Jump to content

Kindling model of epilepsy

Edit links
From Wikipedia, the free encyclopedia

This is an old revision of this page, as edited by Dcirovic (talk | contribs) at 02:45, 27 May 2016 (.). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.

Kindling is a commonly used model for the development of seizures and epilepsy in which the duration and behavioral involvement of induced seizures increases after seizures are induced repeatedly.[1] The kindling model was first proposed in the late 1960s by Goddard and colleagues.[2] Although kindling is a widely used model, its applicability to human epilepsy is controversial.[1]

Method

The word kindling is a metaphor: the increase in response to small stimuli is similar to the way small burning twigs can produce a large fire.[3] It is used by scientists to study the effects of repeated seizures on the brain.[1] A seizure may increase the likelihood that more seizures will occur; an old saying in epilepsy research is "seizures beget seizures".[1] Repeated stimulation "lowers the threshold" for more seizures to occur.[4]

The brains of experimental animals are repeatedly stimulated, usually with electricity, to induce the seizures.[1] Chemicals may also be used to induce seizures.[3] The seizure that occurs after the first such electrical stimulation lasts a short time and is accompanied by a small amount of behavioral effects compared with seizures that result from repeated stimulations.[1] With further seizures, the accompanying behavior intensifies, for example progressing from freezing in early stimulations to convulsions in later ones.[5] The lengthening of duration and intensification of behavioral accompaniment eventually reaches a plateau after repeated stimulation.[1] Even if animals are left unstimulated for as long as 12 weeks, the effect remains; the response to stimulation remains higher than it had been before.[3]

It has been reported that repeated seizure stimulation can result in spontaneous seizures, but studies have had conflicting findings on this question.[1] In humans, some seizure disorders come to an end by themselves even after large numbers of seizures.[1] However, in both human epilepsy and in some animal models, evidence suggests that a process like that found in kindling does occur.[1]

Historical perspective

Already in the 1950s and 1960s, numerous authors recognized the seizure-inducing potential of focal stimulation.[6] Here, Delgado and Sevillano demonstrated that repeated low-intensity stimuli to the hippocampus could lead to progressive increase of electrically evoked seizure activity.[7] Yet, it was not until the late 1960s that Graham Goddard recognized the potential importance of this phenomenon and coined the term 'kindling'.[8] Further research by Goddard on the characteristics of the kindling phenomenon led to his conclusion that kindling can be used to model human epileptogenesis, learning and memory.[9] The publication of these results opened a completely new niche for epilepsy research and has stimulated a significant amount of studies on the subject of kindling and its relevance to human epilepsy[6]

See also

References

  1. ^ a b c d e f g h i j Bertram E (2007). "The relevance of kindling for human epilepsy". Epilepsia. 48 (Supplement 2): 65–74. doi:10.1111/j.1528-1167.2007.01068.x. PMID 17571354.
  2. ^ Sato M (2008). "Kindling: An experimental model of epilepsy" (PDF). Psychiatry and Clinical Neurosciences. 36 (4): 440–441. doi:10.1111/j.1440-1819.1982.tb03123.x.
  3. ^ a b c Abel MS, McCandless DW (1992). "The kindling model of epilepsy". In Adams RN, Baker GB, Baker JM, Bateson AN, Boisvert DP, Boulton AA, et al. (eds.). Neuromethods: Animal Models of Neurological Disease. Totowa, NJ: Humana Press. pp. 153–155. ISBN 0-89603-211-6.
  4. ^ PK Sahoo; KI Mathai; GV Ramdas; MN Swamy (2007). "The pathophysiology of post traumatic epilepsy" (PDF). Indian Journal of Neurotrauma. 4 (1): 11–14. doi:10.1016/s0973-0508(07)80004-9. Temkin NR, Jarell AD, Anderson GD (2001). "Antiepileptogenic agents: how close are we?". Drugs. 61 (8): 1045–55. doi:10.2165/00003495-200161080-00002. PMID 11465868.
  5. ^ Morimoto K, Fahnestock M, Racine RJ (May 2004). "Kindling and status epilepticus models of epilepsy: Rewiring the brain". Prog. Neurobiol. 73 (1): 1–60. doi:10.1016/j.pneurobio.2004.03.009. PMID 15193778.
  6. ^ a b McNamara JO; Byrne MC; Dasheiff RM; JG Fitz (1980). "The Kindling Model of Epilepsy; a Review". Progress in Neurobiology. 15 (2): 139–59. doi:10.1016/0301-0082(80)90006-4. PMID 6109361.
  7. ^ Delgado JM, Sevillano M (1961). "Evolution of repeated hippocampal seizures in the cat". Electroenceph. clin. Neurophys. 13 (2): 722–733. doi:10.1016/0013-4694(61)90104-3.
  8. ^ Goddard GV (1967). "Development of epileptic seizures through brain stimulation at low intensity". Nature. 214: 1020–1. doi:10.1038/2141020a0. PMID 6055396.
  9. ^ Goddard GV, McIntyre DC, Leech CK (1969). "A permanent change in brain function resulting from daily electrical stimulation". Exp Neurol. 25 (3): 295–330. doi:10.1016/0014-4886(69)90128-9. PMID 4981856.
Retrieved from "https://en.wikipedia.org/w/index.php?title=Kindling_model_of_epilepsy&oldid=722283933"