Pain
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Clinical Trial
Muscle palpation with controlled finger pressure: new equipment for the study of tender myofascial tissues.
While manual palpation is the most important method for evaluation of tender myofascial tissues, it lacks reliability. Therefore, we have developed an instrument, called a 'palpometer', which allows the measurement of pressure exerted during palpation. The palpometer consists of a thin pressure-sensitive plastic device attached to the palpating finger, and of a scale recording the pressure applied to the device. ⋯ Thus, a reliable instrument for measuring pressure intensities during palpation of myofascial tissue has been developed. The large variation in palpation pressures between observers indicates that palpation of tender myofascial tissue may be considerably improved by use of the palpometer. This instrument will be indispensable in research studies employing palpation and in the training of physicians to diagnose myofascial pain disorders.
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To address the mechanisms of hyperalgesia and dorsal horn plasticity following peripheral tissue inflammation, the effects of adjuvant-induced inflammation of the rat hindpaw on behavioral nociception and nociceptive neuronal activity in the superficial dorsal horn were examined in neonatally capsaicin-treated rats 6-8 weeks of age. Capsaicin treatment resulted in an 82% loss of unmyelinated fibers in L5 dorsal roots, a dramatic reduction of substance P-like immunoreactivity in the spinal cord, and a significant decrease in the percentage of dorsal horn nociceptive neurons that responded to C-fiber stimulation and noxious heating of the skin. The thermal nociceptive threshold was significantly increased in capsaicin-treated rats, but behavioral hyperalgesia to thermal stimuli still developed in response to inflammation. ⋯ There was no difference in stimulation-induced expansion of the receptive fields for WDR neurons between vehicle- or capsaicin-treated rats. An N-methyl-D-aspartate receptor antagonist, MK-801, attenuated the behavioral hyperalgesia and reduced the receptive field size of dorsal horn neurons in inflamed capsaicin- and vehicle-treated rats. The data suggest that while capsaicin-sensitive primary afferents may be involved in neuronal plasticity induced by peripheral tissue inflammation, changes in the capsaicin-insensitive WDR and NS populations are sufficient to produce thermal and mechanical hyperalgesia after the loss of capsaicin-sensitive primary afferents.
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This study evaluated the pain-related behaviours induced by 2 models of peripheral sciatic nerve injuries in the rat: transient nerve crush and chronic constriction injury (CCI). Various lesions of the saphenous nerve were performed in order to investigate the role of saphenous innervation in behavioural disorders induced by these nerve injuries. Behavioural testing included assessment of responses to phasic stimulation (mechanical and thermal) and observation of 'spontaneous' pain-related behaviour. ⋯ Section without ligation of the saphenous nerve induced comparable results in rats with sciatic crush, but did not significantly modify nociceptive behaviours in rats with CCI. These data emphasise the role of adjacent saphenous nerve in the mechanisms of pain-related disorders induced by these peripheral nerve lesions. On the contralateral paw, pain-related modifications were also observed in both models, suggesting that unilateral nerve lesions induce remote modifications extending beyond the site of the injured nerve.
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Randomized Controlled Trial Clinical Trial
Brief group cognitive-behavioral intervention for temporomandibular disorders.
Temporomandibular disorders (TMD) are currently viewed as an interrelated set of clinical conditions presenting with signs and symptoms in masticatory and related muscles of the head and neck, and the soft tissue and bony components of the temporomandibular joint. Epidemiologic and clinical studies of TMD confirm its status as a chronic pain problem. In this report we present results from a randomized clinical trial which compared, at 3- and 12-month follow-ups, the effects of usual TMD treatment on TMD pain and related physical and psychological variables with the effects of a cognitive-behavioral (CB) intervention delivered to small groups of patients before usual TMD treatment began. ⋯ Such effects were not observed for depression, somatization, or clinical measures of jaw range of motion. Additionally, as hypothesized, dysfunctional chronic pain patients did not appear to benefit from the brief CB intervention. Intent to treat analyses were also performed to assess generalizability of the results.
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Randomized Controlled Trial Clinical Trial
Chronic tension-type headache: amitriptyline reduces clinical headache-duration and experimental pain sensitivity but does not alter pericranial muscle activity readings.
In a double-blind, placebo-controlled trial, the effect of 75 mg of a slow-release formulation of amitriptyline on the clinical severity of chronic tension-type headache and on headache-associated neurophysiological parameters (EMG activity, exteroceptive suppression of temporal muscle activity, contingent negative variation (CNV) and experimental pain sensitivity) was investigated. All of the patients treated had a history of headaches of many years' standing and many of them had failed attempts at treatment. In the amitriptyline group, a significant reduction in daily headache duration was already found in the 3rd week of treatment, while in the placebo group no significant changes in headache duration were to be seen. ⋯ The sensitivity to suprathreshold experimental pain, however, was significantly reduced. The data show a statistically relevant reduction of daily headache duration. However, they also show that amitriptyline can only partly alleviate chronic headaches but cannot cure them.