Chronic back pain continues to be a therapeutic challenge.
This is largely due to the difficulty in arriving at an exact diagnosis. It has been estimated that only 10-15% of patients get a specific diagnosis.
We report here an important clinical observation. While L5 – S1 is generally regarded as the most troublesome segmental level for back pain, in a series of 119 patients, upper lumbar radiculopathy (L1-2, L2-3) was equally common.
We have found upper lumbar radiculopathy to be a common but seldom detected cause of back pain, despite the fact that upper back dysfunction can be quickly diagnosed by clinical examination.
Radiculopathy Findings in Chronic Back Pain
Although ‘low back pain’ has been blamed on a wide spectrum of soft-tissue damage, ranging from minor ligament strain to major disruptions of stabilizing tissues in the entire spine, they may be divided into two main categories: simple mechanical low back pain with no neural involvement and those with radicular involvement.2
In a review of a series of 119 patients admitted to our outpatient clinic for low back pain over a period of 18 months (January 2001 – June 2002). All of them, except for seven, have had back pain for more than 9 weeks, and all had tried other forms of physical therapy without success.
All had musculoskeletal complaints related to the spine, and many had symptoms and/or physical signs at more than one segmental level. Consequently, some patients also had neck pain, shoulder pain, arm pain, dorsal back pain, or pain extending into the leg.
We found signs of radiculopathy (that is, neuropathy at root level) in virtually every patient. It is significant that in 83 of 119 patients signs were most prominent at the upper lumbar spine; 47 of these also presented with L5-S1 findings.
Diagnosing back pain caused by radiculopathy depends almost entirely on the examiner’s clinical experience. The history typically gives little assistance, as reported pain can far exceed that consistent with the injury. Our method of examination searches for signs of peripheral neuropathy – sensory, motor, autonomic, and trophic – which the conventional examination fails to uncover.
Peripheral neuropathy may be defined as a disease that causes disordered function in the peripheral nerve. Although sometimes associated with structural changes in the nerve, a neuropathic nerve can appear deceptively normal: it still conducts nerve impulses, synthesizes and releases transmitted substances and evokes action potentials and muscle contraction.4
Peripheral neuropathy is not exceptional. Of the innumerable causes of nerve damage, such as trauma, metabolic, toxic and others, attrition from spondylosis is by far the most common. The spinal nerve root is notably prone to injury from pressure, stretch, angulation, and friction. Ordinarily, spondylosis follows a gradual, relapsing, and remitting course that is silent until symptoms are precipitated by an incident often so minor that is may pass unnoticed. All gradations of spondylosis can exist, but early spondylotic changes, even when unsuspected, can give rise to radiculopathy. 5,6
Our emphasis on radiculopathy is not without reason: with an acute injury to a healthy nerve, there is prolonged discharge of pain signals, whereas the same injury to a neuropathic nerve can cause a sustained discharge. That is why some people develop severe pain after an apparently minor injury, and why that pain can continue beyond a ‘reasonable’ period.