Traumatic neck injuries are a primary cause of chronic pain, with the cervical facet joint and its capsule being a common source of the pain. During these injuries, the facet capsular ligament undergoes excessive stretching that can initiate pain [1]. Behavioral sensitivity is produced as early as 1 day after facet capsule stretch, which suggests that the excitatory systems in the spinal cord are modulated by certain tissue loading conditions. In particular, the signaling protein PKCε has been implicated in glutamate release in inflammatory pain [2] and is increased in afferents after painful facet injury [3]. Also, neuronal hyperexcitability has been detected after painful, but not nonpainful, facet joint distraction [4]. Despite the involvement of spinal neuronal activation in pain, the time course of its development and its relationship to painful mechanical facet joint injury is unknown.

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