilepsy, a routine awake recording is often pathognomonic. Bursts of frontally predominant, generalized 3-Hz spike-and-wave complexes are seen during the seizures.
      [ 3 ]
      In syndromes with less frequent absence seizures (juvenile absence epilepsy or juvenile myoclonic epilepsy), an awake recording may be normal; a sleep or sleep-deprived recording may be needed.

      Typical absence seizures have generalized 3-Hz spike-and-wave complexes (see image below).

      EEG of a typical absence seizure with 3-Hz spike-a

      EEG of a typical absence seizure with 3-Hz spike-and-wave discharges.

      View Media Gallery

      The spike frequency is often faster at the onset, with a slight deceleration at the end.
      [ 26 ]
      They can range from 2.5-6 Hz, with the faster frequencies seen in syndromes with older age of onset.

      Bursts of generalized polyspikes and waves (multiple spike-and-slow-wave complexes) may also be seen,
      [ 30 ]
      especially during sleep and in syndromes with older age of onset.

      The onset and ending of these seizures are abrupt; no postictal EEG slowing is noted.

      Hyperventilation often provokes these seizures and should be a routine part of all EEGs in children.

      Photosensitivity may be present in idiopathic generalized epilepsies and is more often seen in juvenile myoclonic epilepsy and childhood absence epilepsy than juvenile absence epilepsy.
      [ 29 ]

      EEG video monitoring demonstrates that clinical seizure manifestations may lag behind the start of ictal EEG activity; bursts lasting less than 3 seconds are usually clinically silent. During the absence seizure, rhythmic eye blinks and mild clonic jerks may be present. As a seizure progresses, automatisms may be seen.
      [ 32 ]

      Clinical and EEG features may vary considerably in different children.
      [ 34 ]

      Go to EEG Video Monitoring for procedural information on this topic.

      EEG findings in atypical absence seizures

      Atypical absence seizures are characterized by slow spike-and-wave paroxysms, classically 2.5 Hz (see the image below). The onset may be difficult to discern, and postictal EEG slowing may be noted.

      Slow spike-and-wave discharges (2.5 Hz). This is a

      Slow spike-and-wave discharges (2.5 Hz). This is an interictal pattern in a child with seizures and developmental delay.

      View Media Gallery

      Background activity is often abnormal, reflecting the diffuse or multifocal underlying encephalopathy of symptomatic generalized epilepsy.

      Generalized polyspike-and-wave complexes also may be present, and focal features may be observed.

      The clinical correlation of generalized spike-and-wave complexes with clinical seizures is not as clear-cut as in typical absence seizures. Generalized slow spikes and waves may be present as an interictal pattern, as in Lennox-Gastaut syndrome.

      EEG video monitoring can show a more varied alteration of consciousness than in typical absence seizures. If the patient has underlying mental retardation, discerning changes in mental status may be more difficult in atypical absence.

      Changes in postural tone, most noticeably head nods, are common.

      Ambulatory EEG monitoring over 24 hours may be useful to quantitate the number of seizures per day and their most likely times of occurrence.

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      Pharmacologic Treatment

      Treatment for absence seizures involves antiepileptic drugs (AEDs). Once the proper diagnosis (ie, of the specific epilepsy syndrome) is made, the likelihood of other, coexistent seizure types in the patient, such as myoclonic or tonic-clonic seizures, should be considered and an appropriate medication selected. Since altered awareness occurs with even brief bursts of spike-wave paroxysms on EEG, treatment should be titrated to suppressing all epileptiform activity.

      The decision to start antiepileptic medication must be made with great care. Most AEDs are relatively toxic and can have sedative and cognitive side effects. Children with absence seizures may need to be on medication for many years, and in some cases, for life. EEG can usually confirm the diagnosis, and the presence of spontaneous seizures can be documented on routine EEG or with longer recordings (ie, 24-hour ambulatory EEG or EEG video monitoring).

      Only 2 first-line AEDs have approval from the US Food and Drug Administration (FDA) to be indicated for absence seizures: ethosuximide (Zarontin) and valproic acid (Depakene, Depacon). Ethosuximide has efficacy for absence seizures only and valproic acid has efficacy for absence, generalized tonic-clonic, and myoclonic seizures.

      Ethosuximide (Zarontin) is effective only against absence seizures.

      Valproic acid (Depakene, Depacon, Depakote, Depakote ER) is considered a broad-spectrum AED, because it is effective against absence, myoclonic, tonic-clonic, and partial seizures.

      A study showed that ethosuximide and valproic acid were more effective than lamotrigine in the treatment of childhood absence epilepsy, and that ethosuximide had fewer adverse attentional side effects.
      [ 35 ]

      Symptomatic generalized epilepsies are often refractory to first-line AEDs. Lamotrigine (Lamictal), topiramate (Topamax), and felbamate (Felbatol) are approved by the FDA as adjunctive therapy for the generalized seizures of Lennox-Gastaut syndrome in adult and pediatric patients (>2 y). Clonazepam (Klonopin) and the ketogenic or medium-chain triglyceride diet have been attempted to reduce seizure frequency. However, these adjunctive therapies have limited efficacy.

      Of the newer AEDs, lamotrigine, topiramate, and levetiracetam have been shown to have efficacy against seizures in idiopathic generalized epilepsy
      [ 36 , 37 ]
      and have received FDA approval to be indicated for adjunctive therapy of generalized tonic-clonic seizures in idiopathic generalized epilepsy in children aged 2 years and older (for lamotrigine and topiramate) and in children aged 6 years and older (for levetiracetam). Levetiracetam is indicated as adjunct therapy for generalized tonic-clonic and myoclonic seizures. It has been shown to have only modest efficacy against absence seizures.
      [ 38 , 39 ]

      Lamotrigine and topiramate are also approved as adjunctive therapy in Lennox-Gastaut syndrome in children aged 2 years and older. Rufinamide (Banzel) has been shown effective against typical and atypical absence seizures as well as other seizures in Lennox-Gastaut syndrome
      [ 40 ]
      and is approved as adjunct therapy in children older than 4 years.

      Topiramate has also received FDA approval as initial monotherapy for generalized tonic-clonic seizures in children aged 10 years and older with idiopathic generalized epilepsy. Studies have shown these medications to have antiabsence efficacy, but the data are incomplete.
      [ 41 ]

      Some AEDs can aggravate seizures, especially in cryptogenic or symptomatic generalized epilepsies.
      [ 42 ]
      Treatment with carbamazepine (Tegretol, Tegretol XR, Carbatrol)
      [ 43 , 44 ]
      and oxcarbazepine (Trileptal)
      [ 45 ]
      has been associated with the exacerbation of absence seizures. Gabapentin (Neurontin) is ineffective against absence seizures,
      [ 46 ]
      and tiagabine (Gabitril) and vigabatrin (Sabril) have been associated with the exacerbation of absence or myoclonic seizures in some patients.
      [ 47 ]

      Conception and pregnancy considerations

      Women of childbearing age who are not using adequate birth control should not be treated with valproic acid, if equally effective alternatives are available for them.

      If a woman taking valproic acid wishes to become pregnant, treatment may be crossed over to ethosuximide if only absence seizures are present, and she may be given folic acid 1-5 mg/d before conception. After the first trimester, treatment may be switched back to valproic acid.

      Women with generalized tonic-clonic seizures may be crossed over to lamotrigine, and given folic acid 1-5 mg/d before conception.

      Most clinicians believe that women treated with valproic acid or any hepatic enzyme-inducing AED should be treated with vitamin K before delivery.

