Berthelot Jean-Marie, Douane Frédéric, Ploteau Stéphane, Le Goff Benoît, Darrieutort-Laffite Christelle
Rheumatology Unit, Hôtel-Dieu, Nantes University Hospital, 1, Place Alexis, 44093 Nantes-Cedex 01, France.
Radiology Unit, Hôtel-Dieu, Nantes University Hospital, Place Alexis Ricordeau, 44093 Nantes-Cedex 01, France.
Joint Bone Spine. 2022 Mar;89(2):105291. doi: 10.1016/j.jbspin.2021.105291. Epub 2021 Oct 12.
Compression of roots/nerves can disrupt some of their functions, but does not necessarily cause pain. This is illustrated by the frequency of nearly asymptomatic spinal stenosis or disc herniations. In fact, pain of radiculopathies (and nerve entrapments) may mostly be the consequence of intraneural oedema induced by microscopical venous stasis around roots/spinal ganglia (or nerves) not or poorly shown by imaging. This narrative review first lists arguments for a role of congestion of vasa-nervorum in the pathophysiology of radiculopathies, including those induced by disc herniation and spinal stenosis, but also other sources of overpressures in spinal venous plexuses (pregnancy, vena cava atresia and thrombosis, portal hypertension, epidural varices, arterio-venous fistula, vertebral hemangioma or hemangioblastoma). It also details sources of venous congestion around nerves outside the spine, from pelvis (May-Thurner syndrome, Nut-cracker syndrome) to buttocks (superior and inferior gluteal veins), and even thighs and legs. A better recognition of a preeminent role of venous congestion in radiculopathies, plexopathies, and nerve entrapments, should have major consequences: (i) discard the dogma that compression is mandatory to induce root/nerve suffering, since root/nerve adherences in two locations can impair blood flow in vasa-nervorum through root/nerve stretching; (ii) implementation of sensitive techniques to visualise impingement of blood flow around or within roots and nerves; (iii) better prevention of roots/nerves adherence, or arachnoiditis induced by extravascular fibrin deposition secondary to venous stasis.; (iv) optimizing treatments dampening clot formation and/or extravascular fibrin leakage in the intradural/peridural spaces, or around roots/nerves, like guided injection of tissue plasminogen activator.
神经根/神经受压可能会扰乱其部分功能，但不一定会引起疼痛。这在几乎无症状的脊柱狭窄或椎间盘突出症的发生率中得到了体现。事实上，神经根病（和神经卡压）的疼痛可能主要是由神经根/脊神经节（或神经）周围微小静脉淤滞引起的神经内水肿所致，而影像学检查未显示或显示不佳。本叙述性综述首先列出了神经血管充血在神经根病病理生理学中的作用的论据，包括由椎间盘突出和脊柱狭窄引起的神经根病，以及脊柱静脉丛中其他压力过高的来源（妊娠、腔静脉闭锁和血栓形成、门静脉高压、硬膜外静脉曲张、动静脉瘘、椎体血管瘤或血管母细胞瘤）。它还详细介绍了脊柱外神经周围静脉充血的来源，从骨盆（May-Thurner综合征、胡桃夹综合征）到臀部（臀上静脉和臀下静脉），甚至大腿和小腿。更好地认识静脉充血在神经根病、神经丛病和神经卡压中的突出作用，应该会产生重大影响：（i）摒弃压迫是导致神经根/神经受损的必要条件这一教条，因为两个部位的神经根/神经粘连可通过神经根/神经拉伸损害神经血管的血流；（ii）采用敏感技术来可视化神经根和神经周围或内部的血流受影响情况；（iii）更好地预防神经根/神经粘连或静脉淤滞继发的血管外纤维蛋白沉积引起的蛛网膜炎；（iv）优化治疗方法，减少硬膜内/硬膜外间隙或神经根/神经周围的血栓形成和/或血管外纤维蛋白渗漏，如引导注射组织纤溶酶原激活剂。
