Pain
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This paper describes the development and validation of a measure of strategies used by patients to cope with chronic pain, the Chronic Pain Coping Inventory (CPCI). A 104-item measure of pain coping responses and 3 measures of functioning were completed by 176 chronic pain patients. Two-week retest data were provided by 111 of these patients. ⋯ The results support the reliability of the CPCI scales. Four scales (Guarding, Resting, Asking for Assistance, and Task Persistence) predicted patient- and significant other-reported patient adjustment. Eight scales (Guarding, Opioid Medication Use, NSAID Use, Sedative-Hypnotic Medication Use, Resting, Asking for Assistance, and Exercise/Stretch) demonstrated moderate-to-strong relationships between patient and significant-other versions, further supporting their validity.
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Extending the earlier work of Mikail et al. (1993), a confirmatory factor analysis (CFA; LISREL VII) of a 4-factor model of pain assessment was tested. This model, comprised of the Beck Depression Inventory (BDI) and 13 subscales of the McGill Pain Questionnaire (MPQ) and the West Haven-Yale Multidimensional Pain Inventory (WHYMPI), adequately accounted for the pain experience with minimal overlap. Subjects were 306 outpatient chronic pain patients seen at a multidisciplinary chronic pain clinic. ⋯ The 4 factors were identified as Affective Distress, Support, Pain Description, and Functional Capacity. Results supported the hypothesis that the MPQ, WHYMPI and BDI are representative of the multidimensionality of the pain experience with minimal overlap among measures. Theoretical and clinical implications of reducing the overlap among existing measures in the assessment of pain patients are discussed.
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A patient suffered multiple fractures of the right leg and a left brain-stem infarction involving the anterolateral fasciculus of the central nociceptive system following multiple trauma. Later, the right leg was amputated, resulting in spontaneous and touch-evoked phantom pain and mechanical stump allodynia. However, quantitative sensory testing revealed considerable impairment of sensations normally mediated by cutaneous nociceptors and central spinothalamic systems on the right body side, including the stump but nearly intact touch and vibration senses. ⋯ We concluded the following. (i) Painful somatosensory memories that are responsible for phantom limb pain are located in the brain, most probably in the thalamus or cortex. (ii) Touch-evoked phantom pain and stump allodynia are not mediated by cutaneous nociceptive C and A delta fibers and spinal nociceptive pathways (spinothalamic tract). Activity in the lemniscal system (low-threshold mechanoreceptive A beta afferents, dorsal columns and medial lemnicus system) may be transferred to central pain signaling neurons in the thalamus or cortex resulting in touch-evoked pain sensations. (iii) Ongoing activity in cutaneous nociceptive C fibers and spinal nociceptive systems is not necessary to maintain central processes that account for spontaneous and touch-evoked pain sensations. Activity in nociceptors of deep somatic tissues might be more important.
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In this study, changes in plasma levels of calcitonin gene-related peptide (CGRP) and substance P (SP) during a spontaneous-like cluster headache attack provoked by nitroglycerin were evaluated. Peptide variations after spontaneous or sumatriptan-induced remission were also assessed. Blood was collected from the external jugular vein homolateral to the pain side of 30 male cluster headache patients; 18 men were in an active and 12 in a remission one. ⋯ On the contrary, nitroglycerin neither provoked a cluster headache attack nor altered CGRP-LI in the patients in a remission period. The augmented levels of CGRP-LI measured before and after nitroglycerin administration, when the provoked attack reached the maximum intensity, suggest an activation of the trigeminovascular system during the active period of cluster headache. Moreover, the clinical and biochemical actions showed by sumatriptan stress the involvement of serotonin in cluster headache mechanisms.
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In 40 rats anaesthetized with enflurane, we identified convergent dorsal horn neurones responding to both noxious (pinch) and innocuous (brush) mechanical stimulation of their receptive fields on the tail. We recorded extracellular activity before and during ischaemia of the receptive fields, as well as during subsequent reperfusion. Two NSAIDs, indomethacin and diclofenac sodium, or saline were applied locally to the spinal cord before the induction of ischaemia. ⋯ The neurones became hypersensitive to both pinch and brush during reperfusion of their receptive field, and receptive field size increased. Application of indomethacin and diclofenac sodium to the spinal cord abolished both the hypersensitivity and the increase in receptive field size. Our results indicate that spinal cord prostanoid synthesis facilitates the enhanced excitability of dorsal horn convergent neurones to both noxious and innocuous mechanical stimuli during reperfusion of their receptive fields, but does not affect the neurones' responses to receptive field ischaemia, nor their responses to mechanical stimuli in the absence of a conditioning stimulus.