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Sensi, S.

Publications and source records attributed to Sensi, S..

2 recordsLinked to original sources

A Shared Entropic Axis Spans States of Consciousness Across Pharmacological and Clinical Conditions

A general account of how diverse states of consciousness arise from brain activity requires a quantitative framework that generalises across them. The Entropic Brain Theory proposes that states of consciousness can be ordered along a single dimension defined by the entropy of spontaneous neural activity, but this prediction has not been tested across pharmacological and clinical perturbations within a common analytical pipeline. Here we quantify the temporal irregularity of time-resolved small-world topology using sample entropy, applying the same pipeline to pharmacological (psychedelics, modafinil, propofol anaesthesia) and clinical (schizophrenia) fMRI datasets. Propofol anaesthesia occupied the low-entropy end of the axis; psychedelic states and schizophrenia occupied the high end. The ordering tracks combined modulations of the level and content of consciousness, ranging from reduced awareness under anaesthesia to the heightened arousal and expanded experience of psychedelic states and the disorganised, dysregulated processing of schizophrenia. Crucially, this result was not reducible to fluctuations in mean functional connectivity, and was supported by convergent reorganisation of higher-order association cortex under psychedelics and anaesthesia, alongside a distributed loss of network specificity in schizophrenia. These findings provide cross-condition empirical support for an entropic continuum of brain states and identify the temporal diversity of large-scale network reconfiguration as a primary axis of conscious dynamics.

neuroscience↗

Passive transfer of fibromyalgia pain from patients to mice.

Fibromyalgia syndrome (FMS) is a chronic pain condition characterized by widespread pain and tenderness1,2. The etiology and pathophysiology of fibromyalgia are unknown and there are no effective treatments. Here we show that sensory hypersensitivity in FMS is caused by autoantibodies that act by sensitizing nociceptive sensory neurons. Administration of IgG from FMS patients increased mouse pain sensitivities to stimulation with mechanical pressure and cold. In contrast, transfer of IgG depleted samples from FMS patients or IgG from healthy control subjects had no effect on pain sensitivity. Sensory nerve fibres in ex vivo skin-nerve preparations from mice treated with FMS IgG were hypersensitive to mechanical stimulation. Immunohistochemical analysis revealed that IgG from FMS patients specifically labeled satellite glial cells and myelinated fibre tracts, as well as a small number of macrophages and endothelial cells in mouse dorsal root ganglia but not skin, muscle, spinal cord and brain. Our results demonstrate that fibromyalgia pain is caused by IgG autoantibodies that sensitize peripheral nociceptive afferents neurons and suggest that therapies that reduce patient IgG titres may be effective treatments of fibromyalgia pain.

neuroscience↗