Absence seizure

Last updated
Absence seizure
Other namesPetit mal seizures
Pronunciation
Specialty Neurology

Absence seizures are one of several kinds of generalized seizures. In the past, absence epilepsy was referred to as "pyknolepsy," a term derived from the Greek word "pyknos," signifying "extremely frequent" or "grouped". [1] These seizures are sometimes referred to as petit mal seizures (from the French for "little illness", a term dated to the late 18th century); [2] however, usage of this terminology is no longer recommended. [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). Absence seizures are most common in children. They affect both sides of the brain. [3] [4]

Contents

Childhood absence epilepsy represents a significant portion, accounting for approximately 10 to 17%, of all cases of childhood-onset epilepsy, establishing it as the most common form of pediatric epilepsy. This syndrome is characterized by daily occurrences of frequent but brief episodes of staring spells. These episodes typically commence between the ages of 4 to 8 years and manifest in otherwise seemingly healthy children. On classic electroencephalograms (EEGs), distinct patterns emerge, featuring generalized spike-wave bursts occurring at a frequency of 3 Hz, accompanied by normal background brain activity. Despite sometimes being mistakenly perceived as a benign type of epilepsy, childhood absence epilepsy is associated with varying rates of remission. Children affected by this condition often experience cognitive deficits and encounter enduring psychosocial challenges in the long term. [5]

Epidemiology

The incidence of absence seizures in the United States is 1.9–8 cases per 100,000 population. 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. [6]

Absence seizures affect between 0.7 and 4.6 per 100,000 in the general population and 6 to 8 per 100,000 in children younger than 15 years. Childhood absence seizures account for 10% to 17% of all absence seizures. Onset is between 4 and 10 years and peaks at 5 to 7 years. It is more common in girls than in boys. [7]

Cause

An absence seizure is specifically caused by multifactorial inheritance. The voltage-gated T-type calcium channel is regulated by Gamma-aminobutyric acid receptor subunit gamma-2 (GABRG2), GABRG3, and CACNA1A2 genes. [1] Inheritance of these genes is involved in the etiology (cause) of absence seizure. [7] The commonly held belief is that the genetic factor is the primary cause of childhood absence epilepsy. Furthermore, patients with childhood absence epilepsy have also been reported to exhibit certain copy number variations (CNVs), such as 15q11.2, 15q13.3, and 16p13.11 microdeletions. [1] Almost 25% of children suffering from absence seizure has a relative that suffers from seizures. [8] Some specific anticonvulsant drugs such as phenytoin, carbamazepine, and vigabatrin have been identified to raise the chances of experiencing absence seizures. [9]

Signs and symptoms

The clinical manifestations of absence seizures vary significantly among patients. [10] [11] [12] 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 (postictal state), in contrast to the majority of seizure disorders. [3] If the patient has jerking gestures during the seizure this might be the indication of another type of seizure occurring onward with the absence seizure. [13]

  1. Absence with impairment of consciousness only as per the above description. [3]
  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. [14] [15] [16] The head may tonically draw to one or another side.[ citation needed ]
  5. Absence with automatisms. Purposeful or quasi-purposeful 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. [17]
  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. [3]

Risk factors

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 hyperventilate for three minutes, counting breaths. During hyperventilation, the oxygen and carbon dioxide level will become abnormal. This results in weakening of electrical signal which leads to a reduction in the seizure threshold. [18] 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 seizures. 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. [19]

Pathophysiology

The corticothalamic cortical circuit plays an important role in the pathophysiology of absence seizure. Some of the neurons are important in their occurrence. They are

Abnormal oscillatory rhythms develop in the thalamic nucleus reticularis. This causes inhibition of GABAergic neurotransmission and excitation of glutamate neurotransmission. Abnormal oscillatory spikes are produced by the low threshold T-type calcium channel. This explains how inheritance of gene code for T-type calcium channel leads to an absence seizure. Antiepileptic drugs such as Gabapentin, Tiagabine and Vigabatrin cause inhibition of GABA resulting in exacerbation of absence seizures. [20] [21]

Diagnosis

The primary diagnostic test for absence seizures is electroencephalography (EEG). [22] However, brain scans such as by an MRI can help rule out other diseases, such as a stroke or a brain tumor. [8]

