Pain
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Pain treatment is a crucial aspect in the care of children with cancer and there are many studies demonstrating inefficient pain treatment. In this study, questionnaires dealing with pain treatment of children with malignant diseases were sent to all (47) pediatric departments in Sweden. The aims of this nationwide survey were to evaluate the extent and causes of pain, the use of methods for pain evaluation (e.g. analysis of type of pain and monitoring of pain intensity), principles of pain management, side effects of pain treatment and the educational needs of physicians and nurses regarding these issues. ⋯ According to a majority of physicians and nurses (72%), pain could be treated more effectively than it is presently, and 64% state that they need more time for the management of pain. Both physicians and nurses state that they need additional education in different areas of pain evaluation and pain treatment. Swedish treatment practices for the management of pediatric cancer pain roughly follow the published guidelines, but many improvements are still necessary.
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Comparative Study Clinical Trial
Clinical analgesic equivalence for morphine and hydromorphone with prolonged PCA.
A morphine to hydromorphone equivalence ratio of 7:1 has become the accepted standard, but evidence supporting it comes from single dose studies performed before the advent of patient controlled analgesia (PCA). We compared morphine and hydromorphone use with PCA in bone marrow transplantation patients who required opioids for the control of severe oral mucositis over several days or weeks. An exploratory analysis of clinical records from 102 patients (981 patient days) who used PCA opioids for varying periods of up to 50 days suggested a morphine to hydromorphone use ratio of 3:1. ⋯ Thirty-six patients who used morphine and 21 who used hydromorphone contributed data on pain, satisfaction with pain control, and drug consumption. We observed an average morphine/hydromorphone ratio of 3:1. This differs markedly from historical single dose studies used in published dose equivalency recommendations implying that other equivalency ratios in clinical use may be inappropriate.
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Patients with chronic non-malignant pain are often suspected of reporting medical symptoms that have non-organic as opposed to purely organic origins. According to the somatization hypothesis, non-organic reporting occurs when affective or other benign physical sensations are misconstrued as symptoms of physical disease [corrected]. Psychological tests purporting to assess somatization are limited by their self-report format and may be confounded in patients with physical disease or injury. ⋯ When compared to Minimizers, Amplifiers were disabled for a significantly greater number of days, reported significantly more impairment in domestic functioning, were significantly less active, visited the doctor significantly more often, and were significantly more distressed. The results suggest that substantial differences in disability and medical visitation may exist among patients who may not differ appreciably in their level of organic pathology. Instead, differences in illness behavior may, to some extent, be mediated by differences in somatization.
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Touch evoked agitation (allodynia) can be induced by spinal delivery of strychnine and this effect is antagonized by intrathecal NMDA and non-NMDA receptor antagonists, but not by mu-opiate receptor agonists. In this study, we sought to characterize the effect of focal glycine-receptor inhibition on spontaneous and evoked activity in dorsal horn neurons of the chloralose-anesthetized cat. Strychnine (1 mM) applied near the neurons through a dialysis fiber caused an enhanced response to hair deflection, enlargement of the low threshold receptive fields and in some cells, an increase in afterdischarge. ⋯ Consistent with these data is the contention that under normal circumstances, afferent hair follicle input onto convergent neurons is regulated by a tonic glycinergic circuit. Removal of this regulatory influence leads to a magnification of low threshold tactile throughput in dorsal horn. This model may help to provide pharmacological insights into more efficacious treatments for such pain states that are relatively refractory to opioid therapies.
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Randomized Controlled Trial Clinical Trial
Nimodipine fails to enhance the analgesic effect of slow release morphine in the early phases of cancer pain treatment.
We assessed nimodipine's ability to increase the analgesic effect of morphine in 32 patients suffering from cancer pain in a double-blind, placebo controlled cross-over study. Morphine administration began a few days before the start of the study. The analgesic effects of two combinations were compared: morphine (M) plus placebo (P) and morphine plus 90 mg/24 h of nimodipine (N). ⋯ However, when the same statistical tests were used for comparison of results with pre-treatment baseline values, highly significant differences between mean scores on the scales for pain relief and pain intensity were found. Based on these negative results we conclude that nimodipine given orally at a dose of 30 mg every 8 h does not enhance analgesia when associated with morphine in the early phases of treatment for cancer pain. Our study also gives clear evidence of a placebo effect.