Nout Yvette S, Leedy Gail M, Beattie Michael S, Bresnahan Jacqueline C
Department of Neuroscience, Laboratory of CNS Repair and Spinal Trauma and Repair Laboratories, The Ohio State University College of Medicine and Public Health, Columbus, OH, USA.
Prog Brain Res. 2006;152:359-72. doi: 10.1016/S0079-6123(05)52024-7.
Spinal cord injury often results in loss of normal eliminative and sexual functions. This chapter is focused on defecatory function, although aspects of micturition and erectile function will be covered as well due to the overlap in anatomical organization and response to injury. These systems have both autonomic and somatic components, and are organized in the thoracolumbar (sympathetic), lumbosacral (somatic), and sacral (parasympathetic) spinal cord. Loss of supraspinal descending control and plasticity-mediated alterations at the level of the spinal cord, result in loss of voluntary control and in abnormal functioning of these systems including the development of dyssynergies and spasticity. There are several useful models of spinal cord injury in rodents that exhibit many of the autonomic dysfunctions observed after spinal cord injury in humans. Numerous studies involving these animal models have demonstrated development of abnormalities in bladder, external anal sphincter, and erectile function, such as detrusor-sphincter-dyssynergia and external anal sphincter hyperreflexia. Here we review many of these studies and show some of the anatomical alterations that develop within the spinal cord during the development of these hyperreflexias. Furthermore, we show that spasticity develops in other pelvic floor musculature as well, such as the bulbospongiosus muscle, which results in increased duration and magnitude of pressures developed during erectile events and increased duration of micturition. Advances and continued improvement in the use of current animal models of spinal cord injury should encourage and increase the laboratory work devoted to this relatively neglected area of experimental spinal cord injury.
脊髓损伤常导致正常排泄和性功能丧失。本章重点关注排便功能,不过由于解剖结构和损伤反应存在重叠,排尿和勃起功能方面也会涉及。这些系统既有自主神经成分,也有躯体神经成分,在胸腰段(交感神经)、腰骶段(躯体神经)和骶段(副交感神经)脊髓中组织分布。脊髓以上下行控制的丧失以及脊髓水平可塑性介导的改变,导致这些系统的自主控制丧失以及功能异常,包括协同失调和痉挛的发生。啮齿动物中有几种有用的脊髓损伤模型,它们表现出许多人类脊髓损伤后观察到的自主神经功能障碍。涉及这些动物模型的大量研究已证明膀胱、肛门外括约肌和勃起功能出现异常,如逼尿肌-括约肌协同失调和肛门外括约肌反射亢进。在此,我们回顾其中许多研究,并展示这些反射亢进发展过程中脊髓内发生的一些解剖学改变。此外,我们还表明,其他盆底肌肉组织也会出现痉挛,如球海绵体肌,这会导致勃起过程中产生的压力持续时间和幅度增加,以及排尿时间延长。当前脊髓损伤动物模型应用的进展和持续改进应会鼓励并增加致力于这一相对被忽视的实验性脊髓损伤领域的实验室工作。