Herniated intervertebral disc-associated periradicular fibrosis and vascular abnormalities occur without inflammatory cell infiltration
original abstract †Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.
STUDY DESIGN: Prospective histologic comparison of perineural tissues from patients requiring decompression surgery for herniated intervertebral disc with those from cadaveric controls.
OBJECTIVES: To examine the significance of herniated intervertebral-disc-associated perineural vascular and fibrotic abnormalities with respect to back pain symptom generation.
SUMMARY OF BACKGROUND DATA: Previous cadaveric studies have demonstrated perineural vascular congestion, dilatation, and thrombosis and perineural and intraneural fibrosis occurring in association with herniated intervertebral disc. It was suggested that these neural abnormalities were the result of ischemia, due to venous outflow obstruction, and also represented a possible cause of ongoing back pain symptoms. Criticisms of such a conclusion arose, however, because the possibility could not be excluded that these abnormalities were the result of postmortem artifact.
METHODS: Histologic and immunohistochemical comparison of discal and peridiscal tissues removed from 11 patients with radiographically proven herniated intervertebral disc requiring decompressive surgery and from 6 fresh cadavers without history of back pain in life.
RESULTS: Histology and immunohistochemistry of perineural and extraneural tissues from patients revealed vascular congestion, neovascularization, and endothelial abnormalities including luminal platelet adhesion, in association with reductions in von Willebrand factor levels, together with perivascular and perineural fibrosis. Elevated fibrogenic cytokine concentrations were also detected in patients' tissues. These changes occurred without evidence of inflammation and were absent in cadaveric control tissues.
CONCLUSIONS: The vascular abnormalities detected in patients may represent an important etiopathologic factor predisposing to intraneural and perineural fibrosis, and hence to chronic pain symptoms, after disc herniation. It seems important to preserve the perineural microcirculation following disc herniation.
related content
- “Significance of the small lumbar spinal canal: cauda equina compression syndromes due to spondylosis 3: Intermittent claudication,” Wilson, Journal of Neurosurgery, 1969.
- “Pathophysiology of nerve compression,” Mackinnon, Hand Clin, 2002.
- “Changes in nerve root motion and intraradicular blood flow during an intraoperative straight-leg-raising test,” Kobayashi et al, Spine, 2003.
- “The role of vascular damage and fibrosis in the pathogenesis of nerve root damage,” Jayson, Clinical Orthopaedics & Related Research, 1992.
Cooper 1995 is about:
- “Intervertebral foramen venous obstruction. A cause of periradicular fibrosis?,” Hoyland et al, Spine (Phila Pa 1976), 1989.
This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog. A few highlights:
- Placebo analgesia in physical and psychological interventions: Systematic review and meta-analysis of three-armed trials. Hohenschurz-Schmidt 2024 Eur J Pain.
- Recovery trajectories in common musculoskeletal complaints by diagnosis contra prognostic phenotypes. Aasdahl 2021 BMC Musculoskelet Disord.
- Cannabidiol (CBD) products for pain: ineffective, expensive, and with potential harms. Moore 2023 J Pain.
- Moderators of the effect of therapeutic exercise for knee and hip osteoarthritis: a systematic review and individual participant data meta-analysis. Holden 2023 The Lancet Rheumatology.
- Inciting events associated with lumbar disc herniation. Suri 2010 Spine J.