Beta-bursts and BOLD in health and psychosis: a concurrent EEG-fMRI study

Paul M. Briley, Elizabeth B. Liddle, Molly Simmonite, Marije Jansen, Thomas P. White, Vijender Balain, Lena Palaniyappan, Richard Bowtell, Karen J. Mullinger, Peter F. Liddle

Research output: Contribution to journalArticlepeer-review


Background: There is emerging evidence for abnormal beta oscillations in psychosis. Beta-oscillations are likely to play a key role in the coordination of sensorimotor information, crucial to healthy mental function. Growing evidence suggests that beta oscillations typically manifest as transient “beta-bursts” that increase in probability following a motor response, observable as Post-Movement Beta Rebound (PMBR). Evidence indicates that PMBR is attenuated in psychosis, with greater attenuation associated with greater symptom severity and impairment. Delineating the functional role of beta-bursts may therefore be key to understanding the mechanisms underlying persistent psychotic illness.

Methods: We used concurrent EEG and fMRI to identify BOLD correlates of beta-bursts during the N-back working memory task and intervening rest periods in healthy participants (N = 30) and patients with psychosis (N = 48).
Results: During both task-blocks and intervening rest periods, beta-bursts phasically activated regions implicated in task-relevant content, while suppressing currently tonically active regions. Patients showed attenuated PMBR that was associated with persisting Disorganisation symptoms, as well as impairments in cognition and role function. Patients also showed greater task-related reductions in overall beta-burst rate, and greater, more extensive, beta-burst-related BOLD activation.

Conclusions: Our evidence supports a model in which beta-bursts reactivate latently maintained sensorimotor information and are dysregulated and inefficient in psychosis. We propose that abnormalities in the mechanisms by which beta-bursts coordinate reactivation of contextually appropriate content can manifest as Disorganisation, working memory deficits and inaccurate forward models, and may underlie a “core deficit” associated with persisting symptoms and impairment.
Original languageEnglish
JournalBiological Psychiatry: Cognitive Neuroscience and Neuroimaging
Early online date5 Nov 2020
Publication statusE-pub ahead of print - 5 Nov 2020


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