Department of Anaesthetics, Bradford Royal Infirmary, Bradford BD9 6RJ, UK E-mail: docjohnnyr{at}hotmail.com
Anaesthetics is a broad field. Anaesthetists have provided the basis for many advances in surgical techniques and improvement in outcomes, while allowing ever more traditionally unfit patients to be treated. Not satisfied with that, we expand ever more into the field of surgical pathology, co-developing minimally invasive alternative treatments. There are many examples in the field of chronic spinal pain (Table 1).
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Lumbar spinal stenosis is a reduction in diameter of the spinal canal, lateral nerve canals, or neural foraminae. The usual causes are disc protrusion, spondylolisthesis, ligamentous hypertrophy, and bone hypertrophy, usually in combination. That being the case, how can spinal endoscopy, using flexible instruments without resection, diathermy or laser improve symptoms so effectively, especially in patients with radiculopathic pain?
A clue lies in the poor correlation of the degree of stenosis and severity of symptoms, coupled with the fact that in central canal stenosis (Igarashi and colleagues' patients), 40% of the narrowing is caused by soft tissue hypertrophy.2 Normal soft tissue comprises fat, neurological tissue and vessels. Abnormal soft tissues would be disc material, ligamentous hypertrophy, and fibrosis. Physically, spinal endoscopy, as performed in this study, can only affect the latter. Although not conclusively shown to be causative, adhesion development is associated with back pain and radicular pain. Its ubiquity was demonstrated in this study.
Epiduroscopy is the only true method of determining fibrosis; MRI is disappointing.3 4 But why are there adhesions; these patients had not had surgery? As is the case in lumbar disc disease, does this imply a chemical aetiology? Does the greater degree of vascularity of nerve roots in patients with radicular pain in this study indicate a chemical inflammation of greater magnitude in this group? Does the likely link between excessive bony overgrowth in a physiological attempt to reduce mobility through local arthrodesis,5 also affect the epidural space by producing epidural fibrosis? There is much basic research to be done.
Current theories of epidural adhesion production centre around chronic inflammation as a result of leakage of nucleus pulposus from degenerate intervertebral discs or synovial cytokines from zygapophysial joints.6 7 Mechanisms include: chemical radiculitis; neurogenic inflammation, which is probably an autoimmune response to the nucleus pulposus; and impaired fibrinolysis.68 Nerve root fibrosis ensues from all this as well as chronic oedema encouraged by almost instantaneous thrombosis in the epidural vasculature as a result of contact with the nucleus pulposus.6 7 (Interestingly, this is prevented by steroids and local anaesthetic.) The resulting nerve root ischaemia is described by some in terms of a compartment type syndrome.9
Radiculopathic pain generation is a complex process probably involving most or all of these processes. Nerve compression is a compounding factor, but is not a baseline requirement.10 Adhesions surrounding nerve roots, if they interfere with cerebrospinal fluid nerve growth factor delivery, will lead to demyelination of the whole axon.11 Nerve root ischaemia, directly observable during epiduroscopy, is probably the final common pathway leading to conduction abnormalities and pain.6 7
In contrast, there is little biomechanical knowledge about the nerve root in relation to movement. However, in a recent study, adhesions prevented the normal amount of stretching, slackening, excursion, and pendulum motion needed by nerve roots in order to accommodate back flexion and extension.12 Nerve root blood flow has been directly observed to cease with nerve traction.13 Traction on nerve roots is known to ellicit pain, but this is much more of a potent stimulus in the presence of inflammation.14
So how does epiduroscopy produce such effective pain relief? There are four possible mechanisms listed in Table 2. As Igarashi and colleagues' patients1 had temporarily responded to epidural blocks, but symptoms had recurred within 1 week, it is unlikely that highly accurate placement of steroid alone was the reason.
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Theodore Roosevelt said, I am interested in the man who takes the next step. Igarashi and colleagues1 have done just that by applying epiduroscopy to a particular diagnostic group and obtaining results of great interest.
References
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