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home:diseases:epilepsy [09.22.2018] – [s70] sallieqhome:diseases:epilepsy [09.14.2022] (current) – external edit 127.0.0.1
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 ===== Evidence of infectious cause ===== ===== Evidence of infectious cause =====
  
-  * **An association between epileptic seizures and increased serum bacterial antibody levels -** (({{pubmed>long:6617588}})) +  * **An association between epileptic seizures and increased serum bacterial antibody levels -** (({{pmid>long:6617588}})) 
-  * Innate immune reaction in response to seizures(({{pubmed>long:15193289}})) +  * Innate immune reaction in response to seizures(({{pmid>long:15193289}})) 
-  * Virological and immunological aspects of seizure disorders (({{pubmed>long:12536027}})) +  * Virological and immunological aspects of seizure disorders (({{pmid>long:12536027}})) 
-  * Viruses and the immune system (({{pubmed>long:18205751}})) +  * Viruses and the immune system (({{pmid>long:18205751}})) 
-  * Role of viral infections in the etiology of febrile seizures. (({{pubmed>long:16939854}}))+  * Role of viral infections in the etiology of febrile seizures. (({{pmid>long:16939854}}))
 ===== in the brain's electrical activity ===== ===== in the brain's electrical activity =====
  
-In the majority of  [[http://www.mayoclinic.org/diseases-conditions/epilepsy/home/ovc-20117206|seizure disorders]], no cause is ever found. It wouldn't be surprising if one of the causes of the disturbance in the brain's electrical activity that causes a seizure is Th1 inflammation.+In the majority of  [[https://www.mayoclinic.org/diseases-conditions/epilepsy/home/ovc-20117206|seizure disorders]], no cause is ever found. It wouldn't be surprising if one of the causes of the disturbance in the brain's electrical activity that causes a seizure is Th1 inflammation.
  
 Treatment depends on whether the underlying cause can be determined and how many seizures the person has had. It is fine to continue taking the seizure medications ordered by your doctor. As you progress on the MP, you can discuss the possibility of weaning from the anti-seizure drugs. Treatment depends on whether the underlying cause can be determined and how many seizures the person has had. It is fine to continue taking the seizure medications ordered by your doctor. As you progress on the MP, you can discuss the possibility of weaning from the anti-seizure drugs.
  
-[[http://www.medicinenet.com/diazepam/article.htm|Valium]] is sometimes used to prevent seizures. In our experience, it is important to use brand name Valium rather than a generic. See When and why should I use Valium?+[[https://www.medicinenet.com/diazepam/article.htm|Valium]] is sometimes used to prevent seizures. In our experience, it is important to use brand name Valium rather than a generic. __See [[home:othertreatments:antidepressants#Valium|]]__
  
 Keep in mind that seizure activity could be caused by an immune system reaction at any time while on the MP. To be sure that you are safe, take the usual seizure precautions and work with the study site moderators and your doctor to achieve tolerable immunopathology by the adjustment of meds dosing and schedule while diligently avoiding sun/lights and Vitamin D. Keep in mind that seizure activity could be caused by an immune system reaction at any time while on the MP. To be sure that you are safe, take the usual seizure precautions and work with the study site moderators and your doctor to achieve tolerable immunopathology by the adjustment of meds dosing and schedule while diligently avoiding sun/lights and Vitamin D.
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 +<nodisp>
 ===== Notes and comments ===== ===== Notes and comments =====
  
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   * legacy content   * legacy content
-  * http://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=88633#p88633 s70+  * https://www.marshallprotocol.com/view_topic.php?id=4243&forum_id=37&jump_to=88633#p88633 s70
  
-<blockquote>The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis.(({{pubmed>long:18363708}}))+<blockquote>The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis.(({{pmid>long:18363708}}))
  
-http://emedicine.medscape.com/article/342150-overview+https://emedicine.medscape.com/article/342150-overview
  
 PURPOSE: As reported by several authors, angiotensin II (AngII) is a proinflammatory molecule that stimulates the release of inflammatory cytokines and activates nuclear factor kappaB (NFkappaB), being also associated with the increase of cellular oxidative stress. Its production depends on the activity of the angiotensin converting enzyme (ACE) that hydrolyzes the inactive precursor angiotensin I (AngI) into AngII. It has been suggested that AngII underlies the physiopathological mechanisms of several brain disorders such as stroke, bipolar disorder, schizophrenia, and disease. The aim of the present work was to localize and quantify AngII AT1 and AT2 receptors in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis (MTS) submitted to corticoamygdalohippocampectomy for seizure control. METHOD: Immunohistochemistry, Western blot, and real-time PCR techniques were employed to analyze the expression of these receptors. RESULTS: The results showed an upregulation of AngII AT1 receptor as well as its messenger ribonucleic acid (mRNA) expression in the cortex and hippocampus of patients with MTS. In addition, an increased immunoexpression of AngII AT2 receptors was found only in the hippocampus of these patients with no changes in its mRNA levels. DISCUSSION: These data show, for the first time, changes in components of renin-angiotensin system (RAS) that could be implicated in the physiopathology of MTS. PURPOSE: As reported by several authors, angiotensin II (AngII) is a proinflammatory molecule that stimulates the release of inflammatory cytokines and activates nuclear factor kappaB (NFkappaB), being also associated with the increase of cellular oxidative stress. Its production depends on the activity of the angiotensin converting enzyme (ACE) that hydrolyzes the inactive precursor angiotensin I (AngI) into AngII. It has been suggested that AngII underlies the physiopathological mechanisms of several brain disorders such as stroke, bipolar disorder, schizophrenia, and disease. The aim of the present work was to localize and quantify AngII AT1 and AT2 receptors in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis (MTS) submitted to corticoamygdalohippocampectomy for seizure control. METHOD: Immunohistochemistry, Western blot, and real-time PCR techniques were employed to analyze the expression of these receptors. RESULTS: The results showed an upregulation of AngII AT1 receptor as well as its messenger ribonucleic acid (mRNA) expression in the cortex and hippocampus of patients with MTS. In addition, an increased immunoexpression of AngII AT2 receptors was found only in the hippocampus of these patients with no changes in its mRNA levels. DISCUSSION: These data show, for the first time, changes in components of renin-angiotensin system (RAS) that could be implicated in the physiopathology of MTS.
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 </blockquote> </blockquote>
  
-===== References =====+===== References =====</nodisp> 
home/diseases/epilepsy.txt · Last modified: 09.14.2022 by 127.0.0.1
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