Prevalence and co-occurrence of cognitive impairment in children and young people up to 12-months post-Omicron, 2024, Foret-Bruno, Chalder+

[SNT Gatchaman]

Prevalence and co-occurrence of cognitive impairment in children and young people up to 12-months post infection with SARS-CoV-2 Omicron variant
Foret-Bruno; Shafran; Stephenson; Nugawela; Chan; Ladhani; McOwat; Mensah; Simmons; Fox Smith; D'oelsnitz; Xu; Dalrymple; Heyman; Ford; Segal; Chalder; Rojas; Pinto Pereira

BACKGROUND
Cognitive impairment is often reported after SARS-CoV-2 infection, yet evidence gaps remain. We aimed to (i) report the prevalence and characteristics of children and young people (CYP) reporting “brain fog” (i.e., cognitive impairment) 12-months post PCR-proven SARSCoV-2 infection and determine whether differences by infection status exist and (ii) explore the prevalence of CYP experiencing cognitive impairment over a 12-month period post-infection and investigate the relationship between cognitive impairment and poor mental health and wellbeing, mental fatigue and sleep problems.

METHODS
The Omicron CLoCk sub-study, set up in January 2022, collected data on first-time PCRtest-positive and PCR-proven reinfected CYP at time of testing and at 3-, 6- and 12-months posttesting. We describe the prevalence of cognitive impairment at 12-months, indicating when it was first reported. We characterise CYP experiencing cognitive impairment and use chi-squared tests to determine whether cognitive impairment prevalence varied by infection status. We explore the relationship between cognitive impairment and poor mental health and well-being, mental fatigue and trouble sleeping using validated scales. We examine associations at 3-, 6- and 12-months post-testing by infection status using Mann-Whitney U and chi-square tests.

RESULTS
At 12-months post-testing, 7.0% (24/345) of first-positives and 7.5% (27/360) of reinfected CYP experienced cognitive impairment with no difference between infection-status groups (p=0.78). The majority of these CYP experienced cognitive impairment for the first time at either time of testing or 3-months post-test (no difference between the infection-status groups; p=0.60). 70.8% of first-positives experiencing cognitive impairment at 12-months, were 15-to-17years-old as were 33.3% of reinfected CYP experiencing cognitive impairment (p<0.01). Consistently at all time points post-testing, CYP experiencing cognitive impairment were more likely to score higher on all Strengths and Difficulties Questionnaire subscales, higher on the Chalder Fatigue sub-scale for mental fatigue, lower on the Short Warwick-Edinburgh Mental Wellbeing Scale and report more trouble sleeping.

CONCLUSIONS
CYP have a fluctuating experience of cognitive impairment by 12-months post SARSCoV-2-infection. Cognitive impairment is consistently correlated with poorer sleep, behavioural and emotional functioning over a 12-month period. Clinicians should be aware of cognitive impairment post-infection and its co-occurring nature with poorer sleep, behavioural and mental health symptoms.


HIGHLIGHTS
• 12 months after SARS-CoV-2 infection, around 7% of children and young people report ‘brain fog’ i.e., cognitive impairment.

• 2.4% of children and young people experienced persistent cognitive impairment at 3-, 6- and 12-months after SARS-CoV-2 infection.

• 12 months after SARS-CoV-2 infection, more females, white ethnicities, and older at the time of first infection, children and young people reported cognitive impairment.

• Cognitive impairment co-occurs with poorer mental health, fatigue and sleep problems.

Link | PDF (Brain, Behavior, and Immunity)

 

[Hutan]

At 12-months post-testing, 7.0 % (24/345) of first-positives and 7.5 % (27/360) of reinfected CYP experienced cognitive impairment. Contrary to our original hypothesis, there was no evidence of difference between the infection-status groups (p = 0.78).

That must have challenged Chalder's story-making ability. Somehow the young people who developed brain fog on reinfection had managed to not develop brain fog during the first Covid-19 infection.

75% of the first positives are female; 66% of the reinfected are female

Index of multiple deprivation had basically no relationship with incidence

Importantly, only 2.4 % of included CYP experienced cognitive impairment consistently at 3-, 6- and 12-months suggesting that for most CYP who have this symptom, it is transient.

Third, consistently at all time-points, CYP experiencing cognitive impairment had worse mental health, were more mentally fatigued, had poorer well-being and more trouble sleeping compared to those who did not experience cognitive impairment. Of course, these difficulties are inter-related, and it is likely that these factors influence each other.

These findings highlight that several (potentially distinct) behavioural (e.g., trouble sleeping) and mental health symptoms (e.g., poor well-being) co-occur with cognitive impairment. Corresponding treatments/interventions should thus be multi-disciplinary. Further research is required to elucidate the temporal nature of these associations. For example, we do not yet know how much of the effect of SARS-CoV-2 infection on cognitive impairment is mediated by poor sleep routines. This is feasible because, for example, in adults with PCC, a review demonstrated the overall prevalence of sleep disturbance was 46 %(Chinvararak & Chalder, 2023).

