Disequilibrium, Rather than [POTS], Is the Primary Determinant of Orthostatic Intolerance in Patients with [LC], 2026, Miwa

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Disequilibrium, Rather than Postural Orthostatic Tachycardia Syndrome, Is the Primary Determinant of Orthostatic Intolerance in Patients with Long COVID

Miwa, Kunihisa

Background
Orthostatic intolerance (OI) is an important factor affecting daily functional capacity in patients with long COVID. Traditionally, most OI symptoms have been attributed to exaggerated sympathetic nervous system activation associated with postural orthostatic tachycardia syndrome (POTS). Disequilibrium, also referred to as postural instability, may contribute to the development of OI in patients with long COVID.

Methods
This study evaluated 32 patients with long COVID using neurological examinations and the active 10-min standing test. Disequilibrium was assessed using the Romberg and tandem gait tests. OI was defined as the inability to complete the active 10-min standing test.

Results
Seven patients (22%) were diagnosed with OI. None of them had POTS, whereas six (86%) demonstrated disequilibrium, as detected by the Romberg and/or tandem gait test. POTS was observed in eight patients (25%), none of whom had OI. Disequilibrium was observed in nine patients (28%), six of whom (67%) had OI.

Multiple regression analysis revealed that disequilibrium was positively associated with OI (r = 0.64, p < 0.001), whereas POTS was inversely associated (r = −0.38, p < 0.05).

After 6 weeks of oral minocycline treatment in six patients and 2 weeks of repetitive transcranial magnetic stimulation therapy following minocycline in the other one patient, symptom amelioration was reported in six patients with OI. OI concomitant with disequilibrium recovered in five of the six patients treated and tested, although one patient who experienced symptom recovery failed to undergo the repeated standing test.

Conclusions
Disequilibrium, rather than POTS, was the primary determinant of OI in patients with long COVID.

Web | DOI | PDF | Journal of Clinical Medicine | Open Access
 
Weird stuff. Disequilibrium seems to be mostly analogous to lightheadedness here, but also mostly analogous to what orthostatic intolerance describes, so mostly circular. I have no idea how they make out that this is a primary determinant simply because it's rather common. Thirst is a common symptom of diabetes, this hardly makes it a determinant, primary or even secondary.

I've long had roughly what they describe. My balance is generally fine, I have excellent proprioception, but indeed when I close my eyes my balance becomes much less steady. It's a mostly minor issue, though, so not something I would ever think of mentioning. It seems more of a common symptom, a minor one that rarely gets asked about and seldom mentioned because it's so minor. I don't think it makes sense to think of POTS as a primary determinant of OI, so the premise is, uh, odd.
The paper said:
POTS was observed in eight patients (25%), none of whom had OI
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This seems obviously wrong to me. I can't make sense of POTS that isn't also OI.

Damn is this all a giant mess.
 
rvallee said:
This seems obviously wrong to me. I can't make sense of POTS that isn't also OI.
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If it is just POT it makes perfect sense. Postural tachycardia is not necessarily associated with any orthostatic intolerance.

rvallee said:
My balance is generally fine, I have excellent proprioception, but indeed when I close my eyes my balance becomes much less steady. It's a mostly minor issue,
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The emergence of unsteadiness when closing eyes is an important and pretty reliable neurological sign indicating that the person is relying more on vision and proprioception for stability than is normal. It usually indicates a failure of vestibular function or something more central in midbrain. But in someone with severe 'flu' it may just indicate the severe 'flu'. It would make sense to me that it might show up in ME/CFS without a specific vestibular problem.
 
I have orthostatic intolerance (OI). I thought my symptoms were mostly due to dropping blood pressure. Could disequilibrium be a factor?

I often get an increase in heart rate when standing. I'm not sure if I qualify for POTS now but at one point I did according to my cardiologist. My other diagnosis was NMH (Neurally Mediated Hypotension) but I'm not sure how doctors/researchers view that diagnosis now (too old? outdated?).

Heart rate increases are not much of a problem for me compared to the (delayed) drop in blood pressure. I fainted on the tilt table test after 20 minutes. I get lots of presyncope symptoms if I have to stand still (at worst case I've had to sit down on the ground to avoid fainting). Moving around makes it better but eventually that's not enough and I must sit down. Lying down is even better.

I have no idea how disequilibrium relates to blood pressure drops (if at all) but I thought I'd ask about it.

Sometimes it seems like folks focus more on the heart rate increase part of OI and don't talk about blood pressure drops. But maybe I'm an unusual case? Maybe most patients don't get blood pressure drops? Or is it that blood pressure does not get measured as often?
 
ahimsa said:
Sometimes it seems like folks focus more on the heart rate increase part of OI and don't talk about blood pressure drops. But maybe I'm an unusual case? Maybe most patients don't get blood pressure drops? Or is it that blood pressure does not get measured as often?
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I've come across orthostatic hypotension* a lot but first time hearing about NMH. My ME/CFS was triggered by COVID, so my reading and interactions have been skewed towards LC and only limited to the last few years.

* drop of >20 mm Hg systolic or >10 mm Hg diastolic within 3 minutes of standing
 
ahimsa said:
Sometimes it seems like folks focus more on the heart rate increase part of OI and don't talk about blood pressure drops. But maybe I'm an unusual case? Maybe most patients don't get blood pressure drops? Or is it that blood pressure does not get measured as often?
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You might know this already, but PoTS diagnosic criteria exclude othostatic hypotension and therefore blood pressure should always be measured when testing for PoTS.

I don't know why people focus on PoTS more than OH. It would be interesting to know how prevalent each is in people with ME/CFS and OI.
 
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Jonathan Edwards said:
The emergence of unsteadiness when closing eyes is an important and pretty reliable neurological sign indicating that the person is relying more on vision and proprioception for stability than is normal.
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I've been unable to balance with my eyes shut for as long as I remember, which I thought was just dyspraxia—am one of those people who've never caught a thrown ball or been able to walk down stairs without carefully watching every step.

But I also get so dizzy I can't sit in a rocking chair and have only ever been on one fairground ride (I blacked out), so I suppose it might be vestibular.

Or my mam was right, and I'm just clumsy and hopeless. :emoji_wink:
 
InitialConditions said:
I don't know why people focus on PoTS more than OH.
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Some people always refer to their problem as POTS but if you get into conversation, it turns out they were never diagnosed with POTS but with OI and/or OH. I don't know if they prefer to call it POTS because of disinformation from their doctors or because they think POTS is a more recognised and supported condition.
 
Kitty said:
I've been unable to balance with my eyes shut for as long as I remember, which I thought was just dyspraxia—am one of those people who've never caught a thrown ball or been able to walk down stairs without carefully watching every step.
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It does not have to be vestibular. You work that out by going through all the other neurological signs. But a positive Romberg test (which is this) is abnormal and usually has an identifiable explanation.

Of course, someone with ME/CFS with OI will have OI with their eyes open so the test is not actually showing the mechanism of OI. But the test indicates that your normal set of balance mechanisms is not fully operating and I don't think it would be surprising if it showed up if the mechanism was similar to that in acute infection.
 
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