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Insights into deja vu: Associations between the frequency of experience and amplitudes of low-frequency oscillations in resting-state functional magnetic resonance imaging
Autoři | |
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Rok publikování | 2022 |
Druh | Článek v odborném periodiku |
Časopis / Zdroj | European Journal of Neuroscience |
Fakulta / Pracoviště MU | |
Citace | |
www | https://onlinelibrary.wiley.com/doi/10.1111/ejn.15570 |
Doi | http://dx.doi.org/10.1111/ejn.15570 |
Klíčová slova | ALFF; default mode network; deja vu; fALFF; resting-state fMRI |
Popis | The phenomenon of deja vu (DV) has intrigued scientists for decades, yet its neurophysiological underpinnings remain elusive. Brain regions have been identified in which morphometry differs between healthy individuals according to the frequency of their DV experiences. This study built upon these findings by assessing if and how neural activity in these and other brain regions also differ with respect to DV experience. Resting-state fMRI was performed on 68 healthy volunteers, 44 of whom reported DV experiences (DV group) and 24 who did not (NDV group). Using multivariate analyses, we then assessed the (fractional) amplitude of low-frequency fluctuations (fALFF/ALFF), a metric that is believed to index brain tissue excitability, for five discrete frequency bands within sets of brain regions implicated in DV and those comprising the default mode network (DMN). Analyses revealed significantly lower values of fALFF/ALFF for specific frequency bands in the DV relative to the NDV group, particularly within mesiotemporal structures, bilateral putamina, right caudatum, bilateral superior frontal cortices, left lateral parietal cortex, dorsal and ventral medial prefrontal cortex, and the posterior cingulate cortex. The pattern of differences in fALFF/ALFF measures between the brains of individuals who have experienced DV and those who have not provides new neurophysiological insights into this phenomenon, including the potential role of the DMN. We suggest that the erroneous feeling of familiarity arises from a temporary disruption of cortico-subcortical circuitry together with the upregulation of cortical excitability. |
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