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Absence seizure
ICD-10 G403
ICD-9 345.0
OMIM [1]
DiseasesDB 32994
MedlinePlus 000696
eMedicine neuro/3
MeSH {{{MeshNumber}}}

Petit mal seizures (from the French for "little illness", a term dating from the late 1700s [1])are one of several kinds of seizures. These seizures are sometimes referred to as Absence seizures In absence seizures, the person may appear to be staring into space with or without jerking or twitching movements of the eye muscles. These periods last for seconds, or even tens of seconds. Those experiencing absence seizures sometimes move from one location to another without any purpose. Under normal circumstances thalamocortical oscillations maintain normal consciousness of an individual, however in certain circumstances the normal pattern can become disrupted; thereby leading to an episode of absence. Drugs, such as ethosuximide work by binding to t-type Ca2+ channels on thalamic neurones to modify these oscillations and prevent these episodes from occurring.

Types[edit | edit source]

Absence seizures may occur in several forms of epilepsy. Absence epilepsy refers to epilepsy in which the only seizures are absence seizures. Absence epilepsy is often characterized by age of onset, e.g., childhood absence epilepsy for epilepsy beginning in childhood between the ages of 4 and 12. Absence epilepsy has also been termed pyknolepsy (from the Greek "pyknos", meaning closely packed, dense, or aggregated) and was commonly used in early 20th century German psychiatry[2]

Epilepsy is the most common cause of recurrent seizures, where seizures are single events that reoccur with seemingly random frequency. Single seizures can be caused by blows to the head, fever (febrile seizure), reactions to medications, tumours, or as a symptom of a larger disease, among other causes.

Just as there are many different kinds of seizures, there are many different kinds of epilepsy. Doctors have identified hundreds of different epilepsy syndromes - disorders characterized by a specific set of symptoms that include epilepsy. Some of these syndromes appear to be hereditary. For other syndromes, the cause is unknown. Epilepsy syndromes are frequently described by their symptoms or by where in the brain they originate. People should discuss the implications of their type of epilepsy with their doctors to understand the full range of symptoms, the possible treatments, and the prognosis.

Presentation[edit | edit source]

Some people with absence epilepsy report seeing flashing or blinking lights in the corner of one or both eyes, possibly followed by a 'flash vision change', shortly before they slip into a seizure [How to reference and link to summary or text]. Some have purposeless movements during their seizures, such as a jerking arm or rapidly blinking eyes[3]. Others have no outwardly noticeable symptoms except for brief times when they are "spaced out", as repeated absence seizures can cause momentary lapses of consciousness. Immediately after a seizure, the person will usually resume whatever he or she was doing prior to its onset.

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 other situations requiring sustained, concentrated attention. Childhood absence epilepsy may stop when the child reaches puberty. Absence seizures usually have no lasting effect on intelligence or other brain function. [How to reference and link to summary or text]

It is well known that bright lights, nervous, stressful, uncomfortable situations, or other strong sensory stimuli may trigger seizures.[How to reference and link to summary or text] Hyperventilation is also a common trigger. However, loud noises can help to either bring a person back to consciousness or keep him or her conscious.[How to reference and link to summary or text] Reciting one's name can be very helpful in an emergency as can repetitively asking the victim to "stay with you".[How to reference and link to summary or text] Such can be accomplished by counting methods, alphabets and so on.[4]

A person having an absence seizure shows no emotional expressions during the absent period.[How to reference and link to summary or text] While the ability to express emotion in the face may be dissociated from the experience of emotion, the lack of any emotionally charged facial expression may indicate that a certain level of consciousness and arousal are needed to experience emotions.

A bilateral synchronous, symmetrical 3-Hz spike-and-wave discharge EEG pattern accompanies absence seizures.[5]

Treatment[edit | edit source]

The primary goal of treatment of recurrent absence seizures is to prevent accidental injuries that may occur through the lapses of consciousness that accompany seizures. For those with frequent seizures treatment seeks to prevent the seizures from interfering with learning or other activities of daily life.

The purpose of medication for treatment of absence seizures is to accomplish the goals above, by eliminating or reducing the frequency of the absence seizures, without causing side-effects more serious than the epilepsy itself.