During EEG, hyperventilation can be used to provoke these seizures. [22] Ambulatory EEG monitoring over 24 hours can quantify the number of seizures per day and their most likely times of occurrence. [22]

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. [23] Those most susceptible to this are children, and the first episode usually occurs between 4–14 years old. [24] In the case of JAE, the typical age at which it begins is traditionally within the range of 10 to 19 years, with the highest occurrence observed around the age of 15. Unlike CAE, seizures in JAE are not as frequent but tend to have a longer duration. [1] It is very rare that someone older will experience their first absence seizure. [24] 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. The majority of children experiencing typical absence seizures have an overall normal health condition. However, these absence seizures can disrupt the learning process and hinder concentration in a school environment. This underscores the crucial significance of treatment [13] There are no known before or after effects of absence seizures. [25]

Absence seizures have two essential components: [10] [11] [12]

Absence seizures are broadly divided into typical and atypical types:

Syndromes

Absence seizure 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.

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

Childhood Absence Epilepsy

Childhood absence epilepsy (CAE) is a type of idiopathic epilepsy characterized by its non-convulsive, generalized nature and a genetic origin influenced by multiple factors [26]

Epilepsy with Myoclonic Absences

Myoclonic Absence Epilepsy is an infrequent type of childhood epilepsy characterized by a high occurrence of intellectual impairments and resistance to treatment. [27]

Juvenile Absence Epilepsy

Juvenile Absence Epilepsy is considered an Idiopathic GED (Idiopathic Major Epilepsy) Syndrome and is officially categorized as Idiopathic Generalized Epilepsy by the ILAE. This condition typically begins in adolescents during the puberty stage and is distinguished by the occurrence of absence seizures and Generalized Tonic-Clonic Seizures. [28]

Juvenile Myoclonic Epilepsy

Juvenile Myoclonic Epilepsy (JME), also referred to as Janz Syndrome and Impulsive Petit Mal, is a form of epilepsy that is characterized by absence, Myoclonic, and Generalized Tonic-Clonic Seizures. This epilepsy variant is marked by its idiopathic and hereditary characteristics, as well as its generalization across seizures. The initial documentation of JME dates back to 1867 by Herpin, followed by Janz and Christian labeling it as 'Impulsive Petit Mal' in 1957, and Lund's 1975 designation of 'JME'. [29]

Jeavons Syndrome

Reflex Epilepsy (JS) is a form of epilepsy usually categorized within the spectrum of genetically linked Generalized Epilepsy (GGE). While EM (Epileptic Myoclonus) is commonly acknowledged as a type of seizure, the formal recognition of JS as a separate medical entity by the International League Against Epilepsy (ILAE) has not yet occurred. [30]

Treatment

Treatment of patients with absence seizures only is mainly with ethosuximide or valproic acid, which are of equal efficacy controlling absences in around 75% of patients. Lamotrigine monotherapy is less effective, controlling absences in around 50% of patients. This summary has been recently confirmed by Glauser et al. (2010), [5] 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.

Although ethosuximide is effective in treating only absence seizures, valproic acid is effective in treating multiple seizure types including tonic-clonic seizure and partial seizure, suggesting it is a better choice if a patient is exhibiting multiple types of seizures. [31] Similarly, lamotrigine treats multiple seizure types including partial seizures and generalized seizures, therefore it is also an option for patients with multiple seizure types. [32] 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. [33]

Roughly 70% of children experiencing absence seizures will see these seizures naturally cease before they reach the age of 18. In such instances, the need for medications might no longer be relevant in adulthood. It's worth noting that children who develop absence seizures prior to turning 9 are more inclined to outgrow them compared to those whose absence seizures commence after the age of 10. [34]

Prevention

Appropriate medication is the best way to manage absence seizures, but prevention can be considerably enhanced by life-style changes such as exercise, stress reduction, good sleep hygiene, and healthy diet. [35] In particular, a therapeutic ketogenic diet can be very beneficial. In a review of studies of childhood and juvenile patients, this diet reduced seizure episodes in most patients by more than half; of those with clear outcomes, a quarter to a third became seizure free. [36]

