Mechanical Low Back Pain Causes of mechanical LBP generally are attributed to an acute traumatic event, but they may also include cumulative trauma as an etiology. The severity of an acute traumatic event varies widely, from twisting one's back to being involved in a motor vehicle collision. Mechanical LBP due to cumulative trauma tends to occur more commonly in the workplace.
The pathophysiology of mechanical LBP remains complex and multifaceted. Multiple anatomic structures and elements of the lumber spine (eg, bones, ligaments, tendons, disks, muscle) are all suspected to have a role. Many of these components of the lumber spine have sensory innervation that can generate nociceptive signals representing responses to tissue-damaging stimuli. Other causes could be neuropathic (dysfunction of the nervous system--e.g, sciatica). Most chronic LBP cases most likely involve mixed nociceptive (a sensory receptor that responds to pain) and neuropathic etiologies.
Repetitive, compressive loading of the disks in flexion (eg, lifting) puts the disks at risk for an annular tear and internal disk disruption. Likewise, torsional forces on the disks can produce shear forces that may induce annular tears. The contents of the annulus fibrosis (nucleus pulposus) may leak through these tears. Central fibers of the disk are pain free, so early tears may not be painful. Samples of disk material taken at the time of autopsy reveal that the cross-linked profile of pentosidine, a component of the collagen matrix, declines. This may indicate the presence of increased matrix turnover and tissue remodeling.
Research in the past 20 years suggests that chemical causes may play a role in the production of mechanical LBP. Components of the nucleus pulposus, most notably the enzyme phospholipase A2 (PLA2), have been identified in surgically removed herniated disk material. This PLA2 may act directly on neural tissue, or it may orchestrate a complex inflammatory response that manifests as LBP.
Glutamate, a neuroexcitatory transmitter, has been identified in degenerated disk proteoglycan and has been found to diffuse to the dorsal root ganglion (DRG) affecting glutamate receptors. Substance P (pain) is present in afferent neurons, including the DRG, and is released in response to noxious stimuli, such as vibration and mechanical compression of the nerve. Steady, cyclic, or vibratory loading induces laxity and creep in the viscoelastic structures of the spinal elements. This creep does not recover fully in the in vivo cat model, even when rest periods are equal in duration to the loading period.
The concept of a biomechanical degenerative spiral has an appealing quality and is gaining wider acceptance. This concept postulates the breakdown of the annular fibers allows PLA2 and glutamate, and possibly other as-yet unknown compounds, to leak into the epidural space and diffuse to the DRG. The weakened vertebra and disk segment become more susceptible to vibration and physical overload, resulting in compression of the DRG and stimulating release of substance P. Substance P, in turn, stimulates histamine and leukotriene release, leading to an altering of nerve impulse transmission. The neurons become sensitized further to mechanical stimulation, possibly causing ischemia, which attracts polymorphonuclear cells and monocytes to areas that facilitate further disk degeneration and produce more pain.