The source of low back pain and sciatica

Abstract

M OST ADULTS KNOW that low back pain is common because almost everybody between the ages of 30 and 60 years has had an attack of this aggravating and frequently disabling condition.’ It is second only to the common cold as the reason for time lost from work. An attack of low back pain may be acute, lasting ~2 weeks, or chronic, lasting >3 months. Low back pain attacks may recur over many years, which is usually the case, once they start. Furthermore, back pain is commonly associated with pain in one or both legs. What are the causes of low back pain, and how is this symptom complex related to osteoarthritis (OA)? Disc degeneration is the most common pathological process that effects the low back. Almost everybody develops one or more degenerated discs with aging. Disc degeneration begins in the early 2Os, at the same time the first acute attack of low back pain occurs. The initial attack of low back pain is usually excruciating and disabling and resolves within ten days. It is characterized by deep severe back pain aggravated by change in position and relieved by rest. It seems probable, because almost everybody has low back pain in their middle years, when disc degeneration occurs, that this process is the most likely cause of low back pain. Why then do 37% of totally asymptomatic individuals have an abnormal disc?* On the other hand, disc degeneration with narrowing is the most common x-ray finding associated with low back pain.3 It must be that certain phenomena associated with disc degeneration are the most common causes of low back pain with or without leg pain. What are these phenomena? Disc degeneration begins with loss of waterbinding capacity of the nucleus pulposus and resultant loss of weight-bearing characteristics of the disc.4 Loss of the capacity of the nucleus pulposus cells to produce proteoglycan macromolecules that are able to bind extracellular water leads to a loss of permeability of the disc matrix, cell death, necrosis, disc narrowing, and abnormal weight bearing. The nucleus pulposus under these circumstances is no longer an incompressible hydraulic weight distribution structure but now allows axial loads on the spine to become compressive loads on the annulus fibrosus. With disc narrowing, the annulus fibrosus bulges and becomes relatively unstable with respect to resistance to torsional loads.’ This process is analogous to a poorly inflated radial tire that is susceptible to abnormal stress on the sidewall, leading to cracks and blowouts with continued use. To understand the origin of low back pain and associated leg pain syndromes as the result of OA of the spine, the neuroanatomy of the spine must be reviewed.6‘10 There are two types of receptors of pain stimulus in the low back. The first type are the local nociceptors in the ligaments, peripheral annulus fibrosis, facet joint capsules, and periosteum of the bone. Free nerve endings (pain receptors) and specialized encapsulated nerve endings (proprioceptive and deeply located pain receptors) have been detected in these areas. The second type are the nerve roots, sensory ganglia, and spinal nerves that course through the spinal canals and are not normally nociceptors but become the source of ectopic pain stimulus under pathological conditions.” The sensory innervation of the posterior longitudinal ligament and posterior peripheral layers of the annulus fibrosus comes from the sinuvertebral nerve, which is the first branch of the spinal nerve immediately distal to the sensory root ganglion. Whereas the sensory innervation of the facet joint capsules, interspinous and supraspinous ligaments, periosteum of the bony neural arch of the vertebral bodies, muscle, and overlying skin of the low back comes from the posterior primary ramus of the spinal nerve, the