Pathophysiology of inflammatory, degenerative, and compressive radiculopathies

In answering the patient's question regarding how treatments are likely to "help [her] herniated disc," the mechanical and chemical components of radiculopathy should be addressed. Focal disc abnormalities often can be observed in those without pain, and symptomatic discs can become asymptomatic. Disc lesions can resolve radiologically with time, and patients' symptoms can improve before their radiographs. The literature reviewed in this article suggests that the best opportunity to offer therapies that address the chemical component of injury might be in those patients with acute disc pathology. In the case of degenerative stenosis, gradually evolving mechanical stressors may comprise the primary component of injury. In other instances, patients with radiographic evidence of neural foraminal or lumbar central stenosis may become symptomatic secondary to a superimposed mechanochemical injury. Such stressors can include a focal disc protrusion, leaking nuclear material from an annular tear, or synovial fluid from an adjacent arthrotic zygapophyseal joint. In these patients, the successful treatment of the acute injury process might allow the affected neural elements to return to their state of accommodation in an environment of gradually evolving mechanical compromise. A growing body of literature has helped clinicians to better understand the mechanisms behind radicular disorders. As spine clinicians, we should strive to educate our patients so that they may become more knowledgeable consumers of spine care. As the components of radicular pathology are elucidated further, new biochemical therapies will likely evolve. Similarly, there will probably always be a subset of patients who will require mechanical decompression, and some of these individuals should be offered such treatment without delay. There may a time in the radicular injury process at which a window of opportunity for treatment begins to close. After this point, any therapy offered will not be as likely to result in a more complete symptomatic response. Patients with chronic radicular pain may have neural structural insults and an increased sensitivity of the somatosensory system. Clinicians should strive to avoid this end stage of neural injury, which is less reversible from a chemical or mechanical standpoint and may respond only to chronic pain management modalities.