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      Consultations

      All patients with suspected absence seizures should be examined by a neurologist who has expertise in diagnosing epileptic syndromes. Patients with refractory seizures, especially those with symptomatic epilepsies, may need to be referred to an epileptologist for prolonged EEG video monitoring and medication adjustments.

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      Diet

      A ketogenic
      [ 48 ]
      or medium-chain triglyceride diet
      [ 49 ]
      may be tried in patients with medically intractable seizures. Although these diets are difficult to maintain, there is evidence for their effectiveness.
      [ 50 ]
      Children in whom such diets are being considered should be referred to a center with specialized dietary services.

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      Activity

      Physical activity should not be restricted any more than necessary. Activities in which a seizure might pose a threat, such as swimming or rock climbing, may be allowed with appropriate supervision. A child with epilepsy should not be unnecessarily handicapped. Patients with uncontrolled absence seizures should not be allowed to drive. The situation may be unclear when the patient’s clinical seizures are controlled but the EEG still shows some spike-wave activity.

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      Outpatient Management

      Children with absence seizures should be monitored closely during titration or crossover of AEDs. The dose of the medication should be increased weekly until seizures are controlled or adverse effects develop.

      The aim in therapy is to control seizures completely with the minimum required amount of medication to minimize adverse effects.

      The therapeutic effect of valproic acid for absence seizures may lag several weeks behind reaching a therapeutic level.
      [ 51 ]

      Liver function test, amylase and/or lipase, and complete blood cell (CBC) count results should be monitored during drug treatment to watch for adverse reactions.

      Drug levels should be monitored to ensure treatment compliance and to watch for toxic levels in patients who are too young or too developmentally disabled to articulate subjective adverse effects.

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      Prognosis

      The prognosis for the primary generalized epilepsies depends on the particular epileptic syndrome. Because seizures, particularly generalized tonic-clonic seizures, may occur well after patients appear to achieve good control, a long seizure-free period should be achieved before discontinuation of therapy is considered.

      The remission rate for childhood absence epilepsy is good; 80% of patients respond to medication. Complete remission rates vary widely, perhaps dependent on the length of follow-up.

      Generalized tonic-clonic seizures may develop in up to 40% of children with childhood absence epilepsy.
      [ 26 ]
      Persistence of seizures is more likely in those with generalized tonic-clonic seizures.

      Early onset of absence seizures, quick response to therapy,
      [ 52 ]
      and normal EEG background are good prognostic signs.

      Juvenile myoclonic epilepsy carries a high risk of generalized tonic-clonic seizures. Despite excellent control with relatively small doses of an AED, the relapse rate is greater than 90%.
      [ 53 ]

      Patients with juvenile myoclonic epilepsy generally need to be treated for life, although occasional patients achieve control with careful attention to lifestyle issues (eg, adequate sleep, abstinence from alcohol).

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      Questions & Answers

      Overview

      What are absence seizures?

      How are absence seizures classified?

      What is included in patient education about absence seizures?

      What causes absence seizures?

      What is the pathophysiology of absence seizures?

      What are the risk factors for absence seizures?

      What is the incidence of absence seizures in the US?

      What is the morbidity associated with absence seizures?

      What are the sexual predilections of absence seizures?

      Which age groups have the highest prevalence of absence seizures?

      Which clinical history findings are characteristic of absence seizures?

      Which physical findings are characteristic of absence seizures?

      Which conditions should be included in the differential diagnosis of absence seizures?

      How are absence seizures differentiated from complex partial seizures?

      What is the role of lab testing in the workup of absence seizures?

      What is the role of neuroimaging studies in the diagnosis of absence seizures?

      What is the role of EEG in the diagnosis of absence seizures?

      How are absence seizures treated?

      What is the role of antiepileptic drugs (AEDs) in the treatment of absence seizures?

      How are absence seizures treated during pregnancy?

      Which specialist consultations are beneficial to patients with absence seizures?

      Which dietary modifications are used in the treatment of absence seizures?

      Which activity modifications are used in the treatment of absence seizures?

      What is included in the long-term monitoring of patients with absence seizures?

      What is the prognosis of absence seizures?

      Previous

      References

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      28. Beaumanoir A. Roger J, Bureau M, Dravet, et al, eds. Epileptic Syndromes. London, England: John Libby; 1985. 11: 89-99.

      29. Wolf P. Juvenile absence epilepsy. Roger J, Bureau M, Dravet, et al, eds. Epileptic Syndromes. London, England: John Libby; 1985. 242-6.

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      39. Delanty N, Jones J, Tonner F. Adjunctive levetiracetam in children, adolescents, and adults with primary generalized seizures: open-label, noncomparative, multicenter, long-term follow-up study. Epilepsia. 2012 Jan. 53(1):111-9. [Medline] .

      40. Glauser T, Kluger G, Sachdeo R, Krauss G, Perdomo C, Arroyo S. Rufinamide for generalized seizures associated with Lennox-Gastaut syndrome. Neurology. 2008 May 20. 70(21):1950-8. [Medline] .

      41. Posner EB, Mohamed K, Marson AG. Ethosuximide, sodium valproate or lamotrigine for absence seizures in children and adolescents. Cochrane Database Syst Rev. 2005. (4):CD003032. [Medline] .

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      43. Snead OC 3rd, Hosey LC. Exacerbation of seizures in children by carbamazepine. N Engl J Med. 1985 Oct 10. 313(15):916-21. [Medline] .

      44. Liu L, Zheng T, Morris MJ, Wallengren C, Clarke AL, Reid CA, et al. The mechanism of carbamazepine aggravation of absence seizures. J Pharmacol Exp Ther. 2006 Nov. 319(2):790-8. [Medline] .

      45. Vendrame M, Khurana DS, Cruz M, Melvin J, Valencia I, Legido A, et al. Aggravation of seizures and/or EEG features in children treated with oxcarbazepine monotherapy. Epilepsia. 2007 Nov. 48(11):2116-20. [Medline] .

      46. Guerrini R, Belmonte A, Genton P. Antiepileptic drug-induced worsening of seizures in children. Epilepsia. 1998. 39 Suppl 3:S2-10. [Medline] .

      47. Perucca E. The management of refractory idiopathic epilepsies. Epilepsia. 2001. 42 Suppl 3:31-5. [Medline] .

      48. Hemingway C, Freeman JM, Pillas DJ, Pyzik PL. The ketogenic diet: a 3- to 6-year follow-up of 150 children enrolled prospectively. Pediatrics. 2001 Oct. 108(4):898-905. [Medline] .

      49. Edwards, N. The MCT Diet. epilepsy.com. Available at http://www.epilepsy.com/epilepsy/keto_news_august07 . Accessed: 3/15/09.

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      51. Wheeler MM, Winter ME. Valproic Acid. Winter ME. Basic Clinical Pharmacokinetics. 4. Philadelphia: Lippincott Williams & Wilkins; 2003. 438/14.

      52. Wirrell E, Camfield C, Camfield P, Dooley J. Prognostic significance of failure of the initial antiepileptic drug in children with absence epilepsy. Epilepsia. 2001 Jun. 42(6):760-3. [Medline] .

      53. Delgado-Escueta AV, Enrile-Bacsal F. Juvenile myoclonic epilepsy of Janz. Neurology. 1984 Mar. 34(3):285-94. [Medline] .

