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:
- 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]
- Any alternation in a synaptic characteristics can prone a person to epilepsy. They include:
- Amount of neurotransmitters
- Function of inhibitory neurons
- Function of excitatory neurons
- synaptic structure
- Ion channels involved in neurotransmitter release and conduction of action potential.[6]
- The underlying pathophysiology of focal epilepsy is different than generalized epilepsy.
- Focal epilepsy:
- In these kind of seizures, epileptiform activity starts in a specific area of brain. It can further spread and cause secondary generalized seizure.
- Generalized epilepsy:
- These seizures occur in both cerebral hemispheres simultaneously or spread so fast from one to another that in EEG, we can see bilateral epileptiform activity from the start.[7]
- Focal epilepsy:
Genetics
- There are many genes involved in ion channels and neurotransmitter receptors. The isomorphism of these genes determine a person’s susceptibility for developing epilepsy after an offending injury.[8]
- 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.[9]
- there are some forms of Mendelian syndromes which are the result of mutation in SCN1A gene (Dravet syndrome) or GABR1 gene (autosomal dominant nocturnal frontal lobe epilepsy, juvenile myoclonic epilepsy).[8]
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.[10]
Microscopic Pathology
- On microscopic histopathological analysis:
- In the hippocampus of patients with temporal lobe epilepsy there is evidence of cell loss mainly in CA1 and CA4 sectors, CA1 neuron loss and gliosis and CA4 neuronal cell loss and gliosis.
- In dentate gyrus there is evidence of Substantial granule cell loss and Cell dispersion.[11]
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.
- ↑ Samuels, Martin (2017). Samuels's Manual of neurologic therapeutics. Philadelphia: Wolters Kluwer Health. ISBN 9781496360311.
- ↑ Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
- ↑ 8.0 8.1 Samuels, Martin (2017). Samuels's Manual of neurologic therapeutics. Philadelphia: Wolters Kluwer Health. ISBN 9781496360311.
- ↑ 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.
- ↑ Blümcke I, Thom M, Aronica E, Armstrong DD, Bartolomei F, Bernasconi A, Bernasconi N, Bien CG, Cendes F, Coras R, Cross JH, Jacques TS, Kahane P, Mathern GW, Miyata H, Moshé SL, Oz B, Özkara Ç, Perucca E, Sisodiya S, Wiebe S, Spreafico R (July 2013). "International consensus classification of hippocampal sclerosis in temporal lobe epilepsy: a Task Force report from the ILAE Commission on Diagnostic Methods". Epilepsia. 54 (7): 1315–29. doi:10.1111/epi.12220. PMID 23692496.