Structural abnormalities in the brains of POTS patients-left insula

[adreno]

Also, if they can "prove" that anxiety and depression scores match brain abnormalities, they can send off the patients to CBT.

 

[xchocoholic]

There is no difference between anxiety from POTS, and anxiety from other causes. Anxiety is still anxiety, although the causes vary. What you are saying makes no sense. If patients with POTS state they feel anxiety, they feel anxiety. The feeling of anxiety cannot be separated from it's physical underpinning (the POTS).

I only feel anxious when I'm upright. Esp after standing for 10 plus minutes. By then I'm having a petite mal, sob, overall weakness and tachycardia.

At that point I start frantically looking for a way to lean or sit down. I'm sure people who are unfamiliar with oi don't understand why I suddenly act panicked. And thru no fault of my own, I'm not polite at that point either.

A couple of my drs were surprised that my oi affects me when I'm sitting up too. I was surprised that they were surprised. Lol.

Anxiety from a psychological basis doesn't go away when someone is supine.

 

[adreno]

Anxiety from a psychological basis doesn't go away when someone is supine.

I doubt there is any anxiety (disorder) from a "psychological basis". Everything is reflected in physiology. However, anxiety both with, and without, OI is indeed possible.

And it is not like the brain abnormalities disappear when patients lie down, so they must be assigned to either having, or not having anxiety (or grouped according to severity).

 

[Seven7]

My point was that 2 different groups, w a cohort that has two different deasese but some comorbidy, Have defect in the same part of the brain!!! if we get to the details sure (right finding but bad interpretation) but we can now dig further and soubgroup those w CFS w or W/out POTs. And we can start segragating studies in a better way?!?!??!

Or maybe POTs is at the end the same deasease as CFS but the part of the brain that got attacked / infected(who knows???) is close by but the initial mechanisum is the same???


I am more courious about the implications of the "coincidence" which I am not one to believe in them. So this has to mean something.

 

[adreno]

Well, as I said before, reduced GMV in the left insula is not exactly specific to POTS (or ME) - it has been observed in other clinical groups. Until we have something specific, these studies are only mildly interesting, IMO. The findings also might not be consistent; we need replication.

Lastly, we really don't know what the findings mean. If these changes can be found across the board in many diseases/disorders then perhaps they simply reflect inflammation of certain areas, as I think Marco suggested.

I'm sorry, but I wouldn't set my hopes on neuroimaging studies finding anything really useful in the near future. Researchers have been "looking for the problem in the brain" in depression, ADHD, autism, etc for years without finding any consistent (and specific) biomarkers. Too much heterogeneity, even at the group level.

 

[adreno]

I think our best bet for now is to try to reduce inflammation of the brain. Lithium might be particularly useful, as it has been shown to increase GM volume.

 

[alex3619]

Many people with ME, CFS or POTS have encephalitis.

We need to be careful here. We do NOT have classic encephalitis, which is typically an acute short term major inflammation of the brain. I have had that, due to measles at age 7. What we probably have is diffuse, lower level of intensity, but chronic. In other words, it does not kill us or resolve in a matter of days, but can go on for decades.

The PET scans, qEEG, MRI show something is going on. It does look like microglial activation. Yet we need further research. As it stands the research does not currently meet sufficient standards to be widely accepted. Given what is happening I think it likely its only a matter of time before it does. Further, the fact that we can now find issues using multiple techniques indicates that this might be a robust finding.

 

[adreno]

Reduced insular volume in attention deficit hyperactivity disorder.

Again, non-specific.

 

[Marco]

Reduced insular volume in attention deficit hyperactivity disorder.

Again, non-specific.

Non-specificity would be a problem if you're looking for a biomarker but if it can be found to be directly relevant to the condition then non-specific isn't a problem.

 

[adreno]

Non-specificity would be a problem if you're looking for a biomarker but if it can be found to be directly relevant to the condition then non-specific isn't a problem.

I don't see how this finding tell us anything about POTS, since it is also found in many other conditions. If it's non-specific it might be due to comobidities, and not POTS itself. Perhaps you could elaborate?

