Somatosensory perception in a remote pain‐free area and function of diffuse noxious inhibitory controls (DNIC) in patients suffering from long‐term trapezius myalgia

Leffler, Ann-Sofie; Hansson, Per; Kosek, Eva

doi:10.1053/eujp.2001.0312

Cited by 103 publications

(99 citation statements)

References 42 publications

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“…The association of CLBP with a central disturbance in pain processing is congruent with findings in other chronic pain states. Increased pain sensitivity outside the areas of clinical pain has been reported for other regional pain syndromes, such as tension-type headache (50), temporomandibular disorder (51,52), and localized trapezius myalgia (18). Our findings are also consistent with those of other studies that have demonstrated lowered pain thresholds in patients with low back pain (53) and lowered thresholds in patients with regional or widespread pain who do not have the 11 tender points required for the diagnosis of fibromyalgia (54).…”

Section: Augmented Pain Processing In Idiopathic Chronic Low Back Painsupporting

confidence: 83%

“…A common finding in these and other "central" or "non-nociceptive" pain syndromes is increased tenderness to pressure, which can be classified as mechanical hyperalgesia (i.e., increased pain in response to normally painful stimuli) and/or mechanical allodynia (i.e., pain in response to normally nonpainful stimuli) (16,17). These abnormalities are found even in the absence of any identifiable psychological or behavioral factors, thus implicating central mechanisms that exacerbate pain (e.g., "wind-up") or that attenuate pathways that begin in the brain stem and normally inhibit the ascending transmission of painrelated activity (18)(19)(20).…”

mentioning

confidence: 99%

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Evidence of augmented central pain processing in idiopathic chronic low back pain

Giesecke¹,

Gracely²,

Grant³

et al. 2004

Arthritis & Rheumatism

721

456

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Objective. For many individuals with chronic low back pain (CLBP), there is no identifiable cause. In other idiopathic chronic pain conditions, sensory testing and functional magnetic resonance imaging (fMRI) have identified the occurrence of generalized increased pain sensitivity, hyperalgesia, and altered brain processing, suggesting central augmentation of pain processing in such conditions. We compared the results of both of these methods as applied to patients with idiopathic CLBP (n ‫؍‬ 11), patients with widespread pain (fibromyalgia; n ‫؍‬ 16), and healthy control subjects (n ‫؍‬ 11).Methods. Patients with CLBP had low back pain persisting for at least 12 months that was unexplained by MRI/radiographic changes. Experimental pain testing was performed at a neutral site (thumbnail) to assess the pressure-pain threshold in all subjects. For fMRI studies, stimuli of equal pressure (2 kg) and of equal subjective pain intensity (slightly intense pain) were applied to this same site.Results. Despite low numbers of tender points in the CLBP group, experimental pain testing revealed hyperalgesia in this group as well as in the fibromyalgia group; the pressure required to produce slightly intense pain was significantly higher in the controls (5.6 kg) than in the patients with CLBP (3.9 kg) (P ‫؍‬ 0.03) or the patients with fibromyalgia (3.5 kg) (P ‫؍‬ 0.006).When equal amounts of pressure were applied to the 3 groups, fMRI detected 5 common regions of neuronal activation in pain-related cortical areas in the CLBP and fibromyalgia groups (in the contralateral primary and secondary [S2] somatosensory cortices, inferior parietal lobule, cerebellum, and ipsilateral S2). This same stimulus resulted in only a single activation in controls (in the contralateral S2 somatosensory cortex). When subjects in the 3 groups received stimuli that evoked subjectively equal pain, fMRI revealed common neuronal activations in all 3 groups.Conclusion. At equal levels of pressure, patients with CLBP or fibromyalgia experienced significantly more pain and showed more extensive, common patterns of neuronal activation in pain-related cortical areas. When stimuli that elicited equally painful responses were applied (requiring significantly lower pressure in both patient groups as compared with the control group), neuronal activations were similar among the 3 groups. These findings are consistent with the occurrence of augmented central pain processing in patients with idiopathic CLBP.Chronic low back pain (CLBP) is one of the most common and expensive musculoskeletal disorders in developed countries (1,2). Back pain in general affects 70-85% of all people at some time in their lives, but 90% of affected individuals recover, typically within 12 weeks (3). Recovery after 12 weeks is slow and uncertain, and this subset of patients with CLBP accounts for major expenses in the health care and disability systems (2,4).Despite the magnitude of the problem, little is known about the precise cause of CLBP. There is often a mismatch between objectiv...

