Psychogenic non-epileptic seizures (PNES) are seizure-like episodes that resemble behavioral aspects observed for epileptic seizures but are without the abnormal electrical activity typically seen in epilepsy. The lack of an etiologic model for PNES as well as limitations of available diagnostic methods largely hinders a clear-cut distinction from epilepsy and from a normal functioning brain. In this study, we investigate the brain dynamics of people with PNES and people with epilepsy during phases far-off seizures and seizure-like events as well as the brain dynamics of a control group. Probing for differences between these groups, we utilise the network ansatz and explore local and global characteristics of time-evolving functional brain networks. We observe subject-specific differences in local network characteristics across the groups, highlighting the physiological functioning of specific brain regions. Furthermore, we observe significant differences in global network characteristics-relating to communication, robustness, and stability aspects of the brain. Our findings may provide new insights into the mechanisms underlying PNES and offer a promising diagnostic approach to differentiate them from epilepsy.
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http://dx.doi.org/10.3390/jcm14030666 | DOI Listing |
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Shenzhen-Hong Kong Institute of Brain Science, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China; Guangdong Provincial Key Laboratory of Brain Connectome and Behavior, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China. Electronic address:
In infants, high fever is associated with robust microglial morphological changes, including process retraction and soma enlargement, which contribute to fever-induced seizures. The molecular mechanisms underlying dynamic process retraction during hyperthermia remain poorly understood. Using a hyperthermia-induced microglial activation model in postnatal day 8 mice, we identified the CXCL1-CXCR1 interaction as a key regulator of process retraction.
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