The diagnosis of a somatic symptom disorder must be based on both a negative approach - eliminating another psychiatric or non-psychiatric disorder that would better explain the symptoms - and a positive one, which is, based on the search for characteristic thoughts, emotions or behaviours as well as biological or psychological factors that may promote, trigger or sustain the disorder. Additional tests and specialized medical consultations should not be prescribed solely to reassure the patient; they may actually worsen the condition. The management will move away from the outdated notion of "medically unexplained symptoms" to rely on: the acknowledgment of the painful, debilitating and involuntary nature of the symptoms; the proposal of a positive diagnosis acceptable by the patient and an explanatory model compatible with his or her representations, aimed at putting an end to dysfunctional health care utilization; the proposal of therapeutic objectives aimed at functional rather than symptomatic recovery; the negotiation of pharmacological (selective or mixed serotonin reuptake inhibitor if necessary) and non-pharmacological interventions, especially when it comes to limiting the factors that sustain the disorder; the coordination of the various healthcare professionals.
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Synapse
January 2025
Center for Neural Science, New York University, New York, New York, USA.
Objective: Anorexia nervosa (AN) is an eating disorder with the second highest mortality of all mental illnesses and high relapse rate, especially among adult females, yet with no accepted pharmacotherapy. A small number of studies have reported that adult females who struggled with severe and relapsing AN experienced sustained remission of the illness following ketamine infusions. Two other reports showed that 30 mg/kg IP ketamine can reduce vulnerability of adolescent mice to activity-based anorexia (ABA), an animal model of AN.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
German Center for Neurodegenerative Diseases (DZNE), Munich, Bavaria, Germany.
Background: Progranulin (PGRN) haploinsufficiency is a major risk factor for frontotemporal lobar degeneration with TDP-43 pathology (FTLD-GRN). Multiple therapeutic strategies are in clinical development to restore PGRN levels in the CNS, including gene therapy. However, a limitation of current gene therapy approaches aimed to alleviate FTLD-associated pathologies may be their inefficient brain exposure and biodistribution.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
McGill University, Montreal, QC, Canada.
Background: Activation of the mTOR pathway is pivotal for microglia to induce and sustain neuroprotective functions (Ulland et al., 2017; Wang et al., 2022).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
USC School of Pharmacy, Los Angeles, CA, USA.
Background: Cellular senescence is a hallmark of aging and has been implicated in several neurodegenerative diseases including Alzheimer's disease (AD). Senescence cells undergo changes in gene expression and metabolism and can exhibit a so-called "senescence-associated secretory phenotype" (SASP) characterized by increased secretion of pro-inflammatory molecules and factors which can damage nearby cells, contributing to AD pathology progression.
Method: In this study, we determined mechanisms of cellular senescence using human postmortem brain samples, cellular models, and APOE4 animal models.
Alzheimers Dement
December 2024
Institute of Neurosciences, L'Hospitalet de Llobregat, Barcelona, Spain.
Background: The increased vulnerability of Alzheimer's disease patients to severe SARS-CoV-2 infection raises crucial concerns, especially with the potential transition of the COVID-19 pandemic to an endemic state. Given the rising prevalence of Alzheimer's in an aging world-wide population, elucidating whether SARS-CoV-2 infection may induce or accelerate neurodegeneration becomes imperative.
Method: To investigate the neurodegenerative effects of SARS-CoV-2 infection, we generated brain organoids using human induced pluripotent stem lines from one non-demented control, one with sporadic Alzheimer's, and one with familial Alzheimer's.
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