This article reviews recent human studies of the genetics of acute and chronic pain, which implicate polymorphisms in genes coding for catechol-O-methyltransferase activity and micro-opioid receptors, among a number of others, as influential in explaining variability among the pain responses of individuals.
Cross-sectional data from the population-based Study of Health in Pomerania (SHIP) in Germany were used to estimate additive interactions between depressive symptoms and 22 single-nucleotide polymorphisms (SNPs) of the COMT gene and the neighbouring thioredoxin reductase 2 (TXNRD2) gene on TMD pain.
Genetic variation of the catechol-O-methyltransferase (COMT) gene has been associated with variation in human pain sensitivity and response to analgesics in previous studies.
Since attention and pain both involve the activation of the anterior cingulate gyrus in imaging studies, we compared the Val(108/158)Met influence with the COMT haplotypes and found the latter to be more predictive of attention.
To evaluate the role of COMT gene variants as potential risk factors in a group of patients affected with chronic temporomandibular disorder (TMD) pain.
We performed genotyping for catechol-O-methyltransferase (COMT) Val158Met (rs4680) and dopamine D3 receptor (DRD3) rs6280" genes_norm="1814">Ser9Gly (rs6280) polymorphisms, which were analyzed for associations with pain phenotypes.
In comparison, two pain-related gene SNPs (OPRM1 [rs1799971] and COMT [rs4818]) interacted with psychological factors to predict four shoulder impairment phenotypes (abduction: 5-day average loss; strength loss: 5-day average, peak, and relative loss).
Two other studies investigating gene-environment interactions found that effects of stress on pain were modified by variation in the gene encoding catechol O-methyltransferase.
Our results suggest that the Val158MetCOMT polymorphism modulated some psychological variables but not pressure pain sensitivity in FMS, because women carrying the Met/Met genotype show higher disability, depression, and anxiety but similar PPTs than those with Val/Met or Val/Val genotypes.
To examine the association between COMT and OPRM1 gene polymorphisms and pain and disability at baseline and long-term follow-up in patients treated for chronic low back pain (LBP).
The catechol-O-methyltransferase (COMT) gene contains a functional polymorphism, Val158Met, that has been found to influence human pain perception, and one study has found that migraine was less likely among those with the Val/Val polymorphism.
The primary aim of this study was to investigate the effects of the catechol-O-methyltransferaseVal158Met polymorphism on heat pain perception in a cohort of adults receiving daily opioid therapy for chronic pain.
Our results show that the COMTVal158Met polymorphism contributes to variability in pain sensitivity after cardiac surgery of morphine-treated patients in the intensive care unit, because Met-allele carriers were more sensitive to overall pain and procedure-related pain.
Patients with the COMTG472A-AA genotype (rs4680) and KCNJ6 A1032G-A allele (rs2070995) CLBP responded differently to opioid titration, with higher pain intensity requiring higher dosing.
Heterozygous rare coding variants in CNR1, which encodes the type 1 cannabinoid receptor (CB1), were found to be significantly associated with pain sensitivity (especially migraine), sleep and memory disorders-alone or in combination with anxiety-compared to a set of controls without such CNR1 variants.
Thus, our data show that the val158met polymorphism in the COMT gene contributes significantly to inter-individual differences in neural pain processing: in healthy people, this polymorphism was more related to cognitive aspects of pain processing, whereas BPD patients with reduced pain sensitivity showed an association with activity in brain regions related to affective pain processing.
The aim of this study was to test if genetic variation at the neurokinin 1 receptor gene (TACR1) is associated with pain in individuals with radiographic knee OA.
Genetics-based personalized approaches to pain management have received a setback because of the nonreproducibility of functional genetic associations such as the pain-modulatory effect of the catechol-O-methyl transferase (COMT) gene 472G>A single-nucleotide polymorphism.