Long COVID/CFS/ME Patients

[NeuroTrope]

What do you all think about mild COVID leading to long-term cognitive impairment? I emphasize mild, since severe cases have a clear association with increased neurovascular and pulmonary burden among other signs of systemic damage. I really only see these cases in work comp scenarios where liability is pretty much a joke to establish, which may clue us in as to the motivation of the self-reported symptoms...but some people do seem to genuinely suffer. Of course there are charlatans like this guy SARS-Cov-2 Associated Neurocognitive Decline (SAND) Scan which leads to an iatrogenic effect as well.

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[Fan_of_Meehl]

What do you all think about mild COVID leading to long-term cognitive impairment? I emphasize mild, since severe cases have a clear association with increased neurovascular and pulmonary burden among other signs of systemic damage. I really only see these cases in work comp scenarios where liability is pretty much a joke to establish, which may clue us in as to the motivation of the self-reported symptoms...but some people do seem to genuinely suffer. Of course there are charlatans like this guy SARS-Cov-2 Associated Neurocognitive Decline (SAND) Scan which leads to an iatrogenic effect as well.

Has anyone laid out a specific theory with testable hypotheses regarding the supposed disease process (or neuropathological substrate) that goes from 'SARS-Cov-2 infection' to the direct expression of said distinctive neuropathological process which then uniquely causes some sort of specific and measurable 'cognitive impairment' (with other causes ruled out)?

Or is the text message 'Courtesy of the SARS-Cov-2 virus' somehow stippled onto the neuronal surfaces at a 10nm resolution (font)? That's what the 'scan' detects right?

Seems eerily reminiscient of all the literature on 'neurocognitive disorder due to mild traumatic brain injury (concussion)' to me.

 

[PsyDuck90]

The literature I’ve read has mostly suggested that ongoing cognitive complaints from “long Covid” following mild cases is iatrogenic and more often associated with other factors like mood. So similar to a “Post Concussion Syndrome,” when you treat the anxiety/depression/poor sleep, the cognitive complaints improve. This has been my experience in the few people I’ve assessed with these types of complaints as well.

 

[Fan_of_Meehl]

The literature I’ve read has mostly suggested that ongoing cognitive complaints from “long Covid” following mild cases is iatrogenic and more often associated with other factors like mood. So similar to a “Post Concussion Syndrome,” when you treat the anxiety/depression/poor sleep, the cognitive complaints improve. This has been my experience in the few people I’ve assessed with these types of complaints as well.

I guess this is a new area so hypotheses have to be tested but this also seems like an excellent example of...

When you see hoof prints, think horses not zebras.

 

[NeuroTrope]

I mostly agree but post-viral syndrome from SARS-1, Mono, even the flu is not a new phenomenon. I'm not 100% settled on the "iatrogenic/psychosomatic/misattribution" model yet but do agree that actual "brain damage" is highly unlikely to be present.

 

[PsyDr]

“Long Covid” or PASC can mean anything from “had a hemorrhagic stroke due to Covid” to “was hypoxic forever due to Covid” to “had vague complaints with zero titer evidence of ever being infected”. Oh, and the research base says that there is no discriminatory value between vague complaints and ever being infected.

The cdc and who definitions are pure crap.

 

[neurotic_cow]

I read an article recently (can’t remember where but will try to find and link) where they discussed “long covid” being essentially a subtype of functional neurological disorder, which I thought was interesting and seems pretty accurate in my experience. Also lots of secondary gain in patients I’ve seen who present with the vague “long covid brain fog” as was mentioned above.

Functional neurological disorders after COVID-19 and SARS-CoV-2 vaccines: a national multicentre observational study | Journal of Neurology, Neurosurgery & Psychiatry

 

[AcronymAllergy]

Partly depends on who you ask, what literature you review, and as PsyDr alluded to, how you're defining "long COVID"/PASC. I've certainly seen comparisons to FND, although there are folks who argue that doesn't explain/capture everything or everyone. From a clinical standpoint, I'd probably focus on addressing symptoms and presenting a consistent message of recovery and return to functioning (if there's been a functional disruption).

When there's a variable, at best, relationship between illness severity and persisting symptom report, as has been discussed, it stands to reason there are likely other contributing/causative factors.

 

[PikminOC]

I read an article recently (can’t remember where but will try to find and link) where they discussed “long covid” being essentially a subtype of functional neurological disorder, which I thought was interesting and seems pretty accurate in my experience. Also lots of secondary gain in patients I’ve seen who present with the vague “long covid brain fog” as was mentioned above.

Functional neurological disorders after COVID-19 and SARS-CoV-2 vaccines: a national multicentre observational study | Journal of Neurology, Neurosurgery & Psychiatry

Yes secondary gain I have seen too. In terms of working and disability

 

[futureapppsy2]

I’m really, really wary of calling long COVID/PASC psychosomatic at this point, because it’s literally a novel virus, some long COVID patients do have objective clinical findings (lots of new-onset tachycardias and POTS), and I’m wary of this trend in medicine to jump to “this must be psychosomatic” because we have yet to nail down a sold mechanism of action or diagnostic test yet (we used to call MS and endometriosis psychosomatic and then found that they are very much not). There are certainly patients for whom psychosomatic factors are worsening things, but I don’t think there’s enough evidence yet to say that’s all it is.

