The <scp>COMT rs</scp>4680 <scp>M</scp>et allele contributes to long‐lasting low back pain, sciatica and disability after lumbar disc herniation

Jacobsen, Line M.; Schistad, Elina Iordanova; Storesund, Anette; Pedersen, Linda M.; Rygh, Lars Jørgen; Røe, Cecilie; Gjerstad, Johannes

doi:10.1002/j.1532-2149.2011.00102.x

Cited by 52 publications

(39 citation statements)

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“…Variants of the COMT gene that result in reduced activity of the corresponding enzyme are associated with experimental pain as well as risk of temporomandibular disorder, irritable bowel syndrome, fibromyalgia and low back pain (Diatchenko et al, 2005, Karling et al, 2011, Jacobsen et al, 2012, Martinez-Jauand et al, 2013). These functional genetic variants are also associated with anxiety, depression, and other psychological traits that influence the perception of pain (Fernandez-de-Las-Penas et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Catechol-O-methyltransferase inhibition alters pain and anxiety-related volitional behaviors through activation of β-adrenergic receptors in the rat

et al. 2015

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Reduced catechol-O-methyltransferase (COMT) activity resulting from genetic variation or pharmacological depletion results in enhanced pain perception in humans and nociceptive behaviors in animals. Using phasic mechanical and thermal reflex tests (e.g. von Frey, Hargreaves), recent studies show that acute COMT-dependent pain in rats is mediated by β-adrenergic receptors (βARs). In order to more closely mimic the characteristics of human chronic pain conditions associated with prolonged reductions in COMT, the present study sought to determine volitional pain-related and anxiety-like behavioral responses following sustained as well as acute COMT inhibition using an operant 10–45°C thermal place preference task and a light/dark preference test. In addition, we sought to evaluate the effects of sustained COMT inhibition on generalized body pain by measuring tactile sensory thresholds of the abdominal region. Results demonstrated that acute and sustained administration of the COMT inhibitor OR486 increased pain behavior in response to thermal heat. Further, sustained administration of OR486 increased anxiety behavior in response to bright light, as well as abdominal mechanosensation. Finally, all pain-related behaviors were blocked by the non-selective βAR antagonist propranolol. Collectively, these findings provide the first evidence that stimulation of ARs following acute or chronic COMT inhibition drives cognitive-affective behaviors associated with heightened pain that affects multiple body sites.

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Section: Introductionmentioning

confidence: 99%

Catechol-O-methyltransferase inhibition alters pain and anxiety-related volitional behaviors through activation of β-adrenergic receptors in the rat

et al. 2015

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“…These include age related changes, body weight, smoking and occupational loading (Miranda et al, 2002;Younes et al, 2006;Samartzis et al, 2011). Moreover, psychosocial aspects as well as genetic variability may affect the risk of long-term low back pain and sciatica (Jacobsen et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Pain Intensity the First Year after Lumbar Disc Herniation Is Associated with the A118G Polymorphism in the Opioid Receptor Mu 1 Gene: Evidence of a Sex and Genotype Interaction

Olsen¹,

Jacobsen²,

Schistad³

et al. 2012

Journal of Neuroscience

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Earlier studies have shown that the single nucleotide polymorphism (SNP) A118G (rs1799971) in the opioid receptor mu 1 (OPRM1) gene may affect pain sensitivity. In the present study we investigated whether the A118G SNP could predict clinical outcome regarding progression of pain intensity and disability in patients with low back pain and sciatica after lumbar disc herniation. Patients (n ϭ 258) with lumbar disc herniation and sciatic pain, all European-Caucasian, were recruited from two hospitals in Norway. Pain and disability were rated on a visual analog scale (VAS), by McGill Sensory Questionnaire and by Oswestry Disability Index (ODI) over a 12 months period. The data revealed a significant interaction between sex and A118G genotype regarding the pain intensity during the 12 months (VAS, p ϭ 0.002; McGill, p ϭ 0.021; ODI, p ϭ 0.205, repeated-measures ANOVA). We found that */G women had a slower recovery rate than the */G men. Actually, the */G women had 2.3 times as much pain as the */G men 12 months after the disc herniation (VAS, p ϭ 0.043, one-way ANOVA; p ϭ 0.035, Tukey HSD). In contrast, the A/A women and A/A men seemed to have almost exactly the same recovery rate. The present data suggest that OPRM1 G allele increases the pain intensity in women, but has a protective effect in men the first year after disc herniation.

