Meshreky, Kyrillos and Lewis, Penny ![]() ![]() |
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Abstract
Eye movements (EMs) are a defining feature of rapid eye movement (REM) sleep, yet we are still not clear why they happen. A few hypotheses attempt to explain the possible underlying mechanisms. However, a clear understanding of their functional significance remains lacking. Interestingly, there is an EM component in Eye Movement Desensitization and Reprocessing (EMDR) therapy, that is approved for post-traumatic stress disorder (PTSD). The developer of EMDR, Francine Shapiro described the technique as mimicry of REM. Robert Stickgold built on this by proposing a putative neurobiological model in which the repeated eye movements in EMDR initiate brainstem REM-like mechanisms. In this article, we combine Stickgold's model with the results of a study which showed that alternating bilateral visual stimulation in mice yielded sustained increases in the activities of the Superior Colliculus (SC) and mediodorsal thalamus (MD) which suppressed the activity of basolateral amygdala. We pose a hypothetical question: could EMs during REM sleep similarly inhibit amygdala activity through the SC-MD pathway? And could this be part of the affective modulation mechanisms characteristic of REM sleep?
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Schools > Psychology Research Institutes & Centres > Cardiff University Brain Research Imaging Centre (CUBRIC) |
Publisher: | Elsevier |
ISSN: | 0028-3932 |
Date of First Compliant Deposit: | 22 May 2025 |
Date of Acceptance: | 10 May 2025 |
Last Modified: | 12 Jun 2025 13:07 |
URI: | https://orca.cardiff.ac.uk/id/eprint/178440 |
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