      Media Gallery
      • Percentage of absence seizures with automatisms as a function of duration in seconds. (Data gathered from Penry et al, 1975.)
      • EEG of a typical absence seizure with 3-Hz spike-and-wave discharges.
      • Slow spike-and-wave discharges (2.5 Hz). This is an interictal pattern in a child with seizures and developmental delay.

      of
      3

      Tables

      • Table 1. Clinical and EEG Findings in Typical and Atypical Absence Seizures*
      • Table 2. Differentiating Features of Complex Partial and Absence Seizures

      Table 1. Clinical and EEG Findings in Typical and Atypical Absence Seizures*

      Type of Clinical Seizure

      EEG Findings

      Typical absence

      Impairment of consciousness only

      Usually regular and symmetrical 3 Hz, possible 2- to 4-Hz spike-and-slow-wave complexes, and possible multiple spike-and-slow-wave complexes

      Mild clonic components

      Atonic components

      Tonic component

      Automatisms

      Autonomic components

      Atypical absence

      Changes in tone more pronounced than those of typical absence seizure

      EEG more heterogeneous than in typical absence; may include irregular spike-and-slow-wave complexes, fast activity, or other paroxysmal activity; abnormalities bilateral but often irregular and asymmetrical

      Nonabrupt onset or cessation abrupt

      *May be seen alone or in combination.

      Adapted from Dreifuss FE. Classification of epileptic seizures. In: Engel J Jr, Pedley TA, eds. Epilepsy: A Comprehensive Textbook. Philadelphia, PA: Lippincott-Raven;1997.

      Table 2. Differentiating Features of Complex Partial and Absence Seizures

      Feature

      Complex Partial

      Absence

      Onset

      May have simple partial onset

      Abrupt

      Duration

      Usually >30 s

      Usually < 30 s

      Automatisms

      Present

      Duration dependent

      Awareness

      No

      No

      Ending

      Gradual postictal

      Abrupt

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      Contributor Information and Disclosures

      Author

      Scott Segan, MD Director of SBH Stroke Center and Attending Neurologist, St Barnabas Hospital

      Scott Segan, MD is a member of the following medical societies: American Academy of Neurology , American Epilepsy Society

      Disclosure: Nothing to disclose.

      Specialty Editor Board

      Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

      Disclosure: Received salary from Medscape for employment. for: Medscape.

      Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS, FAES Professor with Tenure, Departments of Neurology, Neuroscience, and Physiology, Assistant Dean for the MD/PhD Program, Program Director of the Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio

      Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS, FAES is a member of the following medical societies: American Academy of Neurology , American Clinical Neurophysiology Society , American Epilepsy Society , American Neurological Association , Society for Neuroscience

      Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Brain Sentinel, consultant.<br/>Stakeholder (<5%), Co-founder for: Brain Sentinel.

      Chief Editor

      Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine

      Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology , American Academy of Sleep Medicine , American Clinical Neurophysiology Society , American Epilepsy Society , American Medical Association

      Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Acorda, Livanova, Eisai, Greenwich, Lundbeck, Neuropace, Sunovion, Upsher-Smith.<br/>Serve(d) as a speaker or a member of a speakers bureau for: Livanova, Eisai, Greenwich, Lundbeck, Neuropace, Sunovion.<br/>Received research grant from: Acorda, Livanova, Greenwich, Lundbeck, Sepracor, Sunovion, UCB, Upsher-Smith.

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      • Sections
        Absence Seizures
      • Overview
      • Etiology
      • Epidemiology
      • Presentation
      • Differential Diagnosis
      • Laboratory Studies
      • Neuroimaging Studies
      • Electroencephalography
      • Pharmacologic Treatment
      • Consultations
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      • Outpatient Management
      • Prognosis
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      Neurology

      Absence Seizures

      Updated: Sep 25, 2018
      • Author: Scott Segan, MD; Chief Editor: Selim R Benbadis, MD  more…
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      Sections
      Absence Seizures
      • Sections
        Absence Seizures
      • Overview
      • Etiology
      • Epidemiology
      • Presentation
      • Differential Diagnosis
      • Laboratory Studies
      • Neuroimaging Studies
      • Electroencephalography
      • Pharmacologic Treatment
      • Consultations
      • Diet
      • Activity
      • Outpatient Management
      • Prognosis
      • Questions & Answers
      • Show All
      • Media Gallery
      • Tables
      • References

      Overview

      Overview

      Absence seizures are a type of generalized non-motor seizures.
      [ 1 ]
      They were first described by Poupart in 1705, and later by Tissot in 1770, who used the term petit access. In 1824, Calmeil used the term absence.
      [ 2 ]
      In 1935, Gibbs, Davis, and Lennox described the association of impaired consciousness and 3-Hz spike-and-slow-wave complexes on electroencephalograms ( EEGs ).
      [ 3 ]

      Absence seizures occur in idiopathic and symptomatic generalized epilepsies.
      [ 4 ]
      Among the idiopathic generalized epilepsies, absence seizures are seen in childhood absence epilepsy (pyknolepsy), juvenile absence epilepsy, and juvenile myoclonic epilepsy (impulsive petit mal).
      [ 5 ]
      The seizures in these conditions are called typical absence seizures and are usually associated with generalized 3-4 Hz spike-and-slow-wave complexes on EEG.
      [ 6 ]

      In childhood absence epilepsy, seizures are frequent and brief, lasting just a few seconds (pyknoleptic). Some children can have many such seizures per day. In other epilepsies, particularly those with an older age of onset, the seizures can last several seconds to minutes and may occur only a few times a day; these are called nonpyknoleptic or spanioleptic absence seizures.

      Myoclonic and tonic-clonic seizures may also be present, especially in syndromes with an older age of onset.

      In the cryptogenic or symptomatic generalized epilepsies, absence seizures are often associated with slow spike-wave complexes of 1.5-2.5 Hz
      [ 5 ]
      ; these are also called sharp-and-slow-wave complexes. These seizures may be associated with loss of axial tone and head nodding; a fall may occur. Increased tone, autonomic features, and automatisms may also be seen. Absence seizures associated with slow spike-wave complexes are called atypical absence seizures.
      [ 7 ]

      See Epilepsy and Seizures for a general overview of these topics.

      Classification

      The International League Against Epilepsy (ILAE) Commission on Classification and Terminology revised the concepts, terminology, and approaches for classifying seizures and epilepsy.
      [ 8 ]

      The classification of absence seizures has been simplified as follows:

      • Typical absence
      • Atypical absence
      • Myoclonic absence
      • Eyelid myoclonia

      Patient education

      Patients who are old enough to drive should be warned about driving and operating heavy machinery. Physicians should be familiar with state laws concerning driving with epilepsy; inform patients concerning these legal matters.

      For patient education information, see the Brain and Nervous System Center , as well as Epilepsy .

      Next:

      Etiology

      The etiology of idiopathic epilepsies with age-related onset is genetic. About 15-40% of patients with these epilepsies have a family history of epilepsy; overall concordance in monozygotic twins is 74%, with a 100% concordance during the peak age of phenotypic expression.
      [ 9 ]
      Family members may have other forms of idiopathic or genetic epilepsy (eg, febrile convulsions, generalized tonic-clonic seizures).

      The idiopathic generalized epilepsies are a group of primary generalized epilepsies with absence, myoclonic, and tonic-clonic seizures. Based on age of onset and seizure types, some can be grouped into well-recognized syndromes, such as childhood absence epilepsy, juvenile absence epilepsy, and juvenile myoclonic epilepsy.

      However, patients with other syndromes, such as generalized epilepsy with febrile seizures plus (GEFS+), as well as patients who have childhood absence epilepsy that leads into juvenile myoclonic epilepsy, illustrate that these syndromes represent a genetically determined lower threshold to have seizures.

      The idiopathic generalized epilepsies are best viewed as a spectrum of clinical syndromes
      [ 10 ]
      with varied genetic causes that affect the function of ion channels.

