Clinical evidence of chemical radiculopathy

Abstract

It is universally accepted that an anatomic abnormality such as a herniated disc or spinal stenosis can lead to radicular leg pain. There is some controversy as to whether radicular pain can be caused by a non-structural, solely biochemical disorder. Prior studies using biochemical analysis of inflammatory mediators of the disc or surrounding structures have enumerated many possible biochemical mediators of radicular pain. However, such studies have not definitively demonstrated whether these inflammatory mediators are the causes of radicular pain or whether these mediators are simply products of the degenerative cascade. The purpose of this paper is to report upon patients who satisfy strict criteria affirming a diagnosis of radiculopathy in the presence of normal imaging studies. The study was designed as a prospective case series of patients fulfilling inclusion and exclusion criteria at a university hospital outpatient physiatric spine practice. Inclusion criteria consisted of symptoms of extremity pain greater than axial pain, examination findings demonstrating a new myotomal deficit that correlates with the root level predicted by the dermatomal pain distribution, and failure to improve after at least 4 weeks of active physical therapy. Magnetic resonance imaging void of local nerve root pathology as per review by the first author and the interpreting radiologist was required. Each patient had to have a positive electromyographic study for an acute radiculopathy. Each patient had to have a positive fluoroscopically guided diagnostic selective nerve root block. In summary, this paper provides clinical evidence that anatomic abnormalities are not required to cause radiculopathy, thus implying that a biochemical etiology is likely to play a significant role in radiculopathy and radicular pain.