首页 » 文章 » 文章详细信息
Neural Plasticity Volume 2016 ,2016-12-08
The Role of Stress Regulation on Neural Plasticity in Pain Chronification
Review Article
Xiaoyun Li 1 Li Hu 1 , 2
Show affiliations
Received 2016-07-27, accepted for publication 2016-11-14, Published 2016-11-14

Pain, especially chronic pain, is one of the most common clinical symptoms and has been considered as a worldwide healthcare problem. The transition from acute to chronic pain is accompanied by a chain of alterations in physiology, pathology, and psychology. Increasing clinical studies and complementary animal models have elucidated effects of stress regulation on the pain chronification via investigating activations of the hypothalamic-pituitary-adrenal (HPA) axis and changes in some crucial brain regions, including the amygdala, prefrontal cortex, and hippocampus. Although individuals suffer from acute pain benefit from such physiological alterations, chronic pain is commonly associated with maladaptive responses, like the HPA dysfunction and abnormal brain plasticity. However, the causal relationship among pain chronification, stress regulation, and brain alterations is rarely discussed. To call for more attention on this issue, we review recent findings obtained from clinical populations and animal models, propose an integrated stress model of pain chronification based on the existing models in perspectives of environmental influences and genetic predispositions, and discuss the significance of investigating the role of stress regulation on brain alteration in pain chronification for various clinical applications.


Copyright © 2016 Xiaoyun Li and Li Hu. 2016
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Li Hu.Key Laboratory of Cognition and Personality, Ministry of Education and Faculty of Psychology, Southwest University, Chongqing, China, swu.edu.cn;CAS Key Laboratory of Mental Health, Institute of Psychology, Beijing, China, cas.cn.huli@psych.ac.cn


Xiaoyun Li,Li Hu. The Role of Stress Regulation on Neural Plasticity in Pain Chronification. Neural Plasticity ,Vol.2016(2016)



[1] K. E. Dixon, B. E. Thorn, L. C. Ward. (2004). An evaluation of sex differences in psychological and physiological responses to experimentally-induced pain: a path analytic description. Pain.112(1-2):188-196. DOI: 10.1056/NEJMra1201534.
[2] N. I. Yarushkina, T. R. Bagaeva, L. P. Filaretova. (2011). Central corticotropin-releasing factor (CRF) may attenuate somatic pain sensitivity through involvement of glucocorticoids. Journal of Physiology & Pharmacology.62(5):541-548. DOI: 10.1056/NEJMra1201534.
[3] L. Gonçalves, R. Silva, F. Pinto-Ribeiro, J. M. Pêgo. et al.(2008). Neuropathic pain is associated with depressive behaviour and induces neuroplasticity in the amygdala of the rat. Experimental Neurology.213(1):48-56. DOI: 10.1056/NEJMra1201534.
[4] R. Peyron, B. Laurent, L. García-Larrea. (2000). Functional imaging of brain responses to pain. A review and meta-analysis (2000). Clinical Neurophysiology.30(5):263-288. DOI: 10.1056/NEJMra1201534.
[5] S. W. G. Derbyshire, A. K. P. Jones, F. Gyulai, S. Clark. et al.(1997). Pain processing during three levels of noxious stimulation produces differential patterns of central activity. Pain.73(3):431-445. DOI: 10.1056/NEJMra1201534.
[6] N. Maleki, L. Becerra, J. Brawn, B. McEwen. et al.(2013). Common hippocampal structural and functional changes in migraine. Brain Structure & Function.218(4):903-912. DOI: 10.1056/NEJMra1201534.
[7] A. E. Metz, H.-J. Yau, M. V. Centeno, A. V. Apkarian. et al.(2009). Morphological and functional reorganization of rat medial prefrontal cortex in neuropathic pain. Proceedings of the National Academy of Sciences of the United States of America.106(7):2423-2428. DOI: 10.1056/NEJMra1201534.
[8] T. Kiritoshi, V. Neugebauer. (2015). Group II mGluRs modulate baseline and arthritis pain-related synaptic transmission in the rat medial prefrontal cortex. Neuropharmacology.95:388-394. DOI: 10.1056/NEJMra1201534.