Medications that should not be used

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. [12] In particular, the GABA agonists vigabatrin and tiagabine are used to induce, not to treat, absence seizures and absence status epilepticus. [37] Similarly, oxcarbazepine, phenytoin, phenobarbital, gabapentin, and pregabalin should not be used in the treatment of absence seizures because these medications may worsen absence seizures. [32]

Data limitations

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. [38] 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 ] A 2019 Cochrane review found that ethosuximide was the best mono-therapy for children and adolescents but noted that if absence seizures co-exist with tonic-clonic seizures then valproate should be preferred. [39] [40]

Related Research Articles

<span class="mw-page-title-main">Epilepsy</span> Group of neurological disorders causing seizures

Epilepsy is a group of non-communicable neurological disorders characterized by recurrent epileptic seizures. An epileptic seizure is the clinical manifestation of an abnormal, excessive, and synchronized electrical discharge in the neurons. The occurrence of two or more unprovoked seizures defines epilepsy. The occurrence of just one seizure may warrant the definition in a more clinical usage where recurrence may be able to be prejudged. Epileptic seizures can vary from brief and nearly undetectable periods to long periods of vigorous shaking due to abnormal electrical activity in the brain. These episodes can result in physical injuries, either directly such as broken bones or through causing accidents. In epilepsy, seizures tend to recur and may have no detectable underlying cause. Isolated seizures that are provoked by a specific cause such as poisoning are not deemed to represent epilepsy. People with epilepsy may be treated differently in various areas of the world and experience varying degrees of social stigma due to the alarming nature of their symptoms.

<span class="mw-page-title-main">Valproate</span> Medication used for epilepsy, bipolar disorder and migraine

Valproate are medications primarily used to treat epilepsy and bipolar disorder and prevent migraine headaches. They are useful for the prevention of seizures in those with absence seizures, partial seizures, and generalized seizures. They can be given intravenously or by mouth, and the tablet forms exist in both long- and short-acting formulations.

<span class="mw-page-title-main">Lamotrigine</span> Medication used for bipolar disorder, epilepsy, & many seizure disorders

Lamotrigine, sold under the brand name Lamictal among others, is a medication used to treat epilepsy and stabilize mood in bipolar disorder. For epilepsy, this includes focal seizures, tonic-clonic seizures, and seizures in Lennox-Gastaut syndrome. In bipolar disorder, lamotrigine has not been shown to reliably treat acute depression for all groups except in the severely depressed; but for patients with bipolar disorder who are not currently symptomatic, it appears to reduce the risk of future episodes of depression.

<span class="mw-page-title-main">Myoclonus</span> Involuntary, irregular muscle twitch

Myoclonus is a brief, involuntary, irregular twitching of a muscle, a joint, or a group of muscles, different from clonus, which is rhythmic or regular. Myoclonus describes a medical sign and, generally, is not a diagnosis of a disease. It belongs to the hyperkinetic movement disorders, among tremor and chorea for example. These myoclonic twitches, jerks, or seizures are usually caused by sudden muscle contractions or brief lapses of contraction. The most common circumstance under which they occur is while falling asleep. Myoclonic jerks occur in healthy people and are experienced occasionally by everyone. However, when they appear with more persistence and become more widespread they can be a sign of various neurological disorders. Hiccups are a kind of myoclonic jerk specifically affecting the diaphragm. When a spasm is caused by another person it is known as a provoked spasm. Shuddering attacks in babies fall in this category.

<span class="mw-page-title-main">Lennox–Gastaut syndrome</span> Rare form of childhood-onset epilepsy

Lennox–Gastaut syndrome (LGS) is a complex, rare, and severe childhood-onset epilepsy syndrome. It is characterized by multiple and concurrent seizure types including tonic seizure, cognitive dysfunction, and slow spike waves on electroencephalogram (EEG), which are very abnormal. Typically, it presents in children aged 3–5 years and most of the time persists into adulthood with slight changes in the electroclinical phenotype. It has been associated with perinatal injuries, congenital infections, brain malformations, brain tumors, genetic disorders such as tuberous sclerosis and numerous gene mutations. Sometimes LGS is observed after infantile epileptic spasm syndrome. The prognosis for LGS is marked by a 5% mortality in childhood and persistent seizures into adulthood.