      Genetic studies have shown that these syndromes are channelopathies, but different gene mutations have been found in the same syndromes. Juvenile myoclonic epilepsy has been linked to chromosome 6,
      [ 11 , 12 ]
      with linkage to chromosome 6p12 in Mexican families.
      [ 13 ]
      Mutations in the EFHC1 gene have been found in Mexican
      [ 14 , 15 ]
      and Italian families
      [ 16 ]
      with juvenile myoclonic epilepsy, but not in a group of Dutch families.
      [ 17 ]

      Childhood absence epilepsy with generalized tonic-clonic seizure has been linked to chromosome 8q24 in a 5-generation family from Bombay, India.
      [ 18 ]
      Childhood absence epilepsy with febrile seizures has been linked to the GABA(A) receptor γ2 subunit (GABRG2) on chromosome 5q3.1-33.1.
      [ 19 ]

      A mutation in the GABA(A) receptor gene GABRB3 was found in Mexican families with childhood absence epilepsy. Mutations showed hyperglycosylation in vitro, with reduced GABA-evoked current density from whole cells. Expression of this gene in the developing brain may help explain an age-related onset and remission in childhood absence epilepsy.
      [ 20 ]

      Pathophysiology

      The pathophysiology of absence seizures is not fully understood. In 1947, Jasper and Droogleever-Fortuyn electrically stimulated nuclei in the thalami of cats at 3 Hz and produced bilaterally synchronous spike-and-wave discharges on EEG.
      [ 21 ]
      In 1953, bilaterally synchronous spike-and-wave discharges were recorded by placing depth electrodes in the thalamus of a child with absence seizures.
      [ 22 ]

      In 1977, Gloor et al demonstrated that the bilaterally synchronous, 3-Hz spike-wave discharges in the feline penicillin model of absence seizures were generated in the cortex. This led to the corticoreticular theory of primarily generalized seizures.

      Abnormal oscillatory rhythms are believed to develop in thalamocortical pathways. This involves gamma-aminobutyric acid (GABA)-B–mediated inhibition alternating with glutamate-mediated excitation.

      The cellular mechanism is believed to involve T-type calcium currents. T channels of the GABAergic reticular thalamic nucleus neurons appear to play a major role in the spike-wave discharges of the GABAergic thalamic neurons.
      [ 23 ]

      GABA-B inhibition appears to be altered in absence seizures, and potentiation of GABA-B inhibition with tiagabine (Gabitril), vigabatrin (Sabril),
      [ 24 ]
      and, possibly, gabapentin (Neurontin), results in exacerbation of absence seizures. Enhanced burst firing in selected corticothalamic networks may increase GABA-B receptor activation in the thalamus, leading to generalized spike-wave activity.

      These data suggest that activity of thalamic networks is necessary for spike-wave discharge rhythmogenesis, and cortical hyperexcitability is necessary for their generation.
      [ 25 ]

      In symptomatic generalized epilepsies, absence seizures are due to a wide variety of causes that at an early stage of neural development, result in diffuse or multifocal brain damage. The causes and management of secondary generalized epilepsies, and the other seizure types that accompany them, are not discussed in this article.

      Risk factors

      After noncompliance with treatment, lack of sleep is the most frequent cause of seizure exacerbations. Drugs that lower the seizure threshold (eg, alcohol, cocaine, high-dose penicillin, isoniazid [INH] overdose, neuroleptics) are most likely to cause seizures in patients with epilepsy. Withdrawal of alcohol, benzodiazepines, and other sedatives are also common causes.

      Previous
      Next:

      Epidemiology

      Incidence in the United States

      The incidence of absence seizures in the United States is 1.9-8 cases per 100,000 population.

      Morbidity and mortality

      The morbidity from typical absence seizures is related to the frequency and duration of the seizures, as well as to the patient’s activities; effective treatment ameliorates these factors.

      Educational and behavioral problems are sequelae of frequent, unrecognized seizures.

      No deaths result directly from absence seizures. However, if an individual suffers an absence seizure while driving or operating dangerous machinery, a fatal accident may occur.

      In children with absence seizures due to secondary generalized epilepsies, death is related to the underlying disease.

      Sex predilection

      Absence seizures are generally believed to be more common in females than in males. Up to two thirds of children with childhood absence epilepsy are girls.
      [ 9 , 26 ]

      Absence epilepsy with myoclonus has a male predominance.
      [ 27 ]

      Age of onset

      The generalized idiopathic epilepsies have age-related onset.

      Onset of absence seizures in children with symptomatic generalized epilepsies depends on the underlying disorder. While many of these disorders may have their onset at an early (prenatal, perinatal, or postnatal) age, absence seizures do not appear until later in childhood. An example is the Lennox-Gastaut syndrome . The cause may be a genetic disorder or a perinatal insult, but the absence seizures do not present until age 1-8 years.
      [ 28 ]

      Childhood absence epilepsy onset is at age 4-8 years, with peak onset at age 6-7 years.
      [ 26 ]

      Juvenile absence epilepsy onset is generally around puberty. Actual age of onset may vary, depending on whether pyknoleptic (8.3 ± 4.5 y) or nonpyknoleptic seizures occur (14.8 ± 8.3 y).
      [ 29 ]

      Juvenile myoclonic epilepsy has a more varied age of onset (8-26 y), but 79% of patients have an onset between the ages of 12 and 18 years.
      [ 30 ]
      Because the absence and myoclonic seizures are brief, they often go unrecognized, and many patients do not present until they experience a tonic-clonic seizure.

      Previous
      Next:

      Clinical Presentation

      Patient history

      Children with idiopathic generalized epilepsies may present with a history of staring spells, but infrequent absence seizures may not be diagnosed until a generalized tonic-clonic seizure has occurred.

      Other symptoms, such as behavioral problems, may be the presenting complaint.
      [ 31 ]
      Whether this is a comorbid condition or a result of brief, unrecognized attacks that cause lapses of awareness and interferes with attention is unknown.

      Decline in school performance may be an indication of the onset or breakthrough of absence seizures.

      In symptomatic generalized epilepsies, atypical absence seizures often occur in the setting of developmental delay or mental retardation. (See Table 1, below, for features of typical and atypical absence seizures.)

      Other seizure types can be present in the patient, such as myoclonic, tonic, atonic, tonic-clonic, and even partial seizures .

      Physical examination

      Physical and neurologic findings are normal in children with idiopathic generalized epilepsies. Having the child hyperventilate for 3-5 minutes can often provoke absence seizures. This procedure can easily be performed in the clinic or office, and the result is diagnostic.

      On clinical examination, typical absence seizures appear as brief staring spells. Patients have no warning or postictal phase, and if engaged in gross motor activity, such as walking, they may stop and stand motionless or they may continue to walk. Children are not responsive during the seizure and have no memory of what happened during the attack; they are generally unaware that a seizure has occurred. (See Table 1, below.)

      Atypical absence seizures, which occur in patients with symptomatic generalized epilepsies, are usually longer than typical absences and often have more gradual onset and resolution.

      In symptomatic generalized epilepsies, physical and neurologic findings may be abnormal, reflecting the underlying disorder. Physical examination may reveal stigmata of a genetic disease, such as a neurocutaneous disorder (eg, tuberous sclerosis) or an inborn error of metabolism. Neurologic examination may show signs of developmental delay or more specific signs, such as spastic paresis in cerebral palsy.

