Anyone had a brain MRS scan?

[hixxy]

Just curious if anyone has had a brain MRS scan? I've had one ordered by a metabolic specialist and supposedly it can detect elevated lactate in the brain. I'll also be having a regular MRI at the same time.

 

[robinhood12345]

I had an MRI but never MRS. it can measure things like choline, creatine, and lots of other compounds in the brain too.

 

[Wolfcub]

I had never heard of MRS before, and had no idea! So I thank you for the heads up @hixxy
I saw a neurologist last week and he has referred me for a CT scan. But I wish I'd known about this then.
It sounds like very helpful technology.

 

[raghav]

I had an MRI/MRS in 2010.It diagnosed that I have left hippocampal sclerosis. The report states there is elevated N acetyl aspartate. The left hippocampus had shrunk 20 % compared to the right hippocampus.

 

[WinterWren]

You might already be aware but the MRS scan is what Jarred Younger used to look at lactate concentrations in the brain, he talked about it at the symposium. It's very interesting!

 

[hixxy]

You might already be aware but the MRS scan is what Jarred Younger used to look at lactate concentrations in the brain, he talked about it at the symposium. It's very interesting!

No, I didn't know this. Thanks for the heads up.

 

[Research 1st]

I had an MRI/MRS in 2010.It diagnosed that I have left hippocampal sclerosis. The report states there is elevated N acetyl aspartate. The left hippocampus had shrunk 20 % compared to the right hippocampus.

Thanks for sharing your experience.

Could you possibly remember if this was a specific test?

Also was it 'non invasive' (just got under a scanner) or did you need an injection to specifically measure ' N acetyl aspartate', because the doctor had a hunch this was related to your symptoms? Or was it a type of scan that measures many things, and doesn't need a specific radioligand/tracer to measure levels or ' N acetyl aspartate'?

I'd love to know as it sounds really interesting. Did you get any help after your abnormal result? I hope so.

 

[Research 1st]

You might already be aware but the MRS scan is what Jarred Younger used to look at lactate concentrations in the brain, he talked about it at the symposium. It's very interesting!

Hello.
Increased ventricular lactate by MRS scanning is shown in the following previous studies in CFS:

1) (Mathew et al, 2008)
2) (Murrough et al, 2010)
3) (Shungu et al, 2012)
4) (Natelson et al, 2017)

It would make sense if you have a metabolic brain disease, then your brain will struggle cognitively, as we say it does after little usage, especially intellectual thinking.

I find I can watch mindless Youtube clips for hours, but short bursts of thinking like this on the forum where I have to think at a higher brain power level, absolutely destroys me and worsens many symptoms such as vertigo, headache and an enhanced sense of feeling 'unreal'.

It's tragic we are mostly all productive capable people, but trapped with in our brains, yet no one believes us.

 

[hixxy]

Thanks for sharing your experience.

Could you possibly remember if this was a specific test?

Also was it 'non invasive' (just got under a scanner) or did you need an injection to specifically measure ' N acetyl aspartate', because the doctor had a hunch this was related to your symptoms? Or was it a type of scan that measures many things, and doesn't need a specific radioligand/tracer to measure levels or ' N acetyl aspartate'?

I'd love to know as it sounds really interesting. Did you get any help after your abnormal result? I hope so.

I can't comment on @raghav's experience but when I spoke to my doctor about the MRS scan she said there was no injection or tracer it's just a scan and the request form didn't specify any particular chemical they were looking to measure (my doctor wanted to know about lactate) so I guess the scan just reports on a whole range of chemicals.

 

[Research 1st]

Thanks for the reply hixxy, it's good to know the scan looks at multiple chemicals, so you only need one scan, so less overall cost than repeating for each individual chemical looked at. This might be of interest, as a significant proportion of CFS patients have elevated brain lactate using MRS scanning...

MRS in Mitochondrial Diseases: Lactate and NAA changes

Mitochondrial disease represents a particularly prominent set of diseases that show MRS changes due to the consequences of impaired OXPHOS. The disruption of the ETC and consequent depletion of NAD+ and NADP+ shifts metabolism from the tricarboxylic acid cycle to glycolysis. The glycolytic by-product lactate is the primary abnormality detected in mitochondrial disease. This can then be measured along with numerous markers of cellular integrity and energetics (e.g. myo-inositol, choline, creatine, and NAA). In mitochondrial diseases, lactate elevations are suggested to range from 3−11 mM (Wilchowski et al., 1999) with other studies reporting average levels of approximately 6 mM (Saitoh et al., 1998; Isobe et al., 2007).

The most consistent MRS change accompanying increased lactate in mitochondrial disease is decreased NAA, suggestive of cellular compromise. While elevations in lactate and decreases in NAA occur in other diseases, for example stroke and seizures (Kingsley et al., 2006), such diseases are typically distinct in clinical work-up and MRI abnormalities. In the following summary, owing to the preponderance of lactate and NAA changes in mitochondrial disease, these metabolites are summarized first, followed by a detailed discussion of myo-inositol, choline, and creatine, with a brief discussion of future studies increasing specificity of measurement. Next, a very specific MRS biomarker in complex II disease, succinate, is described, followed by a summary of how MRS-visible biomarkers may be used to monitor therapeutic interventions in these heterogeneous diseases.
The phenotypic heterogeneity of mitochondrial patients can result in some patients not demonstrating marked lactate elevations (Lin et al., 2003; Bianchi et al., 2003), due to variability in disease state and regional sampling. There is the possibility that variability in regional sampling limits detection in some subjects. In some cases, propan-1,2-diol, localized at 1.1 ppm, can be mistaken for lactate (Figure 7; Cady et al., 1994).

