Pain
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Comparative Study
Acute and remitting painful diabetic polyneuropathy: a comparison of peripheral nerve fibre pathology.
The cause of the neuropathic pain that is experienced by some patients with diabetic neuropathy remains to be established. Early neuropathological reports, based on comparisons between diabetic patients and non-diabetic control subjects, emphasised associations between pathological changes in specific classes of peripheral nerve fibre and the presence of pain. By making comparisons with more appropriate control subjects, namely diabetic patients without neuropathic pain, more recent studies have found that there are few clear morphological correlates for this type of pain. ⋯ However, the inescapable finding of this study was, in fact, the similarity in the nerve fibre pathology in diabetic patients with active and remitting painful neuropathy. We conclude that the occurrence of nerve fibre degeneration and regeneration is in itself unlikely to be sufficient to account fully for diabetic neuropathic pain. However, it is conceivable that events occurring during certain stages in the pathological cycle of degeneration and regeneration create the necessary circumstances which lead to pain.
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Fifteen patients with severe pain due to malignancy were treated by continuous epidural morphine infusions. A disposable external pump was used. Patients were treated in a hospital setting or at home for a total of 906 days. ⋯ Bacterial growth was found in 0.6% of the balloon reservoirs used, while the epidural filters were free from growth. There were no clinical infections. It appears that this delivery system is safe, practical and suitable for use in the home environment.
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Comparative Study
Comparison of cognitive-behavioral group treatment and an alternative non-psychological treatment for chronic low back pain.
This study was designed to investigate the relative efficacy of cognitive-behavioral group treatment, including relaxation training, in comparison with a control condition in a sample of 20 outpatients with chronic low back pain. Subjects in both conditions also received the same physiotherapy back-education and exercise program. ⋯ The combined psychological treatment and physiotherapy condition displayed significantly greater improvement than the attention-control and physiotherapy condition at post-treatment on measures of other-rated functional impairment, use of active coping strategies, self-efficacy beliefs, and medication use. These differences were maintained at 6 month follow-up on use of active coping strategies and, to a lesser degree, on self-efficacy beliefs and other-rated functional impairment.
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Pain responsiveness was investigated experimentally as a function of age and childbirth pain experience. Sensitivity to cold pressor-induced pain was assessed through threshold, tolerance, and visual analog pain ratings. It was hypothesized that childbirth pain experience would mostly modify experimental pain judgment, in accordance with the adaptation-levels model. ⋯ Thus, painful childbirth experience is sufficient to raise cold pressor pain threshold. This finding has never before been reported in the pain literature. It is consistent with anecdotal reports from parous women who, when providing cold pressor pain judgments, say that "nothing compares to labor pain."
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The effects of the major morphine metabolites, morphine-3-glucuronide and morphine-6-glucuronide, on nociception were assessed by the tail-flick, hot-plate and writhing tests in the rat. Morphine-3-glucuronide (M3G) 1.1 x 10(-9) mol (0.5 micrograms) or saline was injected intracerebroventricularly (i.c.v.) or intrathecally (i.t.) followed by a second injection of 2.0 x 10(-10) mol (0.1 microgram) or 2.0 x 10(-11) mol (0.01 microgram) morphine-6-glucuronide (M6G) 10 min later. Administration of M3G (i.c.v.) significantly attenuated the antinociceptive effects of M6G in the hot-plate test. ⋯ In animals receiving M3G there was a prevention or attenuation of the M6G induced depression of respiratory frequency, tidal volume and minute ventilation compared to control groups receiving M6G in combination with saline. These results show that M3G may functionally antagonize the central antinociceptive effects as well as the ventilatory depression induced by M6G. Interestingly, M3G was more potent in antagonizing the M6G-induced analgesia after i.t. administration than that after i.c.v. administration, which may suggest that the spinal cord is more sensitive to the non-opioid excitatory effects of M3G than supraspinal structures.