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51 Trajectories and Predictors of Cognitive Change Following COVID-19
- Daniel K Leibel, Anisha Kohli, Corinna Lathan, James Drane, Ann Parker, Adam Kaplin, Anupama Kumar, Tracy Vannorsdall
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- Journal:
- Journal of the International Neuropsychological Society / Volume 29 / Issue s1 / November 2023
- Published online by Cambridge University Press:
- 21 December 2023, pp. 48-49
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Objective:
Acute cognitive complications following COVID-19 infection have been appreciated in a subset of patients since the early months of the global pandemic. Emerging data reveal that some patients go on to experience cognitive improvement, whereas others may experience further cognitive decline. We aimed to assess trajectories and predictors of cognitive change in a sample of post-COVID-19 patients.
Participants and Methods:This prospective cohort study assessed longitudinal cognitive change in adults receiving care for COVID-19 in the Johns Hopkins Post-Acute COVID-19 Team (JH PACT) clinic. Participants self-administered the Digital Automated Neurobehavioral Assessment (DANA) battery of seven cognitive tests and a performance-based measure of cognitive fatigue on up to six occasions over six weeks. Improvement or decline between the first and last assessment was defined as change of >1 standard deviation of the baseline mean of each outcome. Potential predictors of change included demographic features (age, sex, race/ethnicity, education), COVID-19 illness characteristics (hospitalization or ICU stay, months since symptom onset), and comorbid disease burden. Analyses included measures of central tendency, independent samples t-tests, and chi-square tests of independence.
Results:Of the 36 enrolled participants, 29 (81%) completed at least one DANA assessment (M = 4.7 assessments, SD = 1.8). Those completing at least three assessments (n = 24, 66.7%) were included in the present analyses (71% female; 58% white; M age = 54 years, SD = 10.9; M education = 14.6 years, SD = 2.4; M months since COVID-19 symptom onset at recruitment = 9.8, SD = 4.7; M comorbidities = 2.8, SD = 2.0). Fatigue was the most frequently improved outcome measure, with 41.7% of participants scoring >1 standard deviation above the baseline mean fatigue score at their final assessment. Among cognitive outcomes, the greatest frequency of improvement was observed on tests assessing rapid spatial processing (37.5%), processing speed (33.3%), and memory (33.3%). There were no consistent predictors of improvement, but several subtest-specific findings emerged. Specifically, (a) more comorbidities were positively associated with rate of fatigue reduction (p = .04), (b) longer duration since COVID-19 illness was positively associated with rates of memory improvement (p = .02), (c) older age, male sex, and more comorbidities were positively associated with rate of improvement in reaction time (ps < .05), and (d) more assessments completed was positively associated with rates of improvements in working memory (ps < .05). Response inhibition (12.5%), simple reaction times (16.7%), and working memory (16.7%) showed the lowest rates of improvement over time. Declines in cognition were infrequent, with 4.2 - 8.3% (n = 1 to 2) declining on measures of procedural reaction time, spatial processing, inhibitory control, or working memory.
Conclusions:At an average of >9 months following acute COVID-19 illness, we observed longitudinal improvements in cognitive fatigue as well as processing speed, memory, and spatial reasoning. Consistent predictors of recovery were not identified, although age, sex, comorbid conditions, and time since illness predicted rates of improvement in select domains. Further analyses with a larger sample size and more stringent analyses are needed to confirm and extend these findings.
