ketamine and rtms

[johann1]

Hello,
I'm asking on behalf of a friend who is affected by, among other things, ME/CFS, fibromyalgia/SFPN, and POTS.
Due to her cPTSD, she is considering a ketamine + rTMS treatment.

As far as I know, rTMS can improve symptoms in ME/CFS, fibromyalgia, and even POTS.

Has anyone here had experience with ketamine and/or rTMS therapy?
Did it help you, harm you, or have no effect?

 

[bad1080]

i have no personal experience with ketamine but my therapist said it being a dissociative may not be right for c-ptsd

 

[datadragon]

Ketamine is one of many that may work for ME/CFS due to inhibition of NLRP3 https://pubmed.ncbi.nlm.nih.gov/35925279/ as well as mentioned some benefit to restore impaired myelination https://forums.phoenixrising.me/thr...ic-fatigue-syndrome.91144/page-3#post-2451679

NLRP3 activation would naturally have led to increase of ER Stress, WASF3 levels and Exercise Intolerance/PEM. NLRP3 increases IL-1b/IL-6, INF-y which leads to that WASF3 increase. Heavy exercise, high glucose and fructose and infection all can also increase INF-y increasing WASF3 levels. ER Stress also increases WASF3 Levels. Remember that I found and mentioned how infections, high glucose and fructose, heavy exercise and IFN-y which can increase from inflammation all happen to converge to increase WASF3 levels which is currently shown to cause exercise intolerance/fatigue from research at the NIH. An exercise test indicated the high WASF3 mice produced higher blood lactate levels – which have been found in ME/CFS – and lower glycogen levels. Blocking WASF3 allowed mitochondria to produce energy at normal levels. Glucose deprivation strongly inhibited IFN-gamma (IFN-y) gene expression for example. IFN-y increases expression of GRP78, which is the same GRP78 that increases WASF3 levels. We were discussing in this thread.
https://forums.phoenixrising.me/thr...c-fatigue-syndrome.90582/page-13#post-2469256

The activation of the NLRP3 inflammasome, results in the processing and secretion of active Interleukin 1 (IL-1b) and IL-18. IL-1β induces IL-6 and a Th-17 immune response, whereas IL-18 induces IFN gamma (IFNγ) production by Th-1 lymphocytes An IL-1/IL-6 signature increases neutrophils and C-reactive protein (CRP), whereas an IL-18/IFN-y signature is characterized by hyperferritinemia (excess of an iron storage protein called ferretin in the blood) and cytopenia. https://www.pnas.org/doi/10.1073/pnas.2009017117

There are additional effects of NLRP3 activation such as the lowering of nutrients such as Zinc availability that can lead to many of the other reported downsteam effects In ME/CFS.

Zinc shows up here for one example- In periods of intense muscular activity, zinc is also needed. The ability of the TnT variable N-terminal region to interact through a zinc bridge with the enzyme catalyzing the deamination of AMP to maintain a high energy charge and supply myosin ATPase with ATP could be at the base of a rapid and fine-tuned adaptation to the changes in contractile demands. the zinc-binding protein HPRG we have shown to be candidate to provide the zinc ions to stabilize the AMPD1 native conformation. Furthermore, a clear correlation between the muscle HPRG content and the level of AMPD activity was obtained from the immunological analyses of human skeletal muscle biopsies from patients with AMPD deficiency. AMPD is a zinc enzyme (adenosine monophosphate deaminase) And genetic cause of deficiency can cause ME/CFS
https://forums.phoenixrising.me/thr...aminase-deficiency-type-1.91709/#post-2455574