• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Extremely upsetting SPECT scan results: brain lesions! What now??

xrayspex

Senior Member
Messages
1,111
Location
u.s.a.
@Antares in NYC
What you might like to look into is the ability of quinolinic acid to produce brain lesions. Quinolinic acid, which is a potent neurotoxin, is created in the brain as part of the inflammatory process (during inflammation activated microglia convert L-tryptophan into quinolinic acid). 1

When quinolinic acid is experimentally injected into the brain, it causes lesions to appear. 1 And interestingly, poliovirus induces quinolinic acid, and apparently all the damage resulting from poliomyelitis can be prevented simply by blocking the activity of quinolinic acid. 1

Quinolinic acid has been found to be significantly elevated in Borrelia infection, with dramatically high levels found in Lyme patients with CNS inflammation. 1

There are several supplements and drugs that help protect against quinolinic acid-induced neurotoxicity, including:

selenium, 1 memantine, 1 verapamil, 1 rolipram, 1 minocycline, 1 acyclovir, 1 copper at low doses, 1 COX-2 inhibitors (eg: propolis), 1 ibuprofen, 1 dapsone, 1 saffron, 1 pyruvate, 1 S-allyl-cysteine (from garlic), 1 curcumin, 1 DHEA, 1 EGCG. 1
Hip, a couple random questions---I figured out that I was getting dizzy every time I put selenium in my smoothie lately--I used to be able to tolerate a few drops pulsed on and off but was more religious about it the last couple months and apparently developed an intolerance to it. any thoughts on that?
also am curious, have been able to try amantadine on and off the last 6 years and it makes me depressed---wondering if since memantine is related it could have some of the same properties. I was wondering if amantadine, with being part antiviral, increased quinolinic acid and thus depression.

huh, editing my response to add this, so you put acyclivor in there as quinolinic inhibitor, which confuses me---because another post of yours gave a theory about why depression can happen like with interferon treatment and its related to quinolinic acid---and I think the th 1 th 2 balance---
anything with antiviral properties makes me feel like hell......from valtrex(valcyclivor) to amantadine to lysine....catatonic hopeless mood and increased pain etc
doesnt it seem like immune system and quinolinic acid such a nuanced individualized situation that one person's meat could be another's poison? I was stoked at first tho to see you compiled list of QUIN inhibitors, I am wanting to find more info on that.

here is your post from http://forums.phoenixrising.me/inde...munomodulators-in-cfs.8447/page-6#post-782133

"
Hip said:
Yes, I am pretty sure that the depression is caused by the fact that: the antiviral Th1 response increases interferon gamma (IFN-γ), and IFN-γ then causes an increase in the enzyme indoleamine-2-3-dioxygenase (IDO) in the brain, and IDO breaks down tryptophan, and tryptophan is needed to make serotonin, the happiness neurotransmitter.

In summary:

Th1 Response ➤ Increased IFN-γ ➤ Increased IDO ➤ Reduced Tryptophan ➤ Reduced Serotonin ➤ Depression

(Note however that this study contradicts the above standard explanation of interferon-induced depression, and instead suggests an alternate explanation: that although raised IDO is still responsible for the depression, the mechanism of this depression is via IDO's ability to produce kynurenine and kynurenine metabolites such a quinolinic acid, which is linked to depression. In summary: Th1 Response ➤ Increased IFN-γ ➤ Increased IDO ➤ Increased Kynurenine and its Metabolites such as Quinolinic Acid ➤ Depression)

This type of interferon-induced depression is well-known: this very miserable depression occurs in many hepatitis C patients taking intravenous interferon as a treatment for the hep C virus. Also, Dr John Chia, in his study employing intravenous interferon for ME/CFS patients, found that although interferon was very effective, and was able to place many ME/CFS patients he treated into almost full remission for around 2 to 14 months (which is a spectacular result), he found that many of his patients suffered very significant depression during the treatment period. This problem with interferon-induced depression was one of the reasons I believe Dr Chia has largely stopped using intravenous interferon treatment for ME/CFS (that and the very high cost of intravenous interferon, which is in the order of $15,000 for a course of treatment).


I did try taking IDO inhibitors at the same time as taking my Th1 boosting cocktail, in the hope of preventing this depression from occurring, but this did not seem to help. Perhaps these IDO inhibitors were not potent enough, or perhaps I should have used much higher doses of these IDO inhibitors. (Or perhaps I should have heeded the alternate explanation of how IDO causes depression, and taken quinolinic acid inhibitors instead).



The antidepressant drugs paroxetine and low dose amisulpride have been shown to mitigate interferon-induced depression, so it is worth trying these drugs to combat the depression when you take a Th1 boosting cocktail.

But note that not everybody experiences depression from raised interferon levels, so many ME/CFS patients may be able to take the above Th1 boosting cocktail without getting any depression side effects, and thus may potentially experience an improvement in their ME/CFS symptoms from this antiviral Th1 boosting approach.

Apart from my depression (which I suffer from anyway), I did not get any other side effects from this Th1 boosting cocktail.

I am not sure why the various ME/CFS doctors, such as Dr Cheney and Dr Klimas, have not tried a Th1 boosting cocktail like the one I provided above. These doctors note that ME/CFS patients are stuck in the Th2 mode, and that they need to by shifted into the Th1 mode if they are going clear the viruses likely driving their ME/CFS. So it seems to make sense to try to shift your immune system over to Th1 using several Th1 boosting supplements and drugs, not just one supplement."
 