      Table 1. Clinical and EEG Findings in Typical and Atypical Absence Seizures* (Open Table in a new window)

      Type of Clinical Seizure

      EEG Findings

      Typical absence

      Impairment of consciousness only

      Usually regular and symmetrical 3 Hz, possible 2- to 4-Hz spike-and-slow-wave complexes, and possible multiple spike-and-slow-wave complexes

      Mild clonic components

      Atonic components

      Tonic component

      Automatisms

      Autonomic components

      Atypical absence

      Changes in tone more pronounced than those of typical absence seizure

      EEG more heterogeneous than in typical absence; may include irregular spike-and-slow-wave complexes, fast activity, or other paroxysmal activity; abnormalities bilateral but often irregular and asymmetrical

      Nonabrupt onset or cessation abrupt

      *May be seen alone or in combination.

      Adapted from Dreifuss FE. Classification of epileptic seizures. In: Engel J Jr, Pedley TA, eds. Epilepsy: A Comprehensive Textbook. Philadelphia, PA: Lippincott-Raven;1997.

      Previous
      Next:

      Differential Diagnosis

      Attention Deficit Hyperactivity Disorder ( ADHD )

      Complex Partial Seizures

      Confusional States and Acute Memory Disorders

      Febrile Seizures

      First Pediatric Seizure

      Migraine Variants

      Psychogenic Nonepileptic Seizures

      Reflex Epilepsy

      Shuddering Attacks

      Status Epilepticus

      Breath-holding spells are another differential.

      Staring spells, daydreaming, migraine equivalents, and panic and/or anxiety attacks all may be confused with nonconvulsive seizures.

      Absence versus complex partial seizures

      Absence seizures may be confused with complex partial seizures, especially in cases of prolonged seizures with automatisms (see Table 2, below).

      Table 2. Differentiating Features of Complex Partial and Absence Seizures (Open Table in a new window)

      Feature

      Complex Partial

      Absence

      Onset

      May have simple partial onset

      Abrupt

      Duration

      Usually >30 s

      Usually < 30 s

      Automatisms

      Present

      Duration dependent

      Awareness

      No

      No

      Ending

      Gradual postictal

      Abrupt

      The occurrence of automatisms is dependent on duration of the seizure; the longer the seizure, the more likely automatisms are to occur (see image below).
      [ 32 ]

      Percentage of absence seizures with automatisms as

      Percentage of absence seizures with automatisms as a function of duration in seconds. (Data gathered from Penry et al, 1975.)

      View Media Gallery

      Previous
      Next:

      Laboratory Studies

      When evaluating a child for staring spells, laboratory tests for metabolic abnormalities or toxic or drug ingestion (especially in older children) may be indicated. If a clear history of the episodic nature of the attacks is obtained, then the EEG can be diagnostic and laboratory tests may not be necessary.

      When evaluating a child with a developmental delay, or if the EEG reveals atypical absences, then a full work-up for the underlying cause of a symptomatic generalized epilepsy is indicated.

      Previous
      Next:

      Neuroimaging Studies

      Neuroimaging findings are normal in idiopathic epilepsies by definition, and therefore, neuroimaging is not indicated if the typical clinical pattern is present.

      However, neuroimaging is often ordered by primary care providers and the emergency department, especially if a child presents with a generalized tonic-clonic seizure, to rule out significant structural causes of seizures. A normal result helps to support the diagnosis of idiopathic epilepsy. For cryptogenic and symptomatic generalized epilepsies, neuroimaging can help in the diagnosis of any underlying structural abnormality.

      If imaging is performed, magnetic resonance imaging (MRI) is preferred to computed tomography (CT) scanning. MRI is more sensitive for certain anatomic abnormalities.

      A review of 134 MRI scans in patients with idiopathic generalized epilepsies found nonspecific abnormalities in 24%.
      [ 33 ]

      Previous
      Next:

      Electroencephalography

      The only diagnostic test for absence seizures is the EEG.

      Background activity is normal. In syndromes with frequent absence seizures, such as childhood absence epilepsy, a routine awake recording is often pathognomonic. Bursts of frontally predominant, generalized 3-Hz spike-and-wave complexes are seen during the seizures.
      [ 3 ]
      In syndromes with less frequent absence seizures (juvenile absence epilepsy or juvenile myoclonic epilepsy), an awake recording may be normal; a sleep or sleep-deprived recording may be needed.

      Typical absence seizures have generalized 3-Hz spike-and-wave complexes (see image below).

      EEG of a typical absence seizure with 3-Hz spike-a

      EEG of a typical absence seizure with 3-Hz spike-and-wave discharges.

      View Media Gallery

      The spike frequency is often faster at the onset, with a slight deceleration at the end.
      [ 26 ]
      They can range from 2.5-6 Hz, with the faster frequencies seen in syndromes with older age of onset.

      Bursts of generalized polyspikes and waves (multiple spike-and-slow-wave complexes) may also be seen,
      [ 30 ]
      especially during sleep and in syndromes with older age of onset.

      The onset and ending of these seizures are abrupt; no postictal EEG slowing is noted.

      Hyperventilation often provokes these seizures and should be a routine part of all EEGs in children.

      Photosensitivity may be present in idiopathic generalized epilepsies and is more often seen in juvenile myoclonic epilepsy and childhood absence epilepsy than juvenile absence epilepsy.
      [ 29 ]

      EEG video monitoring demonstrates that clinical seizure manifestations may lag behind the start of ictal EEG activity; bursts lasting less than 3 seconds are usually clinically silent. During the absence seizure, rhythmic eye blinks and mild clonic jerks may be present. As a seizure progresses, automatisms may be seen.
      [ 32 ]

      Clinical and EEG features may vary considerably in different children.
      [ 34 ]

      Go to EEG Video Monitoring for procedural information on this topic.

      EEG findings in atypical absence seizures

      Atypical absence seizures are characterized by slow spike-and-wave paroxysms, classically 2.5 Hz (see the image below). The onset may be difficult to discern, and postictal EEG slowing may be noted.

      Slow spike-and-wave discharges (2.5 Hz). This is a

      Slow spike-and-wave discharges (2.5 Hz). This is an interictal pattern in a child with seizures and developmental delay.

      View Media Gallery

      Background activity is often abnormal, reflecting the diffuse or multifocal underlying encephalopathy of symptomatic generalized epilepsy.

      Generalized polyspike-and-wave complexes also may be present, and focal features may be observed.

      The clinical correlation of generalized spike-and-wave complexes with clinical seizures is not as clear-cut as in typical absence seizures. Generalized slow spikes and waves may be present as an interictal pattern, as in Lennox-Gastaut syndrome.

      EEG video monitoring can show a more varied alteration of consciousness than in typical absence seizures. If the patient has underlying mental retardation, discerning changes in mental status may be more difficult in atypical absence.

      Changes in postural tone, most noticeably head nods, are common.

      Ambulatory EEG monitoring over 24 hours may be useful to quantitate the number of seizures per day and their most likely times of occurrence.

      Previous
      Next:

      Pharmacologic Treatment

      Treatment for absence seizures involves antiepileptic drugs (AEDs). Once the proper diagnosis (ie, of the specific epilepsy syndrome) is made, the likelihood of other, coexistent seizure types in the patient, such as myoclonic or tonic-clonic seizures, should be considered and an appropriate medication selected. Since altered awareness occurs with even brief bursts of spike-wave paroxysms on EEG, treatment should be titrated to suppressing all epileptiform activity.

      The decision to start antiepileptic medication must be made with great care. Most AEDs are relatively toxic and can have sedative and cognitive side effects. Children with absence seizures may need to be on medication for many years, and in some cases, for life. EEG can usually confirm the diagnosis, and the presence of spontaneous seizures can be documented on routine EEG or with longer recordings (ie, 24-hour ambulatory EEG or EEG video monitoring).

