Epilepsy pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.
Overview
Pathophysiology
Physiology
The normal physiology of neuronal action potential can be understood as follows:
Pathogenesis
- It is understood that epileptic seizure is the result of uncontrolled unusual synchronized, localized or widely distributed neuronal electrical discharges.[1]
- The underlying event in all types of seizures is the paroxysmal depolarization shift (PDS) which also causes the EEG changes.[2]
- In a normal circumstance we have a refractory period after every action potential, but in PDS, the absence of refractory period causes a prolonged membrane depolarization.[3]
- The likelihood of PDS happening depends on so many factors such as intrinsic neuronal characteristic (channelopathies) and extrinsic characteristics (excess excitatory or inadequate inhibitory neurotransmitters).
- In order to cause a seizure, so many PDSs most happen in the same time.[4]
Genetics
Mutations in several genes have been linked to some types of epilepsy. Several genes that code for protein subunits of voltage-gated and ligand-gated ion channels have been associated with forms of generalized epilepsy and infantile seizure syndromes.[5]
Associated Conditions
Gross Pathology
Microscopic Pathology
References
- ↑ Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, Engel J (April 2005). "Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE)". Epilepsia. 46 (4): 470–2. doi:10.1111/j.0013-9580.2005.66104.x. PMID 15816939.
- ↑ MATSUMOTO H, AJMONEMARSAN C (April 1964). "CELLULAR MECHANISMS IN EXPERIMENTAL EPILEPTIC SEIZURES". Science. 144 (3615): 193–4. PMID 14107481.
- ↑ Bragin A, Engel J, Wilson CL, Fried I, Mathern GW (February 1999). "Hippocampal and entorhinal cortex high-frequency oscillations (100--500 Hz) in human epileptic brain and in kainic acid--treated rats with chronic seizures". Epilepsia. 40 (2): 127–37. PMID 9952257.
- ↑ Chang BS, Lowenstein DH (September 2003). "Epilepsy". N. Engl. J. Med. 349 (13): 1257–66. doi:10.1056/NEJMra022308. PMID 14507951.
- ↑ Miriam H. Meisler and Jennifer A. Kearney (2005). "Sodium channel mutations in epilepsy and other neurological disorders". Journal of Clinical Investigation. 115 (8): 2010–2017. PMID 16075041 doi:10.1172/JCI25466.