Contributors
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- By Douglas L. Arnold, Laura J. Balcer, Amit Bar-Or, Sergio E. Baranzini, Frederik Barkhof, Robert A. Bermel, Francois A. Bethoux, Dennis N. Bourdette, Richard K. Burt, Peter A. Calabresi, Zografos Caramanos, Tanuja Chitnis, Stacey S. Cofield, Jeffrey A. Cohen, Nadine Cohen, Alasdair J. Coles, Devon Conway, Stuart D. Cook, Gary R. Cutter, Peter J. Darlington, Ann Dodds-Frerichs, Ranjan Dutta, Gilles Edan, Michelle Fabian, Franz Fazekas, Massimo Filippi, Elizabeth Fisher, Paulo Fontoura, Corey C. Ford, Robert J. Fox, Natasha Frost, Alex Z. Fu, Siegrid Fuchs, Kazuo Fujihara, Kristin M. Galetta, Jeroen J.G. Geurts, Gavin Giovannoni, Nada Gligorov, Ralf Gold, Andrew D. Goodman, Myla D. Goldman, Jenny Guerre, Stephen L. Hauser, Peter B. Imrey, Douglas R. Jeffery, Stephen E. Jones, Adam I. Kaplin, Michael W. Kattan, B. Mark Keegan, Kyle C. Kern, Zhaleh Khaleeli, Samia J. Khoury, Joep Killestein, Soo Hyun Kim, R. Philip Kinkel, Stephen C. Krieger, Lauren B. Krupp, Emmanuelle Le Page, David Leppert, Scott Litwiller, Fred D. Lublin, Henry F. McFarland, Joseph C. McGowan, Don Mahad, Jahangir Maleki, Ruth Ann Marrie, Paul M. Matthews, Francesca Milanetti, Aaron E. Miller, Deborah M. Miller, Xavier Montalban, Charity J. Morgan, Ichiro Nakashima, Sridar Narayanan, Avindra Nath, Paul W. O’Connor, Jorge R. Oksenberg, A. John Petkau, Michael D. Phillips, J. Theodore Phillips, Tammy Phinney, Sean J. Pittock, Sarah M. Planchon, Chris H. Polman, Alexander Rae-Grant, Stephen M. Rao, Stephen C. Reingold, Maria A. Rocca, Richard A. Rudick, Amber R. Salter, Paula Sandler, Jaume Sastre-Garriga, John R. Scagnelli, Dana J. Serafin, Lynne Shinto, Nancy L. Sicotte, Jack H. Simon, Per Soelberg Sørensen, Ryan E. Stagg, James M. Stankiewicz, Lael A. Stone, Amy Sullivan, Matthew Sutliff, Jessica Szpak, Alan J. Thompson, Bruce D. Trapp, Helen Tremlett, Maria Trojano, Orla Tuohy, Rhonda R. Voskuhl, Marc K. Walton, Mike P. Wattjes, Emmanuelle Waubant, Martin S. Weber, Howard L Weiner, Brian G. Weinshenker, Bianca Weinstock-Guttman, Jeffrey L. Winters, Jerry S. Wolinsky, Vijayshree Yadav, E. Ann Yeh, Scott S. Zamvil
- Edited by Jeffrey A. Cohen, Richard A. Rudick
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- Book:
- Multiple Sclerosis Therapeutics
- Published online:
- 05 December 2011
- Print publication:
- 20 October 2011, pp viii-xii
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59 - Depression in multiple sclerosis
- from Section IV - Therapy in clinical practice
- Edited by Jeffrey A. Cohen, Richard A. Rudick
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- Book:
- Multiple Sclerosis Therapeutics
- Published online:
- 05 December 2011
- Print publication:
- 20 October 2011, pp 696-706
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Summary
Zamboni hypothesized that venous stasis resulting from cerebrospinal venous insufficiency (CCSVI) leads to increased iron deposition in the brain parenchyma, and that this iron triggers multiple sclerosis (MS) inflammatory activity. A number of authors have challenged the CCSVI hypothesis on several grounds including the redundancy of the venous system. CCSVI has received considerable attention from the mainstream media and the lay public. This has led to increasing pressure on physicians by patients seeking venous imaging and endovascular angioplasty, commonly referred to as the liberation procedure. New therapeutic strategies aimed at reducing venous pressures and venous reflux could be developed and might be more effective than the immunomodulatory and immunosuppressive therapies currently being used. It is, therefore, imperative to confirm and further characterize the association of CCSVI and MS before proceeding with interventional studies and, more importantly, venous procedures in clinical practice.
IL-6 release by LPS-stimulated peripheral blood mononuclear cells as a potential biomarker in Alzheimer's disease
- Adam Kaplin, Katherine A. L. Carroll, Jenn Cheng, Rameeza Allie, Constantine G. Lyketsos, Peter Calabresi, Paul B. Rosenberg
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- Journal:
- International Psychogeriatrics / Volume 21 / Issue 2 / April 2009
- Published online by Cambridge University Press:
- 01 December 2008, pp. 413-414
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There is increasing evidence for the role of activated microglia in the neurotoxic pathways of Alzheimer's disease (AD). Amyloid-β1-42 is a potent activator of microglia (Benveniste et al., 2001), causing them to release pro-inflammatory cytokines including IL-6, IL-1β, TNF-α among others. A peripheral blood marker reflecting CNS inflammatory processes would be useful for treatment development, but the search for such an in vivo marker has been elusive. Peripheral blood and CSF levels of pro-inflammatory cytokines do not consistently differ in AD and controls (reviewed in Rosenberg, 2005). Both microglia and peripheral blood mononuclear cells (PBMCs) release pro-inflammatory cytokines when exposed to immunologic stimuli including lipopolysaccharide (LPS) and phytohemagglutinin (PHA). There are recent data suggesting that PBMCs from AD patients release more cytokines in this paradigm than normal controls (Reale et al., 2004).