Pain
-
A purported pathogenic mechanism for the development of fibromyalgia, a medically unexplained syndrome involving widespread pain, is stress and associated psychiatric disorder. The major stressor of recent World Trade Center terrorist attacks provides a natural experiment for evaluating this mechanism. This study sought to determine whether symptoms consistent with fibromyalgia increased post-September 11 and whether exposure to specific terrorism-related events or prior depression predicted symptom increase. ⋯ Event exposure did not relate to FM-L onset at follow-up, nor did depressive symptoms at baseline interact with event exposure. Depressive symptoms did not predict new onsets better than the extent of their comorbidity with FM-L at baseline. The failure to detect a significant increase in symptoms consistent with a diagnosis of fibromyalgia and the failure of new onsets of such symptoms to be accounted for by exposure to major stressors or prior depressive symptoms suggests that these hypothesized risk factors are unlikely to be of major importance in the pathogenesis of fibromyalgia.
-
The purpose of this study was to describe race/ethnic differences in the use of formal health care services for painful oral symptoms by older adults. We also considered the sex of the respondent rather than assuming that males and females within a specific racial group would use health care services similarly. To our knowledge, these specific utilization patterns have never been reported before in the pain literature. ⋯ Pain at its worst was a positive predictor for four of the five analyses (jaw joint pain, painful oral sores, temperature sensitivity, and toothache pain). The duration variable (years with pain) was a negative predictor of health care use. This is consistent with the conclusion that individuals seek care early in the course of the symptom, i.e. an active care seeking phase, make emotional or physical adjustments, and then resign themselves to the symptoms.
-
This study assessed spatial and temporal aspects of pressure pain during increasing and constant compressions using a cuff algometer and during adaptive compressions using a closed-loop feedback system for maintaining stable pain. Experimental setup consisted of a pneumatic tourniquet cuff, a computer-controlled air compressor, and a 10-cm electronic visual analogue scale (VAS). The first experiment assessed spatial summation for cuff pain by recording the pressure-pain stimulus-response (SR) function during increasing compressions with single and double cuffs. ⋯ The oscillating pressure generated by closed-loop system led to constant rather than adapting pain at intensities of 2, 4, and 6 cm on the VAS. The cuff algometer is highly configurable tool for assessment of pain sensitivity by pressure-pain and time-pain functions. The presented models are useful additions to a researcher's armamentarium for further pharmacological and clinical studies on deep tissue pain and related mechanisms.
-
The current study examined patients with temporomandibular disorders (TMD) (n=20) and pain-free controls (n=28) under stress and relaxation conditions. Interleukin-6 (IL-6), norepinephrine and epinephrine (NE and E) were measured both before and during each of two conditions: a non-stressful relaxation period and a speech stressor. Ischemic pain sensitivity was also assessed after each of these conditions. ⋯ After controlling for depressed mood, TMD patients as a whole showed a significantly blunted response in IL-6 levels produced during stress as compared to controls (beta=0.31*). Although TMD subjects as a whole did not show the expected greater pain sensitivity to the ischemic task, those displaying a less optimistic style did exhibit lower pain tolerance times (beta=-0.61*) and higher pain unpleasantness ratings (beta=0.48*), compared with low optimism controls and high optimism TMD patients. Less optimistic TMD patients also had higher NE and IL-6 levels during stress than other TMD patients, while optimism was unrelated to responses in controls (*P<0.05).
-
Neuropathic pain syndromes are characterized by spontaneous pain and by stimulus-evoked allodynia and hyperalgesia. Stimulus-induced pain, i.e. the capacity of external stimuli to alter sensory processing so as to generate a pain hypersensitivity that outlasts the initiating stimulus, is usually present only after intense activation of nociceptors. In abnormal pain states, however, such as after capsaicin injection or inflammation, a stimulus-induced incremental pain can be generated by repetitive light touch, termed progressive tactile hypersensitivity (PTH). ⋯ However, 10 weeks and after, the same repeated stimulation induced a progressive tactile hypersensitivity that persisted after discontinuation of the tactile stimulation. Following SNI, repeated stimulation of the hypersensitive skin territory, corresponding to the intact spared sural nerve, never induced PTH. Tactile stimulation of regenerating afferents but not spared non-injured afferents, can induce, therefore, PTH and such a stimulus-induced alteration in pain processing may contribute to clinical neuropathic pain.