[9] E. Vachon-Presseau, M.-O. Martel, M. Roy, E. Caron. et al.(2013). Acute stress contributes to individual differences in pain and pain-related brain activity in healthy and chronic pain patients. The Journal of Neuroscience.33(16):6826-6833. DOI: 10.1056/NEJMra1201534.
[10] C. Zimmer, H.-D. Basler, H. Vedder, S. Lautenbacher. et al.(2003). Sex differences in cortisol response to noxious stress. Clinical Journal of Pain.19(4):233-239. DOI: 10.1056/NEJMra1201534.
[11] M. Terada, N. Kuzumaki, N. Hareyama, S. Imai. et al.(2008). Suppression of enriched environment-induced neurogenesis in a rodent model of neuropathic pain. Neuroscience Letters.440(3):314-318. DOI: 10.1056/NEJMra1201534.
[12] P. Schweinhardt, D. A. Seminowicz, E. Jaeger, G. H. Duncan. et al.(2009). The anatomy of the mesolimbic reward System: a link between personality and the placebo analgesic response. Journal of Neuroscience.29(15):4882-4887. DOI: 10.1056/NEJMra1201534.
[13] B. S. McEwen. (1998). Stress, adaptation, and disease: allostasis and allostatic load. Annals of the New York Academy of Sciences.840:33-44. DOI: 10.1056/NEJMra1201534.
[14] D. A. Matre, L. Hernandez-Garcia, T. D. Tran, K. L. Casey. et al.(2010). ‘First pain’ in humans: convergent and specific forebrain responses. Molecular Pain.6(1, article 81). DOI: 10.1056/NEJMra1201534.
[15] A. R. Segerdahl, M. Mezue, T. W. Okell, J. T. Farrar. et al.(2015). The dorsal posterior insula subserves a fundamental role in human pain. Nature Neuroscience.18(4):499-500. DOI: 10.1056/NEJMra1201534.
[16] C. H. Wilder-Smith, D. Schindler, K. Lovblad, S. M. Redmond. et al.(2004). Brain functional magnetic resonance imaging of rectal pain and activation of endogenous inhibitory mechanisms in irritable bowel syndrome patient subgroups and healthy controls. Gut.53(11):1595-1601. DOI: 10.1056/NEJMra1201534.
[17] T. D. Tran, H. Wang, A. Tandon, L. Hernandez-Garcia. et al.(2010). Temporal summation of heat pain in humans: evidence supporting thalamocortical modulation. Pain.150(1):93-102. DOI: 10.1056/NEJMra1201534.
[18] M. Al'Absi, K. L. Petersen, L. E. Wittmers. (2002). Adrenocortical and hemodynamic predictors of pain perception in men and women. Pain.96(1-2):197-204. DOI: 10.1056/NEJMra1201534.
[19] W. B. Hoover, R. P. Vertes. (2007). Anatomical analysis of afferent projections to the medial prefrontal cortex in the rat. Brain Structure & Function.212(2):149-179. DOI: 10.1056/NEJMra1201534.
[20] B. Roozendaal, B. S. McEwen, S. Chattarji. (2009). Stress, memory and the amygdala. Nature Reviews Neuroscience.10(6):423-433. DOI: 10.1056/NEJMra1201534.
[21] K. F. S. Petrelluzzi, M. C. Garcia, C. A. Petta, D. M. Grassi-Kassisse. et al.(2008). Salivary cortisol concentrations, stress and quality of life in women with endometriosis and chronic pelvic pain. Stress.11(5):390-397. DOI: 10.1056/NEJMra1201534.
[22] L. E. Simons, E. A. Moulton, C. Linnman, E. Carpino. et al.(2014). The human amygdala and pain: evidence from neuroimaging. Human Brain Mapping.35(2):527-538. DOI: 10.1056/NEJMra1201534.
