Increased Pain Sensitivity of the Upper Extremities of TMD Patients with Myalgia to Experimentally-evoked Noxious Stimulation: Possibility of Worsened Endogenous Opioid Systems

Kashima, Koji; Rahman, Omar Ibna Faizur; Sakoda, Sumio; Shiba, Ryosuke

doi:10.1080/08869634.1999.11746100

Cited by 65 publications

(56 citation statements)

References 9 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: 91%

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: 91%

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

“…Deficits in pain-evoked hypoalgesia are associated with several chronic pain conditions that disproportionately affect women, including temporomandibular disorder (Kashima et al 1999), irritable bowel syndrome (Wilder-Smith et al 2004), and fibromyalgia (Kosek and Hansson 1997;Lautenbacher and Rollman 1997;Staud et al 2003;Julien et al 2005). These findings suggest that women may have reduced endogenous analgesic system function compared to men, resulting in increased vulnerability to the development or maintenance of chronic pain states.…”

Section: Introductionmentioning

confidence: 80%

“…Pain-evoked hypoalgesia is a psychophysical measure of the function of central endogenous pain modulation systems and has been used experimentally to test these systems in healthy (Willer et al 1979;Price and McHaffie 1988), aged (Edwards et al 2003a), and chronic pain populations (Kashima et al 1999;Staud et al 2003). Pain-evoked hypoalgesic magnitude is inversely related to clinical pain frequency among healthy individuals (Edwards et al 2003b), suggesting that reduced endogenous analgesic system function may be a risk factor for chronic pain.…”

Section: Introductionmentioning

confidence: 99%

Sex differences in endogenous pain modulation by distracting and painful conditioning stimulation

Quiton

Greenspan

2007

Pain

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Sex differences in endogenous pain modulation were tested in healthy volunteers (32 men, 30 women). Painful contact heat stimuli were delivered to the right leg alone, and then in combination with various electrical conditioning stimuli delivered to the left forearm. Four conditioning protocols were applied to each subject in separate sessions: mild, nonpainful (control); distracting; stressfulyet-nonpainful; strongly painful. Thermal stimuli were rated on visual analog scales for pain intensity (INT) and unpleasantness (UNP). Distracting and painful conditioning stimuli significantly reduced heat pain INT and UNP ratings for both sexes, with significantly larger distraction effects on INT ratings for men than women (p=0.004). No sex differences in pain-evoked hypoalgesia were detected (p>0.05). The stress protocol did not consistently reduce heat pain ratings, possibly because the protocol was not sufficiently stressful to activate endogenous modulatory systems. Regression analysis revealed that the magnitude of pain-evoked hypoalgesia was predicted by the perceived distraction (p=0.003) and stress (p=0.04) produced by the painful conditioning stimulation, providing evidence that distraction and stress contribute to pain-evoked hypoalgesia. However, the contribution of stress to pain-evoked hypoalgesia differed by sex (p=0.02), with greater perceived stress associated with greater hypoalgesia in men and the opposite trend in women, suggesting sex differences in the mechanisms underlying pain-evoked hypoalgesia. This study provides indirect evidence that multiple neural mechanisms are involved in endogenous pain modulation and suggests that sex-specific aspects of these systems may contribute to greater pain sensitivity and higher prevalence of many chronic pain conditions among women.

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“…Es liegen Hinweise dafür vor,dass Patienten mit persistierenden MAP im Vergleich zu Nichtpatienten eine erhöhte somatische Schmerzempfindlichkeit (Schmerzschwelle; Schmerztoleranzschwelle) auch an Stellen außerhalb des Kopf-Hals-Bereichs aufweisen [27,34]. Maixner [47] und knapp der Hälfte (46%) [43] der Patienten in Einrichtungen aus,die auf die Behandlung von Gesichtsschmerzen spezialisiert sind.Entsprechend findet man besonders bei dieser Patientengruppe eine psychische Komorbidität,die jedoch eher als Folge denn als Ursache der bestehenden Schmerzen angesehen wird [11].…”

Section: Generalisierte Schmerzhypersensitivität Bei Zentraler Reizveunclassified

Chronische Myoarthropathien des Kausystems

Türp

Schindler

2004

Der Schmerz

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According to the 3rd German Oral Health Study (1999), the prevalence of painful temporomandibular disorders (TMDs) is about 5%. Although limited information about the magnitude of utilization of health care services and expenses for health care in temporomandibular pain patients is available, the financial burden of affected individuals may be considerable. The etiology and pathophysiology of chronic TMDs is still obscure. However, certain (patho)physiological mechanisms may be associated with the genesis and perpetuation of these musculoskeletal facial pains (e. g. disturbances in central nervous system processing; psychosocial factors; hormonal influences). Strong scientific evidence from the dental/medical literature is currently available for the following forms of TMD treatment and management: occlusal appliances (stabilization appliance), clonazepam, diazepam, meprobamate, EMG biofeedback, multimodal approaches (somatic and psychological pain management).

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Increased Pain Sensitivity of the Upper Extremities of TMD Patients with Myalgia to Experimentally-evoked Noxious Stimulation: Possibility of Worsened Endogenous Opioid Systems

Cited by 65 publications

References 9 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

Sex differences in endogenous pain modulation by distracting and painful conditioning stimulation

Chronische Myoarthropathien des Kausystems

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