Pain
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Our previous work indicates that the intrathecal administration of neuropeptide Y (NPY) acts at its cognate receptors to reduce behavioral signs of nociception in several models of inflammatory pain, including the formalin test. The present study extends these findings to a rat model of peripheral neuropathic pain, and then evaluates the hypothesis that NPY inhibits inflammation- and nerve injury-induced activation of spinal nociceptive transmission. Here we show that NPY dose-dependently reduced behavioral signs of mechanical and cold hypersensitivity in the spared nerve injury (SNI) model. ⋯ We found that intrathecal NPY reduced both formalin- and SNI-induced Fos expression. NPY inhibition of SNI-induced Fos expression was localized to the sural (uninjured) innervation territory, and could be blocked by intrathecal BIBO3304 and BIIE0246. We conclude that NPY acts at spinal Y1 and Y2 receptors to reduce spinal neuron activity and behavioral signs of inflammatory or neuropathic pain.
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Multicenter Study Comparative Study
Neurophysiological characterization of postherniotomy pain.
Inguinal herniotomy is one of the most frequent surgical procedures and chronic pain affecting everyday activities is reported in approximately 10% of patients. However, the neurophysiological changes and underlying pathophysiological mechanisms of postherniotomy pain are not known in detail, thereby precluding advances in treatment strategies and prophylaxis. Therefore, we examined forty-six patients reporting moderate to severe postherniotomy pain affecting daily activities for more than a year postoperatively, and compared them with a control group of patients without pain 1 yr postoperatively. ⋯ The specific finding of reduced pain detection threshold over the external inguinal annulus is consistent with damage to the cutaneous innervation territory of nervous structures in the inguinal region. The correspondence between pain location and sensory disturbance suggests that the pain is neuropathic in nature. Whether the underlying pathophysiological mechanisms are related to direct intraoperative nerve injury or nerve injury due to an inflammatory mesh response remains to be determined.
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Comparative Study
Psychosocial risk markers for new onset irritable bowel syndrome--results of a large prospective population-based study.
Irritable bowel syndrome (IBS) affects up to 22% of the general population. Its aetiology remains unclear. Previously reported cross-sectional associations with psychological distress and depression are not fully understood. ⋯ After adjustment for age, gender and baseline abdominal pain status, high levels of illness behaviour (odds ratio (OR)=5.2; 95% confidence interval (95% CI) 2.5-11.0), anxiety (OR=2.0; 95% CI 0.98-4.1), sleep problems (OR=1.6; 95% CI 0.8-3.2), and somatic symptoms (OR=1.6; 95% CI 0.8-2.9) were found to be independent predictors of IBS onset. This study has demonstrated that psychosocial factors indicative of the process of somatisation are independent risk markers for the development of IBS in a group of subjects previously free of IBS. Similar relationships are observed in other "functional" disorders, further supporting the hypothesis that they have similar aetiologies.
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Comparative Study
Exposure to movement in chronic back pain: evidence of successful generalization across a reaching task.
According to the fear-avoidance model, kinesiophobia (pain-related fear) is an important factor in the development of chronic pain and disability through the maintenance of maladaptive avoidance behaviors. Using a paradigm that required repeated exposure to a reaching task, the current study investigated generalization of pain and harm expectancy corrections (i.e., the tendency to bring expectations in line with experience) in chronic low back pain sufferers with high versus low levels of kinesiophobia. Sixty participants were asked to consecutively perform four adaptations of a reaching task, each introducing an element of increased intensity. ⋯ Further, highly kinesiophobic female, but not male, participants demonstrated greater overprediction of harm relative to low kinesiophobic counterparts during the first reaching trial. Finally, in contrast to previous investigations, highly kinesiophobic participants showed successful generalization of pain expectancy corrections across movement tasks. Possible clinical implications of the findings are noted.
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Recently, local morphologic alterations of the brain in areas ascribable to the transmission of pain were detected in patients suffering from phantom pain, chronic back pain, irritable bowl syndrome, fibromyalgia and two types of frequent headaches. These alterations were different for each pain syndrome, but overlapped in the cingulate cortex, the orbitofrontal cortex, the insula and dorsal pons. ⋯ As it seems that chronic pain patients have a common "brain signature" in areas known to be involved in pain regulation, the question arises whether these changes are the cause or the consequence of chronic pain. The author suggests that the gray matter change observed in chronic pain patients are the consequence of frequent nociceptive input and should thus be reversible when pain is adequately treated.