Pain
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Case Reports
Difficult management of pain following sacrococcygeal chordoma: 13 months of subarachnoid infusion.
We report on a patient suffering severe pain following a long-standing sacral chordoma in whom management of therapy and pain was extremely difficult. Because orally administered morphine was observed to be ineffective in the early stages of treatment, we tried to achieve pain relief by using epidural morphine. This was also unsatisfactory. ⋯ Periods of analgesia were followed by occasional crises of intense sharp pain suggesting incomplete relief. No serious complications or meningitis occurred. This case emphasizes the difficulty in managing pain in this type of cancer.
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Hyperalgesia and allodynia in 4 cancer patients treated with morphine disappeared after discontinuing or substituting morphine with other opioid agonists. The first case describes a young female who developed hyperalgesia and myoclonus during intravenous morphine infusion. The hyperalgesia and myoclonus disappeared when the morphine administration was discontinued and she felt comfortable on small and sporadic oral doses of methadone. ⋯ The fourth case describes a boy developing hyperalgesia after high doses of oral and intramuscular morphine. The hyperalgesia disappeared after discontinuing morphine administration but withdrawal symptoms developed due to too small doses of methadone. Possible mechanisms of morphine-induced hyperalgesia are discussed.
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Seventeen drawings of localised low-back pain were analysed by two assessors using 4 systems. Three were grid-based systems and one was by computer. The mean area or 'extent' was calculated to be 7.7%, 4.7%, 3.6% and 2.3% of the body outline using 45, 200, 560 and 61,102 section analyses, respectively. ⋯ Correlation coefficients of extent between the systems varied from 0.46 to 0.94. Correlation was highest between systems of adjacent magnitude of sections. It is concluded that grid-based assessment of small areas overestimates the actual area of pain and this may account for the lack of sensitivity to change in clinical status.
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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.
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Randomized Controlled Trial Clinical Trial
Quantitative sensory examination of epidural anaesthesia and analgesia in man: effects of pre- and post-traumatic morphine on hyperalgesia.
The objectives of the study were: (1) comparison of hypoalgesic effects of pre- and post-traumatic epidural morphine (EM) on primary and secondary hyperalgesia, and (2) comparison of EM hypoalgesia in normal and injured skin. Burn injuries (25 x 50 mm rectangular thermode, 47 degrees C, 7 min) were produced on the calves of healthy volunteers, at 2 different days at least 1 week apart. In randomized order, the subjects received 4 mg of EM administered via the L2-L3 intervertebral space on one day and no treatment on the other day. ⋯ Following NAL, the areas of secondary hyperalgesia expanded beyond control size. It is suggested that the major effect of EM on secondary hyperalgesia is inhibition of C fibre-mediated activity which maintains the altered response properties of central neurons responsible for secondary hyperalgesia. Possible mechanisms of action of NAL in enhancement of hyperalgesia are discussed.