ABSTRACT
The intervertebral disc is now recognized as a common source of chronic axial pain (1-3). They are endowed with necessary innervation to be a source of pain (4,5). Cases of ruptured intervertebral discs have been reported as early as 1896 (6). In 1911, Middleton and Treacher of the United Kingdom (7) and J.E. Goldwait of Boston (8) independently described the entity known as the ruptured intervertebral disc. In 1929, studies by Dandy (9) and Schmorl (10) provided evidence of the possible clinical significance of the ruptured disc. In 1934, a widespread interest was created in the disc as a source of pain (11). This mechanical model by Mixter and Barr became the centralmodel of spine pain, which preoccupied themedical community and diverted attention from other possible causes. The question of the existence of an intradiscal pain mechanism arose in 1984 when Hirsch (12) injected procaine into a herniated disc and reported relief of sciatica. It was Roofes’ description of annulus fibrosus innervation in 1940 that provided an alternative model of the disc as a pain generator independent of a neurocompressive paradigm (13). The clinical validation of Roofes’ discovery came from Vanharanta et al. (14). This paper demonstrated that only an annular fissure which extends from the mid to outer annular region significantly correlates with pain with a provocative injection. Since then, several studies have identified the existence of irritant chemical substances within the disc that could cause sensitization of the disc annulus with mechanical loading (15,16). This sensitivity has been documented both by eliciting the axial pain by pressing on the posterior annulus during lumbar surgery in awake patients (1) and with low pressure (chemical) activation of annular nociceptors (17). The rich innervation of the mid to outer annular layers has been substantiated by four independent studies (18-21) using sophisticated staining and magnification studies.
