What is the pathophysiology of radicular pain in x low back pain (LBP)?

Updated: Aug 22, 2018
  • Author: Jasvinder Chawla, MD, MBA; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
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Answer

Answer

The pathophysiology of spinal nerve root or radicular pain is unclear. Proposed etiologies include neural compression with axonal dysfunction, ischemia, inflammation, and biochemical influences. Spinal nerve roots have unique properties that may explain their proclivity toward producing symptoms. Unlike peripheral nerves, spinal nerve roots lack a well-developed intraneural blood-nerve barrier, and this lack makes them more susceptible to symptomatic compression injury.

Increased vascular permeability caused by mechanical nerve-root compression can induce endoneural edemas. Furthermore, elevated endoneural fluid pressure due to an intraneural edema can impede capillary blood flow and cause intraneural fibrosis. Also, spinal nerve roots receive approximately 58% of their nutrition from surrounding cerebral spinal fluid (CSF). Perineural fibrosis, which interferes with CSF-mediated nutrition, renders the nerve roots hyperesthetic and sensitive to compressive forces.

Research has elucidated several vascular mechanisms that can produce nerve-root dysfunction. Experimental nerve-root compression showed that venous blood flow can be stopped at low pressures, ie, 5-10 mm Hg. The occlusion pressure for radicular arterioles is substantially higher than this, approximating the mean arterial blood pressure and showing a correlation with systolic blood pressure; this factor increases the potential for venous stasis.

Some investigators postulate that venous-then-capillary stasis causes some congestion that, in turn, may induce symptomatic nerve root syndromes. Nerve root ischemia or venous stasis may also generate pathological biochemical changes that cause pain, unlike the progressive sensory-then-motor dysfunction typically seen with peripheral nerve compression. Studies of ischemia experimentally induced with low-pressure nerve root compression demonstrated that compensatory nutrition from CSF diffusion is probably inadequate when epidural inflammation or fibrosis is present. Rapid-onset neural and vascular compromise is more likely than a slow or gradual mechanical deformity to produce symptomatic radiculopathy.


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