Mechanisms of low back pain: a neurophysiologic and neuroanatomic study

• Published in: Clinical orthopaedics and related research no. 335; p. 166
• Main Authors: Cavanaugh, J M, Ozaktay, A C, Yamashita, T, Avramov, A, Getchell, T V, King, A I
• Format: Journal Article
• Language: English
• Published: United States 01.02.1997
• Subjects: Animals; Intervertebral Disc - innervation; Joints - innervation; Low Back Pain - physiopathology; Lumbar Vertebrae; Male; Mechanoreceptors - physiology; Nerve Endings - physiology; Neural Conduction; Neuroanatomy - methods; Neurophysiology - methods; Rabbits; Spinal Nerve Roots - drug effects; Spinal Nerve Roots - physiology; Substance P - physiology
• ISSN: 0009-921X; 1528-1132
• DOI: 10.1097/00003086-199702000-00016

Idiopathic low back pain has confounded health care practitioners for decades. The cellular and neural mechanisms that lead to facet pain, discogenic pain, and sciatica are not well understood. To help elucidate these mechanisms, anesthetized New Zealand white rabbits were used in a series of neurophysiologic and neuroanatomic studies. These studies showed the following evidence in support of facet pain: an extensive distribution of small nerve fibers and endings in the lumbar facet joint, nerves containing substance P, high threshold mechanoreceptors in the facet joint capsule, and sensitization and excitation of nerves in facet joint and surrounding muscle when the nerves were exposed to inflammatory or algesic chemicals. Evidence for pain of disc origin included an extensive distribution of small nerve fibers and free nerve endings in the superficial annulus of the disc and small fibers and free nerve endings in adjacent longitudinal ligaments. Possible mechanisms of sciatica included vigorous and long lasting excitatory discharges when dorsal root ganglia were subjected to moderate pressure, excitation of dorsal root fibers when the ganglia were exposed to autologous nucleus pulposus, and excitation and loss of nerve function in nerve roots exposed to phospholipase A2.