[23] C. Berna, S. Leknes, E. A. Holmes, R. R. Edwards. et al.(2010). Induction of depressed mood disrupts emotion regulation neurocircuitry and enhances pain unpleasantness. Biological Psychiatry.67(11):1083-1090. DOI: 10.1056/NEJMra1201534.
[24] U. Bingel, M. Quante, R. Knab, B. Bromm. et al.(2002). Subcortical structures involved in pain processing: evidence from single-trial fMRI. Pain.99(1-2):313-321. DOI: 10.1056/NEJMra1201534.
[25] K. Bornhövd, M. Quante, V. Glauche, B. Bromm. et al.(2002). Painful stimuli evoke different stimulus-response functions in the amygdala, prefrontal, insula and somatosensory cortex: a single-trial fMRI study. Brain.125(6):1326-1336. DOI: 10.1056/NEJMra1201534.
[26] C. Muhtz, R. Rodriguez-Raecke, K. Hinkelmann, T. Moeller-Bertram. et al.(2013). Cortisol Response to Experimental Pain in Patients with Chronic Low Back Pain and Patients with Major Depression. Pain Medicine (United States).14(4):498-503. DOI: 10.1056/NEJMra1201534.
[27] S. L. Nijhof, J. M. T. M. Rutten, C. S. P. M. Uiterwaal, G. Bleijenberg. et al.(2014). The role of hypocortisolism in chronic fatigue syndrome. Psychoneuroendocrinology.42:199-206. DOI: 10.1056/NEJMra1201534.
[28] M. N. Baliki, D. R. Chialvo, P. Y. Geha, R. M. Levy. et al.(2006). Chronic pain and the emotional brain: specific brain activity associated with spontaneous fluctuations of intensity of chronic back pain. The Journal of Neuroscience.26(47):12165-12173. DOI: 10.1056/NEJMra1201534.
[29] P. Schweinhardt, C. Glynn, J. Brooks, H. McQuay. et al.(2006). An fMRI study of cerebral processing of brush-evoked allodynia in neuropathic pain patients. NeuroImage.32(1):256-265. DOI: 10.1056/NEJMra1201534.
[30] L. Karlsson, B. Gerdle, B. Ghafouri, E. Bäckryd. et al.(2015). Intramuscular pain modulatory substances before and after exercise in women with chronic neck pain. European Journal of Pain.19(8):1075-1085. DOI: 10.1056/NEJMra1201534.
[31] J. Gaab, S. Baumann, A. Budnoik, H. Gmünder. et al.(2005). Reduced reactivity and enhanced negative feedback sensitivity of the hypothalamus–pituitary–adrenal axis in chronic whiplash-associated disorder. Pain.119(1–3):219-224. DOI: 10.1056/NEJMra1201534.
[32] A. A. Mutso, B. Petre, L. Huang, M. N. Baliki. et al.(2014). Reorganization of hippocampal functional connectivity with transition to chronic back pain. Journal of Neurophysiology.111(5):1065-1076. DOI: 10.1056/NEJMra1201534.
[33] M. Ziv, R. Tomer, R. Defrin, T. Hendler. et al.(2010). Individual sensitivity to pain expectancy is related to differential activation of the hippocampus and amygdala. Human Brain Mapping.31(2):326-338. DOI: 10.1056/NEJMra1201534.
[34] I. A. Strigo, A. N. Simmons, S. C. Matthews, A. D. Craig. et al.(2008). Increased affective bias revealed using experimental graded heat stimuli in young depressed adults: evidence of “emotional allodynia”. Psychosomatic Medicine.70(3):338-344. DOI: 10.1056/NEJMra1201534.
[35] A. Ploghaus, I. Tracey, J. S. Gati, S. Clare. et al.(1999). Dissociating pain from its anticipation in the human brain. Science.284(5422):1979-1981. DOI: 10.1056/NEJMra1201534.
[36] R. Riva, P. J. Mork, R. H. Westgaard, U. Lundberg. et al.(2012). Comparison of the cortisol awakening response in women with shoulder and neck pain and women with fibromyalgia. Psychoneuroendocrinology.37(2):299-306. DOI: 10.1056/NEJMra1201534.
