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The Diagnostic Criteria for Psychosomatic Research (DCPR) are those of psychosomatic syndromes that did not find room in the classical taxonomy. More recently, the DCPR were updated, called DCPR-revised (DCPR-R). The present study was conducted to test the criterion-related validity of the DCPR-R.
Two hundred consecutive subjects were enrolled at the Headache Center of Careggi University Hospital (Italy): 100 subjects had a diagnosis of chronic migraine (CM) and 100 had a diagnosis of episodic migraine (EM). Participants received a clinical assessment, which included the DCPR-revised Semi-Structured Interview (DCPR-R SSI), the Structured Clinical Interview for DSM-5 (SCID-5), and the psychosocial index (PSI).
Forty-seven subjects (23.5%) had at least one DSM-5 diagnosis: major depressive disorder (8.5%; n = 17) and agoraphobia (7.5%; n = 15) were the most frequent. One hundred and ten subjects (55%) reported a DCPR-R diagnosis: allostatic overload (29%; n = 58) and type A behavior (10.5%; n = 21) were the most frequent. When the incremental validity of the DCPR system over the DSM system was tested using PSI subscales as the criterion variable, the DCPR-R increased up to 0.11–0.24 the amount of explained variance. Subjects with at least one DCPR-R diagnosis showed lower PSI well-being scores (p = .001), higher PSI stress scores (p
< .001), and higher PSI psychological distress scores (p = .008) than subjects without a DCPR-R diagnosis.
The DCPR-R showed a good criterion-related validity in migraine outpatients. Thus, they might be implemented, together with the DSM-5, in the assessment of migraine subjects.
Substance P(SP), a major peptide neurotransmitter, was first found in the gut, and after two decades from its discovery it was proposed as a mediator of pain at the spinal level. SP belongs to the tachykinin, a family of peptides that share a common C-terminus amino-acid sequence (Phe–X–Gly–Leu– Met–NH2). In mammals the tachykinin are substantially confined to the central and peripheral nervous system. Three main tachykinin peptides have been described: SP, neurokinin A(NKA) and neurokinin B(NKB). SP and NKA are products of the preprotachykinin gene-I that via alternative splicing of the mRNA generates three different precursor proteins from which SP and NKA are produced at different ratios. The sole biologically active product of the preprotachykinin gene-II is NKB. NKB expression is apparently limited to the central nervous system, whereas SP and NKA are also found in a subpopulation of intrinsic neurones of the gut and in a subset of primary sensory neurones, including those of the trigeminal and dorsal root ganglia. Of particular interest for this review is the notion that vagal (nodose and jugular) sensory ganglia are made up of a large proportion of neurones that contain and release tachykinin. Metabolism by membrane-bound peptidases, including neutral endopeptidase (NEP, EC 24.11) and angiotensin converting enzyme (ACE, EC 14.1), is one of the major factors that limit the biological effects of tachykinin.
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