Functional neurological disorders (FND) are symptoms that can affect a variety of functions including motor, sensory and cognitive. These symptoms are genuinely experienced by the patient and are related to a functional disorder rather than a structural one. There is little epidemiological data on these disorders, but their frequency is well established in clinical practice, it is the second most frequent reason for consultation in Neurology. Despite of the frequency of the disorder, general practitioners and specialists are insufficiently trained in the disease, and patients often suffer from stigmatization and/or unnecessary investigations. It is therefore important to be aware of the diagnostic approach to FND, which mostly relies on positive clinical signs. Psychiatric evaluation can help with the characterization of predisposing, precipitating and perpetuating factors of the symptoms (according to the 3P biopsychosocial model related to FND), and guide their management. Finally, diagnosis explanation is a crucial step in the management of the disease, which can in itself have a therapeutic effect, and allow the patient to adhere to the treatments.
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http://dx.doi.org/10.1016/j.encep.2023.06.001 | DOI Listing |
Biosens Bioelectron
January 2025
Department of Physics, Virginia Commonwealth University, Richmond, VA, 23284, USA; Institute for Sustainable Energy and Environment, Virginia Commonwealth University, Richmond, VA, 23284, USA. Electronic address:
Wearable devices designed for the somatosensory system aim to provide event-cue feedback electronics and therapeutic stimulation to the peripheral nervous system. This prompts a neurological response that is relayed back to the central nervous system. Unlike virtual reality tools, these devices precisely target peripheral mechanoreceptors by administering specific stimuli.
View Article and Find Full Text PDFSci Adv
January 2025
Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Mitochondrial electron transport chain (ETC) function modulates macrophage biology; however, mechanisms underlying mitochondria ETC control of macrophage immune responses are not fully understood. Here, we report that mutant mice with mitochondria ETC complex III (CIII)-deficient macrophages exhibit increased susceptibility to influenza A virus (IAV) and LPS-induced endotoxic shock. Cultured bone marrow-derived macrophages (BMDMs) isolated from these mitochondria CIII-deficient mice released less IL-10 than controls following TLR3 or TLR4 stimulation.
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January 2025
State Key Laboratory of Environment Criteria and Risk Assessment, Chinese Research Academy of Environmental Sciences, Beijing, China.
Human health is being threatened by environmental microplastic (MP) pollution. MPs were detected in the bloodstream and multiple tissues of humans, disrupting the regular physiological processes of organs. Nanoscale plastics can breach the blood-brain barrier, leading to neurotoxic effects.
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January 2025
Lee Kong Chian School of Medicine, Nanyang Technological University, 11 Mandalay Road, Singapore 308232, Singapore.
Reward prediction errors (RPEs) quantify the difference between expected and actual rewards, serving to refine future actions. Although reinforcement learning (RL) provides ample theoretical evidence suggesting that the long-term accumulation of these error signals improves learning efficiency, it remains unclear whether the brain uses similar mechanisms. To explore this, we constructed RL-based theoretical models and used multiregional two-photon calcium imaging in the mouse dorsal cortex.
View Article and Find Full Text PDFPLoS Genet
January 2025
Waksman Institute, Rutgers University, Piscataway, New Jersey, United States of America.
Mutations of the Cullin-3 (Cul3) E3 ubiquitin ligase are associated with autism and schizophrenia, neurological disorders characterized by sleep disturbances and altered synaptic function. Cul3 engages dozens of adaptor proteins to recruit hundreds of substrates for ubiquitination, but the adaptors that impact sleep and synapses remain ill-defined. Here we implicate Insomniac (Inc), a conserved protein required for normal sleep and synaptic homeostasis in Drosophila, as a Cul3 adaptor.
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