[37] R. Ikeda, Y. Takahashi, K. Inoue, F. Kato. et al.(2007). NMDA receptor-independent synaptic plasticity in the central amygdala in the rat model of neuropathic pain. Pain.127(1-2):161-172. DOI: 10.1056/NEJMra1201534.
[38] D. Niddam, S. Lee, Y. Su, R. Chan. et al.(2016). Brain structural changes in patients with chronic myofascial pain. European Journal of Pain. DOI: 10.1056/NEJMra1201534.
[39] L. J. Crofford. (1998). The hypothalamic-pituitary-adrenal stress axis in fibromyalgia and chronic fatigue syndrome. Zeitschrift fur Rheumatologie.57, S2:S67-S71. DOI: 10.1056/NEJMra1201534.
[40] M. Tajerian, D. Leu, Y. Zou, P. Sahbaie. et al.(2014). Brain neuroplastic changes accompany anxiety and memory deficits in a model of complex regional pain syndrome. Anesthesiology.121(4):852-865. DOI: 10.1056/NEJMra1201534.
[41] D. Catley, A. T. Kaell, C. Kirschbaum, A. A. Stone. et al.(2000). A naturalistic evaluation of cortisol secretion in persons with fibromyalgia and rheumatoid arthritis. Arthritis Care & Research.13(1):51-61. DOI: 10.1056/NEJMra1201534.
[42] A. R. Mansour, M. N. Baliki, L. Huang, S. Torbey. et al.(2013). Brain white matter structural properties predict transition to chronic pain. Pain.154(10):2160-2168. DOI: 10.1056/NEJMra1201534.
[43] P. Y. Geha, M. N. Baliki, R. N. Harden, W. R. Bauer. et al.(2008). The brain in chronic CRPS pain: abnormal gray-white matter interactions in emotional and autonomic regions. Neuron.60(4):570-581. DOI: 10.1056/NEJMra1201534.
[44] S. Benson, L. Rebernik, A. Wegner, J. Kleine-Borgmann. et al.(2015). Neural circuitry mediating inflammation-induced central pain amplification in human experimental endotoxemia. Brain, Behavior, & Immunity.48(1):222-231. DOI: 10.1056/NEJMra1201534.
[45] U. Blankstein, J. Chen, N. E. Diamant, K. D. Davis. et al.(2010). Altered brain structure in irritable bowel syndrome: potential contributions of pre-existing and disease-driven factors. Gastroenterology.138(5):1783-1789. DOI: 10.1056/NEJMra1201534.
[46] W. Valfrè, I. Rainero, M. Bergui, L. Pinessi. et al.(2008). Voxel-based morphometry reveals gray matter abnormalities in migraine. Headache.48(1):109-117. DOI: 10.1056/NEJMra1201534.
[47] E. Vachon-Presseau, M. Roy, M.-O. Martel, E. Caron. et al.(2013). The stress model of chronic pain: evidence from basal cortisol and hippocampal structure and function in humans. Brain.136(3):815-827. DOI: 10.1056/NEJMra1201534.
[48] J. C. Choi, J. Kim, E. Kang, J.-H. Choi. et al.(2016). Step-down vs. step-up noxious stimulation: differential effects on pain perception and patterns of brain activation. Acta Anaesthesiologica Scandinavica.60(1):117-127. DOI: 10.1056/NEJMra1201534.
[49] M. N. Baliki, B. Petre, S. Torbey, K. M. Herrmann. et al.(2012). Corticostriatal functional connectivity predicts transition to chronic back pain. Nature Neuroscience.15(8):1117-1119. DOI: 10.1056/NEJMra1201534.
[50] J. A. Hashmi, M. N. Baliki, L. Huang, A. T. Baria. et al.(2013). Shape shifting pain: chronification of back pain shifts brain representation from nociceptive to emotional circuits. Brain.136(9):2751-2768. DOI: 10.1056/NEJMra1201534.
[51] T. Schmidt-Wilcke, E. Leinisch, A. Straube, N. Kämpfe. et al.(2005). Gray matter decrease in patients with chronic tension type headache. Neurology.65(9):1483-1486. DOI: 10.1056/NEJMra1201534.
