Scioli-Salter Erica R, Forman Daniel E, Otis John D, Gregor Kristin, Valovski Ivan, Rasmusson Ann M
*Research Division ∥Department of Anesthesiology, VA Boston Healthcare System, Jamaica Plain Departments of †Psychiatry §Psychiatry and Psychology, Boston University School of Medicine ‡New England Geriatric Research, Education, and Clinical Center, Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School ¶Department of Psychiatry, National Center for PTSD, Women's Health Science Division, VA Boston Healthcare System, Boston University School of Medicine, Boston, MA.
Clin J Pain. 2015 Apr;31(4):363-74. doi: 10.1097/AJP.0000000000000115.
Chronic pain and posttraumatic stress disorder (PTSD) are disabling conditions that affect biological, psychological, and social domains of functioning. Clinical research demonstrates that patients who are affected by chronic pain and PTSD in combination experience greater pain, affective distress, and disability than patients with either condition alone. Additional research is needed to delineate the interrelated pathophysiology of chronic pain and PTSD, with the goal of facilitating more effective therapies to treat both conditions more effectively; current treatment strategies for chronic pain associated with PTSD have limited efficacy and place a heavy burden on patients, who must visit various specialists to manage these conditions separately. This article focuses on neurobiological factors that may contribute to the coprevalence and synergistic interactions of chronic pain and PTSD. First, we outline how circuits that mediate emotional distress and physiological threat, including pain, converge. Secondly, we discuss specific neurobiological mediators and modulators of these circuits that may contribute to chronic pain and PTSD symptoms. For example, neuropeptide Y, and the neuroactive steroids allopregnanolone and pregnanolone (together termed ALLO) have antistress and antinociceptive properties. Reduced levels of neuropeptide Y and ALLO have been implicated in the pathophysiology of both chronic pain and PTSD. The potential contribution of opioid and cannabinoid system factors also will be discussed. Finally, we address potential novel methods to restore the normal function of these systems. Such novel perspectives regarding disease and disease management are vital to the pursuit of relief for the many individuals who struggle with these disabling conditions.
慢性疼痛和创伤后应激障碍（PTSD）是致残性病症，会影响生理、心理和社会功能领域。临床研究表明，同时患有慢性疼痛和创伤后应激障碍的患者比仅患其中一种病症的患者经历更强烈的疼痛、情感痛苦和功能障碍。需要进一步研究来阐明慢性疼痛和创伤后应激障碍相互关联的病理生理学，以便促进更有效的疗法来更有效地治疗这两种病症；目前针对与创伤后应激障碍相关的慢性疼痛的治疗策略疗效有限，给患者带来沉重负担，患者必须分别拜访不同专科医生来管理这些病症。本文重点关注可能导致慢性疼痛和创伤后应激障碍共病及协同相互作用的神经生物学因素。首先，我们概述介导情绪困扰和生理威胁（包括疼痛）的神经回路是如何汇聚的。其次，我们讨论这些神经回路中可能导致慢性疼痛和创伤后应激障碍症状的特定神经生物学介质和调节因子。例如，神经肽Y以及神经活性甾体化合物别孕烯醇酮和孕烯醇酮（统称为ALLO）具有抗应激和抗伤害感受特性。神经肽Y和ALLO水平降低与慢性疼痛和创伤后应激障碍的病理生理学有关。还将讨论阿片类和大麻素系统因素的潜在作用。最后，我们探讨恢复这些系统正常功能的潜在新方法。这种关于疾病和疾病管理的新观点对于为许多与这些致残性病症作斗争的个体寻求缓解至关重要。