      Only 2 first-line AEDs have approval from the US Food and Drug Administration (FDA) to be indicated for absence seizures: ethosuximide (Zarontin) and valproic acid (Depakene, Depacon). Ethosuximide has efficacy for absence seizures only and valproic acid has efficacy for absence, generalized tonic-clonic, and myoclonic seizures.

      Ethosuximide (Zarontin) is effective only against absence seizures.

      Valproic acid (Depakene, Depacon, Depakote, Depakote ER) is considered a broad-spectrum AED, because it is effective against absence, myoclonic, tonic-clonic, and partial seizures.

      A study showed that ethosuximide and valproic acid were more effective than lamotrigine in the treatment of childhood absence epilepsy, and that ethosuximide had fewer adverse attentional side effects.
      [ 35 ]

      Symptomatic generalized epilepsies are often refractory to first-line AEDs. Lamotrigine (Lamictal), topiramate (Topamax), and felbamate (Felbatol) are approved by the FDA as adjunctive therapy for the generalized seizures of Lennox-Gastaut syndrome in adult and pediatric patients (>2 y). Clonazepam (Klonopin) and the ketogenic or medium-chain triglyceride diet have been attempted to reduce seizure frequency. However, these adjunctive therapies have limited efficacy.

      Of the newer AEDs, lamotrigine, topiramate, and levetiracetam have been shown to have efficacy against seizures in idiopathic generalized epilepsy
      [ 36 , 37 ]
      and have received FDA approval to be indicated for adjunctive therapy of generalized tonic-clonic seizures in idiopathic generalized epilepsy in children aged 2 years and older (for lamotrigine and topiramate) and in children aged 6 years and older (for levetiracetam). Levetiracetam is indicated as adjunct therapy for generalized tonic-clonic and myoclonic seizures. It has been shown to have only modest efficacy against absence seizures.
      [ 38 , 39 ]

      Lamotrigine and topiramate are also approved as adjunctive therapy in Lennox-Gastaut syndrome in children aged 2 years and older. Rufinamide (Banzel) has been shown effective against typical and atypical absence seizures as well as other seizures in Lennox-Gastaut syndrome
      [ 40 ]
      and is approved as adjunct therapy in children older than 4 years.

      Topiramate has also received FDA approval as initial monotherapy for generalized tonic-clonic seizures in children aged 10 years and older with idiopathic generalized epilepsy. Studies have shown these medications to have antiabsence efficacy, but the data are incomplete.
      [ 41 ]

      Some AEDs can aggravate seizures, especially in cryptogenic or symptomatic generalized epilepsies.
      [ 42 ]
      Treatment with carbamazepine (Tegretol, Tegretol XR, Carbatrol)
      [ 43 , 44 ]
      and oxcarbazepine (Trileptal)
      [ 45 ]
      has been associated with the exacerbation of absence seizures. Gabapentin (Neurontin) is ineffective against absence seizures,
      [ 46 ]
      and tiagabine (Gabitril) and vigabatrin (Sabril) have been associated with the exacerbation of absence or myoclonic seizures in some patients.
      [ 47 ]

      Conception and pregnancy considerations

      Women of childbearing age who are not using adequate birth control should not be treated with valproic acid, if equally effective alternatives are available for them.

      If a woman taking valproic acid wishes to become pregnant, treatment may be crossed over to ethosuximide if only absence seizures are present, and she may be given folic acid 1-5 mg/d before conception. After the first trimester, treatment may be switched back to valproic acid.

      Women with generalized tonic-clonic seizures may be crossed over to lamotrigine, and given folic acid 1-5 mg/d before conception.

      Most clinicians believe that women treated with valproic acid or any hepatic enzyme-inducing AED should be treated with vitamin K before delivery.

      Previous
      Next:

      Consultations

      All patients with suspected absence seizures should be examined by a neurologist who has expertise in diagnosing epileptic syndromes. Patients with refractory seizures, especially those with symptomatic epilepsies, may need to be referred to an epileptologist for prolonged EEG video monitoring and medication adjustments.

      Previous
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      Diet

      A ketogenic
      [ 48 ]
      or medium-chain triglyceride diet
      [ 49 ]
      may be tried in patients with medically intractable seizures. Although these diets are difficult to maintain, there is evidence for their effectiveness.
      [ 50 ]
      Children in whom such diets are being considered should be referred to a center with specialized dietary services.

      Previous
      Next:

      Activity

      Physical activity should not be restricted any more than necessary. Activities in which a seizure might pose a threat, such as swimming or rock climbing, may be allowed with appropriate supervision. A child with epilepsy should not be unnecessarily handicapped. Patients with uncontrolled absence seizures should not be allowed to drive. The situation may be unclear when the patient’s clinical seizures are controlled but the EEG still shows some spike-wave activity.

      Previous
      Next:

      Outpatient Management

      Children with absence seizures should be monitored closely during titration or crossover of AEDs. The dose of the medication should be increased weekly until seizures are controlled or adverse effects develop.

      The aim in therapy is to control seizures completely with the minimum required amount of medication to minimize adverse effects.

      The therapeutic effect of valproic acid for absence seizures may lag several weeks behind reaching a therapeutic level.
      [ 51 ]

      Liver function test, amylase and/or lipase, and complete blood cell (CBC) count results should be monitored during drug treatment to watch for adverse reactions.

      Drug levels should be monitored to ensure treatment compliance and to watch for toxic levels in patients who are too young or too developmentally disabled to articulate subjective adverse effects.

      Previous
      Next:

      Prognosis

      The prognosis for the primary generalized epilepsies depends on the particular epileptic syndrome. Because seizures, particularly generalized tonic-clonic seizures, may occur well after patients appear to achieve good control, a long seizure-free period should be achieved before discontinuation of therapy is considered.

      The remission rate for childhood absence epilepsy is good; 80% of patients respond to medication. Complete remission rates vary widely, perhaps dependent on the length of follow-up.

      Generalized tonic-clonic seizures may develop in up to 40% of children with childhood absence epilepsy.
      [ 26 ]
      Persistence of seizures is more likely in those with generalized tonic-clonic seizures.

      Early onset of absence seizures, quick response to therapy,
      [ 52 ]
      and normal EEG background are good prognostic signs.

      Juvenile myoclonic epilepsy carries a high risk of generalized tonic-clonic seizures. Despite excellent control with relatively small doses of an AED, the relapse rate is greater than 90%.
      [ 53 ]

      Patients with juvenile myoclonic epilepsy generally need to be treated for life, although occasional patients achieve control with careful attention to lifestyle issues (eg, adequate sleep, abstinence from alcohol).

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      Questions & Answers

      Overview

      What are absence seizures?

      How are absence seizures classified?

      What is included in patient education about absence seizures?

      What causes absence seizures?

      What is the pathophysiology of absence seizures?

      What are the risk factors for absence seizures?

      What is the incidence of absence seizures in the US?

      What is the morbidity associated with absence seizures?

      What are the sexual predilections of absence seizures?

      Which age groups have the highest prevalence of absence seizures?

      Which clinical history findings are characteristic of absence seizures?

      Which physical findings are characteristic of absence seizures?

      Which conditions should be included in the differential diagnosis of absence seizures?

      How are absence seizures differentiated from complex partial seizures?

      What is the role of lab testing in the workup of absence seizures?

      What is the role of neuroimaging studies in the diagnosis of absence seizures?

      What is the role of EEG in the diagnosis of absence seizures?

      How are absence seizures treated?

      What is the role of antiepileptic drugs (AEDs) in the treatment of absence seizures?

      How are absence seizures treated during pregnancy?

      Which specialist consultations are beneficial to patients with absence seizures?

      Which dietary modifications are used in the treatment of absence seizures?

