Discography probably provokes pain by three mechanisms: (1) stimulation of nerve endings, (2) biomechanical or neurochemical stimulation, and (3) deflection of vertebral body endplates.
It is believed that pain generated by discography occurs when annular fissures or nuclear herniations extend into the outer third of the annulus fibrosis (22). Nerve endings from branches of the lumbar ventral rami, gray rami communicantes, and the sinuvertebral nerves innervate the outer third of the ventral, lateral, and dorsal annulus, respectively (23). Histological and immunocytochemical studies have demonstrated the presence of a variety of nerve endings in the outer annulus, and neurotransmitters associated with pain perception (nociception) have been detected in the annulus and posterior longitudinal ligament (23). The injection of contrast into the disc may increase intradiscal pressure, stretch the annulus, and stimulate nerve endings.
Histochemical studies have shown that nerve endings in the annulus contain peptides, such as calcitonin gene related peptide, vasoactive intestinal peptide, and substance P. These peptides have been shown to be associated with nociception (24-26). The pain response provoked by concordant discography may be secondary to the stimulation of these nociceptive nerve endings by enzymes such as phospholipase A2 and nuclear degradation products (27). To simplify, the injection of contrast into the disc may result in some biochemical or neurochemical stimulation that causes pain.
The last proposed mechanism for pain provoked with discography is endplate deflection. Heggeness and Doherty have documented endplate deflection during intradiscal injection, which could explain a mechanical component for discogenic back pain (28).
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