Facet joints are implicated as a major source of neck and low-back pain.
Both cervical and lumbar facet syndromes have been described in the medical
literature. Biomechanical studies have shown that lumbar and cervical
facet-joint capsules can undergo high strains during spine-loading.
Neuroanatomic studies have demonstrated free and encapsulated nerve endings in
facet joints as well as nerves containing substance P and calcitonin
gene-related peptide. Neurophysiologic studies have shown that facet-joint
capsules contain low-threshold mechanoreceptors, mechanically sensitive
nociceptors, and silent nociceptors. Inflammation leads to decreased
thresholds of nerve endings in facet capsules as well as elevated baseline
discharge rates. Recent biomechanical studies suggest that rear-end
motor-vehicle impacts give rise to excessive deformation of the capsules of
lower cervical facet joints. Still unresolved is whether this stretch is
sufficient to activate nociceptors in the joint capsule.
To answer this question, recent studies indicate that low stretch levels
activate proprioceptors in the facet-joint capsule. Excessive capsule stretch
activates nociceptors, leads to prolonged neural afterdischarges, and can
cause damage to the capsule and to axons in the capsule. In instances in which
a whiplash event is severe enough to injure the joint capsule, facet capsule
overstretch is a possible cause of persistent neck pain.