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Simon B. Eickhoff

5 papers in the library · 675 citations · publishing 2009-2025

Papers

Investigating the Functional Heterogeneity of the Default Mode Network Using Coordinate-Based Meta-Analytic Modeling

Journal of Neuroscience November 18, 2009 Angela R. Laird, Simon B. Eickhoff, Karl Li et al. 577 citations

The default mode network (DMN) is a set of brain regions active at rest and less active during many tasks, but these regions also show task-related increases. By combining activation likelihood estimation meta-analysis with the BrainMap database, core DMN regions were identified and their functional heterogeneity examined. Meta-analytic coactivation maps showed each region connects with both DMN and non-DMN areas. Behavioral domain analysis revealed that DMN subnetworks are differentially specialized: affective, perceptual, and motor-processing cliques were identified. The results provide a connectivity model of DMN interactions during diverse tasks.

The architecture of the human default mode network explored through cytoarchitecture, wiring and signal flow

Nature Neuroscience January 28, 2025 Casey Paquola, Margaret Garber, Stefan Frässle et al. 58 citations

The default mode network (DMN) is a set of brain regions important for complex thought and behavior. By combining postmortem tissue analysis and brain scans, researchers found that the DMN contains different types of cells, some specialized for processing single senses, others for combining information, and still others for memory. The DMN includes regions that receive input from sensory areas and a core that is relatively cut off from direct sensory information. Analysis of how signals flow through the DMN showed it uniquely balances output across different levels of sensory processing. These findings provide a structural basis for understanding the DMN's broad role in brain function and cognition.

Effects of ketamine and midazolam on resting state connectivity and comparison with ENIGMA connectivity deficit patterns in schizophrenia

Human Brain Mapping October 21, 2019 Bhim M. Adhikari, Juergen Dukart, Joerg F. Hipp et al. 24 citations

Ketamine, given at subanesthetic doses to healthy volunteers, produces psychosis-like symptoms and reduces functional connectivity in the salience network, auditory network, and default mode network (DMN). Midazolam, a sedative, only reduces DMN connectivity. The pattern of connectivity deficits caused by ketamine positively correlates with the pattern seen in schizophrenia, whereas midazolam's effects do not. After subtracting midazolam's effects, the remaining ketamine-specific disconnectivity pattern still correlates with schizophrenia deficits. This suggests that ketamine's psychosis-like effects have a brain functional basis that overlaps with schizophrenia-related connectivity disruptions.

Functional imaging studies of acute administration of classic psychedelics, ketamine, and MDMA: Methodological limitations and convergent results.

Neuroscience and Biobehavioral Reviews November 1, 2023 Sophia Linguiti, Jacob W Vogel, Valerie J Sydnor et al. 15 citations

A systematic review of 91 fMRI studies on acute psychedelic effects found substantial methodological heterogeneity. Only 51 unique samples were used across the 91 papers, and 54% of studies did not meet current standards for correcting Type I errors or controlling motion artifacts. Psilocybin and LSD consistently modulated connectivity along the sensorimotor-association cortical axis. Ketamine consistently increased activation in the dorsomedial prefrontal cortex. The review calls for future adoption of pre-registration, standardized processing and statistical testing, and data sharing to improve rigor.

Local activity alterations in autism spectrum disorder correlate with neurotransmitter properties and ketamine induced brain changes.

medRxiv : the preprint server for health sciences October 21, 2024 Pascal Grumbach, Jan Kasper, Joerg F. Hipp et al. 1 citation preprint

Autism spectrum disorder involves altered resting-state brain function, and an imbalance between excitation and inhibition is a proposed mechanism. In two large independent cohorts, individuals with autism consistently showed reduced local brain activity in default mode network nodes and increased activity in temporal regions, cerebellum, and brainstem. These activity changes spatially overlapped with multiple neurotransmitter systems, including dopamine, glutamate, GABA, and acetylcholine. The NMDA-antagonist ketamine, but not the GABA-potentiator midazolam, induced activity changes resembling those seen in autism, suggesting that pharmacologically shifting the excitation-inhibition balance can mimic autism-related brain alterations.