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Epilepsy (seizures)

Seizures are Th1-related. For example, one member had a grand-mal seizure after mistakenly taking a full tablet of Azithromycin at the start of Phase 2.

Safety

If you have a history of seizures, be sure to take all seizure precautions.

Seizures

In my opinion, seizure disorders are very common in Th1 diseasesThe chronic inflammatory diseases caused by bacterial pathogens.. However, frank grand mal seizures are the least common. Variants of petit mal, 'spacing out', loss of train of thought, muscle twitches, restless leg syndrome etc are all seizure disorders. The 'blacking out' that I have described and which are not uncommon as immune system reactions, are seizures, IMO. Also, emotional outbursts, again common in Th1 diseases, may be temporal lobe seizures. ~Greg Blaney, MD

-Because seizures are caused by the Th1 immune pathogens, EVERY epilepsy drug will affect the immune system in a way which will retard or halt progress to cure. It is clear that epilepsy is only controlled by either 1. getting rid of the pathogens, or 2. a lifetime of immune suppression

Dr. Trevor Marshall, Ph.D

- Valium seems to be effective to prevent seizures when taken at the start of a seizure headache. ~Caitlin's mother

Evidence of infectious cause

  • An association between epileptic seizures and increased serum bacterial antibody levels - 1)
  • Innate immune reaction in response to seizures2)
  • Virological and immunological aspects of seizure disorders 3)
  • Viruses and the immune system 4)
  • Role of viral infections in the etiology of febrile seizures. 5)

in the brain's electrical activity

In the majority of 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 inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue..

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.

Valium is sometimes used to prevent seizures. In our experience, it is important to use brand name Valium rather than a generic. See 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 immunopathologyA state in which a patient has maintained an acceptable intensity of bacterial die-off reaction. The primary goal of the Marshall Protocol. by the adjustment of meds dosing and schedule while diligently avoiding sun/lights and Vitamin D.

Seizure disorders are common in Th1 diseases

In my opinion, seizure disorders are very common in Th1 diseases including borrelia. However, frank grand mal seizures are the least common. Variants of petit mal, 'spacing out', loss of train of thought, muscle twitches, restless leg syndrome etc are all seizure disorders.

The 'blacking out' that I have described and which are not uncommon as Herx reactions, are seizures, IMO. Also, emotional outbursts, again common in Th1 diseases, may be temporal lobe seizures. ~Greg Blaney, MD

Monitor serum depokote closely

Meds, such as depakote, whose doses are determined by blood levels need more frequent serum measurements to monitor possible changing needs as inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. resolves and biochemistry changes.

Patients experiences with seizures while on the MP

At least one member of the MP cohort has epilepsy, and the epileptic activity seems to modulated by immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed.. Epilepsy is probably a Th1 diseaseAny of the chronic inflammatory diseases caused by bacterial pathogens..

..Trevor..

I have myoclonic seizures, fewer now since I have been on antibiotics, actually TREATING the disease, instead of pallative measures. I believe they are due to the disease, as the onset of seizure activity coincided with the onset of my illness.

We know bacteria reside in the CNS, and that neurotransmitters, hormones, regulatory functions are all disrupted by these infections. I am fortunate, in that they are not sudden onset, I feel them coming on, and can take medication. As the critters croak—the manifestations of the disease will lessen. ~hrts4me

I had a seizure 6 weeks ago, first ever in my life. I got up early, started down the stairs and fell. I was unconscious when my husband went to pick me up but then had the seizure. I saw a neurologist today who is pretty sure it's from neuro-sarc.

I guess I'm just surprised that I had a seizure after being on the MP for this long, my life is so much better for being on the MP I wouldn't have imagined anything going awry. ~Sue K

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===== Notes and comments =====

<DiseaseHierarchy>

The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis.6)

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 cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. 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.

