Pain
-
Randomized Controlled Trial Comparative Study Clinical Trial
The Amsterdam Pain Management Index compared to eight frequently used outcome measures to evaluate the adequacy of pain treatment in cancer patients with chronic pain.
There is no 'gold standard' to assess the adequacy of pain treatment in cancer patients. The purpose of the study is to explore the Amsterdam Pain Management Index, a newly designed measure to evaluate the adequacy of cancer pain treatment, and to compare it with eight frequently used outcome measures. The Amsterdam Pain Management Index compares patients' Present Pain Intensity, Average Pain Intensity, and Worst Pain Intensity with a composite score of analgesics used, while correcting for what a patient considers as a tolerable level of pain. ⋯ The ability of the outcome measures to detect changes over time was clearly demonstrated by all outcome measures. Effects of the intervention were only found for the Amsterdam Pain Management Index and patients' Substantial Worst Pain score. Although support was provided for the use of the Amsterdam Pain Management Index, more research is warranted.
-
Comparative Study
TMJ disorders and myogenic facial pain: a discriminative analysis using the McGill Pain Questionnaire.
Our aim was to assess the discriminative capacity of the McGill Pain Questionnaire (MPQ) in patients with temporomandibular joint (TMJ) disorders or with myogenous facial pain (MP). The MPQ was administered to 57 TMJ and 28 MP patients who were also asked to assess the level of pain using the Visual Analog Scale (VAS). Weighted MPQ item scores, subscale Pain Rating Indexes (PRI), total PRI and the number of words chosen were calculated. ⋯ In conclusion, the MPQ consistently discriminated between TMJ and MP patients. Although the higher affective scores in the MP patients may be partly induced by higher levels of anxiety in these patients, the data convincingly show that the system's discriminative capacity relates to all MPQ subscores and to the majority of the MPQ items. Moreover, within the same item, the choice of verbal descriptors varies consistently between the two groups of patients.
-
Research among persons with cancer pain suggests that the association between pain intensity and pain interference is non-linear. That is, pain begins to have a serious impact on functioning when it reaches a certain threshold level (about 5 on 0--10 scales). Often, a second pain threshold can be identified which, once reached, shows an even greater proportional negative impact on functioning. ⋯ Moreover, the degree of pain interference appeared to vary as a function of pain type. The same level of back pain interfered more significantly with daily function than phantom limb pain did after pain levels reached five or more (on a 0--10 scale). These findings have implications for understanding the meaning of pain intensity levels, as well as for the assessment of pain intensity in persons with amputation-related pain.
-
This study used concordant behavioral and electrophysiological approaches to examine the actions of the prototypic kappa opioid receptor agonist U69593 in the rostral ventromedial medulla (RVM). In vitro whole-cell voltage clamp recordings indicated that bath application of U69593 produced outward currents in primary cells in the RVM. In secondary cells, which comprised 80% of the population, U69593 produced a concentration-dependent and norbinaltorphimine (norBNI)-reversible inhibition of evoked excitatory postsynaptic currents (EPSCs) in the absence of any postsynaptic effect. ⋯ The highly test-dependent nature of U69593's effects suggests that the mechanisms by which neurons in the RVM modulate thermal nociceptive responses evoked from the tail and hindpaw are not uniform. Collectively, these data suggest that the RVM is a primary site of action for the antinociceptive actions of kappa opioid receptor agonists and that the mechanism most likely involves a presynaptic inhibition of excitatory inputs to secondary cells. Thus, disinhibition of pain inhibitory neurons in the RVM is likely to be a common mechanism by which opioid receptor agonists produce antinociception, whether by the direct inhibition of inhibitory secondary cells, as in the case of mu opioid receptor agonists, or by a reduction in the excitatory drive to these neurons, as in the case of kappa opioid receptor agonists.