Epilepsy pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
===Physiology=== | ===Physiology=== | ||
The normal physiology of neuronal action potential can be understood as follows: | The normal physiology of neuronal action potential can be understood as follows:<ref>{{cite book | last = Pollard | first = Thomas | title = Cell biology | publisher = Elsevier | location = Philadelphia, PA | year = 2017 | isbn = 9780323341264 }}<ref> | ||
===Pathogenesis=== | ===Pathogenesis=== | ||
Revision as of 14:43, 4 December 2018
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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:
- The underlying event in all types of seizures is the paroxysmal depolarization shift (PDS) which also causes the EEG changes.[1]
- 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.[2]
- 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.[3]
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.[4]
Gross Pathology
On gross pathology, slight opacity and thickening of the meninges, signs of meningitis, vascular disturbances, ecchymoses on the surface of various organs and fatty changes in the heart and striated muscles are characteristic findings of epilepsy.[5]
Microscopic Pathology
On microscopic pathology, there are no characteristic findings present.
References
- ↑ 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.
- ↑ GOWERS, FirstName (2016). EPILEPSY AND OTHER CHRONIC CONVULSIVE DISEASES : their causes, symptoms, and treatment (classic... reprint. S.l: FORGOTTEN BOOKS. ISBN 1334720053.