Why is mesial temporal lobe epilepsy with Ammon's horn sclerosis becoming less common?

2014 ◽  
Vol 22 (1) ◽  
pp. e12-e12 ◽  
Author(s):  
T. A. Butler ◽  
P. Dugan ◽  
J. French
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Mesial Temporal Lobe Epilepsy ◽  
Ammon's Horn ◽  
Ammon's Horn Sclerosis ◽  
Ammon’S Horn ◽  
Mesial Temporal Lobe ◽  
Ammon’S Horn Sclerosis

Limbic P300s in temporal lobe epilepsy with and without Ammon's horn sclerosis

1999 ◽  
Vol 11 (6) ◽  
pp. 1899-1906 ◽  
Author(s):  
T. Grunwald ◽  
H. Beck ◽  
K Lehnertz ◽  
I. Blümcke ◽  
N. Pezer ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Ammon's Horn ◽  
Ammon's Horn Sclerosis ◽  
Ammon’S Horn ◽  
Ammon’S Horn Sclerosis

Mitochondrial dysfunction in neurodegenerative disorders

2007 ◽  
Vol 35 (5) ◽  
pp. 1228-1231 ◽  
Author(s):  
M. Baron ◽  
A.P. Kudin ◽  
W.S. Kunz
Keyword(s):  
Mitochondrial Dna ◽  
Temporal Lobe Epilepsy ◽  
Respiratory Chain ◽  
Temporal Lobe ◽  
Neurodegenerative Disorders ◽  
Mitochondrial Protein ◽  
Ammon's Horn ◽  
Ammon's Horn Sclerosis ◽  
Ammon’S Horn ◽  
Ammon’S Horn Sclerosis

There is compelling evidence for the direct involvement of mitochondria in certain neurodegenerative disorders, such as Morbus Parkinson, FRDA (Friedreich's ataxia), ALS (amyotrophic lateral sclerosis), and temporal lobe epilepsy with Ammon's horn sclerosis. This evidence includes the direct genetic evidence of pathogenic mutations in mitochondrial proteins in inherited Parkinsonism {such as PARK6, with mutations in the mitochondrial PINK1 [PTEN (phosphatase and tensin homologue deleted on chromosome 10)-induced kinase 1]} and in FRDA (with mutations in the mitochondrial protein frataxin). Moreover, there is functional evidence of impairment of the respiratory chain in sporadic forms of Parkinsonism, ALS, and temporal lobe epilepsy with Ammon's horn sclerosis. In the sporadic forms of the above-mentioned neurodegenerative disorders, increased oxidative stress appears to be the crucial initiating event that affects respiratory chain function and starts a vicious cycle finally leading to neuronal cell death. We suggest that the critical factor that determines the survival of neurons in neurodegenerative disorders is the degree of mitochondrial DNA damage and the maintenance of an appropriate mitochondrial DNA copy number. Evidence for a depletion of intact copies of the mitochondrial genome has been provided in all above-mentioned neurodegenerative disorders including ALS and temporal lobe epilepsy with Ammon's horn sclerosis. In the present study, we critically review the available data.

scholarly journals Increased leak conductance in dentate gyrus granule cells of temporal lobe epilepsy patients with Ammon’s horn sclerosis

Epilepsia ◽  
2009 ◽  
Vol 50 (4) ◽  
pp. 646-653 ◽  
Author(s):  
Michael Stegen ◽  
Christina C. Young ◽  
Carola A. Haas ◽  
Josef Zentner ◽  
Jakob Wolfart
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Dentate Gyrus ◽  
Temporal Lobe ◽  
Granule Cells ◽  
Ammon's Horn ◽  
Ammon's Horn Sclerosis ◽  
Ammon’S Horn ◽  
Ammon’S Horn Sclerosis
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