Trevor Marshall to Amy, me, C, jrfoutin, Jcwat101, kzd1000show details 12:50 PM (12 minutes ago) Review

Nature Reviews Neurology 7, 31-40 (January 2011) | doi:10.1038/nrneurol.2010.178

Subject Categories: Epilepsy | Neuroimmunology and neuroinflammation | Injury, repair and rehabilitation

The role of inflammation in epilepsy

Annamaria Vezzani, Jacqueline French, Tamas Bartfai & Tallie Z. Baram About the authors

Abstract

Epilepsy is the third most common chronic brain disorder, and is characterized by an enduring predisposition to generate seizures. Despite progress in pharmacological and surgical treatments of epilepsy, relatively little is known about the processes leading to the generation of individual seizures, and about the mechanisms whereby a healthy brain is rendered epileptic. These gaps in our knowledge hamper the development of better preventive treatments and cures for the ≈30% of epilepsy cases that prove resistant to current therapies. Here, we focus on the rapidly growing body of evidence that supports the involvement of inflammatory mediators—released by brain cells and peripheral immmune cells—in both the origin of individual seizures and the epileptogennic process. We first describe aspects of brain inflammation and immunity, before exploring the evidence from clinical and experimental studies for a relationship between inflammation and epilepsy. Subsequently, we discuss how seizures cause inflammation, and whether such inflammation, in turn, influences the occurrence and severity of seizures, and seizure-related neuronal death. Further insight into the complex role of inflammation in the generation and exacerbation of epilepsy should yield new molecular targets for the design of antiepileptic drugs, which might not only inhibit the symptoms of this disorder, but also prevent or abrogate disease pathogenesis.

In my opinion, seizure disorders are very common in Th1 diseases including Borrelia. However, frank grand mal seizures are the least common. Variants of petit mal, “spacing out”, loss of train of thought, muscle twitches, restless leg syndrome etc are all seizure disorders. The “blacking out” that I have described and which are not uncommon as immune system reactions, are seizures, IMO. Also, emotional outbursts, again common in Th1 diseases, may be temporal lobe seizures.

One physiological causation for panic attacks is the depletion of intracellular magnesium by the infection. I believe this is primarily due to vitamin D dysregulation but could also be caused by the direct depleting effect of the physical stress of the illness. Therefore, taking extra magnesium but without calcium or vitamin D, can lessen some of these reactions.

Greg Blaney, MD

===== References =====

1)
Iivanainen M, Hietala J, Malkamäki M, Waltimo O, Valtonen VV. An association between epileptic seizures and increased serum bacterial antibody levels. Epilepsia. 1983 Oct;24(5):584-7. doi: 10.1111/j.1528-1157.1983.tb03422.x.
[PMID: 6617588] [DOI: 10.1111/j.1528-1157.1983.tb03422.x]
2)
Turrin NP, Rivest S. Innate immune reaction in response to seizures: implications for the neuropathology associated with epilepsy. Neurobiol Dis. 2004 Jul;16(2):321-34. doi: 10.1016/j.nbd.2004.03.010.
[PMID: 15193289] [DOI: 10.1016/j.nbd.2004.03.010]
3)
Eeg-Olofsson O. Virological and immunological aspects of seizure disorders. Brain Dev. 2003 Jan;25(1):9-13. doi: 10.1016/s0387-7604(02)00162-6.
[PMID: 12536027] [DOI: 10.1016/s0387-7604(02)00162-6]
4)
Getts DR, Balcar VJ, Matsumoto I, Müller M, King NJC. Viruses and the immune system: their roles in seizure cascade development. J Neurochem. 2008 Mar;104(5):1167-76. doi: 10.1111/j.1471-4159.2007.05171.x. Epub 2008 Jan 17.
[PMID: 18205751] [DOI: 10.1111/j.1471-4159.2007.05171.x]
5)
Millichap JG, Millichap JJ. Role of viral infections in the etiology of febrile seizures. Pediatr Neurol. 2006 Sep;35(3):165-72. doi: 10.1016/j.pediatrneurol.2006.06.004.
[PMID: 16939854] [DOI: 10.1016/j.pediatrneurol.2006.06.004]
6)
Argañaraz GA, Konno AC, Perosa SR, Santiago JFC, Boim MA, Vidotti DB, Varella PPV, Costa LG, Canzian M, Porcionatto MA, Yacubian EM, Sakamoto AC, Carrete HJ, Centeno RS, Amado D, Cavalheiro EA, Junior JAS, Mazzacoratti MdGN. The renin-angiotensin system is upregulated in the cortex and hippocampus of patients with temporal lobe epilepsy related to mesial temporal sclerosis. Epilepsia. 2008 Aug;49(8):1348-57. doi: 10.1111/j.1528-1167.2008.01581.x. Epub 2008 Mar 21.
[PMID: 18363708] [DOI: 10.1111/j.1528-1167.2008.01581.x]
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