Intracranial hypertension? already heard that in PFS studies

Yes, I had an MRI done of my brain after a blood test showed more than double the reference value of prolactin. They were looking for anything that might look like a hyperprolactinoma.

Doctors said the MRI did not show any abnormalities whatsoever and sent me home with viagra.

Unsure how this is related ach ganglionic antibodies…could you explain?

Im pretty sure he was replying to the original poster.

Btw heres what ive been looking at as far as natural treatment using GBS as an example.
They dont mention an exact strain though.
GBS is a classic example of an autoimmune neuropathy.

Bifidobacterium alleviates guillain-barré syndrome by
regulating the function of T17 cells

In summary, our data show higher levels of
IL-17 in plasma and CSF of patients with GBS.
The concentrations of IL-17A in plasma and
CSF were correlated positively with the GDSS in
GBS patients and negatively correlated with
Bifidobacterium. Treatment with Bifidobacterium not only significantly alleviated the disease activity, but also reduced the levels of
IL-17A. Our findings may provide new insights
into the regulation of inflammatory responses during the pathogenic process of GBS and
suggest that the levels of plasma and CSF
IL-17A may be important for evaluating the disease severity and therapeutic efficacy in GBS

I would also be looking at this as well, now it starts to look like a blood disorder also.
Ive tested positive for this at one point.

Neurological manifestations of antiphospholipid
Neurologic disorders are among the most common and important clinical manifestations
associated with the antiphospholipid syndrome (APS). It is characterized by diverse neurological manifestations.
These include stroke, transient ischaemic attack, Sneddon’s syndrome, convulsions ⁄ epilepsy, dementia,
cognitive deficits, headaches ⁄ migraine, chorea, multiple sclerosis-like, transverse myelitis, ocular symptoms
and Guillain–Barre´ syndrome.

I was diagnosed with this from accutane, it was my first side effect. I had to have a spinal tap, don’t remember what the specific number was, but my pressure was high, hurt like hell.

Ok, but how did thesituation evolved? were you able to remove the spinal tap? did the situation recover?

Felt some relief with the Spinal Tap but didn’t resolve 100%, took percocet for a couple days after the spinal tap which relieved the pain 100%.

Had an MRI 2 months later, everything was fine.

How much time ago did you take the MRI? I had the first done 7 years ago, and the meds were not very concordant that there was something strange. Now that I took a new MRI the report was pretty clear. I will talk with my endo and make a comparison, but It seems the situation has evolved for the worse.


So you had headaches? I don’t but I feel some kind of pressure, I would call that something like “peripheral head numbness”.

So you definitely got the spinal tap removed correct?

Yes, the pain was unbearable, the spinal tap was just to check my pressure, it was a one time thing.

ok got it thx

Thanks for all the material, I am studying the question. I apparently don’t have symptoms of autoimmune ganglionopathy, apart from a possible autonomic dysfunction but I’m taking a look.

Yes, I’ve had a finding of abnormal pituitary activity when I was a “mild” case. At that time I only had physical problems, e.g. muscle wasting/worsening with exercise, until rechallenge years later after which I severely crashed and developed severe neurological and sexual symptoms, and progressive atrophic changes. I have not had an MRI since.

I’ve given some thoughts in the literature review awor and myself provided in 2020 if you’re interested. O’Reilly et al. provided an important paper determining a role of androgen signaling in CSF pressure in IIH patients, and further demonstrated this in animal cell modelling:

"A central and potentially causative role of androgen signaling was recently demonstrated in idiopathic intracranial hypertension (IIH), which entails an increase of CSF pressure. O’Reilly et al. identified a pattern of androgen excess in female IIH patients. Like human choroid plexus, rat cells expressed AR along with androgen-metabolising enzymes. It was demonstrated that testosterone drove CSF output in rodent choroid plexus cells ​(O’Reilly et al., 2019)​. O’Reilly et al. noted that while a determinant role for androgens in IIH may seem biologically implausible considering IIH occurs less frequently in men, androgens are now known to exert sexually dimorphic effects on metabolism. The metabolic phenotype of hypogonadal men resembles that of women with androgen excess, including an increased risk of type 2 diabetes, non-alcoholic fatty liver disease and cardiovascular mortality ​(Ding et al., 2006; Kautzky-Willer et al., 2016)​. O’Reilly et al. suggest epigenetic modifications to local androgen action or differences in AR signaling in both sexes as a plausible explanation, with IIH potentially representing a distinctive manifestation of these sex specific differences ​(O’Reilly et al., 2019)​.

Interestingly, male IIH patients are more likely to have symptoms typically associated with androgen insufficiency including obstructive sleep apnoea, erectile dysfunction and loss of libido ​(Fraser et al., 2010)​. As well, androgen deprivation therapy or hypogonadism can induce IIH symptomatology ​(Valcamonico et al., 2013)​. Although in males the metabolic parabola of AR signaling is shifted far to the right compared with females ​(Ding et al., 2006; Morford et al., 2018)​, significant increases in AR signaling in men are likely to recapitulate this symptomatology, and we therefore consider it plausible IIH occurs in PFS and contributes to commonly reported symptoms, including feelings of intense pressure in the head.

