Brain Plasticity of Primary Dysmenorrhea: Functional and Structural Brain Imaging Studies

• Main Authors: Cheng-Hao Tu, 杜政昊
• Other Authors: Jen-Chuen Hsieh
• Format: Others
• Language: en_US
• Published: 2010
• Online Access: http://ndltd.ncl.edu.tw/handle/47805788550920053499

博士 === 國立陽明大學 === 神經科學研究所 === 98 === Primary dysmenorrhea (PDM, menstrual pain without pelvic abnormality) is the most common gynecological disorder in the reproductive age. Typical PDM patients suffer from cramping pain in the lower abdomen that starts with the menstruation and lasts for 24 to 72 hours. Between 40 to 90% of female adolescents have experienced PDM, and 15% have had severe pain. The abnormal uterine activity in PDM is thought to be caused by excessive production of prostaglandins and leukotrienes which mediate hyperalgesia and inflammatory pain and cause vasoconstriction, ischemia and myometrial contraction. Evidence point to the presence of central sensitization in PDM as indicated by hyperalgesia, especially in deep tissue, throughout the menstrual cycle and extends to non-referred pain areas. Moreover, during the menstrual period hyperalgesia also presents in cutaneous tissue and also extends to non-referred pain areas. Thus, an enhanced pain perception in patients with PDM may possibly as a result of both peripheral and central sensitization. However, it remains unknown whether brain plastic alterations are associated with PDM. Prolonged nociceptive input to the central nervous system can induce both functional and structural alterations throughout the central nervous system and is known to result in central sensitization. Hence, the aim of this thesis is to investigate the possible brain alterations in both functional and structural aspects associated with PDM. In the first study, using 18F-labaled fluoro-deoxyglucose positron emission tomography the brain activity was investigated in both PDM patients and healthy controls across different menstrual phases. The results show that ongoing menstrual pain in PDM is accompanied by abnormal brain metabolism in several brain regions involved in various aspects of pain processing. The disinhibition of thalamo-orbitofrontal-prefrontal networks may contribute to the generation of pain and hyperalgesia in PDM possibly by maintaining spinal and thalamic sensitization while increasing negative affect. In the second study, the possible regional gray matter volume changes were examined using optimized voxel-based morphometry method. The results suggest that PDM is underpinned by structural changes in brain regions responsible for a combination of impaired pain inhibition, increased pain facilitation and increased affect. These changes were in part related to the severity of the experienced PDM pain. The third study probed the difference in the cortical thickness between PDM patients and healthy controls and the relationship between regional alterations and the severity of menstrual pain. The results demonstrated that regional cortical thinning exists in the pain-modulation areas in PDM patients, and the brain resilience of structural plasticity for an intermittent menstrual pain of regular and cyclic nature. Taken together, these studies demonstrated that long-term cyclic recurrent PDM accompanied with functional and structural abnormalities in brain. Such abnormalities are unique in PDM. The functional and structural alterations may contribute to the generation of pain and hyperalgesia in PDM with a combination of impaired pain inhibition, increased pain facilitation and increased affect.