Pathophysiology of inflammatory, degenerative, and compressive XXXX .

@entity1 @entity179 @entity74 @entity158 @entity614 @entity1118 @entity130 @entity890
In answering the @entity1 's question regarding how treatments are likely to "help [her] @entity890 ," the mechanical and chemical components of @entity614 should be addressed. Focal disc abnormalities often can be observed in those without @entity158 , and symptomatic discs can become asymptomatic. Disc lesions can resolve radiologically with time, and @entity1 ' symptoms can improve before their radiographs. The literature reviewed in this article suggests that the best opportunity to offer therapies that address the chemical @entity130 might be in those @entity1 with acute disc pathology. In the case of @entity179 , gradually evolving mechanical stressors may comprise the primary @entity130 . In other instances, @entity1 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 @entity1 , 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 @entity74 . As spine clinicians, we should strive to educate our @entity1 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 @entity1 who will require mechanical decompression, and some of these individuals should be offered such treatment without delay. There may a time in the @entity130 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. @entity1 with chronic @entity158 may have neural structural insults and an increased sensitivity of the somatosensory system. Clinicians should strive to avoid this end stage of @entity130 , which is less reversible from a chemical or mechanical standpoint and may respond only to @entity1118 management modalities.