Last edited:

Hip

Senior Member
Messages
17,871
Hip, a couple random questions---I figured out that I was getting dizzy every time I put selenium in my smoothie lately--I used to be able to tolerate a few drops pulsed on and off but was more religious about it the last couple months and apparently developed an intolerance to it. any thoughts on that?

Nothing comes to mind that might explain it. A lot of people find higher doses of selenium over-stimulating, but not sure about dizziness.


also am curious, have been able to try amantadine on and off the last 6 years and it makes me depressed---wondering if since memantine is related it could have some of the same properties. I was wondering if amantadine, with being part antiviral, increased quinolinic acid and thus depression.

Amantadine has antidepressant properties as well as being an antiviral, so strange that it makes you depressed. What dose are you taking, because Dr David Bell found amantadine 25 mg to 50 mg daily helps ME/CFS, but says higher doses can exacerbate symptoms. Ref: 1 When I take amantadine, I use a 25 mg dose.



anything with antiviral properties makes me feel like hell......from valtrex(valcyclivor) to amantadine to lysine....catatonic hopeless mood and increased pain etc

Valtrex for me ramped up anxiety, and so I could not take it. I don't do that well on lysine either, but am fine with amantadine 25 mg.
 

dannybex

Senior Member
Messages
3,564
Location
Seattle
why do you think there are not as many studies on nutrition since 1975? just curious.....have noticed a lot of useful research decreased over the years. wondered if some of the politics discussed in that lymes film under our skin alludes to some of reasons.

My guess is that drug companies found a lot more profit in creating new drugs that just (temporarily) suppress symptoms, instead of some nutritional approaches that actually address and repair the problems. Sure, some drugs can be helpful -- like antifungals, antibiotics -- but most (In my opinion) just make it seem like the problems are 'better', when all they're doing is suppressing symptoms....
 

SK2018

SK
Messages
239
Location
Asia wide + UK
I'm so upset and shaken I can't even type this note right. I just read the reports from two tests that I had at a major hospital last week. I haven't talked to any of my doctors yet (waiting lists) but left them voicemails to call me back when they can. The test were conducted to assess my increasing brainfog and worsening cognitive issues, and results of both tests are quite upsetting:

MRI Spectrography:
A few nonspecific white matter lesions are noted which could be related to prior ischemic or inflammatory sequela. No mass, mass effect or midline shift. There is no hydrocephalus or acute ischemia. Intracranial flow voids are maintained.
Impression: Minimal nonspecific white matter lesions are noted which could be related to prior ischemic or inflammatory sequela.

Nuclear Medicine Brain SPECT Scan:
Moderate decrease in cerebral cortical perfusion in a heterogeneous pattern. These findings are nonspecific and may be seen with meningitis/encephalitis, Lyme disease or connective tissue disorders such as lupus.​

I don't even know where to start.
Am I brain damaged?
Is this progressive? Will it get worse?
Is this reversible? Is there a treatment to reverse it or make it better?
If this is not reversible or it continues to progress, what am I to expect?

I'm broken down emotionally. I'm extremely upset and scared. I can't even begin to wrap my head around the consequences that these findings may have for the rest of my life.

If someone knows a bit more about these lesions and decreased cortical blood flow, I would appreciate some advice, next steps, or recommendations of other doctors that I should see. Thanks.
I would suggest getting a full anti neuronal antibody panel done and consider a trial of immune therapy as soon as possible if you have no sign of infective markers it's most likely immune mediated in some form,the immune system is over complex and many things can go wrong.Of course be aware of the risks of immune therapy first.

About Brain Damage ,I had some hypoperfusion on my SPECT Initially but that's mostly cleared up now as my baseline improved,I think we may be left with some slight deficits but nothing major i.e. not being 100% but racking up to 80-90% would be enough ,but it's hard to say for sure ,at least one positive note is there doesn't seem to be any important "structural"damage.
 
Last edited:
Messages
3
This paper found that "Serum quinolinic acid was increased only in the cobalamin-deficient rats."

http://www.jnutbio.com/article/S0955-2863(97)89666-0/abstract

Many of us have high B12 levels, but perhaps there's a functional deficiency?

Also, this study found 'folic acid' protected 'susceptible retinal neurons from the neurotoxic effects' of quinolinic acid in chick retinas.

http://www.ncbi.nlm.nih.gov/pubmed/3297751
------------------------------------------------------------------------------------------------
I guess this was discussed on this forum before but just in case:


Probably MTHFR Genetic Mutation
by: Kerri Knox, RN- The Immune Queen!


Here's some information about this from a natural practitioner who effectively deals with this regularly. Here's something that may be of help for you.
______________________________________________

This girl may have chronic fatigue syndrome, which does occur in young people. In chronic fatigue syndrome (CFS), it is common to see elevated B12 and folate in the blood serum, but this type of measurement is misleading in this disorder, because there is a functional deficiency of B12 in the cells, and folates drain from the cells to the blood in response, via the "methyl trap" mechanism due to MTHFR Gene Mutation.

Most of the B12 in the blood serum has been exported from the cells and is bound to haptocorrin, not transcobalamin, so it is accessible only to the liver cells, as
part of a salvage pathway for recycling B12 back to the gut for reabsorption, not to the cells of the body in general.

This occurs because of glutathione depletion, which removes the normal protection from B12 inside the cells. The glutathione depletion therefore leads to hijacking of B12 by toxins, and this in turn causes a functional deficiency of B12. That produces a partial block in the methionine synthase enzyme, which leads to the
folate draining and also sets up a vicious circle mechanism with glutathione depletion, which is what makes CFS a chronic condition.


Rich Van Konynenburg, Ph.D.
Independent CFS Researcher