Reflex seizures are epileptic seizures that are consistently induced by a specific stimulus or trigger, making them distinct from other epileptic seizures, which are usually unprovoked. Reflex seizures are otherwise similar to unprovoked seizures and may be focal, generalized, myoclonic, or absence seizures. Epilepsy syndromes characterized by repeated reflex seizures are known as reflex epilepsies. Photosensitive seizures are often myoclonic, absence, or focal seizures in the occipital lobe, while musicogenic seizures are associated with focal seizures in the temporal lobe.

Myoclonic epilepsy refers to a family of epilepsies that present with myoclonus. When myoclonic jerks are occasionally associated with abnormal brain wave activity, it can be categorized as myoclonic seizure. If the abnormal brain wave activity is persistent and results from ongoing seizures, then a diagnosis of myoclonic epilepsy may be considered.

In the field of neurology, seizure types are categories of seizures defined by seizure behavior, symptoms, and diagnostic tests. The International League Against Epilepsy (ILAE) 2017 classification of seizures is the internationally recognized standard for identifying seizure types. The ILAE 2017 classification of seizures is a revision of the prior ILAE 1981 classification of seizures. Distinguishing between seizure types is important since different types of seizures may have different causes, outcomes, and treatments.

Dravet syndrome (DS), previously known as severe myoclonic epilepsy of infancy (SMEI), is an autosomal dominant genetic disorder which causes a catastrophic form of epilepsy, with prolonged seizures that are often triggered by hot temperatures or fever. It is very difficult to treat with anticonvulsant medications. It often begins before one year of age, with six months being the age that seizures, char­ac­ter­ized by prolonged convulsions and triggered by fever, usually begin.

Childhood absence epilepsy (CAE), formerly known as pyknolepsy, is an idiopathic generalized epilepsy which occurs in otherwise normal children. The age of onset is between 4–10 years with peak age between 5–7 years. Children have absence seizures which although brief, they occur frequently, sometimes in the hundreds per day. The absence seizures of CAE involve abrupt and severe impairment of consciousness. Mild automatisms are frequent, but major motor involvement early in the course excludes this diagnosis. The EEG demonstrates characteristic "typical 3Hz spike-wave" discharges. The presence of any other seizure type at time of diagnosis rules out the diagnose of CAE. Prognosis is usually good in well-defined cases of CAE with most patients "growing out" of their epilepsy.

Idiopathic generalized epilepsy (IGE) is a group of epileptic disorders that are believed to have a strong underlying genetic basis. IGE is considered a subgroup of Genetic Generalized Epilepsy (GGE). Patients with an IGE subtype are typically otherwise normal and have no structural brain abnormalities. People also often have a family history of epilepsy and seem to have a genetically predisposed risk of seizures. IGE tends to manifest itself between early childhood and adolescence although it can be eventually diagnosed later. The genetic cause of some IGE types is known, though inheritance does not always follow a simple monogenic mechanism.

Juvenile myoclonic epilepsy (JME), also known as Janz syndrome or impulsive petit mal, is a form of hereditary, idiopathic generalized epilepsy, representing 5–10% of all epilepsy cases. Typically it first presents between the ages of 12 and 18 with myoclonic seizures. These events typically occur after awakening from sleep, during the evening or when sleep-deprived. JME is also characterized by generalized tonic–clonic seizures, and a minority of patients have absence seizures. It was first described by Théodore Herpin in 1857. Understanding of the genetics of JME has been rapidly evolving since the 1990s, and over 20 chromosomal loci and multiple genes have been identified. Given the genetic and clinical heterogeneity of JME some authors have suggested that it should be thought of as a spectrum disorder.

<span class="mw-page-title-main">Generalized epilepsy</span> Epilepsy syndrome that is characterised by generalised seizures with no apparent cause

Generalized epilepsy is a form of epilepsy characterised by generalised seizures with no apparent cause. Generalized seizures, as opposed to focal seizures, are a type of seizure that impairs consciousness and distorts the electrical activity of the whole or a larger portion of the brain.

Progressive Myoclonic Epilepsies (PME) are a rare group of inherited neurodegenerative diseases characterized by myoclonus, resistance to treatment, and neurological deterioration. The cause of PME depends largely on the type of PME. Most PMEs are caused by autosomal dominant or recessive and mitochondrial mutations. The location of the mutation also affects the inheritance and treatment of PME. Diagnosing PME is difficult due to their genetic heterogeneity and the lack of a genetic mutation identified in some patients. The prognosis depends largely on the worsening symptoms and failure to respond to treatment. There is no current cure for PME and treatment focuses on managing myoclonus and seizures through antiepileptic medication (AED).

