About 10 Percent Of COVID-19 Infected Individuals Will Suffer Executive Dysfunction Issues

A new study by researchers from University of Waterloo- Ontario, Canada has found that roughly 10 percent of post-COVID individuals are like to suffer from executive dysfunction.

Executive dysfunction is a term for the range of cognitive, emotional and behavioral difficulties which often occur after injury to the frontal lobes of the brain or in some cases due to injury caused as a result of viral pathogens.

Impairment of executive functions is common after acquired brain injury and has a profound effect on many aspects of everyday life. Executive function is a set of skills that enable you to do things such as:

-paying attention
-remembering information
-multitasking
 
These skills are important for planning, organization, strategizing, paying attention to little details and time management.

Common symptoms of executive dysfunction include:

-misplacing papers, homework, or work or school materials.
-difficulty with time management.
-difficulty organizing schedules.
-trouble keeping one’s office or bedroom organized.
-constantly losing personal items.
-difficulty dealing with frustration or setbacks.
-trouble with memory recall or following multistep directions
-inability to self-monitor emotions or behavior
(I know it sounds like some things we see in Biden!)
 
The study was aimed at determining whether SARS-CoV-2 infection and COVID-19 symptom severity were associated with executive dysfunction among members of the general population, including those not hospitalized or exposed to intubation.
 
The NEUROCOVID study involved cross-sectional observation research with data from an ongoing national cohort study of young and middle-aged adults. The Canadian COVID-19 Experiences Survey (CCES) involves 1,958 adults with equal representation of vaccinated and vaccine hesitant adults between the ages of 18 and 54 years.
 
The study was a population-based survey of community dwelling adults, representative of the broader Canadian population. The participants included men and women between 18 and 54 years of age from English and French speaking provinces. The sample comprised 1,958 adults with a mean age of 37 years (SD=10.4); 60.8% were female.
 
SARS-CoV-2 infection with COVID-19 symptoms of any severity, ranging from negligible to life-threatening infection requiring hospitalization.

The symptoms of cognitive dysfunction were assessed via an abbreviated form of the Barkley Deficits in Executive Functioning Scale (BDEFS).
 
The study findings showed that of those who reported a prior SARS-CoV-2 infection regardless of COVID-19msymptom severity (Madj=1.89, SE=0.08, CI: 1.74, 2.04; n=175) reported a significantly higher number of symptoms of executive dysfunction than their non-infected counterparts (Madj=1.63, SE=0.08, CI: 1.47,1.80; n=1,599; β=0.26, p=.001).
 
Among those infected, there was a dose-response relationship between COVID-19 symptom severity and level of executive dysfunction, with moderate (β=0.23, CI: 0.003-0.46) and very/extremely severe (β= 0.69, CI: 0.22-1.16) COVID-19 symptoms being associated with significantly greater dysfunction.
 
These effects remained reliable and of similar magnitude after removing those who had been received intubation.
 
The study findings concluded that positive SARS-CoV-2 infection history and COVID-19 symptom severity are associated with executive dysfunction among young and middle-aged adults with no history of medically induced coma.
 
The study findings were published on a preprint server and are currently being peer reviewed. https://www.medrxiv.org/content/10.1101/2022.01.01.22268614v1
 
Accordingly, there are several hypothesized mechanisms by which SARS-CoV-2 infection may produce cognitive dysfunction, including encephalitis, coagulopathy, cytokine storm, hypoxia, and megakaryocyte invasion. https://pubmed.ncbi.nlm.nih.gov/33576767/
 
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7801840/
 
https://www.nature.com/articles/s41582-020-00453-w
 
This present study cannot distinguish among these neurophysiological mechanisms, or others that may yet be identified.
 
The study findings do not preclude the possibility that symptoms of cognitive dysfunction are influenced by reporting biases among those who are continuing to experience emotional distress following the measurement period. Given that the effects of negative mood on symptom reporting is causally established, and given that mood impacts of the COVID-19 pandemic are well-documented, this possibility cannot be definitively excluded.
 
At least one prior population-based study however has found similar dose response effects using performance-based measures of cognitive function (i.e., cognitive tasks rather than reported symptoms).
https://www.cuimc.columbia.edu/rehab/frequency-and-profile-objective-cognitive-deficits-hospitalized-patients-recovering-covid-19

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Cognitive dysfunction is one of the potential adverse consequences of SARS-CoV-2 infection. It is understood that SARS-CoV-2 could impact the brain through a number of non-exclusive, indirect mechanisms including hypoxia, thrombosis, coagulopathy, cytokine storm, and megakaryocyte invasion^1-6 .