[52] C. J. L. Murray, A. D. Lopez. (2013). Measuring the global burden of disease. New England Journal of Medicine.369(5):448-457. DOI: 10.1056/NEJMra1201534.
[53] B. S. McEwen. (2007). Physiology and neurobiology of stress and adaptation: central role of the brain. Physiological Reviews.87(3):873-904. DOI: 10.1056/NEJMra1201534.
[54] J. F. Bernard, G. F. Huang, J. M. Besson. (1992). Nucleus centralis of the amygdala and the globus pallidus ventralis: electrophysiological evidence for an involvement in pain processes. Journal of Neurophysiology.68(2):551-569. DOI: 10.1056/NEJMra1201534.
[55] L. J. Crofford, S. R. Pillemer, K. T. Kalogeras, J. M. Cash. et al.(1994). Hypothalamic-pituitary-adrenal axis perturbations in patients with fibromyalgia. Arthritis & Rheumatism.37(11):1583-1592. DOI: 10.1056/NEJMra1201534.
[56] W. Li, V. Neugebauer. (2004). Differential roles of mGluR1 and mGluR5 in brief and prolonged nociceptive processing in central amygdala neurons,. Journal of Neurophysiology.91(1):13-24. DOI: 10.1056/NEJMra1201534.
[57] A. A. Mutso, D. Radzicki, M. N. Baliki, L. Huang. et al.(2012). Abnormalities in hippocampal functioning with persistent pain. The Journal of Neuroscience.32(17):5747-5756. DOI: 10.1056/NEJMra1201534.
[58] K. Wingenfeld, D. Wagner, I. Schmidt, G. Meinlschmidt. et al.(2007). The low-dose dexamethasone suppression test in fibromyalgia. Journal of Psychosomatic Research.62(1):85-91. DOI: 10.1056/NEJMra1201534.
[59] A. V. Apkarian, P. S. Thomas, B. R. Krauss, N. M. Szeverenyi. et al.(2001). Prefrontal cortical hyperactivity in patients with sympathetically mediated chronic pain. Neuroscience Letters.311(3):193-197. DOI: 10.1056/NEJMra1201534.
[60] G. A. McCain, K. S. Tilbe. (1989). Diurnal hormone variation in fibromyalgia syndrome: a comparison with rheumatoid arthritis. The Journal of Rheumatology.16(19):154-157. DOI: 10.1056/NEJMra1201534.
[61] R. Zhang, M. Tomida, Y. Katayama, Y. Kawakami. et al.(2004). Response durations encode nociceptive stimulus intensity in the rat medial prefrontal cortex. Neuroscience.125(3):777-785. DOI: 10.1056/NEJMra1201534.
[62] J. S. Labus, C. S. Hubbard, J. Bueller, B. Ebrat. et al.(2013). Impaired emotional learning and involvement of the corticotropin-releasing factor signaling system in patients with irritable bowel syndrome. Gastroenterology.145(6):1253-1261.e3. DOI: 10.1056/NEJMra1201534.
[63] G. Neeck, W. Riedel. (1999). Hormonal pertubations in fibromyalgia syndrome. Annals of the New York Academy of Sciences.876:325-339. DOI: 10.1056/NEJMra1201534.
[64] V. Neugebauer, W. Li. (2003). Differential sensitization of amygdala neurons to afferent inputs in a model of arthritic pain. Journal of Neurophysiology.89(2):716-727. DOI: 10.1056/NEJMra1201534.
[65] G. Blackburn-Munro, R. E. Blackburn-Munro. (2001). Chronic pain, chronic stress and depression: coincidence or consequence?. Journal of Neuroendocrinology.13(12):1009-1023. DOI: 10.1056/NEJMra1201534.
[66] B. S. McEwen, M. Kalia. (2010). The role of corticosteroids and stress in chronic pain conditions. Metabolism: Clinical and Experimental.59(1):-S15. DOI: 10.1056/NEJMra1201534.