<span class="mw-page-title-main">Rolandic epilepsy</span> Most common epilepsy syndrome in childhood, usually subsiding with age

Benign Rolandic epilepsy or self-limited epilepsy with centrotemporal spikes is the most common epilepsy syndrome in childhood. Most children will outgrow the syndrome, hence the label benign. The seizures, sometimes referred to as sylvian seizures, start around the central sulcus of the brain.

Myoclonic astatic epilepsy (MAE), also known as myoclonic atonic epilepsy or Doose syndrome, and renamed "Epilepsy with myoclonic-atonic seizures" in the ILAE 2017 classification, is a generalized idiopathic epilepsy. It is characterized by the development of myoclonic seizures and/or myoclonic astatic seizures. Some of the common monogenic causes include mutations in the genes SLC6A1 (3p25.3),CHD2 (15q26.1), AP2M1 (10q23.2).

Jeavons syndrome is a type of epilepsy. It is one of the most distinctive reflex syndromes of idiopathic generalized epilepsy characterized by the triad of eyelid myoclonia with and without absences, eye-closure-induced seizures, EEG paroxysms, or both, and photosensitivity. Eyelid myoclonia with or without absences is a form of epileptic seizure manifesting with myoclonic jerks of the eyelids with or without a brief absence. These are mainly precipitated by closing of the eyes and lights. Eyelid myoclonia is the defining seizure type of Jeavons syndrome.

An epilepsy syndrome is defined as "a characteristic cluster of clinical and EEG features, often supported by specific etiological findings ."

SLC6A1 epileptic encephalopathy is a genetic disorder characterised by the loss-of-function of one copy of the human SLC6A1 gene. SLC6A1 epileptic encephalopathy can typically manifest itself with early onset seizures and it can also be characterised by mild to severe learning disability. Not all manifestations of the conditions are present in one given patient.

People with epilepsy can have safe, healthy pregnancies and healthy babies. However, proper planning and care is essential. The goal of planning is to minimize the risk of congenital malformations and neurodevelopmental disorders for the fetus while maintaining the parent's seizure control.

