Many of us tend to associate LBP with the disc, more specifically with a ‘herniated’ disc. However research which began in the mid 1970s’ and was described in depth in the 1987 text Clinical Anatomy of the Lumbar Spine (Bogduk & Twomey) explicated the most compelling source of acute LBP: internal disc disruption promulgating annular ‘tears’. Not coincidentally these “tears” create a pain profile mimicking a ligament sprain.
Sato et al (Eur Spine 2005) further delineates this likely mechanism of acute (non-radicular) LBP; a “re-reputure of a previously repaired region in the posterior annulus of a moderately degenerated disc with an annular tear”.
Torsional injuries along-side degenerative changes create circumferential tears, these tears typically do not change the outer architecture of the disc so direction-preference is absent and an often “unendurable” (discogenic) pain persists until slowly healed with granulation tissue (type III collagen).
Only ~10% show ‘leakage’ thru the tear.
Sato found nearly 50% of patients developed the acute LBP with “casual” movements…further validating the “weakened” annular fiber theory and susceptibility to torsional strains; the disc’s weak link.