Have you noticed that after your body temperature rises, for example from taking a bath, shower, or eating warm/hot food or other things, - tremors, weakness, and partly cognitive symptoms also become significantly worse and a little easier after you cool down again?

i looking for some kind of Uhthoff's phenomenon if you interested you can research this also

Have you noticed that after your body temperature rises, for example from taking a bath, shower, or eating warm/hot food or other things, - tremors, weakness, and partly cognitive symptoms also become significantly worse and a little easier after you cool down again?

i looking for some kind of Uhthoff's phenomenon if you interested you can research this also

Specifically, stimulation of the somatosensory cortex and the motor cortex of the legs and hands reduces the general symptoms of PFS/PSSD, including tremors, weakness, and analgesia over the body, as well as taste, smell, and sound perception. It even partially helps with libido and sexual function, to the surprise of my neurologist and me,

as short update at 7 session seems this even somehow affected emotion blunting and anhedonia it also improved quite significantly, for now i continue sessions

i want to mention classical rTMS protocol for depression/ocd did absolutely nothing for me, i did 20 session into DLPFC, nothing changes at all nor better nor worse

update seems like even my personality drug response and emotions slowly coming back online

Specifically, stimulation of the somatosensory cortex and the motor cortex of the legs and hands reduces the general symptoms of PSSD, including tremors, weakness, and analgesia over the body, as well as taste, smell, and sound perception. It even partially helps with libido and sexual function, to the surprise of my neurologist and me.

Yes this is for PSSD but maybe some in PFS also can get some idea for that especially if you have real neurological symptoms(tremors weakens loss of coordination) just like me

I should say upfront: none of this is a cure. It's just a collection of things that have helped me survive and, in some cases, regain a bit of function.

I've been dealing with severe PSSD for about 6 years now, triggered by escitalopram. Over time I've had to figure out my own approach because the medical system in my country has been hostile (they tried to label me schizophrenic at one point). I finally found a neurologist who is open-minded and willing to look at my documented evidence, but most of what I do is still self-directed out of necessity. I wanted to share the rough protocol that I've slowly put together, in case any of it is useful for others to discuss with their own doctors.

As symptoms goes i have ("Full Blown PSSD") - this means all of it.

The model I've been working from is based on the idea that SSRIs like escitalopram are possibly mitochondrial toxins. There's some published research showing they can inhibit Complex I of the electron transport chain, at least in vitro. In a susceptible person, that might cause an energy deficit in the longest, thinnest nerve fibers—the C-fibers—leading to a kind of length-dependent small-fiber neuropathy. This would likely affect axonal transport, so the delivery of ion channels like TRPV1 (the capsaicin receptor) to the nerve endings slows down or stops. That might explain the selective sensory loss pattern a lot of us see, like a delayed or absent capsaicin response but a preserved menthol response, because TRPM8 seems less dependent on that transport pathway. The autonomic problems like orthostatic hypotension could be from damaged C-fibers failing to help constrict blood vessels properly. That's my best guess, anyway; it's hard to prove.

Given that framework, my stack has a couple layers.

First was, tranylcypromine (Parnate). It's an older MAOI antidepressant. Without it, I can't even get out of bed. It doesn't fix the PSSD symptoms, but it keeps the baseline depression at a level where I can function. It seems to be a lifeline for me. Yes Serotonin but in my case don't cause worsening of PSSD symptoms but helps depression and cognition

For the orthostatic hypotension and blood pressure crashes, I stumbled onto fludrocortisone. It's a mineralocorticoid that expands blood volume. My labs showed high renin with inappropriately normal aldosterone and high hematocrit, so it looked like I was chronically hypovolemic. Fludrocortisone brought my resting heart rate down from the 90s–100s to the 70s–80s, which was a clear sign it was doing something. Combined with iron supplements (my ferritin was suboptimal), it made the orthostatic stuff more manageable.

Then there's the rTMS Not just classical rTMS for depression - I've been mapping my own cortex, essentially. The most dramatic response is from the motor cortex; stimulating the hand area makes my tremor and weakness disappear on the contralateral side almost instantly, which my neurologist saw. That was huge because it showed the problem isn't just psychiatric. The frontal pole stimulation, targeting orbitofrontal and rostromedial prefrontal areas, seems to bring back smells, tastes, hearing clarity, and even a bit of libido for a while. The somatosensory association area stimulation is intense - it improves bodily awareness and multisensory integration for up to two days, but the session itself causes overstimulation and a crash. It seems like those higher-order sensory integration hubs are intact but in some kind of hibernation, probably from lack of input.

I also use mitochondrial support. A mix of peptides - SS-31 for cardiolipin stabilization, MOTS-c for biogenesis, Humanin for anti-apoptotic protection, and BPC-157 for nerve repair and angiogenesis. And BAM15 as a pulsed, very low-dose mitochondrial uncoupler, which seems to create a hormetic rebound. I've noticed that after a meal, I no longer get the crushing postprandial fatigue; instead I have a little more energy, which is a big change.