      Which activity modifications are used in the treatment of absence seizures?

      What is included in the long-term monitoring of patients with absence seizures?

      What is the prognosis of absence seizures?

      Previous

      References

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      2. Temkin O. The Falling Sickness. Johns Hopkins Press: Baltimore, MD; 1971. 250.

      3. Gibbs FA, Davis H, Lennox WG. The EEG in epilepsy and in conditions of impaired consciousness. Arch Neurol Psychiat. 1935. 34:1134-48.

      4. Proposal for revised classification of epilepsies and epileptic syndromes. Commission on Classification and Terminology of the International League Against Epilepsy. Epilepsia. 1989 Jul-Aug. 30(4):389-99. [Medline] .

      5. Benbadis SR, Berkovic SF. Absence Seizures. Wyllie E, Gupta A and Lachhwani DK. The Treatment of Epilepsy. Principles and Practice. 4th ed. Philadelphia: Lippincott, Williams and Wilkins; 2006. 305-315.

      6. Panayiotopoulos CP. Typical Absence Seizures. The International League Against Epilepsy. Available at http://www.ilae-epilepsy.org/Visitors/Centre/ctf/typical_absence.cfm . Accessed: March 16, 2008.

      7. Dulac O. Atypical Absence. The International League Against Epilepsy. Available at http://www.ilae-epilepsy.org/Visitors/Centre/ctf/atypical_absence.cfm . Accessed: March 16, 2008.

      8. Fisher RS, Cross JH, French JA, Higurashi N, Hirsch E, Jansen FE, et al. Operational classification of seizure types by the International League Against Epilepsy: Position Paper of the ILAE Commission for Classification and Terminology. Epilepsia. 2017 Apr. 58 (4):522-530. [Medline] .

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      11. Greenberg DA, Delgado-Escueta AV, Widelitz H, Sparkes RS, Treiman L, Maldonado HM, et al. Juvenile myoclonic epilepsy (JME) may be linked to the BF and HLA loci on human chromosome 6. Am J Med Genet. 1988 Sep. 31(1):185-92. [Medline] .

      12. Liu AW, Delgado-Escueta AV, Gee MN, Serratosa JM, Zhang QW, Alonso ME, et al. Juvenile myoclonic epilepsy in chromosome 6p12-p11: locus heterogeneity and recombinations. Am J Med Genet. 1996 Jun 14. 63(3):438-46. [Medline] .

      13. Bai D, Alonso ME, Medina MT, Bailey JN, Morita R, Cordova S, et al. Juvenile myoclonic epilepsy: linkage to chromosome 6p12 in Mexico families. Am J Med Genet. 2002 Dec 1. 113(3):268-74. [Medline] .

      14. Stogmann E, Lichtner P, Baumgartner C, Bonelli S, Assem-Hilger E, Leutmezer F, et al. Idiopathic generalized epilepsy phenotypes associated with different EFHC1 mutations. Neurology. 2006 Dec 12. 67(11):2029-31. [Medline] .

      15. Suzuki T, Delgado-Escueta AV, Aguan K, Alonso ME, Shi J, Hara Y, et al. Mutations in EFHC1 cause juvenile myoclonic epilepsy. Nat Genet. 2004 Aug. 36(8):842-9. [Medline] .

      16. Annesi F, Gambardella A, Michelucci R, Bianchi A, Marini C, Canevini MP. Mutational analysis of EFHC1 gene in Italian families with juvenile myoclonic epilepsy. Epilepsia. 2007 Sep. 48(9):1686-90. [Medline] .

      17. Pinto D, Louwaars S, Westland B, Volkers L, de Haan GJ, Trenité DG, et al. Heterogeneity at the JME 6p11-12 locus: absence of mutations in the EFHC1 gene in linked Dutch families. Epilepsia. 2006 Oct. 47(10):1743-6. [Medline] .

      18. Fong GC, Shah PU, Gee MN, Serratosa JM, Castroviejo IP, Khan S, et al. Childhood absence epilepsy with tonic-clonic seizures and electroencephalogram 3-4-Hz spike and multispike-slow wave complexes: linkage to chromosome 8q24. Am J Hum Genet. 1998 Oct. 63(4):1117-29. [Medline] .

      19. Wallace RH, Marini C, Petrou S, Harkin LA, Bowser DN, Panchal RG, et al. Mutant GABA(A) receptor gamma2-subunit in childhood absence epilepsy and febrile seizures. Nat Genet. 2001 May. 28(1):49-52. [Medline] .

      20. Tanaka M, Olsen RW, Medina MT, Schwartz E, Alonso ME, Duron RM. Hyperglycosylation and reduced GABA currents of mutated GABRB3 polypeptide in remitting childhood absence epilepsy. Am J Hum Genet. 2008 Jun. 82(6):1249-61. [Medline] .

      21. Jasper HH, Droogleever-Fortuyn J. Experimental studies on the functional anatomy of petit mal epilepsy. Assoc Res Nerv Ment Dis. 1947. 26:272-98.

      22. Williams, D. A study of thalamic and cortical rhythms in petit mal. Brain. 1953. 76:50-69.

      23. Panayiotopoulos CP. Absence epilepsies. Engel J Jr, Pedley TA, eds. Epilepsy: A Comprehensive Textbook. Philadelphia, PA: Lippincott-Raven; 1997. 2327-46.

      24. Arzimanoglou A, Ostrowsky-Coste K. Absence Seizures. Wyllie E, Casino GD, Gidal BE, Goodkin HP. Wyllie’s Treatment of Epilepsy: Principles and Practice. Philadelphia: Lippincott Williams & Wilkins; 2012. 198/15.

      25. Avoli M. A brief history on the oscillating roles of thalamus and cortex in absence seizures. Epilepsia. 2012 May. 53(5):779-89. [Medline] .

      26. Loiseau P. Childhood absence epilepsy. Roger J, Bureau M, Dravet, et al, eds. Epileptic Syndromes. London, England: John Libby; 1985: 106-20.

      27. Tassinari CA, Bureau M. Epilepsy with myoclonic absences. Roger J, Bureau M, Dravet, et al, eds. Epileptic Syndromes. London, England: John Libby; 1985. 121-9.

      28. Beaumanoir A. Roger J, Bureau M, Dravet, et al, eds. Epileptic Syndromes. London, England: John Libby; 1985. 11: 89-99.

      29. Wolf P. Juvenile absence epilepsy. Roger J, Bureau M, Dravet, et al, eds. Epileptic Syndromes. London, England: John Libby; 1985. 242-6.

      30. Wolf P. Juvenile myoclonic epilepsy. Roger J, Bureau M, Dravet, et al, eds. Epileptic Syndromes. London, England: John Libby; 1985. 247-58.

      31. Hamiwka LD, Wirrell EC. Comorbidities in pediatric epilepsy: beyond “just’ treating the seizures. J Child Neurol. 2009 Jun. 24(6):734-42. [Medline] . [Full Text] .

      32. Penry JK, Porter RJ, Dreifuss RE. Simultaneous recording of absence seizures with video tape and electroencephalography. A study of 374 seizures in 48 patients. Brain. 1975 Sep. 98(3):427-40. [Medline] .

      33. Betting LE, Mory SB, Lopes-Cendes I, Li LM, Guerreiro MM, Guerreiro CA, et al. MRI reveals structural abnormalities in patients with idiopathic generalized epilepsy. Neurology. 2006 Sep 12. 67(5):848-52. [Medline] .

      34. Sadleir LG, Farrell K, Smith S, Connolly MB, Scheffer IE. Electroclinical features of absence seizures in childhood absence epilepsy. Neurology. 2006 Aug 8. 67(3):413-8. [Medline] .

