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The role of vascular damage and fibrosis in the pathogenesis of nerve root damage

PainSci » bibliography » Jayson 1992
Tags: etiology, neat, back pain, neurology, pro, pain problems, spine

Three articles on PainSci cite Jayson 1992: 1. The Complete Guide to Trigger Points & Myofascial Pain2. The Complete Guide to Low Back Pain3. Can Massage Damage Nerves?

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.

Vascular damage and fibrosis are common within the vertebral canal and intervertebral foramen. The grossest examples occur in patients who have previously undergone oil-based myelography or spinal surgery. The mechanisms of fibrosis in the latter instance may be related to persisting cotton debris from sponges used during the operation. This debris may act as a fibrogenic stimulus. However, in cadaveric studies of nonoperated spines, the author and his colleagues have found clear evidence of vascular damage and fibrosis within the spines, and this vascular damage is significantly related to the severity of degenerative disk disease. Degenerative disk disease with osteophytic proliferation and disk protrusion may lead to compression of epidural veins with dilation of noncompressed veins. There is a significant statistical relationship between the extent of the disk degeneration and prolapse and the evidence of venous compression and dilatation. The dilatated veins may contain antemortem thromboses. In turn, there is a significant statistical relationship between the evidence for venous obstruction and perineural fibrosis. Such a relationship also exists between perineural fibrosis and neuronal atrophy. If therefore appears likely that venous obstruction with resultant hypoxia is an important mechanism leading to nerve root damage. In the peripheral blood, significant defects in the fibrinolytic system correlate with the severity of the symptoms. However, it was not possible to correlate these changes with individual clinical or imaging features. These fibrinolytic changes are recognized as markers of vascular damage and may reflect the pathologic processes that the author and his colleagues have demonstrated. It is uncertain whether they play any secondary pathogenic role in the chronicity of these back problems. Exercise is known to stimulate the fibrinolytic system, and the author is currently examining whether the benefit that is obtained from intensive physical rehabilitation programs may, at least in part, be the result of this stimulation.

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