 

[Hutan]

Gosh, there is entertainment of the possibility of physical damage:

Although the origins of cognitive dysfunction following SARS-CoV-2 infection has yet to be established, several hypotheses have been proposed that involve direct or indirect damage to the central nervous system by the virus, leading to chronic inflammation of brain tissues as well as neural injury via hypoxia or vascular dysfunction(Nouraeinejad, 2022). There is also an increasing literature highlighting increased brain injury after SARS-CoV-2 infection and abnormal brain imaging many months post-infection (Granholm, 2023). For example, 56 adult convalescent participants with neurological complications following COVID-19 showed elevated Glial Fibrillary Acidic Protein (a marker of astrocyte injury) and Neurofilament Light (a marker of axonal and dendritic injury) more than 6 weeks after their original infection (Michael et al., 2023). In 18 adults, longitudinal MRI data exploring brain structural changes of patients recovered from COVID-19 showed grey matter volume reduction persisted in the cerebellum, vermis, and right temporal lobe after two years (Du et al., 2023).

But, of course, it could just be due to the behavioural issues:

Alternatively, the observed cognitive dysfunction could be, in part, due to indirect effects resulting from changes in CYP’s daily life and routines during the pandemic.

Interesting that the words 'deep phenotyping' are used:

Deep phenotyping studies and neuroimaging of CYP might elucidate any underlying biological mechanisms.

An acknowledgement that their data collection approach needs improvement:

Furthermore, our single-item question, provided only a brief explanation of “confusion/memory loss” and may not fully capture the complexity of cognitive impairment that has been shown in adults with ‘brain fog’ after SARS-CoV-2 infection (e.g., Jennings et al., 2022, Hampshire et al., 2024). This may also explain why we did not observe a dose effect relationship between viral infections (reinfection vs first-positives) and their downstream effects on the brain.

 

[NelliePledge]

Chalder being an author is not associated with useful output this may be due to behavioural factors

 

[Hutan]

They are actually calling for more objective measurement of cognitive dysfunction:

An objective assessment of cognitive functioning would allow for a more nuanced understanding of the link between brain fog and everyday functioning as measured by questionnaires such as the SDQ. Importantly, we are uncertain that the concept of ‘brain fog’ existed pre-pandemic, or if it did what it was called, and the corresponding pre-pandemic prevalence. Similarly, we are unaware of pre-pandemic normative data on the mental fatigue sub-scale of the CFS.

So, all up, this paper could be worse. I'd go so far to suggest it is an anomaly - a paper with Chalder as an author that is not dreadful. Of course, a big problem, and they acknowledge this, is that they don't know what percentage of young people would report brain fog without an infection. But, they aren't immediately assuming that the cause of the brain fog is young people getting into poor sleep habits and other bad routines that can be fixed with sleep hygiene. They are allowing for the possibility of a biological mechanism. (Although I expect the paper will be used to justify behavioural improvement such as sleep hygiene interventions).

 

[Sean]

Corresponding treatments/interventions should thus be multi-disciplinary.

All roads lead to multi-disciplinary trans-diagnostic rehabilitation.

Chalder being an author is not associated with useful output this may be due to behavioural factors

 

[NelliePledge]

They do have history of providing evidence that is useful to be fair the PACE paper showing nobody returned to previous levels of work and more were receiving benefits being the one that sticks in my mind.

Not so useful in validating their own hypothesis

 

[NelliePledge]

Weaknesses in the questionnaire

Militant thinking creeping in

 

[rvallee]

Could be worse, but there is the usual "multidisciplinary teams because mental health and behavioral", but they frame sleep issues as behavioral, which is absurd, and the poor mental health is clearly a result of the illness, so that without addressing the illness, addressing the mental health is useless. So it's really just the same old, but this time they can't reasonably be dismissive and apply their "viruses don't do that" dogma. At least not fully, deniers and minimizers will keep milking the few months of restrictions for years.

Data show a commonly-found lull where impairments are lower at 6 months, but increase back to close to what they were at 3 months by the 12 month mark. Relapses are pretty common, we are usually talking about remissions rather than recoveries in many cases, all lost without long-term follow-up.

In isolation this would be unremarkable, but happening after decades of making stuff up about alternative explanations for this it just comes off as absurd. This is from a team whose first paper basically concluded: "Long Covid? I don't know, doesn't seem like there's anything here". Ladhani has been especially vocally dismissive that LC even exists.

But, hey, it was an easy paper and when you get funding, you gotta spend it. That's how you get more funding to waste in the future.

 

[Amw66]

They are actually calling for more objective measurement of cognitive dysfunction:


So, all up, this paper could be worse. I'd go so far to suggest it is an anomaly - a paper with Chalder as an author that is not dreadful. Of course, a big problem, and they acknowledge this, is that they don't know what percentage of young people would report brain fog without an infection. But, they aren't immediately assuming that the cause of the brain fog is young people getting into poor sleep habits and other bad routines that can be fixed with sleep hygiene. They are allowing for the possibility of a biological mechanism. (Although I expect the paper will be used to justify behavioural improvement such as sleep hygiene interventions).

Given the myriad of physical research anomalies ( albeit mostly in adults) they would risk becoming irrelevant if they didn't acknowledge it..