Increased synchronization during cognitive flexibly task in Sickle Cell Disease: A Feasibility Study
Poster No:
237
Submission Type:
Abstract Submission
Authors:
Nahom Mossazghi1, Sid Roy2, Joel Dzidzorvi Kwame Disu3, Elizabeth Meinert-Spyker3, Lara Abdelmohsen3, Antara Titikhsha3, Sossena Wood3
Institutions:
1Carnegie Mellon University, PIttsburgh, PA, 2Carnegie Mellon University, Pittsburrgh, PA, 3Carnegie Mellon University, Pittsburgh, PA
First Author:
Co-Author(s):
Introduction:
Sickle Cell Disease (SCD) is a genetic blood disorder caused by a beta-globin gene mutation, leading to impaired oxygen delivery and neurovascular dysfunction(Kato, 2018; Sundd, 2018). These disruptions cause neurological complications, including strokes, silent cerebral infarcts, and reduced cognitive flexibility-a core executive function enabling adaptation to changing demands(Solomou, 2013). Prior studies in children with SCD have identified deficits in early attention modulation using auditory ERP paradigms (Downes, 2018). However, no task-based EEG studies have examined neural dynamics in adult patients with SCD. Additionally, resting-state EEG findings indicate altered theta, beta, and alpha band activity in SCD, but how these changes affect task-related neural processes remains unclear(Case, 2017). Here, we use event-related synchronization/desynchronization (ERS/ERD) during a Digit Symbol Substitution Task to investigate cognitive flexibility in adults with SCD(Jaeger, 2018). We hypothesize increased ERS in frontoparietal networks as cognitive flexibility rises, reflecting impaired neural activation patterns fundamental to executive function.
Methods:
We recruited 5 controls (mean age 25.8±2.68) and 5 SCD (mean age 34.0±7.09). Two controls were excluded from EEG analysis due to poor data quality. Participants view a digit-symbol prompt and press distinct keys to indicate whether the pair is congruent (matches the reference table) or incongruent (does not match). EEG data were recorded using a 32-channel BrainAmp system at 5000Hz. Preprocessing in EEGLAB included down sampling to 250Hz, filtering at 1–50Hz, removing bad channels, and ICA to remove artifacts. Epochs were extracted from -200 to 1000ms with respect to stimulus onset. ERD/ERS was calculated across delta (1–4Hz), theta (4–8Hz), alpha (8–12Hz), beta (12–30Hz), and gamma (30–50Hz) using a 4th-order Butterworth filter and the Hilbert transform. Baseline normalization (-200 to 0ms) produced percent-change values. Difference scores (congruent–incongruent) per condition were derived and visualized using topographic maps.
·DSST Task Design
Results:
The topographic maps, Fig. 2, illustrate ERD/ERS differences across frequency bands and EEG component and time windows. At earlier time points (P1, N1, P2), significant theta ERD is observed in both groups, with the strongest effects localized to the parietal regions during the N2 window (orange box; p < 0.05). At later time points (P3, N400), significant theta ERS emerges, with patients showing stronger congruent ERS in frontal and parietal regions compared to controls (red box; p < 0.05). In the alpha band, controls exhibit moderate ERS in the incongruent condition during P3 and N400, while patients show greater congruent ERS. These results highlight distinct temporal dynamics, with early theta ERD reflecting cognitive engagement and later theta ERS indicating sustained activation and network-level differences in patients with SCD.
·EEG ERS/ERD Analysis
Conclusions:
ERS/ERD analysis reveals distinct temporal and frequency-specific differences in patients with SCD. Increased theta ERD in earlier time windows may suggest heightened engagement of parietal attentional networks to process task prompts. In later time windows, stronger theta ERS in the frontoparietal network indicates increased cognitive processing and decision-making demands. Our findings may suggest that patients with SCD require greater task-related cognitive effort than controls, as reflected by sustained neural activation across time points. Our results partially support our hypothesis, showing increased theta and alpha ERS in SCD. However, these observations are limited to congruent tasks, which are less cognitively demanding, potentially reflecting inefficient neurocircuitry. Our small sample size is a limitation of this study and ongoing recruitment will help confirm the consistency of these findings in a larger cohort and provide deeper insights into the neural mechanisms underlying cognitive deficits in SCD.
Disorders of the Nervous System:
Neurodegenerative/ Late Life (eg. Parkinson’s, Alzheimer’s) 1
Higher Cognitive Functions:
Executive Function, Cognitive Control and Decision Making
Modeling and Analysis Methods:
EEG/MEG Modeling and Analysis 2
Exploratory Modeling and Artifact Removal
Keywords:
ADULTS
Cognition
Computational Neuroscience
Cortex
Data analysis
DISORDERS
Electroencephaolography (EEG)
Modeling
Psychiatric Disorders
Other - Sickle Cell Disease; Executive Function; Task-based fMRI;
1|2Indicates the priority used for review
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Provide references using APA citation style.
Case, M. (2017). Increased theta band EEG power in sickle cell disease patients. Journal of Pain Research, 11, 67–76.
Couette, M. (2023). Early strokes are associated with more global cognitive deficits in adults with sickle cell disease. Journal of Clinical Medicine, 12(4).
Downes, M. (2018). Altered neurophysiological processing of auditory attention in preschool children with sickle cell disease. Journal of Pediatric Psychology, 43(8), 856–869.
Jaeger, J. (2018). Digit symbol substitution test. Journal of Clinical Psychopharmacology, 38(5), 513–519.
Jorgensen, D. R. (2017). Disease severity and slower psychomotor speed in adults with sickle cell disease. Blood Advances, 1(21), 1790–1795.
Kato, G. J. (2018). Sickle cell disease. Nature Reviews Disease Primers, 4.
Solomou, E. (2013). Extent of silent cerebral infarcts in adult sickle-cell disease patients on magnetic resonance imaging: Is there a correlation with the clinical severity of disease? Hematology Reports, 5(1), 8–12.
Sundd, P. (2018). Pathophysiology of sickle cell disease. Annual Review of Pathology: Mechanisms of Disease, 14, 263–292.