Studies of hospitalized patients have revealed cognitive deficits in the areas of memory, spatial navigation, attention, short- term memory, and executive function^5,7 Further, the cognitive impairments following SARS-Cov-2 infection may persist after the acute phase of infection ⁵, a phenomenon known as “long covid”^8,9.

Several studies have reported reliable evidence of cognitive dysfunction among those previously infected with SARS-CoV-2.^{7, 10-14} However, some of these studies are limited by non-representative samples and lack of comparison to non-infected controls in the general population.

Examination of a population-based sample including asymptomatic and minimally symptomatic individuals, coupled with a control sample of non-infected individuals from the same population facilitates quantification of the reliability and magnitude of SARS-CoV-2 infection impacts on cognition, if they do indeed exist. Beyond the above, relatively little is known about the extent to which cognitive deficits are predicted by age or sex, as demographic moderators.

The current study reports findings from a population survey of 1,958 adults in the general population, who reported cognitive status, SARS-CoV-2 infection history, and COVID-19 symptom severity. It was hypothesized based on prior research^{7, 10-14} that (1) SARS-CoV-2 infection history would be associated with greater symptoms of executive dysfunction, and (2) severity of COVID-19 symptoms would be positively correlated with severity of cognitive dysfunction, in a dose response manner.

Based on the increased sensitivity of higher cognitive functions to environmental and systemic insults, it was expected that older adults would be more susceptible to infection-related executive dysfunction than younger adults.

Discussion

In this population-representative cohort of community-dwelling adults, those with a positive history of SARS-CoV-2 infection reported more symptoms of cognitive dysfunction than those with no such history. This effect was stronger for men than for women, and for younger versus older adults.

A dose-response relationship between COVID-19 symptom severity and magnitude of cognitive dysfunction was evident such that increasing infection severity was associated with greater symptoms of cognitive dysfunction. Importantly, reliable effects of positive SARS-CoV-2 infection history and COVID-19 symptom severity on cognitive dysfunction were evident even in this sample of individuals not typically subject to age-related cognitive decline (ages 18 to 54) and not exposed to medically induced coma via hospital-based treatment for severe COVID-19. Our findings were similar to a prior report of executive dysfunction as correlated with COVID-19 symptom severity in a large population sample¹³.

There are several hypothesized mechanisms by which SARS-CoV-2 infection may produce cognitive dysfunction, including encephalitis, coagulopathy, cytokine storm, hypoxia, and megakaryocyte invasion^4,5,6. The current investigation cannot distinguish among these neurophysiological mechanisms, or others that may yet be identified.

The current findings do not preclude the possibility that symptoms of cognitive dysfunction are influenced by reporting biases among those who are continuing to experience emotional distress following the measurement period. Given that the effects of negative mood on symptom reporting is causally established¹⁸, and given that mood impacts of the COVID-19 pandemic are well-documented^19-23, this possibility cannot be definitively excluded. However, at least one prior population-based study has found similar dose- response effects using performance-based measures of cognitive function (i.e., cognitive tasks rather than reported symptoms).⁷

It is not clear why there appeared to be a stronger link between SARS-CoV-2 infection and cognitive dysfunction in younger- as compared with middled aged adults. It is possible that such deficits were more obvious to younger adults, given that a higher proportion would be in educational programs wherein lapses in attention and concentration may have been more salient to them.

In either case, it is not clear how consequential symptoms of cognitive dysfunction would be expected to be, even if reliable across studies. It is not uncommon for other types of viral infections to cause symptoms of cognitive dysfunction, including the seasonal flu, herpes, MERS, Zika and Varicella (chickenpox)^24-28. Documenting the stability and functional impact of any SARS-CoV-2 infection impairments in cognition will be important.

Finally, given that the predominant SARS-CoV-2 variant during the time of the survey was Delta, the findings are applicable only to the Delta and earlier variants. Moreover, the retrospective nature of the study does not allow us to determine with confidence which infections were attributable to Delta versus earlier variants. We also cannot conclude that the same associations would be observed with the Omicron variant, in particular because of the lower COVID-19 symptom severity apparent with

Omicron in comparison with earlier variants, at least based on early data^29-31. In the current (pre-Omicron) sample, we found that only moderate and higher COVID-19 symptom severities were associated with significantly elevated symptoms of executive dysfunction. Further analyses of follow-up waves of the CCEP data will enable examination of the relative impact of the Omicron variant on symptoms of executive dysfunction.