Based on the experimental and clinical results in the literatures and the author's experience, a working hypothesis for the pathomechanism of radicular pain is proposed. When the nerve root is involved, mechanical and circulatory changes are produced. Inflammatogenic materials may leak from the degenerative disc and facet into the nerve root, causing chemical radiculitis. These changes can be followed by nerve fiber and cell changes including blockage of axonal flow and demyelination, causing ectopic discharges and cross talk. Disturbed or enhanced synthesis and transport of neuropeptides can also be elicited. These multifactorial changes may finally result in sensitization of both the central and peripheral nervous systems, causing radicular pain.