Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The American Psychiatric Association recently published the fourth edition of its Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). Although earlier editions included pain-related diagnosis, inherent problems in their construction limited their applicability. This article discusses how DSM-IV deals with pain, with a specific focus on the new diagnostic category of Pain Disorder.
Clin J Pain 1995 Sep
PMID:Review: DSM-IV and pain. 853 35

This paper will present an overview of pain problems associated with lesions, disorder or dysfunction of the central nervous system (CNS). The incidence, qualities of the pain experience, associated sensory abnormalities, and other characteristics will be discussed. Particular attention will be paid to central pain (CP) associated with stroke as the most prominent and best studied of the many CP problems. In general, there is poor understanding of the pathophysiology of CP, problems are often severe and intractable, and treatment is typically difficult. The concept of CP is increasingly being invoked to account for various presentations not traditionally considered, e.g. fibromyalgia. It is suggested that processes associated with CP might also contribute to the presentation in psychiatric Pain Disorders or other atypical pain problems. Finally, although perhaps not as problematic, a number of CNS disorders or lesions may be associated with reduced sensitivity to pain.
 ...
PMID:An overview of pain problems associated with lesions, disorder or dysfunction of the central nervous system. 1145 63

SCN9Aencodes the voltage-gated sodium channel Na(v)1.7, a protein highly expressed in pain-sensing neurons. Mutations in SCN9A cause three human pain disorders: bi-allelic loss of function mutations result in Channelopathy-associated Insensitivity to Pain (CIP), whereas activating mutations cause severe episodic pain in Paroxysmal Extreme Pain Disorder (PEPD) and Primary Erythermalgia (PE). To date, all mutations in SCN9A that cause a complete inability to experience pain are protein truncating and presumably lead to no protein being produced. Here, we describe the identification and functional characterization of two novel non-truncating mutations in families with CIP: a homozygously-inherited missense mutation found in a consanguineous Israeli Bedouin family (Na(v)1.7-R896Q) and a five amino acid in-frame deletion found in a sporadic compound heterozygote (Na(v)1.7-DeltaR1370-L1374). Both of these mutations map to the pore region of the Na(v)1.7 sodium channel. Using transient transfection of PC12 cells we found a significant reduction in membrane localization of the mutant protein compared to the wild type. Furthermore, voltage clamp experiments of mutant-transfected HEK293 cells show a complete loss of function of the sodium channel, consistent with the absence of pain phenotype. In summary, this study has identified critical amino acids needed for the normal subcellular localization and function of Na(v)1.7.
 ...
PMID:Congenital insensitivity to pain: novel SCN9A missense and in-frame deletion mutations. 2063 6

The degree to which psychological factors are believed to influence the experience of pain has evolved significantly through history. Over the past 100 years, the trend has shifted from a focus on the study of sensory aspects of pain perception to one where psychological factors play a prominent role. Pain is now viewed as a complex subjective experience consisting of sensory, affective, and cognitive components. Psychological presentations of pain are commonly reduced to a differential among Pain Disorder, Somatization Disorder, and Malingering. Limitations in the use of the current DSM-IV-TR diagnostic classifications for pain will lead to changes in the upcoming DSM-V. Psychological testing is becoming increasingly recognized as a valuable evidence-based method for making diagnoses of psychological factors influencing pain presentations. There is a shift from the use of brief measures of pain intensity to multidimensional scales including assessment of affect and perceived functional disability. There is also increased attention to the use of validity scales for assessing symptom exaggeration and other types of response bias. Neuropsychologists, with specialized knowledge and background in evidence based assessment methods, are particularly well equipped to provide valuable input regarding psychological presentations of pain in forensic contexts and in consultation to multidisciplinary treatment teams.
 ...
PMID:Differential diagnosis of psychological factors evoked by pain presentations. 2339 34

Chronic pain is common; it is found in up to 15% of randomly selected population samples, and psychosocial factors including those provoked by physical trauma associated with industrial and motor vehicular accidents are very common in etiology. The diagnosis of post-traumatic stress disorder may be appropriate in many of these cases. The objectives of this paper are to review the psychological and social factors which contribute to the etiology of chronic pain syndromes. It reviews also the relationship of pain to Depressive, Anxiety and Substance Abuse Disorders and the principles of management of Pain Disorder. Supportive psychotherapy, pharmacotherapy (in particular tricyclic antidepressant medication) and behavioral rehabilitation programs may all be helpful in producing symptomatic improvement. An interdisciplinary pain clinic, particularly one which involves non-medical health professionals such as psychologists, social workers, occupational therapists and physiotherapists are very helpful in the management of complex cases.
...
PMID:Somatoform pain disorder. 2452 48

The Nav1.7 voltage-gated sodium channel, encoded by SCN9A, is critical for human pain perception yet the transcriptional and post-transcriptional mechanisms that regulate this gene are still incompletely understood. Here, we describe a novel natural antisense transcript (NAT) for SCN9A that is conserved in humans and mice. The NAT has a similar tissue expression pattern to the sense gene and is alternatively spliced within dorsal root ganglia. The human and mouse NATs exist in cis with the sense gene in a tail-to-tail orientation and both share sequences that are complementary to the terminal exon of SCN9A/Scn9a. Overexpression analyses of the human NAT in human embryonic kidney (HEK293A) and human neuroblastoma (SH-SY5Y) cell lines show that it can function to downregulate Nav1.7 mRNA, protein levels and currents. The NAT may play an important role in regulating human pain thresholds and is a potential candidate gene for individuals with chronic pain disorders that map to the SCN9A locus, such as Inherited Primary Erythromelalgia, Paroxysmal Extreme Pain Disorder and Painful Small Fibre Neuropathy, but who do not contain mutations in the sense gene. Our results strongly suggest the SCN9A NAT as a prime candidate for new therapies based upon augmentation of existing antisense RNAs in the treatment of chronic pain conditions in man.
...
PMID:Regulation of Nav1.7: A Conserved SCN9A Natural Antisense Transcript Expressed in Dorsal Root Ganglia. 2603 78