Pain is the somatic symptom par excellence, legitimizing more than any other the sick role and illness behavior. The functions and implications of pain are clearest in situations of acute illness or injury or in chronic, organically based conditions in which actual or threatened tissue damage is signaled by its report. Much greater complexity is found in a variety of clinical presentations (conversion hysteria, hypochondriasis, chronic pain syndromes, Briquet's syndrome, Munchausen's syndrome) in which pain may form part or all of the clinical picture. In such conditions the relationship of the patient's report of pain to other phenomena (tissue damage, physiopathology, perceptual and cognitive styles, personality type, individual and family psychodynamics, anxiety, depression, behavioral patterns, social and economic factors, cultural influences) is important in elucidating pathogenetic mechanisms of which several may be operating in any one case. Awareness of the existence and interaction of these mechanisms facilitates the development and integration of treatment approaches.

Download full-text PDF

Source
http://dx.doi.org/10.1159/000287826DOI Listing

Publication Analysis

Top Keywords

pathogenetic mechanisms
8
tissue damage
8
pain
6
relationship pathogenetic
4
mechanisms treatment
4
treatment patients
4
patients pain
4
pain pain
4
pain somatic
4
somatic symptom
4

Similar Publications

Introduction: In recent years, the understanding of atopic dermatitis (AD) pathogenetic mechanisms has expanded and now it is recognized that Th2 immune axis dysregulation is pivotal to AD pathogenesis. The advent of biological drugs and small molecules have marked a revolution in the treatment of AD. Dupilumab, targeting IL-4 and IL-13, has been the first to demonstrate efficacy in treating moderate to severe AD by modulating type-2 inflammation pathways.

View Article and Find Full Text PDF

The endothelium at the interface between tissues and in the bloodstream.

Clin Microbiol Rev

January 2025

Laboratory of Pathology of Implant Infections, Laboratory of Immunorheumatology and Tissue Regeneration, IRCCS Istituto Ortopedico Rizzoli, Bologna, Italy.

SUMMARY is a major human pathogen. It can cause many types of infections, in particular bacteremia, which frequently leads to infective endocarditis, osteomyelitis, sepsis, and other debilitating diseases. The development of secondary infections is based on the bacterium's ability to associate with endothelial cells lining blood vessels.

View Article and Find Full Text PDF

The heart employs a specialized ribosome in its muscle cells to translate genetic information into proteins, a fundamental adaptation with an elusive physiological role. Its significance is underscored by the discovery of neonatal patients suffering from often fatal heart failure caused by rare compound heterozygous variants in RPL3L, a muscle-specific ribosomal protein that replaces the ubiquitous RPL3 in cardiac ribosomes. -linked heart failure represents the only known human disease arising from mutations in tissue-specific ribosomes, yet the underlying pathogenetic mechanisms remain poorly understood despite an increasing number of reported cases.

View Article and Find Full Text PDF

Pathogenic variants of GDAP1 cause Charcot-Marie-Tooth disease (CMT), an inherited neuropathy characterized by axonal degeneration. GDAP1, an atypical glutathione S-transferase, localizes to the outer mitochondrial membrane (OMM), regulating this organelle's dynamics, transport, and membrane contact sites (MCSs). It has been proposed that GDAP1 functions as a cellular redox sensor.

View Article and Find Full Text PDF

Background: Mutations in the structural domain of the epidermal growth factor receptor (EGFR) kinase represent a critical pathogenetic factor in non-small cell lung cancer (NSCLC). Small-molecule EGFR-tyrosine kinase inhibitors (TKIs) serve as first-line therapeutic agents for the treatment of EGFR-mutated NSCLC. But the resistance mutations of EGFR restrict the clinical application of EGFR-TKIs.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!