Epileptogenesis
Epileptogenesis is the gradual process by which a typical
Causes
The causes of epilepsy are broadly classified as genetic, structural/metabolic, or unknown.[4] Anything that causes epilepsy causes epileptogenesis, because epileptogenesis is the process of developing epilepsy. Structural causes of epilepsy include neurodegenerative diseases, traumatic brain injury, stroke, brain tumor, infections of the central nervous system, and status epilepticus (a prolonged seizure or a series of seizures occurring in quick succession).[5]
Latent period
After a brain injury occurs, there is frequently a "silent" or "latent period" lasting months or years in which seizures do not occur;[6] Canadian neurosurgeon Wilder Penfield called this time between injury and seizure "a silent period of strange ripening".[7] During this latent period, changes in the physiology of the brain result in the development of epilepsy.[6] This process, during which hyperexcitable neural networks form, is referred to as epileptogenesis.[6] If researchers come to better understand epileptogenesis, the latent period may allow healthcare providers to interfere with the development of epilepsy or to reduce its severity.[6]
Pathophysiology
Changes that occur during epileptogenesis are poorly understood but are thought to include cell death, axonal sprouting, reorganization of neural networks, alterations in the release of neurotransmitters, and neurogenesis.[5] These changes cause neurons to become hyperexcitable and can lead to spontaneous seizures.[5]
Brain regions that are highly sensitive to insults and can cause epileptogenesis include temporal lobe structures such as the hippocampus, the amygdala, and the piriform cortex.[6]
Neural reorganization
In addition to chemical processes, the physical structure of neurons in the brain may be altered. In
Hyperexcitability, a characteristic feature of epileptogenesis in which the likelihood that
Another proposed mechanism for epileptogenesis in TBI is that damage to white matter causes hyperexcitability by effectively undercutting the cerebral cortex.[8]
Glutamate receptor activation
It is believed that activation of
Excessive release of the neurotransmitter
Blood brain barrier disruption
Treatment
A major goal of epilepsy research is the identification of therapies to interrupt or reverse epileptogenesis. Studies largely in animal models have suggested a wide variety of possible antiepileptogenic strategies although, to date, no such therapy has been demonstrated to be antiepileptogenic in clinical trials.
History
Throughout most of history for which written records exist on the subject, it was probably generally believed that epilepsy came about through a supernatural process.[22] Even within the medical profession, it was not until the 18th century that ideas of epileptogenesis as a supernatural phenomenon were abandoned.[22] However, biological explanations have also long existed, and sometimes explanations contained both biological and supernatural elements.[22]
Research
Epileptogenesis that occurs in human brains has been modeled in a variety of
See also
- Kindling model
- Post-traumatic epilepsy
- Post-traumatic seizure
References
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McNamara JO, Huang YZ, Leonard AS (October 2006). "Molecular signaling mechanisms underlying epileptogenesis". Sci. STKE. 2006 (356): re12. S2CID 42882078.
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Armijo JA, Valdizán EM, De Las Cuevas I, Cuadrado A (2002). "Advances in the physiopathology of epileptogenesis: Molecular aspects". Rev Neurol (in Spanish). 34 (5): 409–29. PMID 12040510.
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Aroniadou-Anderjaska V, Fritsch B, Qashu F, Braga MF (February 2008). "Pathology and pathophysiology of the amygdala in epileptogenesis and epilepsy". Epilepsy Res. 78 (2–3): 102–16. PMID 18226499.
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"Post-traumatic epilepsy". Br Med J. 2 (6132): 229. 1978. PMID 98198.
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Firlik KS, Spencer DD (2004). "Surgery of post-traumatic epilepsy". In Dodson WE, Avanzini G, Shorvon SD, Fish DR, Perucca E (eds.). The Treatment of Epilepsy. Oxford: Blackwell Science. p. 775. ISBN 0-632-06046-8. Retrieved 2008-06-09.
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Beghi E (2004). "Aetiology of epilepsy". In Dodson WE, Avanzini G, Shorvon SD, Fish DR, Perucca E (eds.). The Treatment of Epilepsy. Oxford: Blackwell Science. p. 61. ISBN 0-632-06046-8. Retrieved 2008-06-09.
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Eadie MJ, Bladin PF (2001). "The interpretation of the epileptic process". A Disease Once Sacred: A History of the Medical Understanding of Epilepsy. London: John Libbey. p. 80. ISBN 0-86196-607-4. Retrieved 2008-06-12.
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Leśkiewicz M, Lasoń W (2007). "The neurochemical mechanisms of temporal lobe epilepsy: an update". Prz. Lek. (in Polish). 64 (11): 960–4. PMID 18409413.