Certain anticonvulsant drugs are used to minimize the number of seizures episodes. Absence seizures appear to respond well to divalproex sodium (trade name: Depakote), ethosuximide (trade name: Zarontin), and lamotrigine (Lamictal). Each of these medications has potential side effects, some of them possibly serious, which makes it important that the patient and/or their caregivers understand the specific medication they have been prescribed.

For treatment of absence seizures there is insufficient evidence to know if any of the available medications is best. i.e., which has the best combination of safety and efficacy for a particular patient.[6] Nor is it known how long medication must be continued before an off-medication trial should be conducted to determine if the individual has outgrown the absence seizures, as is often the case with 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.[How to reference and link to summary or text]

The U.S. government is currently sponsoring such a study.[7] The purpose of this study is to determine the best initial treatment for childhood absence epilepsy from among valproic acid, ethosuximide and lamotrigine. In addition, the researchers hope to develop methods that may be used in the future to help choose the best medicine for each child diagnosed with absence seizures. The 5-year study began in 2004, and is expected to involve more than 400 children.

Also included in the study will be pharmacokinetics and pharmacogenetics research. Pharmacokinetics is the study of how the body absorbs, distributes, metabolizes, and excretes drugs. Pharmacogenetics is the study of genetic determinants of the response to drugs. Knowledge gained from this study may lead to individualized treatment for children with absence seizures.

See also[edit | edit source]

References[edit | edit source]

  1. Daly, D. D. (1968). Reflections on the Concept of Petit Mai. Epilepsia 9 (3): 175-178.
  2. Sauer, H.. Uber gehaufte kleine Anfalle by Kindern (pyknolepsie). Mschr Psychiatr Neurol 40: 276-300.
  3. Symptoms of Petit mal seizures
  4. Epilepsy.
  5. (1941) Electroencephalographic classification of the epilepsies. Arch Neurol Psychiatry 45.
  6. Ethosuximide, sodium valproate or lamotrigine for absence seizures in children and adolescents.
  7. Childhood Absence Epilepsy Rx PK-PD-Pharmacogenetics Study - Full Text View -

2. Patten, John [1996]. "22" Neurological Differential Diagnosis., 2 Rev Ed, 380-1, London: Springer-Verlag London Limited.

Further reading[edit | edit source]

Books[edit | edit source]

  • Ramaratnam, S., & Marson, A. (2007). Epilepsy. Malden, MA: Blackwell Publishing.

Papers[edit | edit source]

