Most journals display a picture of low back pain with a picture of a patient with a herniated disc and, although this is uncommon, it is the image most often portrayed. Rosomoff et al. This percentage was confirmed by the Quebec Task Force on Spinal Disorders report of 45,000 patients. Obvious to all should be the fact that nociceptive input is the result of a dysfunctional state. The nerve membrane will be stretched.
Ionic flow occurs with depolarization and the generation of an action potential.
In other words, nerve root compression from whatever source is painful only briefly, and sustained pressures lead to electrical silence and absence of sensation. It is worth reminding the reader that vital to the transmission of pain is the induction of the state or condition of hyperalgesia and sensitization of nerve endings. The injury need not be gross. Microscopic tissue damage, as in inflammation, may be enough. Once hyperalgesia has been established, tissue breakdown substances, such as bradykinin, histamine, and other neuropeptides, are released, which in the presence of hyperalgesia, combine to produce pain.5 The herniated disc or bony stenosis causing pain can easily be explained in these same terms.