[67] R. Melzack. (1999). Pain and stress: a new perspective. Psychological Factors in Pain:89-106. DOI: 10.1056/NEJMra1201534.
[68] J. P. Herman, M. M. Ostrander, N. K. Mueller, H. Figueiredo. et al.(2005). Limbic system mechanisms of stress regulation: hypothalamo-pituitary- adrenocortical axis. Progress in Neuro-Psychopharmacology and Biological Psychiatry.29(8):1201-1213. DOI: 10.1056/NEJMra1201534.
[69] D. Borsook, N. Maleki, L. Becerra, B. McEwen. et al.(2012). Understanding migraine through the lens of maladaptive stress responses: a model disease of allostatic load. Neuron.73(2):219-234. DOI: 10.1056/NEJMra1201534.
[70] E. R. de Kloet, M. Joëls, F. Holsboer. (2005). Stress and the brain: from adaptation to disease. Nature Reviews Neuroscience.6(6):463-475. DOI: 10.1056/NEJMra1201534.
[71] S. Khanna. (1997). Dorsal hippocampus field CA1 pyramidal cell responses to a persistent versus an acute nociceptive stimulus and their septal modulation. Neuroscience.77(3):713-721. DOI: 10.1056/NEJMra1201534.
[72] Z. Wang, S. Bradesi, J.-M. I. Maarek, K. Lee. et al.(2008). Regional brain activation in conscious, nonrestrained rats in response to noxious visceral stimulation. Pain.138(1):233-243. DOI: 10.1056/NEJMra1201534.
[73] V. Sveinsdottir, H. R. Eriksen, H. Ursin, Å. M. Hansen. et al.(2016). Cortisol, health, and coping in patients with nonspecific low back pain. Applied Psychophysiology Biofeedback.41(1):9-16. DOI: 10.1056/NEJMra1201534.
[74] R. F. Smallwood, A. R. Laird, A. E. Ramage, A. L. Parkinson. et al.(2013). Structural brain anomalies and chronic pain: a quantitative meta-analysis of gray matter volume. Journal of Pain.14(7):663-675. DOI: 10.1056/NEJMra1201534.
[75] A. May. (2008). Chronic pain may change the structure of the brain. Pain.137(1):7-15. DOI: 10.1056/NEJMra1201534.
[76] S. Khanna, J. G. Sinclair. (1989). Noxious stimuli produce prolonged changes in the CA1 region of the rat hippocampus. Pain.39(3):337-343. DOI: 10.1056/NEJMra1201534.
[77] B. S. McEwen. (2001). Plasticity of the hippocampus: adaptation to chronic stress and allostatic load. Annals of the New York Academy of Sciences.933:265-277. DOI: 10.1056/NEJMra1201534.
[78] M. Burgmer, M. Gaubitz, C. Konrad, M. Wrenger. et al.(2009). Decreased gray matter volumes in the cingulo-frontal cortex and the amygdala in patients with fibromyalgia. Psychosomatic Medicine.71(5):566-573. DOI: 10.1056/NEJMra1201534.
[79] S. Sudhaus, B. Fricke, S. Schneider, A. Stachon. et al.(2007). The cortisol awakening response in patients with acute and chronic low back pain: relations with psychological risk factors of pain chronicity. Schmerz.21(3):202-211. DOI: 10.1056/NEJMra1201534.
[80] K. Wingenfeld, C. Heim, I. Schmidt, D. Wagner. et al.(2008). HPA axis reactivity and lymphocyte glucocorticoid sensitivity in fibromyalgia syndrome and chronic pelvic pain. Psychosomatic Medicine.70(1):65-72. DOI: 10.1056/NEJMra1201534.
[81] G. Ji, V. Neugebauer. (2014). CB1 augments mGluR5 function in medial prefrontal cortical neurons to inhibit amygdala hyperactivity in an arthritis pain model. European Journal of Neuroscience.39(3):455-466. DOI: 10.1056/NEJMra1201534.
