Epilepsy pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
* It is understood that epileptic seizure is the result of uncontrolled unusual synchronized, localized or widely distributed neuronal electrical discharges.<ref name="pmid15816939">{{cite journal |vauthors=Fisher RS, van Emde Boas W, Blume W, Elger C, Genton P, Lee P, Engel J |title=Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE) |journal=Epilepsia |volume=46 |issue=4 |pages=470–2 |date=April 2005 |pmid=15816939 |doi=10.1111/j.0013-9580.2005.66104.x |url=}}</ref> | |||
* The underlying event in all types of seizures is the paroxysmal depolarization shift (PDS) which also causes the EEG changes.<ref name="pmid14107481">{{cite journal |vauthors=MATSUMOTO H, AJMONEMARSAN C |title=CELLULAR MECHANISMS IN EXPERIMENTAL EPILEPTIC SEIZURES |journal=Science |volume=144 |issue=3615 |pages=193–4 |date=April 1964 |pmid=14107481 |doi= |url=}}</ref> | |||
* 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.<ref name="pmid9952257">{{cite journal |vauthors=Bragin A, Engel J, Wilson CL, Fried I, Mathern GW |title=Hippocampal and entorhinal cortex high-frequency oscillations (100--500 Hz) in human epileptic brain and in kainic acid--treated rats with chronic seizures |journal=Epilepsia |volume=40 |issue=2 |pages=127–37 |date=February 1999 |pmid=9952257 |doi= |url=}}</ref> | |||
*It is understood that | * 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 PDS s most happen in the same time.<ref name="pmid14507951">{{cite journal |vauthors=Chang BS, Lowenstein DH |title=Epilepsy |journal=N. Engl. J. Med. |volume=349 |issue=13 |pages=1257–66 |date=September 2003 |pmid=14507951 |doi=10.1056/NEJMra022308 |url=}}</ref> | |||
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*The | |||
[[Mutation]]s in several [[gene]]s have been linked to some types of epilepsy. Several genes that code for [[protein]] subunits of [[voltage-gated ion channel|voltage-gated]] and [[ligand-gated ion channel|ligand-gated]] [[ion channel]]s have been associated with forms of generalized epilepsy and infantile seizure syndromes.<ref name="JClinInvestigation2005-Miriam">{{cite journal | author=Miriam H. Meisler and Jennifer A. Kearney | title=Sodium channel mutations in epilepsy and other neurological disorders | journal=Journal of Clinical Investigation | volume=115 | issue=8 | year=2005 | pages=2010–2017 | id=PMID 16075041 {{Doi|10.1172/JCI25466}}}}</ref> Several ligand-gated ion channels have been linked to some types of frontal and generalized epilepsies. Epilepsy-related mutations in some non-ion channel genes have also been identified. | [[Mutation]]s in several [[gene]]s have been linked to some types of epilepsy. Several genes that code for [[protein]] subunits of [[voltage-gated ion channel|voltage-gated]] and [[ligand-gated ion channel|ligand-gated]] [[ion channel]]s have been associated with forms of generalized epilepsy and infantile seizure syndromes.<ref name="JClinInvestigation2005-Miriam">{{cite journal | author=Miriam H. Meisler and Jennifer A. Kearney | title=Sodium channel mutations in epilepsy and other neurological disorders | journal=Journal of Clinical Investigation | volume=115 | issue=8 | year=2005 | pages=2010–2017 | id=PMID 16075041 {{Doi|10.1172/JCI25466}}}}</ref> Several ligand-gated ion channels have been linked to some types of frontal and generalized epilepsies. Epilepsy-related mutations in some non-ion channel genes have also been identified. | ||
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==Microscopic Pathology== | ==Microscopic Pathology== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]
Overview
Pathophysiology
Physiology
The normal physiology of [name of process] 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 PDS s most happen in the same time.[4]
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] Several ligand-gated ion channels have been linked to some types of frontal and generalized epilepsies. Epilepsy-related mutations in some non-ion channel genes have also been identified.
One interesting finding in animals is that repeated low-level electrical stimulation to some brain sites can lead to permanent increases in seizure susceptibility: in other words, a permanent decrease in seizure "threshold." This phenomenon, known as kindling (by analogy with the use of burning twigs to start a larger fire) was discovered by Dr. Graham Goddard in 1967. Chemical stimulation can also induce seizures; repeated exposures to some pesticides have been shown to induce seizures in both humans and animals. One mechanism proposed for this is called excitotoxicity. The roles of kindling and excitotoxicity, if any, in human epilepsy are currently hotly debated.
Other causes of epilepsy are brain lesions, where there is scar tissue or another abnormal mass of tissue in an area of the brain.
Genetics
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.