  • Abad Alegria, F., Miravete Fuertes, P., & Gonzalez Matilla, P. (1984). Malignant, repeated transient unconsciousness in petit mal attacks of epilepsy: Comunicacion Psiquiatrica Vol 12 1984-1985, 75-86.
  • Abramovich, G. B., & Tets, I. S. (1967). On Several Debatable Questions of Petit Mal in Children: Zhurnal Nevropatologii i Psikhiatrii 67(10) 1967, 1535-1539.
  • Ahmed, R., & Varghese, T. (2006). Unusual presentation of absence seizures: A case report: Journal of Pediatric Neurology Vol 4(1) 2006, 45-47.
  • Amit, R., Amit, Y., & Amit, D. J. (2006). Blockage of eye-closure-generated generalized paroxysms by mental activity: Journal of Pediatric Neurology Vol 4(1) 2006, 53-56.
  • Arushanian, E. B., & Avakian, R. M. (1978). Metrazol-induced petit mal: The role played by monoaminergic mechanisms and striatum: Pharmacology, Biochemistry and Behavior Vol 8(2) Feb 1978, 113-117.
  • Assael, M. I. (1972). Petit mal status without impairment of consciousness: Diseases of the Nervous System Vol 33(8) Aug 1972, 526-528.
  • Beck, U., Wenzel, D., & Sauer, M. (1977). Selective deprivation of sleep in pycnoleptic children: Effects of deprivation of slow-wave sleep and REM sleep on the frequency and duration of petit mal attacks: Archiv fur Psychiatrie und Nervenkrankheiten Vol 223(2) 1977, 107-115.
  • Browne, T. R., & et al. (1975). Ethosuximide in the treatment of absence (petit mal) seizures: Neurology Vol 25(6) Jun 1975, 515-524.
  • Charlton, M. H., & Yahr, M. D. (1967). Long-Term Follow-up of Patients with Petit Mal: Archives of Neurology 16(6) 1967, 595-598.
  • Cleeland, C. S., & Booker, H. E. (1967). Petit Mal Evoked by Arousal During Sensory Restriction: Archives of Neurology 17(3) 1967, 324-330.
  • Conte, A., Gilio, F., Iacovelli, E., Bettolo, C. M., Di Bonaventura, C., Frasca, V., et al. (2007). Effects of repetitive transcranial magnetic stimulation on spike-and-wave discharges: Neuroscience Research Vol 57(1) Jan 2007, 140-142.
  • Dondey, M. (1983). Transverse topographical analysis of petit mal discharges: Diagnostical and pathogenic implications: Electroencephalography & Clinical Neurophysiology Vol 55(4) Apr 1983, 361-371.
  • Drury, I., & Dreifuss, F. E. (1985). Pyknoleptic petit mal: Acta Neurologica Scandinavica Vol 72(4) Oct 1985, 353-362.
  • Dubikaitis, V. V. (1970). Dynamics of the cerebral potential field in normals and epileptics with petit mal type of attacks: Zhurnal Nevropatologii i Psikhiatrii Vol 70(8) Aug 1970, 1167-1171.
  • Dubikaitis, V. V. (1971). The mechanism and possible physiological significance of reconstruction of the fields of potentials in the brain of epileptic patients during a petit mal attack: Zhurnal Nevropatologii i Psikhiatrii Vol 71(3) 1971, 371-378.
  • Faber, J., Dusek, J., Tosovsky, J., & Taichmanova, Z. (1977). EEG periodogram during waking, synchronized sleep and petit mal attack: Activitas Nervosa Superior Vol 19(3) 1977, 210.
  • Faber, J., Tosovsky, J., Mestan, J., & Tuhacek, M. (1972). Statistical and mathematical analysis of clinical and sub-clinical paroxysms petit mal: Activitas Nervosa Superior Vol 14(1) 1972, 61-63.
  • Faber, J., Tosovsky, J., Taichmanova, Z., & Taberyova, M. (1974). EEG and vigilance during the petit mal attack: Activitas Nervosa Superior Vol 16(2) May 1974, 134-140.
  • Fox, H. A., Kantor, S., Dell'Aria, S., Campbell, R. J., & et al. (1988). Petit mal-grand mal ECT: A method to induce seizures without barbiturate anesthesia: Convulsive Therapy Vol 4(3) 1988, 243-247.
  • Gruneberg, F., & Helmchen, H. (1969). Impulsive petit-mal state and paranoid psychosis: Nervenarzt Vol 40(8) Aug 1969, 381-385.
  • Hasan, M., Lerman-Sagie, T., Lev, D., & Watemberg, N. (2006). Recurrent absence status epilepticus (spike-and-wave stupor) associated with lamotrigine therapy: Journal of Child Neurology Vol 21(9) Sep 2006, 807-809.
  • Herman, K. R. (1977). Petit mal status: Clinical and electrographic features: American Journal of EEG Technology Vol 17(4) Dec 1977, 177-185.
  • King, A. G. (1980). A pharmacological investigation of an animal model of the petit mal seizure: Dissertation Abstracts International.
  • King, G. A., & Burnham, W. M. (1980). Effects of d-amphetamine and apomorphine in a new animal model of petit mal epilepsy: Psychopharmacology Vol 69(3) Aug 1980, 281-285.