In this context, it is of interest that the pilot study of Melcangi et al. evaluating CSF methylation in PFS patients and controls found only one member of the control group with methylation of SRD5A2, and this patient had normal-pressure hydrocephalus. The majority of PFS patient samples exhibited variable methylation of this gene ​(Melcangi et al., 2019)​."

citations in original text.

Also @tab, please could you complete the survey? It’s important symptoms like yours are recorded in this data set, and every submission really helps. You can take it by clicking the graph icon in the top right of the forum when on a desktop or laptop. Thank you very much.


About 6 months ago. I have not had a hormonal blood test done since, but at the time my prolactin was increasing. Perhaps it would be wise to do another blood test soon as my symptoms have not really changed much over time and to see if my prolactin levels have significantly increased since and if a new MRI is warranted.

Have you been prescribed medication for the hyperprolactinoma, like cabergoline? I’ve heard people mention (short-term) increase in libido and sexual functioning while taking cabergoline. Although in my view taking cabergoline would be symptom relief instead of actual treatment.

If you have a similar condition to mine, I have taken many prolactin tests during the years, I also took a prolactin curve test.
I have seen it vary from normal to 97 ng/ml (near prolactinoma limit). Sometimes it is down, sometimes it is up. I couldn’t find any clue on this behavior. My sexual condition too is not stable, I sometimes have problems keeping it up, sometimes I’m pretty hard. I have no clue why these changes happen from day to day. In my limited knowledge of erectile physiology, there probably is something fkdup in the hypotalamus too as when I experience ejaculation the penis immediately softens during ejaculation. I can see this only as nervous mediated effect from the hypotalamus, through the spine and then to the penis. But this again is only my hypothesis as I’m not an MD I’d have to study much more in order to be fairly sure about that.

So yes, if I were you, I would take a prolactin test from time to time just to understand what is it’s behavior.

I only made a short cabergoline cycle many years ago. I restarted a cycle a couple months ago. Prolactine goes down, T increases, but honestly the benefits seem to be limited. I hope that by waiting a bit more the symptoms will fade. Howver considering the recent finding from the MRI I’m not all that positive anymore as the pituitary compression probably hinders all other pituitary hormones. That being said, I don’t like cabergoline as it brings risks of heart fibrosis and similar, at least at higher dosages. But who trusts leaflets anymore? Big Pharma is a joke and they should go and fk themselfes. I don’t think I’m going to take it lifelong. You might try it out to check if it does something for you.
Either way, at least in my case, I don’t have a lot of hopes for a real healing treatment anymore. As you can see the problems are many. I will do all what I can anyway and I’m still prone to holistic/behavioral therapies. I’m reconsidering my workout and diet routine as in these years I wasn’t able succeed in the body fat/muscle recomposition, and I have muscle wastage and gynoid fat deposits from Fin that surely act as hormonal organ. Not to mention my real gynecomastia (another gift from FIn). I’m getting some results with the new routine but it’s too early to tell if this translates into stable improvements.

Thanks for the elaboration on your experience. I will push to get a new hormone measurement.

I do agree with axolotl though: Would you please contribute to the survey, because it’s not going to be open for much longer and it’s very important that as many patients as possible contribute to the data.


I do not feel to complete the survey as I took also an antipressant and benzos during my finasteride therapy. The data I can provide would probably be misleading. Also more than 10 years have passed since the start of Fin. It’s very hard for me to recall the answer to many questions which are very detailed. I think my survey would only be misleading to researchers.

I have been found a few days ago to have very high semen leukocytes. Leukocytospermia is a sign of infection/inflammation in seminal vescicles/prostate. I will do a seminal colture and see what happens.

I am pretty sure that PFS is nothing more than an antibody that somehow attacks the androgen receptors and in the worst cases, even estrogen receptors, preventing them from binding to the hormone. I can’t understand why the researchers don’t want to move in this direction. The answer to PFS would be around the corner.


Anti-AChR antibodies disrupt communication between nerve fibers and skeletal muscles, inhibit muscle contraction and prevent activation of acetylcholine receptors, resulting in rapid muscle fatigue. The action of the anti-AChR antibodies is threefold:

Binding antibodies bind to exposed receptors on nerve cells and can cause inflammation that destroys the receptors;

Blocking antibodies can “mask” the receptors, preventing acetylcholine from binding to them;

Modulating antibodies cause cross-reactivity between receptors, with consequent internalization of receptors within muscle cells and elimination from the neuromuscular junction

This is the most interesting part, because in the first PFS studies the researchers found an increase in the density of the androgen receptor. It seems to me a fairly rational mechanism: The antibody binds to the receptors, preventing them from working, but without destroying them. The body is not responding to the hormone and what is the most logical move? It produces other receptors, which are blocked again. This would also explain why partial recoveries last so short. It seems really crazy to me that no research has moved in this direction. It seems too obvious.

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