Epilepsy pathophysiology: Difference between revisions
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* In order to cause a seizure, so many PDSs 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> | * In order to cause a seizure, so many PDSs 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> | ||
==Genetics== | ==Genetics== | ||
[[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> | * [[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> | ||
==Gross Pathology== | ==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 muscle|striated muscles]] can be seen in epilepsy.<ref>{{cite book | last = GOWERS | first = FirstName | title = EPILEPSY AND OTHER CHRONIC CONVULSIVE DISEASES : their causes, symptoms, and treatment (classic... reprint | publisher = FORGOTTEN BOOKS | location = S.l | year = 2016 | isbn = 1334720053 }}</ref> | |||
==Microscopic Pathology== | ==Microscopic Pathology== | ||
* On microscopic pathology, there are no characteristic findings present. | |||
On microscopic pathology, there are no characteristic findings present. | |||
==References== | ==References== | ||
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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:
- When an action potential reaches the plasma membrane of a neuron cell, voltage gated Na+ channels will open and Na+ flows into the cell and makes it depolarized. When plasma membrane potential reaches a specific level, K+ channel opening will hyperpolarize the neuronal membrane.[1]
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Pathogenesis
- It is understood that epileptic seizure is the result of uncontrolled unusual synchronized, localized or widely distributed neuronal electrical discharges.[2]
- The underlying event in all types of seizures is the paroxysmal depolarization shift (PDS) which also causes the EEG changes.[3]
- 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.[4]
- 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.[5]
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.[6]
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 can be seen in epilepsy.[7]
Microscopic Pathology
- On microscopic pathology, there are no characteristic findings present.
References
- ↑ Pollard, Thomas (2017). Cell biology. Philadelphia, PA: Elsevier. ISBN 9780323341264.
- ↑ 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.
- ↑ GOWERS, FirstName (2016). EPILEPSY AND OTHER CHRONIC CONVULSIVE DISEASES : their causes, symptoms, and treatment (classic... reprint. S.l: FORGOTTEN BOOKS. ISBN 1334720053.