 

[futureapppsy2]

“Long Covid” or PASC can mean anything from “had a hemorrhagic stroke due to Covid” to “was hypoxic forever due to Covid” to “had vague complaints with zero titer evidence of ever being infected”. Oh, and the research base says that there is no discriminatory value between vague complaints and ever being infected.

The cdc and who definitions are pure crap.

Hasn’t 95%+ of the population in the US been infected by COVID at this point, based on titer studies? I could see COVID being somewhat like EBV, where almost everyone gets infected, the vast majority are fine (ranging from mild/asymptomatic illness to severe illness), but some have ongoing or later stage complications.

 

[cara susanna]

Wasn't there a study showing that mental health symptoms accounted for a lot of long COVID?

 

[WisNeuro]

Wasn't there a study showing that mental health symptoms accounted for a lot of long COVID?

I saw something to this effect. Not surprising, it's the same for chronic lyme's or people with a mild TBI who have continuing symptoms, personality characteristics and previous MH stuff seems to soak up most of the variance.

 

[PsyDr]

Hasn’t 95%+ of the population in the US been infected by COVID at this point, based on titer studies? I could see COVID being somewhat like EBV, where almost everyone gets infected, the vast majority are fine (ranging from mild/asymptomatic illness to severe illness), but some have ongoing or later stage complications.

If you can have “long Covid” without EVER having Covid, and there is no predictive value in developing “long Covid” from actual Covid infection, then I fail to see how prevalence has any relevance.

That’s the same reason why PCS got thrown out of the DSM.

 

[Fan_of_Meehl]

If you can have “long Covid” without EVER having Covid, and there is no predictive value in developing “long Covid” from actual Covid infection, then I fail to see how prevalence has any meaning.

That’s the same reason why PCS got thrown out of the DSM.

The fundamental distinction between the task of scientific description vs. scientific explanation. Quite apt here.

 

[futureapppsy2]

If you can have “long Covid” without EVER having Covid, and there is no predictive value in developing “long Covid” from actual Covid infection, then I fail to see how prevalence has any relevance.

That’s the same reason why PCS got thrown out of the DSM.

My point is that it's hard to say that people are developing long COVID without ever having been infected if almost everyone has been infected at least once. You don't really have a control group at that point.

 

[PsyDr]

My point is that it's hard to say that people are developing long COVID without ever having been infected if almost everyone has been infected at least once. You don't really have a control group at that point.

Despite your speculation, there is actually a body of literature that contradicts your position.

 

[futureapppsy2]

Despite your speculation, there is actually a body of literature that contradicts your position.

Not speculation, those are published infection estimates I’ve read. If you other references stating much lower infection rates, please share them. (Btw, there’s a surprising number of infectious agents with extremely high cumulative infection rates—HPV, EBV, HSV-1, etc, and a small proportion of people get long-term effects from those). Of course there are some people that have “long-term effects” that are highly or entirely psychosomatic (IMO, the strong majority of CFS/ME is heavily psychosomatic). On the other hand, one can’t really fake a new-onset arrhythmia.

 

[erg923]

if almost everyone has been infected at least once.

what's the evidence for this?

 

[futureapppsy2]

what's the evidence for this?

IHME studies out of UW give a 90% infection rate. Other estimates from the CDC seem to be about 60-70% (though those are earlier 2022 and likely underestimates due to that), so IHME may be high. We know about 20-45% of infections are asymptomatic and many others are mildly symptomatic, so a lot of these are missed unless the person happens to be enrolled in a study that does blood-based antibody testing. Honestly, COVID-19 is pretty much built for high penetration—it’s a virus that can spread both asymptomatically and pre-symptomatically, is highly contagious, and usually doesn’t debilitate people enough to completely isolate them.

 

[NeuroTrope]

I have no doubt some people will claim long COVID without ever actually contracting the disease. That doesn't explain the actual cases though.

 

[PsyDr]

Not speculation, those are published infection estimates I’ve read. If you other references stating much lower infection rates, please share them. (Btw, there’s a surprising number of infectious agents with extremely high cumulative infection rates—HPV, EBV, HSV-1, etc, and a small proportion of people get long-term effects from those). Of course there are some people that have “long-term effects” that are highly or entirely psychosomatic (IMO, the strong majority of CFS/ME is heavily psychosomatic). On the other hand, one can’t really fake a new-onset arrhythmia.

You are speculating. Prevalence does not matter if there is an actual control group. For example:

Matta, J., et al. (2021). "Association of Self-reported COVID-19 Infection and SARS-CoV-2 Serology Test Results With Persistent Physical Symptoms Among French Adults During the COVID-19 Pandemic." JAMA Intern Med.


Arguing from prevalence will not meet Freighner criteria. It's like saying FSIQ is useless, because the average FSIQ of everyone who has ever lived is 0.