Objective
to investigate the relationships between self-reported cognitive abilities, psychological symptoms and neuropsychological outcomes in PSS.
Methods
PSS patients and healthy controls completed a comprehensive neuropsychometric battery and questionnaires: the Centers for Epidemiological Scale-Depression, the Profile of Fatigue- mental domain (Prof-M) for cognitive symptoms, Fatigue Severity Scale and the Short-Form McGill Pain Questionnaire.
Results
Female PSS patients (N=39) were similar to controls (N=17) in estimated pre-morbid intellectual function, age and education. Depression (p=.002), cognitive symptoms (p=.001), fatigue (p=.000003) and pain (p=.024) scores were greater in the patient group. PSS patients demonstrated inferior performance relative to controls in psychomotor processing (p=.027) and verbal reasoning (p=.007). PSS patients with and without depression had similar performance on multiple tests, but depressed patients had significantly lower scores for executive function (p=.041). Cognitive symptoms correlated with verbal memory (p=.048), whereas pain correlated with executive function measures (Stroop, p=.017) and working memory (Trails B, p=.036). In the regression model, depression and verbal memory were independent predictors that accounted for 61 % of the variance in cognitive symptoms.
Conclusion
The Prof-M is a simple self-report measure which could be useful in screening PSS subjects who may benefit from detailed psychometric evaluation. Our results are consistent with the hypothesis that depression and verbal memory impairment are overlapping but independent aspects of neural involvement in PSS. While pain and depression are significant confounders of cognitive function in PSS, this study suggests that impaired verbal reasoning ability in PSS is not attributable to pain or depression.
Objective: To date, very few studies investigating neurocognitive deficits in COVID-19 have been published. This case series addresses cognition in post-COVID-19 patient by describing three patients in acute rehabilitation to inform a model of cognitive sequelae of COVID-19. Methods: Three English-speaking inpatients with severe symptoms and long-term intensive care unit (ICU) treatment are described. All patients had a premorbid history of hypertension and hyperlipidemia and experienced delirium and hypoxemia when hospitalized. Patient 1 is a 62-year-old male with 15 years of education with additional history of obstructive sleep apnea and type 2 diabetes. Patient 2 is a 73-year-old female with 12 years of education with a premorbid medical history of alcohol use disorder and Guillain-Barre syndrome. Patient 3 is a 75-year-old male with 14 years of education. No patients had premorbid psychiatric histories. Results: The three patients demonstrated deficits on formal neuropsychological testing, particularly with encoding and verbal fluency. Memory measures improved with a more structured story memory task compared to a lessstructured verbal list-learning task, suggesting executive dysfunction impacted learning. None of the patients demonstrated rapid forgetting of information. Two patients endorsed new depressive and/or anxiety symptoms. Conclusions: The results suggest evidence for neurocognitive deficits after severe COVID-19 infection, particularly in encoding and verbal fluency. These results were interpreted with caution given the limited number of patients and the telephone-based battery. The specific mechanism that caused these cognitive deficits in these individuals remains unclear. A proposed three-stage model of cognitive dysfunction is described to help guide future research.
In this exploratory study, frontal region WM microstructure alterations accompanied cognitive symptoms and were associated with mild cognitive impairment in PSS. While additional study is warranted to assess the specificity and stability of these results, DTI could provide novel insight into the pathological processes accompanying the subtle cognitive dysfunction commonly experienced by PSS patients.
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