LBP has been recorded as a common human complaint since the time of Hipocrates.

Back pain has been variously attributed to local structures (lumbago) or generalized malady(athrtritis) (1). Determining the cause of LBP in most instances is unimportant,however,because the symptoms are most often transient and do not seriously interfere with function. Even severe episodes are most often self-limited in duration. Although LBP may be the secondmost common cause of visit to physician in the US, evidence available suggests many more episodes of LBP are never evaluated by a health professional and no formal diagnosis is considered. This chapter concerns the differential diagnosis ofLBP in clinical practice. Particular emphasis is placed on chronic,nonspecific back pain and the role of discography in diagnosis. There is, however , no practical list of diferential diagnosis that apply in all LBP. In fact, applying a generalized approach to diagnosing all LBP has resulted in much of the confusion seen in the field. In the initial stages of an evaluation, the goal of differential diagnosis is to identify or exclude serious condition (ex., tumors,infection,neurologic injury ,visceral disease,etc.) The physician can then direct specific treatment, if those potentially catastrophic causes of LBP are found , or initiate nonspecific supportive treatment if no specific pathologic process is identified. This is fundamentally different than evaluation of chronic LBP illness.When a practioner sees a patient with persistent LBP that is functionally debilitating, the practical differencial diagnosis becomes a more complex affair. In the situation, a precise diagnosis is important if possible because a more invasive or morbid treatment may be considered. This chapter discusses the practical approaches to the diagnosis of LBP complaints in the acute and chronic phases. Significant limitation in the data that estimate the incidence of specific causes of LBP and the tests used to establish a diagnosis are also discussed. Particular emphasis is given to discography, which si commonly used to define the cause of LBP. The goal of this chapter is to place the strengths and limitation of diagnosis strategies in perspective for acute and chronic back pain assessments. Diagnosis Historically ,LBP has been attributed to a variety of causes. It is interesting to note that throughout history, most LBP was not associated with trauma or injury. Rather,LBP was thought to have a humoral or rheumatic cause. It has been only in the past century that LBP as an injury has become a popular supposition. The reality is that few patients with acute or chronic LBP symptoms have experienced serious trauma;however,low intensity, repetitive movements and forces are postulated to produce traumatic injuries over time.(1) A comprehensive differential diagnosis(Table 1) of LBP lists many causes,the majority of which are associated with systematic disease. However, an exhaustive listing of diseases associated with LBP is of little practical value to the clinician attempting to make a diagnosis. To be useful in practice, the practical differential diagnosis should help direct evaluation and weigh the implication of various treatments. To be meaningful, a practical approach to the diagnosis of LBP must be epidemiologically and therapeutically balanced. Table 1 gives a listing of potencial anatomic sites from which nociceptor stimulation may be centrally interpred as LBP, regardless of the nociceptive site, is modulated by local, regional,central, and systemic factors. The following factors are important in understanding the clinical expression of LBP syndromes:

Adjacent tissue injury. Significant injury to nearby structures may increase the perception of pain in a hyperalgesic effect. This is a well known phenomen that may amplify pain perception by increased local inflammatory processes or neurologic sensitization (2,3). Local anesthetic. Local anesthetic or anti-inflammatory (steroid) injection may decrease the perception of pain. Interesting work on local anesthetic blocks has shown that percutaneous injection to areas of reffered pain, but not the true pain generator, can provide pain relief. It has been also shown that local local anesthetics applied distal to a lesion can modulate pain perception. The mechanisms of these remote actions to mitigate pain sensation are not clear but affect the fundamental premise of diagnostic blocks as used in practice. Nearby tissue injury. Tissue injury the same or adjacent sclerotomal afferents as lower spinal elements may increase LBP sensitivity. This effect is though to be due to physiologic or histologic changes at the level of the dorsal root ganglion or spinal cord ascending tracts (5). Chronic regional pain syndromes. Chronic pain processes from regional pathology may increase pain sensitivity at lower spinal elements. This effect may be regional or global and may be related to physiologic changes at multiple levels, including the spinal cord and brain(3).