Acute pain is a warning protective sensation for any impending harm.However,chronic pain syndromes are often resistant diseases that may consume large amount of health care costs.It has been suggested by recent studies that pain perception may be formed in central neural networks via large-scale coding processes,which involves sensory,affective,and cognitive dimensions.Many central areas are involved in these processes,including structures from the spinal cord,the brain stem,the limbic system,to the cortices.Thus,chronic painful diseases may be the result of some abnormal coding within this network.A thorough investigation of coding mechanism of pain within the central neuromatrix will bring us great insight into the mechanisms responsible for the development of chronic pain,hence leading to novel therapeutic interventions for pain management.
Objective Recently,there has been growing interest in the interaction between depressive disorders and pain.The purpose of this study was to examine whether depression would lead to a decreased sensitivity to noxious stimuli in rats with spontaneous pain.Methods The olfactory bulbectomized rats were used as a model of depression.The depression-like behaviors were assessed by open field test and changes in body weight.Formalin solution was injected into the rat hindpaw to produce ongoing pain.Noxious thermal stimuli were applied onto the hindpaw contralateral to formalin injection,and the withdrawal thresholds were measured.Results In non-depressive rats,the formalin-treated paw developed hypoalgesia to noxious stimuli while the contralateral paw was not affected.The depressive rats,however,showed a significantly lower sensitivity to noxious thermal stimulus,represented as higher withdrawal thresholds of the contralateral paw,when compared to the non-depressive rats.Conclusion These results demonstrate that depression can alleviate the stimulus-evoked pain even in the context of formalin inflammatory pain,consistent with the previous clinical observations that patients suffering from both depression and persistent pain have decreased sensitivities to noxious experimental stimuli.
To review the literature on the use of brain imaging, including functional magnetic resonance imaging （fMRI）, positron emission tomography （PET）, magnetic resonance spectroscopy （MRS） and voxel-based morphometry （VBM） in investigation of the activity in diverse brain regions that creates and modulates chronic neuropathic pain. Data sources English literatures from January 1, 2000 to July 31, 2007 that examined human brain activity in chronic neuropathic pain were accessed through MEDLINE/CD ROM, using PET, fMRI, VBM, MRS and receptor binding. Study selection Published articles about the application of fMRI, PET, VBM, MRS and chronic neuropathic pain were selected. Data extraction Data were mainly extracted from 40 representative articles as the research basis. Results The PET studies suggested that spontaneous neuropathic pain is associated with changes in thalamic activity. Both PET and fMRI have been used to investigate the substrate of allodynia. The VBM demonstrated that brain structural changes are involved in chronic neuropathic pain, which is not seen in a matched control group. However, the results obtained had a large variety, which may be due to different pain etiology, pain distribution, lesion tomography, symptoms and stimulation procedures. Conclusions Application of the techniques of brain imaging plays a very important role in the study of structural and functional reorganization in patients with neuropathic pain. However, a unique “pain matrix” has not been defined. Future studies should be conducted using a prospective longitudinal research design, which would guarantee the control for many confounding factors.
Background Previous brain imaging studies suggested that the brain activity underlying the perception of chronic pain may differ from that underlying acute pain. To investigate the brain regions involved in chronic spontaneous pain due to brachial plexus avulsion （BPA）, fluorine-18^fluorodeoxyglucose （18^F-FDG） positron emission tomography （PET） scanning was applied to determine the glucose metabolic changes in patients with pain due to BPA.Methods Six right-handed patients with chronic spontaneous pain due to left-BPA and twelve right-handed age- and sex-matched healthy control subjects participated in the 18^F-FDG PET study. The patients were rated by visual analog scale （VAS） during scanning and Hamilton depression scale and Hamilton anxiety scale after scanning. Statistical parametric mapping 2 （SPM2） was applied for data analysis. Results Compared with healthy subjects, the patients had significant glucose metabolism decreases in the right thalamus and SI （P 〈0.001, uncorrected）, and significant glucose metabolism increases in the right orbitofrontal cortex （OFC） （BAll）, left rostral insula cortex and left dorsolateral prefrontal cortex （DLPFC） （BA10/46） （P 〈0.001, uncorrected）. Conclusion These findings suggest that the brain areas involved in emotion, attention and internal modulation of pain may be related to the chronic spontaneous pain due to BPA.