It's a long story i also use PEA+TCP , but PEA itself made me worse - caused paradoxical hypotension and weakness, likely because my peripheral norepinephrine stores are depleted. But its N,N-dimethyl derivative (N,N-DMPEA) had a positive effect, possibly because it bypasses the broken nerve terminals and acts more directly.

All of this is documented with detailed notes, lab tests, and videos. My neurologist is now on board and we're pursuing skin biopsy, QST, and autoantibody panels to try to get objective evidence of SFN. The capsaicin test with its delayed length-dependent response was the key that got him to take me seriously.

I don't know if any of this will help others, It's possible some of these ideas are off base, and I'm just one person self-experimenting under absurd circumstances. But maybe some of it might spark a useful conversation with a doctor or a researcher.

I as me for evryoine else think rTMS a very first priority thing to try for this all
As effect for me goes:
(TCP>rTMS>PEA>PEP)

Yes this is for PSSD but maybe some in PFS also can get some idea for that

I should say upfront: none of this is a cure. It's just a collection of things that have helped me survive and, in some cases, regain a bit of function.

I've been dealing with severe PSSD for about 6 years now, triggered by escitalopram. Over time I've had to figure out my own approach because the medical system in my country has been hostile (they tried to label me schizophrenic at one point). I finally found a neurologist who is open-minded and willing to look at my documented evidence, but most of what I do is still self-directed out of necessity. I wanted to share the rough protocol that I've slowly put together, in case any of it is useful for others to discuss with their own doctors.

As symptoms goes i have ("Full Blown PSSD") - this means all of it.

The model I've been working from is based on the idea that SSRIs like escitalopram are possibly mitochondrial toxins. There's some published research showing they can inhibit Complex I of the electron transport chain, at least in vitro. In a susceptible person, that might cause an energy deficit in the longest, thinnest nerve fibers—the C-fibers—leading to a kind of length-dependent small-fiber neuropathy. This would likely affect axonal transport, so the delivery of ion channels like TRPV1 (the capsaicin receptor) to the nerve endings slows down or stops. That might explain the selective sensory loss pattern a lot of us see, like a delayed or absent capsaicin response but a preserved menthol response, because TRPM8 seems less dependent on that transport pathway. The autonomic problems like orthostatic hypotension could be from damaged C-fibers failing to help constrict blood vessels properly. That's my best guess, anyway; it's hard to prove.

Given that framework, my stack has a couple layers.

First was, tranylcypromine (Parnate). It's an older MAOI antidepressant. Without it, I can't even get out of bed. It doesn't fix the PSSD symptoms, but it keeps the baseline depression at a level where I can function. It seems to be a lifeline for me. Yes Serotonin but in my case don't cause worsening of PSSD symptoms but helps depression and cognition

For the orthostatic hypotension and blood pressure crashes, I stumbled onto fludrocortisone. It's a mineralocorticoid that expands blood volume. My labs showed high renin with inappropriately normal aldosterone and high hematocrit, so it looked like I was chronically hypovolemic. Fludrocortisone brought my resting heart rate down from the 90s–100s to the 70s–80s, which was a clear sign it was doing something. Combined with iron supplements (my ferritin was suboptimal), it made the orthostatic stuff more manageable.

Then there's the rTMS Not just classical rTMS for depression - I've been mapping my own cortex, essentially. The most dramatic response is from the motor cortex; stimulating the hand area makes my tremor and weakness disappear on the contralateral side almost instantly, which my neurologist saw. That was huge because it showed the problem isn't just psychiatric. The frontal pole stimulation, targeting orbitofrontal and rostromedial prefrontal areas, seems to bring back smells, tastes, hearing clarity, and even a bit of libido for a while. The somatosensory association area stimulation is intense - it improves bodily awareness and multisensory integration for up to two days, but the session itself causes overstimulation and a crash. It seems like those higher-order sensory integration hubs are intact but in some kind of hibernation, probably from lack of input.

I also use mitochondrial support. A mix of peptides - SS-31 for cardiolipin stabilization, MOTS-c for biogenesis, Humanin for anti-apoptotic protection, and BPC-157 for nerve repair and angiogenesis. And BAM15 as a pulsed, very low-dose mitochondrial uncoupler, which seems to create a hormetic rebound. I've noticed that after a meal, I no longer get the crushing postprandial fatigue; instead I have a little more energy, which is a big change.

It's a long story i also use PEA+TCP , but PEA itself made me worse - caused paradoxical hypotension and weakness, likely because my peripheral norepinephrine stores are depleted. But its N,N-dimethyl derivative (N,N-DMPEA) had a positive effect, possibly because it bypasses the broken nerve terminals and acts more directly.

All of this is documented with detailed notes, lab tests, and videos. My neurologist is now on board and we're pursuing skin biopsy, QST, and autoantibody panels to try to get objective evidence of SFN. The capsaicin test with its delayed length-dependent response was the key that got him to take me seriously.

I don't know if any of this will help others, It's possible some of these ideas are off base, and I'm just one person self-experimenting under absurd circumstances. But maybe some of it might spark a useful conversation with a doctor or a researcher.

I as me for evryoine else think rTMS a very first priority thing to try for this all
As effect for me goes:
(TCP>rTMS>PEA>PEP)