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Coronavirus: Information from the Front Lines
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Re: Correlation To Significant Cognitive Reduction Post Covid Found In Large UK Studymeisha, that's why I put "Correlation" in the title of the post. However, your assertions about experimental design are unnecessarily restrictive. The study authors recognize and do not ignore the issues involved in drawing inferences about causal relationships from cross-group studies. If you are familiar with the use of linear models in statistical analysis, please read (or re-read) the Methods, Results, and Discussion sections of the actual study (linked in my previous post). A couple of excerpts: The GLM [Generalized Linear Model] was re-estimated including confirmation of COVID-19 by biological test as a main effect (Table S5a). In proportion with the number of UK confirmed cases when the bulk of data were collected, 386 people reported a positive biological test, including 86% of the hospitalised with ventilator sub-group. There were significant main effects of positive test (F(1,81,326) = 12.487 p = 0.0004 estimate = −0.19SDs) and respiratory severity (F(5,81,326) = 6.7 p = 3.165e-06). Intriguingly though, the interaction was non-significant (F(4,81,326) = 0.81 p = 0.51), indicating a possible deficit for mild cases who were bio-positive for COVID-19. A further GLM restricted to those who reported no breathing difficulties (bio-positive = 212 vs. suspected = 8,726) confirmed this (Fig. 2b, Table S5b), with a robustly greater global performance deficit for bio-positive cases (t=−2.592 p = 0.0048 (one tailed) estimate = −0.18SDs). Repeating the analysis for people who reported staying at home with breathing difficulty bio-positive = 100 suspected 0.4745 estimate = 0.0531SDs). Taken together, these findings indicate that the cognitive impairments detected in COVID-19 survivors were unlikely to reflect pre-morbid differences. A common challenge in studies of COVID-19 is that differences between people who have vs. have not been ill could relate to premorbid differences. To address this issue, a linear model was trained on the broader independent GBIT dataset (N = 269,264) to predict general cognitive performance based on age (to the third order), sex, handedness, ethnicity, first language, country of residence, occupational status and earnings. Predicted and observed general performance correlated substantially r = 0.53), providing a proxy measure of premorbid intelligence of comparable performance to common explicit tests such as the National Adult Reading Test []. Regression of the same linear model with respiratory severity as the predictor indicated that people who were ill would on average be expected to have marginally higher as opposed to lower cognitive performance (Table S6). This relationship did not vary in a simple linear manner with symptom severity. Furthermore, when a follow up questionnaire was deployed in late December 2020, 275 respondents indicated that they had subsequently been ill with COVID-19 and received a positive biological test. Their baseline global cognitive scores did not differ significantly from the 7522 respondents who had not been ill (t = 0.7151, p = 0.4745 estimate = 0.0531SDs). Taken together, these findings indicate that the cognitive impairments detected in COVID-19 survivors were unlikely to reflect pre-morbid differences. One possibility was that the observed cognitive deficits related to ongoing symptoms of COVID-19 infection, e.g., high temperature or respiratory problems. 4.8% of participants who were ill reported having residual symptoms, including 84.1% of the ventilator group, 12.2% hospitalised, 9.2% assisted at home, 5.8% unassisted and 3.8% without respiratory problems. Notably, 24.4% of participants who had positive biological tests reported persistent symptoms of illness compared with 4.2% who had not. When report of residual COVID-19 symptoms was included in the GLM (Table S7), the main effect of respiratory severity was undiminished (F(5, 81,287) = 8.2422 p = 8.54E-08). The main effect of residual symptoms was formally non-significant and of small effect size (F(1, 81,287) = 1.0633 p = 0.302 estimate = −0.0440 SDs). We further examined whether there was a relationship between cognitive performance and time since symptom onset (Fig. S1) amongst bio-confirmed cases who did not report residual symptoms. In this sub-group, mean time from symptom onset was 1.96 months +/- 1.65SDs with an upper limit of 9 months. Analyzing this sub-group with time since symptom onset as the predictor showed no significant correlation (F(1,290) = 0.222 p = 0.638). Furthermore, expanding the analysis include those who were not bio-confirmed (mean time = 2.4610, SD=1.3481, max = 11) also showed no significant relationship between time and the magnitude of the observed deficit (F(1,12078) = 2.1196 p = 0.14545). Another possibility was that the observed cognitive deficits had a basis in pre-existing conditions. When a GLM was estimated with additional predictors for common pre-existing conditions and 12 mood self-assessment items capturing aspects including depression, anxiety, insomnia, tiredness (Table S8), a number of them showed the expected association with reduced cognitive performance. However, the statistical significance and scale of the respiratory severity main effect remained approximately the same (F(5, 81,304) = 9.3355 p = 6.65E-09). Furthermore, the effect size for those who had been hospitalized was substantial relative to the other conditions examined.= 3,286) showed a similar scaled deficit (t = −2.25 p = 0.012 (one tailed) estimate = −0.23SDs). A larger relationship was evident amongst cases who went to hospital but were not put on a ventilator (bio-positive = 22 vs suspected = 126, t=−1.7923 p = 0.0375 (one tailed) estimate = −0.41SDs). And Our analyses provide converging evidence to support the hypothesis that COVID-19 infection is associated with cognitive deficits that persist into the recovery phase. The observed deficits varied in scale with respiratory symptom severity, related to positive biological verification of having had the virus even amongst milder cases, could not be explained by differences in age, education or other demographic and socioeconomic variables, remained in those who had no other residual symptoms and was of greater scale than common pre-existing conditions that are associated with virus susceptibility and cognitive problems. The scale of the observed deficit was not insubstantial; the 0.47 SD global composite score reduction for the hospitalized with ventilator sub-group was greater than the average 10-year decline in global performance between the ages of 20 to 70 within this dataset. It was larger than the mean deficit of 480 people who indicated they had previously suffered a stroke (−0.24SDs) and the 998 who reported learning disabilities (−0.38SDs). For comparison, in a classic intelligence test, 0.47 SDs equates to a 7-point difference in IQ. |
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