Pain
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Chronic pain, lymphoedema, post-irradiation neuropathy and other symptoms are reported in as many as 75% of women following breast cancer treatment. This study examined pain and sensory abnormalities in women following breast cancer surgery. Sensory tests were carried out on operated and contralateral sides in 15 women with spontaneous pain and sensory abnormalities and 11 pain-free women. ⋯ Pinprick-evoked pain was correlated to spontaneous pain but not to flux. Spontaneous pain was not correlated to flux. Sensitization seems to be a feature in breast cancer-operated women with pain, but not in pain-free women.
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Complete or partial spinal section at T(8) has been shown to block tactile allodynia but not thermal hyperalgesia following L(5)/L(6) spinal nerve ligation (SNL), suggesting the supraspinal integration of allodynia in neuropathic pain. In the present study, the possibility of mediation of nerve injury-associated pain through tonic activity of descending nociceptive facilitation arising from the rostroventromedial medulla (RVM) was investigated. Specifically, the actions of brainstem cholecystokinin and the possible importance of sustained afferent input from injured nerve fibers were determined using pharmacological and physiological approaches in rats with SNL. ⋯ These results suggest that changes in supraspinal processing are likely to contribute to the observed poor efficacy of opioids in clinical states of neuropathic pain. These data also indicate that the activation of descending nociceptive facilitatory pathways is important in the maintenance of neuropathic pain, appears to be dependent on CCK release, and may be driven from sustained afferent input from injured nerves to brainstem sites. Collectively, these data support the hypothesis that abnormal tonic activity of descending facilitation mechanisms may underlie chronic pain from peripheral nerve injury.
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One hundred and sixty-eight patients with osteoarthritis (OA) of the knees participated in this study. Of the participants, 72 were men and 96 were women. All participants completed the Arthritis Impact Measurement Scales (AIMS), underwent a 10 min standardized observation session to assess their pain behavior, and completed the Catastrophizing Scale of the Coping Strategies Questionnaire (CSQ) and the Depression Scale of the Symptom Checklist 90 Revised (SCL-90R). ⋯ Once catastrophizing was entered into the analyses, the previously significant effects of gender were no longer found. Interestingly, catastrophizing still mediated the gender-pain relationship even after controlling for depression. These findings underscore the importance of both gender and catastrophizing in understanding the OA pain experience and may have important implications for pain assessment and treatment.
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We examined whether cerebral activation to two different intense and painful stimuli could be detected using functional magnetic resonance imaging (fMRI) in alpha-chloralose anesthetized rats. Experiments were performed using a 9.4 T magnet and a surface coil centered over the forebrain. A set of gradient echo images were acquired and analyzed using our software based on fuzzy cluster analysis (EvIdent). ⋯ All these regions of activation were markedly reduced during nitrous oxide inhalation. Treatment with morphine resulted in an inhibition of the activation response to electrical stimulation in most regions except for sensory-motor cortex. Thus, electrical and chemical noxious stimuli activated regions that are known to be involved in the central processing of pain and morphine modified the activation observed. fMRI combined with appropriate exploratory data analysis tools could provide an effective new tool with which to study novel analgesics and their effects on the CNS processing of pain in animal models.
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Transection of the L5 spinal nerve in rats results in allodynia- and hyperalgesia-like behavior to mechanical stimulation which are thought to be mediated by ectopic activity arising in lesioned afferent neurons mainly in the dorsal root ganglion (DRG). It has been suggested that the neuropathic pain behavior is dependent on the sympathetic nervous system. In rats 3-56 days after L5 spinal nerve lesion, we tested responses of axotomized afferent fibers recorded in the dorsal root of the lesioned segment to norepinephrine (NE, 0.5 microg/kg) injected intravenously and to selective electrical stimulation of the lumbar sympathetic trunk (LST). ⋯ These results show that sympathetic-sensory coupling occurs only in a minority of axotomized afferents after L5 spinal nerve injury. Like previous studies, they cast doubt on the notion that the L5 spinal nerve lesion is a good model for sympathetically maintained pain. Since responses of lesioned afferent neurons to LST stimulation and NE could be provoked with high reliability after inducing vasoconstriction in the DRG, and since they mirrored stimulation-induced vasoconstrictions in the DRG, it appears that in this model the association of sympathetic activity with afferent discharge occurs mainly when perfusion of the DRG is impaired.