Whiplash injury can produce pain in the neck, arm, and hand, and has been associated with inflammation. However, the relationship between inflammatory responses and pain symptoms remains unknown, hindering the development of appropriate therapeutics for whiplash symptoms. Two joint loading paradigms were used separately in an established rat model of painful cervical facet joint distraction to apply: (1) gross failure, and (2) subfailure distraction of the facet capsular ligament. Behavioral outcomes were compared to determine whether more severe mechanical loading produces greater pain by measuring mechanical hyperalgesia in the shoulder and forepaws. Inflammatory mediators (glia and cytokines) were quantified in the spinal cord and dorsal root ganglion (DRG) after injury. Subfailure loading produced sustained hyperalgesia in the shoulder and forepaw that was significantly greater (p < 0.042) than sham, while an induced capsule failure produced only transient, yet significant (p < 0.021), mechanical hyperalgesia. The absence of hyperalgesia after ligament failure suggests this type of injury may interrupt nociceptive input from the capsule, which is likely necessary to produce sustained pain symptoms. Glial mRNA was significantly increased (p < 0.043) in the spinal cord after ligament failure, but remained unchanged in the DRG. Cytokine mRNA levels in the spinal cord and DRG were also significantly elevated after facet ligament failure, but not after painful subfailure loading. Findings suggest that different joint loading scenarios produced varied inflammatory responses in the CNS. These data support existing clinical reports suggesting that therapeutic interventions directed at the facet capsule may be effective in treating this painful injury.