Failure of somatosensory-evoked-potential monitoring in sensorimotor neuropathy.
Failure of somatosensory-evoked-potential monitoring in sensorimotor neuropathy.
复制标题
感觉运动神经病体感诱发电位监测失败。
DOI：
10.1097/00007632-199104000-00018
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发表时间：
1991
期刊：
影响因子：
3
通讯作者：
D. Young
中科院分区：
文献类型：
--
作者：
M. Krishna;John F. A. Taylor;M. C. Brown;J. Farrell;T. Morley;M. Edgar;D. Young
M.Krishna，MS(Orth)“J，F，Taylor，MD，MCH(Orth)，FRCS，”M，C，Brown，MC，Phd，BSc，*J，Farrell，f T，R，Morley，Ez A，Edgar，FRCS，and D.Young|1972年首次描述*今天，它被认为是正确检测大肠菌病手术中神经功能障碍的关键。它的基础是背柱传递一种冲动，该冲动起源于刺激窝内的神经。记录电极放置在仪器区上方的硬膜外间隙中。然后对信号进行平均，并记录幅度和潜伏期。将SSEPM失败的患者作为监测系统进行研究具有重要意义。在这篇报告中，我们描述了5例Charcot-Marie-Tooth病(遗传性感觉运动神经病[HSMN]I型)患者，他们的术中监测失败困扰着外科医生，我们讨论了这些患者的临床特征和可用于评估脊髓功能的替代方案。CASɛ报道病例1。1987年7月，一名12岁女孩出现特发性胸腰椎侧弯61例。检查外科医生没有发现神经缺陷。在前路生长停止后，行Harrington棒内固定和脊柱融合。在这例患者中，SSEPM显示无信号。当时无法确定失败的原因，很快就被遗忘了，因为她没有术后神经功能障碍。1989年2月，她回来了，抱怨膝盖弯曲。杆子的上钩移位了，畸形又一次达到了60。她被发现患有下丘疹和反射障碍。神经传导研究证实了夏科-玛丽-图斯病(HSMNI型)的诊断。哈灵顿被更换了，但SSEPM再次没有显示任何信号。她没有后来的神经缺陷。这促使我们研究了150例脊柱侧弯患者在矫形手术中进行SSEPM检查的记录。又有四名患者被发现患有夏科-玛丽-图斯病。所有患者术中均未行脊髓监测。其中两人是在手术后才被确诊的。其中一例术后出现一过性神经功能障碍。年龄从11岁到16岁不等。
M. KRISHNA, MS (Orth)" J, F, TAYLOR, MD, MCh (Orth), FRCS," M, C, BROWN, MC, PhD, BSc,* J, FARRELL, f T, R, MORLEY, eZ A, EDGAR, FRCS, and D. YOUNG| first described in 1972* Today, it is accepted as essential in the proper detection of intraoperative neurologic deficit during scoli-osis instrumentation. It is based on the dorsal column transmission ofan impulse originating from the stimulation ofnerves in the popliteal fossa. The recording electrode is placed in the epidural space above the instrumented area. The signals are then averaged and the amplitude and latency recorded. It is important to study the patients in whom SSEPM failed as a monitoring system. In this report we describe five patients with Charcot-Marie-Tooth disease (hereditary sensorimotorneuropathy [HSMN] Type I) in whom intraoperative monitoring failure puzzled the surgeons, and we discuss the clinical features and alternatives available to evaluate cord function in these patients. casɛ REPors ano ueroosCase 1. In July 1987 a 12-year-old girl presented with “idiopathic” thoracolumbar scoliosis of 61. The examining surgeon detected no neurologic deficit. After anterior growth arrest, Harrington rod instrumentation and spinal fusion were done. In this patient, SSEPM showed no signal. At the time the cause for this failure could not be determined, and it was soon forgotten because she had no postoperative neurologic deficit. In February 1989 she returned complaining of buckling oftheknees. The upperhookofthe rodhaddisplaced, and the deformity was once again 60. She was found to have pes cavus and areflexia. Nerve conduction studies confirmed a diagnosis of Charcot-Marie-Tooth disease (HSMNType I). The Harrington was replaced, but SSEPM again did not show any signal. She had no subsequent neurologic deficit. This promptedustostudytherecords of 150scoliosis patients who hadSSEPM during corrective surgery. Four more patients were found with Charcot-Marie-Tooth disease. All had failure of spinal cord monitoring during surgery. Two were diagnosed only after surgery. One had a transient postoperative neurologic deficit. Their ages ranged from 11 to 16 years.