Orthostatic intolerance without postural tachycardia: how much dysautonomia?, 2013, Parsaik et al.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902804/

Ajay K Parsaik, Wolfgang Singer, Thomas G Allison, David M Sletten, Michael J Joyner, Eduardo E Benarroch, Phillip A Low, Paola Sandroni (Department of Neurology, Mayo Clinic, Rochester, Minnesota)

Received 19 November 2012, Accepted 09 May 2013, Published 01 June 2013

Background
Chronic symptoms of orthostatic intolerance occur in postural tachycardia syndrome (POTS) and patients with orthostatic intolerance (OI) without tachycardia. We recently reported that deconditioning is almost universal in both patient groups. In this study, we focussed on the question of how much dysautonomia, besides orthostatic tachycardia, is there in POTS vs. OI, and how the two groups compare in regards to clinical, autonomic, laboratory, and exercise variables.

Methods
We retrospectively studied all patients referred for orthostatic intolerance at Mayo Clinic between January 2006 and June 2011, who underwent standardized autonomic and exercise testing.

Results
Eighty-four POTS and 100 OI fulfilled inclusion criteria, 89 % were females. The mean age was 25 and 32 years, respectively. Clinical presentation, autonomic parameters, laboratory findings, and degree of deconditioning were overall similar between the two groups, except for the excessive orthostatic heart rate (HR) rise and mild vasomotor findings observed in POTS but not in OI (slightly larger Valsalva ratio and incomplete blood pressure recovery during Valsalva). Both groups responded poorly to various medications. Severely deconditioned patients were similar to non-deconditioned patients, except for 24 h urine volume (1,555 vs. 2,417 ml), sweat loss on thermoregulatory sweat test (1.5 vs. 0.5 %), and few respiratory parameters during exercise, which are likely clinically insignificant.

Conclusion
Though similar in clinical presentation, POTS and OI are different entities with greater, albeit still mild, dysautonomia in POTS. The clinical and pathophysiological relevance of minimal dysautonomia in the absence of orthostatic tachycardia as seen in OI remain uncertain.

 

Being written in 2012, this is showing its age. To give an example of one outdated assumption made in this paper:

In 2014 we had this study:
REDUCED CEREBRAL BLOOD FLOW WITH ORTHOSTASIS PRECEDES HYPOCAPNIC HYPERPNEA, SYMPATHETIC ACTIVATION AND POTS (nih.gov)

But aside from that specific point, the author's general emphasis on deconditioning is far too strong. We know from other work now that any deconditioning is secondary in most cases, something that is only being reinforced with very recent post-COVID case studies that include immediate dysautonomia onset.

 

I was curious about what they mean by deconditioning and:

Is that an official thing? Or just something people use because it sounds relevant? Or are those patients just sicker? How do they tell the difference?

Further down there's this:

Very few people actually experience this. In the discussion around this sentence I see no examination of whether they checked those things in their participants, which seems like a gross oversight. Sounds like a mere assumption. And it's followed by:

So it sounds like deconditioning is nothing but an assumption that no one actually checks and that the disease state, still a mystery, is a much more likely explanation.

Because this is always framed around exercise intolerance, understood as people being unable to go jogging and sustain a reasonable performance, rather than exertion from even the lightest of daily activities. Any exercise arduous enough to do a VO2 measurement will be far and above that level of exertion. We're talking about people struggling to do the most minimal things, not people annoyed that they can't run or party all night like they used to when they were 20 year-olds.