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“…Six studies analysed Nordic populations [6,14,22,23,27,36], five analysed other European populations[2,4,15,20,41], three analysed Japanese [37,43,46], two analysed Israeli Jewish [12,35] and South African black, Caucasian and Indian [21,49], one analysed Chinese (Taiwan) [8] and one analysed Caucasian-, African- and Hispanic-American populations [47]. One study included five cohorts with various neuropathic pain conditions from four populations (Danish, Finnish, Israeli-Jewish, and Caucasian-, African- and Hispanic-American) [11].…”

Section: Resultsmentioning

confidence: 99%

“…Two studies on postherpetic neuralgia (PHN) recruited participants from the same Japanese population [37,46]. Several studies reused the same cohorts to investigate different polymorphisms, namely two studies on a South African HIV-positive cohort comprising African black, Caucasian and Indian [21,49], two studies on a Norwegian cohort with discogenic sciatic pain [22,23], two studies on Caucasian-, African- and Hispanic-American patients with persistent pain after surgery for discogenic sciatic pain [11,47], and three studies on a Finnish cohort with discogenic pain [11,27,36]. …”

Section: Resultsmentioning

confidence: 99%

“…The identified studies could be classified into three broad categories, according to their reason for phenotyping neuropathic pain, to: (1) determine whether any pain was neuropathic (identification of cases and controls) [2,4,8,12,14,15,20,22,23,35–37,43,46,49]; (2) identify endo-phenotypes within cohorts with neuropathic pain (i.e. phenomics) [6,11,21,27,41,47,49]; and (3) identify pain (not specifically neuropathic) in a neurological condition, e.g.…”

Section: Resultsmentioning

confidence: 99%

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Neuropathic pain phenotyping by international consensus (NeuroPPIC) for genetic studies

Hecke

Kamerman

Attal

et al. 2015

Pain

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For genetic research to contribute more fully to furthering our knowledge of neuropathic pain we require an agreed, valid and feasible approach to phenotyping, in order to allow collaboration and replication in samples of sufficient size. Results from genetic studies on neuropathic pain have been inconsistent and have met with replication difficulties, in part because of differences in phenotypes used for case ascertainment. Since there is no consensus on the nature of these phenotypes, nor the methods of collecting them, this study aimed to provide guidelines on collecting and reporting phenotypes in cases and controls for genetic studies. Consensus was achieved through a staged approach: (1) systematic literature review to identify all neuropathic pain phenotypes used in previous genetic studies; (2) Delphi survey to identify the most useful neuropathic pain phenotypes, their validity and feasibility; and (3) meeting of experts to reach consensus on the optimal phenotype(s) to be collected from neuropathic pain patients for genetic studies. A basic ‘entry-level’ set of phenotypes was identified for any genetic study of neuropathic pain. This set identifies cases of ‘possible’ neuropathic pain, and controls, and includes: (1) a validated symptom-based questionnaire to determine whether any pain is likely to be neuropathic; (2) body chart or checklist to identify whether the area of pain distribution is neuroanatomically logical; and (3) details of pain history (intensity, duration, any formal diagnosis). This NeuroPPIC ‘entry-level’ set of phenotypes can be expanded by more extensive and specific measures, as determined by scientific requirements and resource availability.

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The COMT rs4680 Met allele contributes to long‐lasting low back pain, sciatica and disability after lumbar disc herniation

Abstract: We conclude that the functional COMT Val158Met SNP contributes to long lasting low back pain, sciatica and disability after lumbar disc herniation.

Cited by 52 publications

References 25 publications

Catechol-O-methyltransferase inhibition alters pain and anxiety-related volitional behaviors through activation of β-adrenergic receptors in the rat

Catechol-O-methyltransferase inhibition alters pain and anxiety-related volitional behaviors through activation of β-adrenergic receptors in the rat

Pain Intensity the First Year after Lumbar Disc Herniation Is Associated with the A118G Polymorphism in the Opioid Receptor Mu 1 Gene: Evidence of a Sex and Genotype Interaction

Neuropathic pain phenotyping by international consensus (NeuroPPIC) for genetic studies

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