Wiginton James G, Brazdzionis James, Mohrdar Cyrus, Sweiss Raed, Lawandy Shokry
Neurosurgery, Riverside University Health System Medical Center, Moreno Valley, USA.
Medicine, Western University of Health Sciences, Pomona, USA.
Cureus. 2019 Jul 30;11(7):e5279. doi: 10.7759/cureus.5279.
A rare complication of cervical spine decompression is acute paralysis following the procedure. This neurologic deficit is thought to be due to reperfusion injury of a chronically ischemic spinal cord and is referred to as "white cord syndrome" given the pathognomonic finding of hyperintensity on T2-weighted MRI. Three prior cases have been reported. We present a case of transient quadriplegia following posterior cervical decompression. A 41-year-old male with cervical spondylotic myelopathy presented with bilateral progressive upper extremity weakness, hyperreflexia, and cervical spine MRI showing severe cord compression at C1 and partial hyperintense signal. Intraoperatively, after C1 bony decompression and without perceptible technical cause, the patient experienced a complete loss of both somatosensory evoked potentials (SSEPs) and motor evoked potentials (MEPs) with an eventual return to baseline prior to completing the operation. The patient awoke from surgery with acute quadriplegia without perceptible technical cause (intraoperative compression or evident anatomic compromise). An immediate postoperative MRI revealed a more pronounced hyperintensity in the central cervical cord on T2-weighted sequences. Treatment with increased mean arterial pressure (MAP) therapy and dexamethasone resulted in the patient regaining some movement over a period of hours and full strength over a period of months. The mechanism of acute weakness following cervical spine decompression in the absence of perceptible technical cause is not fully understood, but current theory suggests that a reperfusion injury is most likely the cause. It remains a diagnosis of exclusion. Familiarity with this potential postoperative complication can aid in appropriate postoperative therapy with early diagnosis and intervention leading to restored spinal cord function and excellent prognosis.
颈椎减压术的一种罕见并发症是术后急性瘫痪。这种神经功能缺损被认为是由于慢性缺血性脊髓的再灌注损伤所致,鉴于T2加权磁共振成像(MRI)上有特征性的高信号表现,故称为“白脊髓综合征”。此前已有3例相关病例报道。我们报告1例颈椎后路减压术后出现短暂性四肢瘫痪的病例。一名41岁患有颈椎病性脊髓病的男性,表现为双侧进行性上肢无力、反射亢进,颈椎MRI显示C1水平脊髓严重受压且部分信号高增强。术中,在C1椎体减压后,无明显技术原因,患者体感诱发电位(SSEP)和运动诱发电位(MEP)完全消失,最终在完成手术前恢复至基线水平。患者术后苏醒时出现急性四肢瘫痪,无明显技术原因(术中压迫或明显的解剖结构受损)。术后即刻MRI显示T2加权序列上颈髓中央高信号更明显。采用提高平均动脉压(MAP)治疗和地塞米松治疗后,患者在数小时内恢复了一些运动能力,并在数月内恢复了全部力量。在无明显技术原因的情况下,颈椎减压术后急性无力的机制尚不完全清楚,但目前理论认为最可能的原因是再灌注损伤。它仍然是一种排除性诊断。熟悉这种潜在的术后并发症有助于进行适当的术后治疗,早期诊断和干预可恢复脊髓功能并带来良好预后。