  • Labate, A., Briellmann, R. S., Abbott, D. F., Waites, A. B., & Jackson, G. D. (2005). Typical childhood absence seizures are associated with thalamic activation: Epileptic Disorders Vol 7(4) Dec 2005, 373-377.
  • Lange, H. U., & Rabe, F. (1978). Problems of symptomatic pyknoleptic and impulsive petit mal epilepsy: A discussion of epilepsy classification: Nervenarzt Vol 49(1) Jan 1978, 41-46.
  • Lipman, I. J., Isaacs, E. R., & Suter, C. G. (1971). Petit mal status: A variety of non-convulsive status epilepticus: Diseases of the Nervous System Vol 32(5) May 1971, 342-345.
  • Luborsky, L., & et al. (1975). A context analysis of psychological states prior to petit mal EEG paroxysms: Journal of Nervous and Mental Disease Vol 160(4) Apr 1975, 282-298.
  • Moore, D. P. (1981). A case of petit mal epilepsy aggravated by lithium: American Journal of Psychiatry Vol 138(5) May 1981, 690-691.
  • Novak, J., Corke, P., & Fairley, N. (1971). "Petit mal status" in adults: Diseases of the Nervous System Vol 32(4) Apr 1971, 245-248.
  • Orren, M. M., & Mirsky, A. F. (1975). Relation between ocular manifestations and onset of spike-and-wave discharges in petit mal epilepsy: Epilepsia Vol 16(5) Dec 1975, 771-779.
  • Penry, J. K., & Dreifuss, F. E. (1969). Automatisms associated with the absence of petit mal epilepsy: Archives of Neurology 21(2) 1969, 142-149.
  • Polack, P.-O., Guillemain, I., Hu, E., Deransart, C., Depaulis, A., & Charpier, S. (2007). Deep layer somatosensory cortical neurons initiate spike-and-wave discharges in a genetic model of absence seizures: Journal of Neuroscience Vol 27(24) Jun 2007, 6590-6599.
  • Pontius, A. A. (1990). Infanticide in Limbic (?) Psychotic Trigger Reaction in a man with Jacksonian and petit mal (?) seizures: "Kindling" by traumatic experiences: Psychological Reports Vol 67(3, Pt 1) Dec 1990, 935-945.
  • Repolt, J., Deibold, M., & Binnert, D. (1967). Appearance of Petit Mal after a Traumatism: Annales Medico-Psychologiques 1(1) 1967, 134.
  • Samardzhiev, A. K., & Sirakov, A. A. (1967). A Clinico-Electroencephalographic Study of the Action of Zarontine in Attacks of Petit Mal in Children: Zhurnal Nevropatologii i Psikhiatrii 67(10) 1967, 1544-1548.
  • Shearer, D. E., Fleming, D. E., & Bigler, E. D. (1976). The photically evoked afterdischarge: A model for the study of drugs useful in the treatment of petit mal epilepsy: Epilepsia Vol 17(4) Dec 1976, 429-435.
  • Shev, E. E. (1967). Western Electroencephalography Society: EEG in adult petit mal with special reference to status epilepticus: Electroencephalography & Clinical Neurophysiology 22(3) 1967, 294-295.
  • Stegemann, H., & Wendland, K. L. (1972). Alternating psychotic episodes in impulsive petit mal: Psychiatrie, Neurologie und Medizinische Psychologie Vol 24(11) Nov 1972, 646-656.
  • Stevens, J. R. (1970). Focal abnormality in petit mal epilepsy: Neurology Vol 20(11) Nov 1970, 1069-1076.
  • Stevens, J. R. (1977). New Concepts in Petit Mal Epilepsy: PsycCRITIQUES Vol 22 (12), Dec, 1977.
  • Tansey, M. A. (1985). The response of a case of petit mal epilepsy to EEG sensorimotor rhythm biofeedback training: International Journal of Psychophysiology Vol 3(2) Nov 1985, 81-84.
  • Terzano, M. G., Gemignani, F., & Mancia, D. (1978). Petit mal status with myoclonus: Case report: Epilepsia Vol 19(4) Aug 1978, 385-392.
  • Tovia, E., Goldberg-Stern, H., Shahar, E., & Kramer, U. (2006). Outcome of children with Juvenile Absence Epilepsy: Journal of Child Neurology Vol 21(9) Sep 2006, 766-768.
  • Van Luijtelaar, G., & Sitnikova, E. (2006). Global and focal aspects of absence epilepsy: The contribution of genetic models: Neuroscience & Biobehavioral Reviews Vol 30(7) 2006, 983-1003.
  • Warter, J.-M., Tranchant, C., Marescaux, C., Depaulis, A., & et al. (1990). Immediate effects of 14 non-MAOI antidepressants in rats with spontaneous petit mal-like seizures: Progress in Neuro-Psychopharmacology & Biological Psychiatry Vol 14(2) 1990, 261-270.
  • Weissberg, M. P. (1975). A case of petit-mal status: A diagnostic dilemma: American Journal of Psychiatry Vol 132(11) Nov 1975, 1

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