Pain
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A hypothesis is presented concerning the neuronal mechanisms which subserve the sympathetically maintained pains such as causalgia and reflex sympathetic dystrophy. The hypothesis rests on two assumptions: that a high rate of firing in spinal wide-dynamic-range (WDR) or multireceptive neurons results in painful sensations; and that nociceptor responses associated with trauma can produce long-term sensitization of WDR neurons. The hypothesis states that chronic sympathetically maintained pains are mediated by activity in low-threshold, myelinated mechanoreceptors, that this afferent activity results from sympathetic efferent actions upon the receptors or upon afferent fibers ending in a neuroma and that these afferent fibers evoke sufficient activity in sensitized spinal WDR neurons to produce a painful sensation. ⋯ This hypothesis does not require nerve injury or dystrophic tissue. It explains both the continuous pain and the allodynia that are common to these syndromes and their abolition by sympathetic block. Specific changes are proposed in the diagnosis and treatment of post-traumatic pains.
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Seventy-four chronic low back pain patients in a study assessing the effectiveness of group outpatient cognitive-behavioral and operant behavioral treatment completed the Coping Strategy Questionnaire (CSQ) and measures of pain, depression, and functional disability pre- and post-treatment. The previously reported factor structure of the CSQ was generally replicated, and significant associations were found between use of ignoring and reinterpretation strategies and downtime, between use of attention diversion strategies and pain intensity, and between tendency to catastrophize and physical and psychosocial impairment. ⋯ Increased use of praying and hoping strategies was significantly related to decreases in pain intensity. Decreased catastrophizing was also significantly related to decreases in pain intensity, as well as to decreases in physical and psychosocial impairment.
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In an attempt to unravel the relationship between chronic pain and depression, the authors studied the incidence of depression, alcoholism, and chronic pain in first degree relatives of 100 chronic pain patients with and without depression. A higher incidence of major depression was found in first degree relatives of those patients with depression than those without depression. Familial incidence of alcohol dependence was similar in both groups of patients. These findings confirm an earlier report and raise questions about the notion of considering chronic pain simply as a variant of depression and suggest the possibility that the occurrence of major depression in chronic back pain might be related to genetic vulnerability to depression in these patients.
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DADL was administered to a patient who was analgetically tolerant to continuously infused, intrathecal morphine sulfate. DADL restored analgesia without respiratory depression but opiate withdrawal syndrome was not prevented. ⋯ Clonidine hydrochloride and decreasing doses of oral morphine were used to successfully treat the withdrawal syndrome, including somnolence. Further research is indicated to verify the findings of this one patient and investigate the efficacy of DADL to provide analgesia for morphine-tolerant patients.
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Comparative Study
A simultaneous comparison of fentanyl's analgesic effects on experimental and clinical pain.
Intravenous administration of 0.8 microgram/kg and 1.1 micrograms/kg fentanyl in low back pain patients reduced both sensory intensity and unpleasantness visual analogue scale (VAS) responses to experimental pain evoked by graded 5-sec nociceptive temperature stimuli (45-51 degrees C) as well as VAS-sensory and VAS-affective responses to clinical pain. Fentanyl produced similar decreases in VAS-sensory responses to experimental and clinical pain. ⋯ This interaction of type of pain (experimental versus clinical) and pain dimension (sensory versus affective) results from either a steeper sensory intensity-unpleasantness relationship for clinical pain as compared to experimental pain or additional selective influences of opiates on affective factors uniquely related to clinical pain. These results indicate that low to moderate doses of opiates reduce both sensory and affective dimensions of pain and strongly suggest that changes in pain affect occur mainly as a direct consequence of reductions in pain sensation intensity.