Research progress on the mechanisms of impaired neurological recovery after cauda equina syndrome and long-term functional reconstruction strategies for neurogenic bladder

Guo Jie; Zhou Lina; Lei Ling; Zhang Yanjun

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Research progress on the mechanisms of impaired neurological recovery after cauda equina syndrome and long-term functional reconstruction strategies for neurogenic bladder

更新时间：2026-10-23

- Research progress on the mechanisms of impaired neurological recovery after cauda equina syndrome and long-term functional reconstruction strategies for neurogenic bladder
- Journal of Chongqing Medical University Pages: 1-9(2026)
- 作者机构：
  
  1.甘肃中医药大学中医临床学院，兰州 730050
  2.甘肃省中医院脊柱骨二科，兰州 730000
- 作者简介：
- 基金信息：
- DOI：
  CLC： R681.5
- Received：26 July 2026，
  
  Revised：2026-09-19，
  
  Accepted：20 September 2026，
  
  Published：23 October 2026
- 稿件说明：
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Guo Jie,Zhou Lina,Lei Ling,et al.Research progress on the mechanisms of impaired neurological recovery after cauda equina syndrome and long-term functional reconstruction strategies for neurogenic bladder[J].Journal of Chongqing Medical University,
DOI：

Guo Jie,Zhou Lina,Lei Ling,et al.Research progress on the mechanisms of impaired neurological recovery after cauda equina syndrome and long-term functional reconstruction strategies for neurogenic bladder[J].Journal of Chongqing Medical University, DOI：10.13406/j.cnki.cyxb..

摘要

马尾综合征（cauda equina syndrome，CES）是由腰骶神经根受压或损伤引起的严重神经功能障碍，部分患者经减压治疗后仍遗留排尿、排便及鞍区感觉等功能障碍。本文以“临床问题—机制解释—评估分层—长期干预”为主线，围绕CES减压术后神经功能恢复障碍及神经源性膀胱长期管理进行综述。现有证据表明，持续性神经功能障碍可能与机械压迫及缺血、沃勒变性、施万细胞表型转换、神经免疫微环境、细胞外基质重塑及脑—膀胱网络可塑性等多种因素相关，但部分机制证据主要来源于外周神经或脊髓损伤模型，尚缺乏CES特异性临床证据。治疗方面，早期磁共振成像（magnetic resonance imaging，MRI）评估并尽快减压仍是急性CES的基础策略；术后应结合尿动力学检查、残余尿量测定及神经功能评定进行动态评估，规范开展清洁间歇导尿、药物治疗和康复训练，必要时考虑骶神经调控等治疗。干细胞、外泌体、神经导管及人工智能等新技术仍面临安全性隐患、标准化缺失和临床证据不足等转化障碍。未来应建立以CES分型和膀胱功能为基础的分层管理体系，并通过多中心前瞻性研究完善长期预后评价和治疗策略。

Abstract

Cauda equina syndrome （CES） is a severe neurological disorder caused by compression or injury of the lumbosacral nerve roots. Some patients continue to experience dysfunction in urination，defecation，and saddle sensation after decompression. This review follows a thematic framework of “clinical problem，mechanistic explanation，stratified assessment，and long-term intervention” and summarizes impaired neurological recovery and long-term management of neurogenic bladder after decompression for CES. Current evidence suggests that persistent neurological dysfunction may be associated with multiple factors，including mechanical compression and ischemia，Wallerian degeneration，Schwann cell phenotypic switching，neuroimmune microenvironment，extracellular matrix remodeling，and brain-bladder network plasticity. However，some of the mechanistic evidence is derived primarily from peripheral nerve or spinal cord injury models，and CES-specific clinical evidence remains scarce. In terms of treatment，early magnetic resonance imaging assessment and prompt decompression remain the fundamental strategies for acute CES. After surgery，patients should undergo dynamic assessment based on urodynamic testing，measurement of post-void residual volume，and neurological evaluation. Standardized interventions，including clean intermittent catheterization，pharmacological therapy，and rehabilitation training，should be implemented. Sacral neuromodulation and other therapies may be considered when indicated. Emerging technologies，such as stem cells，exosomes，nerve conduits，and artificial intelligence，still face translational challenges such as safety concerns，a lack of standardization，and insufficient clinical evidence. Future research should establish a stratified management system based on CES classification and bladder function and should use multicenter prospective studies to refine long-term prognostic evaluation and therapeutic strategies.

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references

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