References

  1. 1 2 3 4 5 Albuja, A. C., & Khan, G. Q. (2022). Absence Seizure. In StatPearls. StatPearls Publishing.
  2. ↑ 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. S2CID   45169328.
  3. 1 2 3 4 "Absence Seizures". Epilepsy Foundation. Retrieved 2021-12-18.
  4. ↑ "Ethosuximide - an overview | ScienceDirect Topics". www.sciencedirect.com. Retrieved 2021-12-18.
  5. 1 2 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.
  6. ↑ Scott Segan. (2018). Absence Seizures. Medscape.https://reference.medscape.com/article/1183858-overview?form=fpf
  7. 1 2 Albuja, Ana C.; Khan, Gulam Qutubuddin (2021), "Absence Seizure", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   29763042 , retrieved 2021-12-20
  8. 1 2 Mayo Clinic > Absence seizure (petit mal seizure) June 23, 2011
  9. ↑ Posner E. (2013). Absence seizures in children. BMJ clinical evidence, 2013, 0317.
  10. 1 2 "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. S2CID   22190102.
  11. 1 2 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. S2CID   36248499.
  12. 1 2 3 Panayiotopoulos, C. P. (2010). A clinical guide to epileptic syndromes and their treatment (2nd ed.). London: Springer.[ page needed ]
  13. 1 2 "Absence Seizures". www.hopkinsmedicine.org. 22 August 2023. Retrieved 2023-08-22.
  14. ↑ 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.
  15. ↑ John S. Duncan (1996). Eyelid Myoclonia with Absences. John Libbey Eurotext. pp. 52–. ISBN   978-0-86196-550-2.
  16. ↑ Antonio V. Delgado-Escueta (2005). Myoclonic Epilepsies. Lippincott Williams & Wilkins. pp. 104–. ISBN   978-0-7817-5248-0.
  17. ↑ Myers, Kenneth (May 2018). "Myoclonic absence seizures with complex gestural automatisms". European Journal of Paediatric Neurology. 22 (3): 532–535. doi:10.1016/j.ejpn.2017.12.003. PMID   29325826.
  18. ↑ "Seizure Threshold Is Controlled by Breathing Pattern and Blood Gases". Epilepsy Foundation. Archived from the original on 2021-12-20. Retrieved 2021-12-20.
  19. ↑ Perucca, Gram, Avanzini, and Dulac, 1998, "Antiepileptic drugs as a cause of worsening seizures."
  20. ↑ "What is the pathophysiology of absence seizures?". www.medscape.com. Retrieved 2021-12-21.
  21. ↑ Albuja, Ana C.; Khan, Gulam Qutubuddin (2021), "Absence Seizure", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   29763042 , retrieved 2021-12-21
  22. 1 2 3 Absence Seizures at eMedicine
  23. ↑ Carlson, Neil R. (2013). Physiology of Behavior.
  24. 1 2 "Absence Seizures". www.hopkinsmedicine.org. 22 August 2023. Retrieved 2023-08-16.
  25. ↑ Epilepsy Therapy Project. "Absence Seizures". Epilepsy Foundation. Retrieved 8 May 2013.
  26. ↑ V. Crunelli, N. Leresche Childhood absence epilepsy: genes, channels, neurons and networks Nat Rev Neurosci, 3 (2002), pp. 371-382
  27. ↑ Manonmani V, Wallace SJ. Epilepsy with myoclonic absences. Arch Dise Child 1994; 70: 288–90.
  28. ↑ Yadala, S., & Nalleballe, K. (2023). Juvenile Absence Epilepsy. In StatPearls. StatPearls Publishing.
  29. ↑ Amrutkar, C., & Riel-Romero, R. M. (2023). Juvenile Myoclonic Epilepsy. In StatPearls. StatPearls Publishing.
  30. ↑ Nilo, Annacarmen; Crespel, Arielle; Genton, Pierre; Macorig, Greta; Gigli, Gian Luigi; Gelisse, Philippe (April 2021). "Epilepsy with eyelid myoclonias (Jeavons syndrome): An electro-clinical study of 40 patients from childhood to adulthood". Seizure. 87: 30–38. doi: 10.1016/j.seizure.2021.02.028 . PMID   33677402. S2CID   232060130.
  31. ↑ Kahan, Scott; Brillman, Jon (2005). In A Page Neurology. Hagerstwon, MD: Lippincott Williams & Wilkins. p. 47. ISBN   978-1-4051-0432-6.
  32. 1 2 "NICE Guidelines". 11 January 2012. Retrieved 3 November 2014.
  33. ↑ 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. S2CID   37633941.
  34. ↑ "Absence Seizures". Epilepsy Foundation. Retrieved 08-22-2023
  35. ↑ "Absence Seizures". www.hopkinsmedicine.org. 19 November 2019. Retrieved 2021-12-19.
  36. ↑ Groomes, Laura B.; Pyzik, Paula L.; Turner, Zahava; Dorward, Jennifer L.; Goode, Victoria H.; Kossoff, Eric H. (February 2011). "Do Patients With Absence Epilepsy Respond to Ketogenic Diets?". Journal of Child Neurology. 26 (2): 160–165. doi:10.1177/0883073810376443. PMID   20647578. S2CID   21958807.
  37. ↑ Knake, S; Hamer, H.M; Schomburg, U; Oertel, W.H; Rosenow, F (August 1999). "Tiagabine-induced absence status in idiopathic generalized epilepsy". Seizure. 8 (5): 314–317. doi: 10.1053/seiz.1999.0303 . PMID   10486298.
  38. ↑ 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 (4): CD003032. doi:10.1002/14651858.CD003032.pub2. PMID   16235312.
  39. ↑ Brigo, Francesco; Igwe, Stanley C.; Lattanzi, Simona (2021-01-21). "Ethosuximide, sodium valproate or lamotrigine for absence seizures in children and adolescents". The Cochrane Database of Systematic Reviews. 1 (1): CD003032. doi:10.1002/14651858.CD003032.pub5. ISSN   1469-493X. PMC   8095003 . PMID   33475151.
  40. ↑ 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.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.