 

[Marco]

I don't see how this finding tell us anything about POTS, since it is also found in many other conditions. If it's non-specific it might be due to comobidities, and not POTS itself. Perhaps you could elaborate?

There seems to an emerging consensus that despite being given discrete names, the 'major psychiatric disorders' (schizophrenia, MDD, bipolar, ASD, ADHD) may all have the same biological underpinnings but present differently in different people.

As I'd written previously (on the subject of 'ME/CFS') :

‘Atypical presentations and co-morbidity’

The situation is further complicated (if you conform to the convention that each labelled condition is a specific and discrete disease state) by ‘atypical’ presentations and ‘co-morbid’ conditions. Indeed, the high levels of atypical presentations found in these disorders suggests a fluidity is present that transcends traditional disease boundaries. In the proposed schema there is no ‘atypical’ or ‘co-morbidity’, only individuals where the symptom complex (including symptoms that do or do not fit within neat diagnostic boundaries) directly results from a neuroinflammatory state. This is a far more parsimonious explanation than to suggest that each ‘co-morbid’ condition arose simultaneously but from different underlying pathophysiologies.

 

[Research 1st]

Regarding this paper, there are many questions I'd like to know. Some of which include:

1: Where were these POTS patients recruited from.
2: Did any of them have CFS/Lyme like variants.
3: If they did not have CFS, how do they know they don't have CFS/Lyme like variants.
4: How disabled are they? Able to attend outpatients clinics? Working? Housebound?
5: As detailed below, what subset of POTS were these patients? Was deconditioning POTS excluded.
6: If a subset is known, what tests were used in addition to a TILT test to come to any definite conclusion.

People might be a little alarmed about an association to psychiatric symptoms and POTS, because of the conclusion of the authors. I wouldn't be especially. I'd note it, but not unduly worry. This is only one study.

Firstly POTS or CFS isn't categorized as psychological. Secondly a link to psychiatric symptoms in these POTS patients studies isn't necessarily a bad thing. Behavioral changes are common or indeed universal in neurological disorders. One could argue it would abnormal to have a neurological disorder, and not develop behavioral/psychological changes! People living with MS for example commonly experience mood swings and depression/anxiety.

As someone with POTS I won't 'celebrate' early from the results of one study, in a condition with multiple subsets. This is because of how POTS is diagnosed.

POTS diagnosis only requires a TILT test as the required screening tool, despite many other ways to measure autonomic dysfunction/damage in addition to the TILT test. In my view this is critically important to consider when trying to associate any possible biomarker to the POTS syndrome.


Without considering this, it's easy to get excited about structural brain abnormalities in POTS, to my knowledge it's a first and thus is exciting to some especially as already noted by other posters here, that CFS now has some similar evidence too using cutting edge imaging software.

However, when any researcher finds future imaging defects in POTS, we would ideally like to know in their published paper, what subsets of POTS these POTS patients have. To me, this would increase the value to the scientific community of any piece of POTS research, especially one with potential biomarkers.

Subsets of POTS (not universally accepted, used as a screening tool, or part of a POTS diagnosis):

Hypovolemia POTS requiring a radiology scan to assess blood volume.
Hyperadregenic POTS requring a baseline and then a standing up after a prolonged period, urine test.
Mast Cell Activation POTS - self explanatory.
Deconditioning POTS - not an uncommon claim for why people with CFS have POTS, often incorrectly.
Genetic POTS - patients with certain shared genes that make people more prone to dysautonomia.
Neuropathic/autoimmune POTS - patients have antibodies to Nicotinic Acetylcholine Receptors.

All of these questions need answering, and more importantly, the patients need assessing and diagnosed with the correct POTS subset they have or everyone remains confused, including the researchers.

 

[Seven7]

To be honest, I hang on POTs forums and some I can say do not have CFS (not overactivity issues) others I don't even know how they don't believe they have cfs, when I hear symptoms I am like hmmmmmm "just POTs?"!!!! Some complain of tiredness, lymph pain and just too many things that indicate inmune issues too.

So I am starting to wonder if a lot of them have something like CFS.