Source:
Neuroimaging of Mitochondrial Disease, 4.1, page 8.
Russell P. Saneto, Seth D. Friedman, and Dennis W. W. Shaw
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2600593/

 

[raghav]

@Research 1st There was no injection. I had had an EEG and the neurologist a professor and very highly rated said it was due to hippocampal sclerosis and he said the seizures (partial in my case) could be caused by both hippocampus firing abnormally or it could be restricted to one side only. If it had been on my right brain he said it could be surgically removed (Anterior Temporal Lobectomy ATLE).

So when I went for the scan (it was part of an epilepsy package) I told the radiologist in advance to look for problems in the hippocampus. So maybe that helped him to focus on the hippocampus. The report states I had dense mossy fiber in my left hippocampus and the volume had shrunk by 20% compared to the right. It stated elevated levels of N acetyl aspartate. I dont know whether the spectroscopy could automatically scan for various suspected chemicals. At that time I did not know that it was ME / CFS that I had.

Anyway when I went back to the neuro with the scan report he said surgery was ruled out since left brain was my dominant and it controlled many aspects like memory and language skills. He also said there was not much known about the role of hippocampus(in 2010).

I had had an MRI in 1995. It turned out normal. At that time I had an abnormal VEP test result (Visually Evoked Potential). One optic nerve it was 100 milliseconds and in the other it was 125 . So the neuro at that time suspected MS due to my vision symptoms of after images and sensitivity to light. But six months later the test was normal. So he did not know what to do and put me on alprazolam. They had absolutely no clue as to what was happening.

 

[raghav]

@Research 1st You have mentioned that NAA levels are low in mito diseases. But in Jarred Younger's presentation he found elevated levels of Lactate, N acetyl aspartate, Cr(I suppose that is creatinine) and Cho (Choline ?) from the graph he presented.

 

[Research 1st]

@Research 1st You have mentioned that NAA levels are low in mito diseases. But in Jarred Younger's presentation he found elevated levels of Lactate, N acetyl aspartate, Cr(I suppose that is creatinine) and Cho (Choline ?) from the graph he presented.

Hi. Yes I was showing that a mito disease that shares our high Lactate BUT, as a classic metabolic disease like in neurological disease also (e.g. MS) has reduced NAA - the opposite of the Younger et al CFS study. However, not everyone is in agreement NAA is a reliable indicator for neuronal viability, such as from the findings in this study in sickle cell.

Our findings call into question the role of NAA as a marker of the number of viable neurons in brain tissue. Many other observations may also be problematic if NAA is to be interpreted as a marker of neuronal viability. The key issue is that if NAA is a neuronal marker, it should be present whenever neurons are present, and it should be stable under conditions in which neuronal number is stable. Yet, a case report of a child with only mild developmental disability described no NAA resonance at all in the brain (1). The NAA peak is also known to transiently decrease after acute brain injury (19), and NAA can show stable increases after therapy for moyamoya disease (20), amyotrophic lateral sclerosis (21), or Wernicke encephalopathy (22). The finding that NAA deficits can be reversed over a relatively short period argues strongly that NAA is not a reliable marker of neuronal loss. Furthermore, NAA levels can be chronically elevated in disease states not associated with neuronal proliferation, including Canavan disease (23), Pelizaeus-Merzbacher disease (24), and familial bipolar I disorder (25). In aggregate, these results suggest that NAA is not a reliable marker of viable neurons (19, 26).

Source:
Abnormally High Levels of Brain N-Acetylaspartate in Children with Sickle Cell Disease
R. Grant Steen and Robert J. Ogg
American Journal of Neuroradiology March 2005, 26 (3) 463-468;
Source: http://www.ajnr.org/content/26/3/463.long

What they're saying is if sickle cell can injure you brain neurons, so NAA should be low, then why in their study is it high...

Either way, the Younger et al/Nakatomi neuroinflammation studies (that compliment each other) need to be repeated on very severely affected CFS patients which is a catch 22 if the patient is in a dark room, can't be moved/touched and is expected to lay in a claustrophobic tube in a brightly lit room with a loud machine!

Sometimes I think we all forget this, the most sick CFS patients never get in a research study involving brain scanning, or exercise studies. Yet in other conditions, they do. Even patients who survive heart attacks do exercise studies and stroke patients also get scanned. Our illness is very specific in how it's hidden, and also because if a research uses strict CDC CFS criteria, then patients with diagnosable organic diseases are then removed from participating in CFS research. Naturally if you do that, you remove the most interesting findings.

Imagine studying HIV and removing patients who develop dementia ,cancer, or pneumonia as they 'don't have pure AIDS'. This is why our research discovery has been held back for so long, not just because of research funding. It seems the only person to be aware of this, due to his own son, is Ron Davis who had the idea recently of looking at the severely affected. So for me, I'd love to know if the severely affected have the same level of changes on brain scans, including MRS.

 

[Research 1st]

@Research 1st

I had had an MRI in 1995. It turned out normal. At that time I had an abnormal VEP test result (Visually Evoked Potential). One optic nerve it was 100 milliseconds and in the other it was 125 . So the neuro at that time suspected MS due to my vision symptoms of after images and sensitivity to light. But six months later the test was normal. So he did not know what to do and put me on alprazolam. They had absolutely no clue as to what was happening.

Optic neuritis (ON) can do that. Fluctuating results if you were having an attack of ON during the VEP test. If you were, it would explain why on repeat, the test was normal.