In their thoughtful perspectives article, Finnerup et al. 4 challenge the idea that there is a transition or shift from an acute nociceptive pain to another chronic pain type that is driven by central sensitization, spinal amplification, and altered descending pain modulation. As an alternative idea, they argue that after resolution of the original physiological cause, new types of pain can be Figure 1. Development of chronic pain after injury (based on ref.
1). (A)A simplified presentation of the common cause model: symptoms (fear, pain, avoidance, disability…) are assumed to be caused by a common cause (E1 and E2, eg, a physiological event such as injury or inflammation). If the common cause resolves, the symptoms also disappear. (B) A simplified presentation of dynamics of the network model: symptoms influence each other and can be maintained even when the nociceptive or neuropathic contributions are resolved. For example, a physiological event (E) that is external to the network activates a dormant network of observable and connected symptoms such as pain and fear, which may spread to other symptoms, such as avoidance and disability. In a strongly connected network, removal of the physiological event does not lead to recovery as the network is self-sustaining.