Type 1 diabetes affects the structure and function of the brain, with psychomotor speed as the most commonly reported deficit. The current study sought to uncover the dynamics underlying motor processing in the brain of adults with type 1 diabetes using an arrow-based Flanker task. Adults (ages 19-35, N = 39) with type 1 diabetes and no major complications and a matched control group (N = 40) underwent magnetoencephalography (MEG) while performing the task. During the task, participants were presented with a row of five arrows facing right or left, and participants were instructed to respond by button press to the direction of the middle arrow. Analyses focused on the time period around movement execution to examine motor-related dynamics. Time series analyses were performed on the peak beta and gamma responses from the motor cortices. An ANOVA model and follow-up regression analyses were used to delineate the predictive value of each neural response in driving behavioral outcomes. Subsequent t-tests between frequent (3+ episodes per week) and infrequent (0-1 episodes per week) hypoglycemic groups were performed to examine response differences within the adults with type 1 diabetes. Responses driving behavior differed between adults with and without type 1 diabetes. In adults with type 1 diabetes, beta frequency responses were significant predictors of reaction time, where greater ipsilateral recruitment led to faster reaction times (b = .58, t = 3.64, p = .001). In contrast, gamma drove behavioral outcomes in the control group (b = -.43, t = -2.96, p = .005). Further, within group analyses revealed that more frequent episodes of hypoglycemia were associated with alterations specific to beta responses during the pre-movement baseline period (p < .05). These results show frequency specific alterations in motor dynamics in adults with type 1 diabetes, with an added effect of increased hypoglycemia. These findings strongly indicate that diabetes directly impacts motor control components in the brain, regulating behavioral outcomes.


C.M. Embury: None. V.A. Were: None. G.H. Lord: None. A. Drincic: Board Member; Self; Corcept Therapeutics. C. Desouza: Consultant; Self; Novo Nordisk A/S, Sanofi US. T.W. Wilson: None.


National Institutes of Health (R01MH103220, R01MH116782)

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