      35. Glauser TA, Cnaan A, Shinnar S, Hirtz DG, Dlugos D, Masur D. Ethosuximide, valproic acid, and lamotrigine in childhood absence epilepsy. N Engl J Med. 2010 Mar 4. 362(9):790-9. [Medline] .

      36. Berkovic SF, Knowlton RC, Leroy RF, Schiemann J, Falter U. Placebo-controlled study of levetiracetam in idiopathic generalized epilepsy. Neurology. 2007 Oct 30. 69(18):1751-60. [Medline] .

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      39. Delanty N, Jones J, Tonner F. Adjunctive levetiracetam in children, adolescents, and adults with primary generalized seizures: open-label, noncomparative, multicenter, long-term follow-up study. Epilepsia. 2012 Jan. 53(1):111-9. [Medline] .

      40. Glauser T, Kluger G, Sachdeo R, Krauss G, Perdomo C, Arroyo S. Rufinamide for generalized seizures associated with Lennox-Gastaut syndrome. Neurology. 2008 May 20. 70(21):1950-8. [Medline] .

      41. Posner EB, Mohamed K, Marson AG. Ethosuximide, sodium valproate or lamotrigine for absence seizures in children and adolescents. Cochrane Database Syst Rev. 2005. (4):CD003032. [Medline] .

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      43. Snead OC 3rd, Hosey LC. Exacerbation of seizures in children by carbamazepine. N Engl J Med. 1985 Oct 10. 313(15):916-21. [Medline] .

      44. Liu L, Zheng T, Morris MJ, Wallengren C, Clarke AL, Reid CA, et al. The mechanism of carbamazepine aggravation of absence seizures. J Pharmacol Exp Ther. 2006 Nov. 319(2):790-8. [Medline] .

      45. Vendrame M, Khurana DS, Cruz M, Melvin J, Valencia I, Legido A, et al. Aggravation of seizures and/or EEG features in children treated with oxcarbazepine monotherapy. Epilepsia. 2007 Nov. 48(11):2116-20. [Medline] .

      46. Guerrini R, Belmonte A, Genton P. Antiepileptic drug-induced worsening of seizures in children. Epilepsia. 1998. 39 Suppl 3:S2-10. [Medline] .

      47. Perucca E. The management of refractory idiopathic epilepsies. Epilepsia. 2001. 42 Suppl 3:31-5. [Medline] .

      48. Hemingway C, Freeman JM, Pillas DJ, Pyzik PL. The ketogenic diet: a 3- to 6-year follow-up of 150 children enrolled prospectively. Pediatrics. 2001 Oct. 108(4):898-905. [Medline] .

      49. Edwards, N. The MCT Diet. epilepsy.com. Available at http://www.epilepsy.com/epilepsy/keto_news_august07 . Accessed: 3/15/09.

      50. Lefevre F, Aronson N. Ketogenic diet for the treatment of refractory epilepsy in children: A systematic review of efficacy. Pediatrics. 2000 Apr. 105(4):E46. [Medline] .

      51. Wheeler MM, Winter ME. Valproic Acid. Winter ME. Basic Clinical Pharmacokinetics. 4. Philadelphia: Lippincott Williams & Wilkins; 2003. 438/14.

      52. Wirrell E, Camfield C, Camfield P, Dooley J. Prognostic significance of failure of the initial antiepileptic drug in children with absence epilepsy. Epilepsia. 2001 Jun. 42(6):760-3. [Medline] .

      53. Delgado-Escueta AV, Enrile-Bacsal F. Juvenile myoclonic epilepsy of Janz. Neurology. 1984 Mar. 34(3):285-94. [Medline] .

      Media Gallery
      • Percentage of absence seizures with automatisms as a function of duration in seconds. (Data gathered from Penry et al, 1975.)
      • EEG of a typical absence seizure with 3-Hz spike-and-wave discharges.
      • Slow spike-and-wave discharges (2.5 Hz). This is an interictal pattern in a child with seizures and developmental delay.

      of
      3

      Tables

      • Table 1. Clinical and EEG Findings in Typical and Atypical Absence Seizures*
      • Table 2. Differentiating Features of Complex Partial and Absence Seizures

      Table 1. Clinical and EEG Findings in Typical and Atypical Absence Seizures*

      Type of Clinical Seizure

      EEG Findings

      Typical absence

      Impairment of consciousness only

      Usually regular and symmetrical 3 Hz, possible 2- to 4-Hz spike-and-slow-wave complexes, and possible multiple spike-and-slow-wave complexes

      Mild clonic components

      Atonic components

      Tonic component

      Automatisms

      Autonomic components

      Atypical absence

      Changes in tone more pronounced than those of typical absence seizure

      EEG more heterogeneous than in typical absence; may include irregular spike-and-slow-wave complexes, fast activity, or other paroxysmal activity; abnormalities bilateral but often irregular and asymmetrical

      Nonabrupt onset or cessation abrupt

      *May be seen alone or in combination.

      Adapted from Dreifuss FE. Classification of epileptic seizures. In: Engel J Jr, Pedley TA, eds. Epilepsy: A Comprehensive Textbook. Philadelphia, PA: Lippincott-Raven;1997.

      Table 2. Differentiating Features of Complex Partial and Absence Seizures

      Feature

      Complex Partial

      Absence

      Onset

      May have simple partial onset

      Abrupt

      Duration

      Usually >30 s

      Usually < 30 s

      Automatisms

      Present

      Duration dependent

      Awareness

      No

      No

      Ending

      Gradual postictal

      Abrupt

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      Contributor Information and Disclosures

      Author

      Scott Segan, MD Director of SBH Stroke Center and Attending Neurologist, St Barnabas Hospital

      Scott Segan, MD is a member of the following medical societies: American Academy of Neurology , American Epilepsy Society

      Disclosure: Nothing to disclose.

      Specialty Editor Board

      Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

      Disclosure: Received salary from Medscape for employment. for: Medscape.

      Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS, FAES Professor with Tenure, Departments of Neurology, Neuroscience, and Physiology, Assistant Dean for the MD/PhD Program, Program Director of the Clinical Neurophysiology Fellowship, University of Texas School of Medicine at San Antonio

      Jose E Cavazos, MD, PhD, FAAN, FANA, FACNS, FAES is a member of the following medical societies: American Academy of Neurology , American Clinical Neurophysiology Society , American Epilepsy Society , American Neurological Association , Society for Neuroscience

      Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Brain Sentinel, consultant.<br/>Stakeholder (<5%), Co-founder for: Brain Sentinel.

      Chief Editor

      Selim R Benbadis, MD Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida Morsani College of Medicine

      Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology , American Academy of Sleep Medicine , American Clinical Neurophysiology Society , American Epilepsy Society , American Medical Association

      Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Acorda, Livanova, Eisai, Greenwich, Lundbeck, Neuropace, Sunovion, Upsher-Smith.<br/>Serve(d) as a speaker or a member of a speakers bureau for: Livanova, Eisai, Greenwich, Lundbeck, Neuropace, Sunovion.<br/>Received research grant from: Acorda, Livanova, Greenwich, Lundbeck, Sepracor, Sunovion, UCB, Upsher-Smith.

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      • Sections
        Absence Seizures
      • Overview
      • Etiology
      • Epidemiology
      • Presentation
      • Differential Diagnosis
      • Laboratory Studies
      • Neuroimaging Studies
      • Electroencephalography
      • Pharmacologic Treatment
      • Consultations
      • Diet
      • Activity
      • Outpatient Management
      • Prognosis
      • Questions & Answers
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      • References

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