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Section: Augmented Pain Processing In Idiopathic Chronic Low Back Painsupporting

confidence: 83%

mentioning

confidence: 99%

Evidence of augmented central pain processing in idiopathic chronic low back pain

Giesecke¹,

Gracely²,

Grant³

et al. 2004

Arthritis & Rheumatism

721

456

View full text Add to dashboard Cite

show abstract

“…The authors concluded from these data that chronic pain could be caused in part by a deficient pain inhibitory system (137). Deficits in DNIC have been demonstrated in patients with a number of chronic pain syndromes, including, for example, osteoarthritis of the knee (138), chronic pancreatitis (139), rheumatoid arthritis (140), and long-term trapezius myalgia (141).…”

Section: Loss Of Dnic and Chronic Painmentioning

confidence: 99%

Central modulation of pain

Ossipov¹,

Dussor²,

Porreca³

2010

J. Clin. Invest.

908

728

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It has long been appreciated that the experience of pain is highly variable between individuals. Pain results from activation of sensory receptors specialized to detect actual or impending tissue damage (i.e., nociceptors). However, a direct correlation between activation of nociceptors and the sensory experience of pain is not always apparent. Even in cases in which the severity of injury appears similar, individual pain experiences may vary dramatically. Emotional state, degree of anxiety, attention and distraction, past experiences, memories, and many other factors can either enhance or diminish the pain experience. Here, we review evidence for "top-down" modulatory circuits that profoundly change the sensory experience of pain.

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“…TMD patients often experience hyperalgesia on palpation and/or thermal stimulation. This hyperalgesia is present in the orofacial region and also at remote, asymptomatic sites, like the forearm 9, 17, 18, 87, 93, 94, 95, 96. Evidence also supports perceptual amplification of nonpainful auditory tones in TMD patients 97.…”

Section: Qst In Orofacial Pain and Dentistrymentioning

confidence: 90%

Applications of sensory and physiological measurement in oral‐facial dental pain

Dabiri

Harper

Kapila

et al. 2018

Special Care in Dentistry

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Dentists regularly employ a variety of self‐report and sensory techniques to aid in the diagnosis and treatment of tooth‐related disease. Many of these techniques leverage principles borrowed from psychophysics, the quantitative measurement of the relationship between stimuli and evoked sensations, which falls under the larger umbrella of quantitative sensory testing (QST). However, most clinicians fail to meet the bar for what could be considered quantitative sensory testing, and instead focus on qualitative and dichotomous “yes/no” aspects of sensory experience. With our current subjective measurements for pain assessments, diagnosis and treatment of dental pain in young children and individuals (any age) with severe cognitive impairment rely extensively on third‐party observations. Consequently, the limitation of inadequate pain diagnosis can lead to poor pain management. In this review, it discusses mechanisms that underlie acute and chronic dental pain. It details the measurement of somatosensory responses and pulpal blood flow as objective measures of tooth health and pain. It proposes that bridging these varied methodologies will significantly improve diagnosis and treatment of orofacial pain and pathology. It concludes that improving the precision of sensory measurements could yield important improvements in diagnostic challenges in pulpal pathology for noncommunicative and cognitively impaired individuals.

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Somatosensory perception in a remote pain‐free area and function of diffuse noxious inhibitory controls (DNIC) in patients suffering from long‐term trapezius myalgia

Cited by 103 publications

References 42 publications

Evidence of augmented central pain processing in idiopathic chronic low back pain

Evidence of augmented central pain processing in idiopathic chronic low back pain

Central modulation of pain

Applications of sensory and physiological measurement in oral‐facial dental pain

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