[82] G. Ji, H. Sun, Y. Fu, Z. Li. et al.(2010). Cognitive impairment in pain through amygdala-driven prefrontal cortical deactivation. The Journal of Neuroscience.30(15):5451-5464. DOI: 10.1056/NEJMra1201534.
[83] M. Joëls, H. Karst, R. DeRijk, E. R. de Kloet. et al.(2008). The coming out of the brain mineralocorticoid receptor. Trends in Neurosciences.31(1):1-7. DOI: 10.1056/NEJMra1201534.
[84] J. A. Macedo, J. Hesse, J. D. Turner, J. Meyer. et al.(2008). Glucocorticoid sensitivity in fibromyalgia patients: decreased expression of corticosteroid receptors and glucocorticoid-induced leucine zipper. Psychoneuroendocrinology.33(6):799-809. DOI: 10.1056/NEJMra1201534.
[85] I. N. Karatsoreos, B. S. McEwen. (2011). Psychobiological allostasis: resistance, resilience and vulnerability. Trends in Cognitive Sciences.15(12):576-584. DOI: 10.1056/NEJMra1201534.
[86] H. Cardoso-Cruz, D. Lima, V. Galhardo. (2013). Impaired spatial memory performance in a rat model of neuropathic pain is associated with reduced hippocampus-prefrontal cortex connectivity. The Journal of Neuroscience.33(6):2465-2480. DOI: 10.1056/NEJMra1201534.
[87] D. M. Lyons, C. Yang, A. M. Sawyer-Glover, M. E. Moseley. et al.(2001). Early life stress and inherited variation in monkey hippocampal volumes. Archives of General Psychiatry.58(12):1145-1151. DOI: 10.1056/NEJMra1201534.
[88] Y. M. Ulrich-Lai, W. Xie, J. T. A. Meij, C. M. Dolgas. et al.(2006). Limbic and HPA axis function in an animal model of chronic neuropathic pain. Physiology & Behavior.88(1-2):67-76. DOI: 10.1056/NEJMra1201534.
[89] S. J. Linton. (2000). A review of psychological risk factors in back and neck pain. Spine.25(9):1148-1156. DOI: 10.1056/NEJMra1201534.
[90] T. Hayashi, M. Miyata, T. Nagata, Y. Izawa. et al.(2009). Intracerebroventricular fluvoxamine administration inhibited pain behavior but increased Fos expression in affective pain pathways. Pharmacology Biochemistry & Behavior.91(3):441-446. DOI: 10.1056/NEJMra1201534.
[91] R. M. Sapolsky, H. Uno, C. S. Rebert, C. E. Finch. et al.(1990). Hippocampal damage associated with prolonged glucocorticoid exposure in primates. Journal of Neuroscience.10(9):2897-2902. DOI: 10.1056/NEJMra1201534.
[92] M. Lehner, E. Taracha, A. Skórzewska, P. Maciejak. et al.(2006). Behavioral, immunocytochemical and biochemical studies in rats differing in their sensitivity to pain. Behavioural Brain Research.171(2):189-198. DOI: 10.1056/NEJMra1201534.
[93] J. S. Labus, I. D. Dinov, Z. Jiang, C. Ashe-Mcnalley. et al.(2014). Irritable bowel syndrome in female patients is associated with alterations in structural brain networks. Pain.155(1):137-149. DOI: 10.1056/NEJMra1201534.
[94] M. C. Bushnell, M. Čeko, L. A. Low. (2013). Cognitive and emotional control of pain and its disruption in chronic pain. Nature Reviews Neuroscience.14(7):502-511. DOI: 10.1056/NEJMra1201534.
[95] T. Nakagawa, A. Katsuya, S. Tanimoto, J. Yamamoto. et al.(2003). Differential patterns of c-fos mRNA expression in the amygdaloid nuclei induced by chemical somatic and visceral noxious stimuli in rats. Neuroscience Letters.344(3):197-200. DOI: 10.1056/NEJMra1201534.
[96] C. P. Mao, H. J. Yang. (2015). Smaller amygdala volumes in patients with chronic low back pain compared with healthy control individuals. Journal of Pain.16(12):1366-1376. DOI: 10.1056/NEJMra1201534.
