Integrating electrophysiological, mechanical, and optical methods to define the mechanisms of painful facet joint injury

Persistent pain is a common occurrence following whiplash injuries produced during motor vehicle crashes. The cervical facet joint and its capsule have often been identified as the source of chronic pain in patients with whiplash-associated disorders. However, for the majority of patients, no radiographic evidence of cervical spine injury is present. A capsular ligament stretch-based mechanism for initiating facet-mediated pain has been proposed based on human cadaveric studies of the facet joint kinematics during whiplash stimulations. However, without direct evidence of capsule damage during whiplash, the biomechanical and physiological mechanisms by which altered vertebral kinematics produce a facet capsule injury have not been fully elucidated. The goal of this thesis was to identify the facet joint loading conditions that produce microstructural damage to the facet capsular ligament and determine whether such loading can initiate neuronal plasticity in the spinal cord. Using a rat model of cervical facet joint loading, spinal neuron hyperexcitability was quantified from extracellular voltage recordings after imposing joint loading conditions that do and do not produce persistent pain symptoms. To determine whether neuronal hyperexcitability corresponds to a detectable change in the microstructure of the facet capsular ligament, a quantitative polarized light imaging technique was employed to define collagen fiber kinematics during capsule loading. A vector correlation analysis technique was developed to localize anomalies in the fiber kinematics of the human facet capsular ligament during tensile loading and was compared to changes in the mechanical response of the tissue during loading. The collagen fiber kinematics of the rat facet capsular ligament were also defined and compared to the joint loading conditions that produce neuronal plasticity and persistent pain symptoms. Altered fiber alignment and changes in the mechanical function of the human facet capsule were quantified after a subfailure vertebral retraction to determine the potential for microstructural damage in the facet capsule following whiplash-like motion. This work demonstrates that facet capsule stretch can cause microstructural changes to the capsular ligament in the absence of capsule rupture and establishes a framework to identify the mechanisms of facet joint injury and the development of central sensitization and persistent pain.