Risk factors and abnormal cerebrospinal fluid associate with cognitive symptoms after mild COVID-19, 2022, Apple et al

Wyva

Wyva

Senior Member (Voting Rights)
Abstract

Cognitive post-acute sequelae of SARS-CoV-2 (PASC) can occur after mild COVID-19. Detailed clinical characterizations may inform pathogenesis. We evaluated 22 adults reporting cognitive PASC and 10 not reporting cognitive symptoms after mild SARS-CoV-2 infection through structured interviews, neuropsychological testing, and optional cerebrospinal fluid (CSF) evaluations (53%).

Delayed onset of cognitive PASC occurred in 43% and associated with younger age. Cognitive PASC participants had a higher number of pre-existing cognitive risk factors (2.5 vs. 0; p = 0.03) and higher proportion with abnormal CSF findings (77% vs. 0%; p = 0.01) versus controls. Cognitive risk factors and immunologic mechanisms may contribute to cognitive PASC pathogenesis.

Open access: https://onlinelibrary.wiley.com/doi/full/10.1002/acn3.51498
 
This looks like well intentioned research. The kind we hoped would shed light on post viral syndromes. However, probably due to practical problems like age-control matching and total control numbers, it's not particularly convincing. Some interesting results anyway

Abnormal oligoclonal banding (OCB) patterns were identified in 69% (9/13) of participants with cognitive PASC compared to 0% of cognitive controls (p = 0.03). The abnormal OCB patterns reflected matched bands in CSF and serum for 8/9 participants.
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In this small study, we identified that adults reporting new, persistent cognitive symptoms after mild SARS-CoV-2 infection had delayed symptom onset in 43% of cases, a higher median number of pre-existing cognitive risk factors and a higher proportion with CSF abnormalities compared to cognitive controls who also recovered from SARS-CoV-2 infection. The large proportion of participants reporting a delayed onset of cognitive PASC implies that events occurring after the acute period of SARS-CoV-2 infection may contribute to pathogenesis and respond to early intervention.
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The section I bolded piqued my interest. Most me/cfs patients report onset after an infection, but I do not know of any data about how long after infection. If symptoms develop in half the patients 2 months later (the timeframe referred to above), it might tell us something about what kinds of pathology are taking place and eliminate others. After all, what happens in those 2 months? If that held for me/cfs I think it would be of massive potential interest. Of course, I wasn't clear if the covid patients were still experiencing their original covid symptoms for a longer tail of say, 4 weeks, and only then reported the onset of post-covid symptoms. As I said, I would be very interested in this data in me/cfs patients. Many of us develop it after mono, where the original infection symptoms can linger and blur the line between onset of me/cfs.
 
Wyva said:
The study is explained in this article:

Cerebrospinal Fluid Offers Clues to Post-COVID ‘Brain Fog’
Over-Stimulated Immune System May Be Impetus to Cognitive Symptoms, UCSF-Led Study Shows
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“If people tell us they have new thinking and memory issues, I think we should believe them rather than require that they meet certain severity criteria.”

Cognitive symptoms have been identified in other viruses, in addition to COVID-19 and HIV. These include the coronaviruses SARS and MERS, hepatitis C and Epstein-Barr virus.
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EBV done a number on my brain.
 
My cognitive issues are a result of energy depletion and autonomic impairment. The virus I contracted didn't have a negative impact on my memory.
 
The study had a very small number of participants, so hard to draw any conclusions I think.

(CSF was taken only from 13 particpants out of the 22 in the 'cognitive' group; the control group had only 10 particpants and CSF was taken from only 4 of them .)

Two points that I found of interest:

From the article (post #2) :

"All participants underwent an in-person cognitive testing battery with a neuropsychologist, applying equivalent criteria used for HIV-associated neurocognitive disorder (HAND).

"Surprisingly, the researchers found that 13 of the 22 participants (59 percent) with cognitive symptoms met HAND criteria, compared with seven of the 10 control participants (70 percent).

" 'Comparing cognitive performance to normative references may not identify true changes, particularly in those with a high pre-COVID baseline, who may have experienced a notable drop but still fall within normal limits,' said Hellmuth."

" 'If people tell us they have new thinking and memory issues, I think we should believe them rather than require that they meet certain severity criteria.'

Good to see they acknowledge that. Even better if they searched for or developed appropriate testing.


A couple of risk-factors for cognitive issues could be relevant, too :


"The researchers also found that the participants with cognitive symptoms had an average of 2.5 cognitive risk-factors, compared with an average of less than one risk factor for participants without the symptoms.

"These risk-factors included diabetes and hypertension, which can increase the risk of stroke, mild cognitive impairment and vascular dementia; and a history of ADHD, which may make the brain more vulnerable to executive functioning issues. Other risk factors included anxiety, depression, a history of heavy alcohol or repeated stimulant use, and learning disabilities."

(Table 2 in the paper: https://onlinelibrary.wiley.com/doi/10.1002/acn3.51498 )
 
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