[97] S. Khanna, L. S. Chang, F. Jiang, H. C. Koh. et al.(2004). Nociception-driven decreased induction of Fos protein in ventral hippocampus field CA1 of the rat. Brain Research.1004(1-2):167-176. DOI: 10.1056/NEJMra1201534.
[98] S. J. Lupien, B. S. McEwen, M. R. Gunnar, C. Heim. et al.(2009). Effects of stress throughout the lifespan on the brain, behaviour and cognition. Nature Reviews Neuroscience.10(6):434-445. DOI: 10.1056/NEJMra1201534.
[99] M. J. Millan. (1999). The induction of pain: an integrative review. Progress in Neurobiology.57(1):1-164. DOI: 10.1056/NEJMra1201534.
[100] R. Rodriguez-Raecke, A. Niemeier, K. Ihle, W. Ruether. et al.(2009). Brain gray matter decrease in chronic pain is the consequence and not the cause of pain. The Journal of Neuroscience.29(44):13746-13750. DOI: 10.1056/NEJMra1201534.
[101] A. V. Apkarian, M. C. Bushnell, R.-D. Treede, J.-K. Zubieta. et al.(2005). Human brain mechanisms of pain perception and regulation in health and disease. European Journal of Pain.9(4):463-484. DOI: 10.1056/NEJMra1201534.
[102] R. M. Sapolsky, L. C. Krey, B. S. Mcewen. (1986). The neuroendocrinology of stress and aging: the glucocorticoid cascade hypothesis. Endocrine Reviews.7(3):284-301. DOI: 10.1056/NEJMra1201534.
[103] H. Merskey, N. Bogduk. (1994). Classification of Chronic Pain: Descriptions of Chronic Pain Syndromes and Definitions of Pain Terms. DOI: 10.1056/NEJMra1201534.
[104] K. B. Jo, Y. J. Lee, I. G. Lee, S. C. Lee. et al.(2016). Association of pain intensity, pain-related disability, and depression with hypothalamus–pituitary–adrenal axis function in female patients with chronic temporomandibular disorders. Psychoneuroendocrinology.69:106-115. DOI: 10.1056/NEJMra1201534.
[105] E. Vachon-Presseau, P. Tétreault, B. Petre, L. Huang. et al.(2016). Corticolimbic anatomical characteristics predetermine risk for chronic pain. Brain.139(7):1958-1970. DOI: 10.1056/NEJMra1201534.
[106] D. P. Hibar, J. L. Stein, M. E. Renteria. (2015). Common genetic variants influence human subcortical brain structures. Nature.520(7546):224-229. DOI: 10.1056/NEJMra1201534.
[107] M. W. Gilbertson, M. E. Shenton, A. Ciszewski, K. Kasai. et al.(2002). Smaller hippocampal volume predicts pathologic vulnerability to psychological trauma. Nature Neuroscience.5(11):1242-1247. DOI: 10.1056/NEJMra1201534.
[108] L. E. Simons, I. Elman, D. Borsook. (2014). Psychological processing in chronic pain: a neural systems approach. Neuroscience and Biobehavioral Reviews.39:61-78. DOI: 10.1056/NEJMra1201534.
[109] S. J. Lupien, F. Maheu, M. Tu, A. Fiocco. et al.(2007). The effects of stress and stress hormones on human cognition: implications for the field of brain and cognition. Brain and Cognition.65(3):209-237. DOI: 10.1056/NEJMra1201534.
[110] M. N. Baliki, A. V. Apkarian. (2015). Nociception, pain, negative moods, and behavior selection. Neuron.87(3):474-491. DOI: 10.1056/NEJMra1201534.
[111] A. V. Apkarian, Y. Sosa, S. Sonty, R. M. Levy. et al.(2004). Chronic back pain is associated with decreased prefrontal and thalamic gray matter density. The Journal of Neuroscience.24(46):10410-10415. DOI: 10.1056/NEJMra1201534.
浏览 31次
下载全文 5次
评分次数 0次
用户评分 0.0分
分享 0次