Atkinson P P, Atkinson J L
Department of Neurology, Mayo Clinic Rochester, MN 55905 USA.
Mayo Clin Proc. 1996 Apr;71(4):384-9. doi: 10.4065/71.4.384.
The term "spinal shock" applies to all phenomena surrounding physiologic or anatomic transection of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity below the level of the injury. Hypotension due to loss of sympathetic tone is a possible complication, depending on the level of the lesion. The mechanism of injury that causes spinal shock is usually traumatic in origin and occurs immediately, but spinal shock has been described with mechanisms of injury that progress over several hours. Spinal cord reflex arcs immediately above the level of injury may also be severely depressed on the basis of the Schiff-Sherrington phenomenon. The end of the spinal shock phase of spinal cord injury is signaled by the return of elicitable abnormal cutaneospinal or muscle spindle reflex arcs. Autonomic reflex arcs involving relay to secondary ganglionic neurons outside the spinal cord may be variably affected during spinal shock, and their return after spinal shock abates is variable. The returning spinal cord reflex arcs below the level of injury are irrevocably altered and are the substrate on which rehabilitation efforts are based.
“脊髓休克”一词适用于围绕脊髓生理或解剖横断所产生的所有现象,这种横断会导致损伤平面以下全部或大部分脊髓反射活动暂时丧失或抑制。取决于损伤平面,因交感神经张力丧失导致的低血压是一种可能的并发症。导致脊髓休克的损伤机制通常源于创伤且立即发生,但脊髓休克也曾在数小时内进展的损伤机制中被描述。基于希夫-谢灵顿现象,损伤平面上方紧邻的脊髓反射弧也可能受到严重抑制。脊髓损伤脊髓休克期的结束以可引出的异常皮脊髓或肌梭反射弧的恢复为信号。涉及中继至脊髓外二级神经节神经元的自主反射弧在脊髓休克期间可能受到不同程度的影响,脊髓休克消退后其恢复情况也各不相同。损伤平面以下恢复的脊髓反射弧发生了不可逆转的改变,是康复努力所基于的基础。