Livingston theorized that severe lasting pain induces functional and organic changes in the nervous system, thereby producing a chronic pain state.
The thalamus is a site where activations would most be expected in the acute pain state.
Important questions to ask are: Why does acute pain transition into a chronic pain state in some patients?
Thus, identifying and treating their pain aggressively after surgery could positively impact their long-term pain state [104].
However, potential mechanisms promoting the establishment of a persistent pain state and the increased pain vulnerability remain unknown.
More importantly, in comparison to the PET study on spontaneous migraine [21], no brainstem activity was found during the acute pain state compared to the resting state.
FM is characterized by chronic, widespread pain along with various clinical symptoms that reflect a centralized pain state, including fatigue, insomnia, cognitive dysfunction, headache, and depression [2].
Whether these mechanisms are causally related to pain, or just reflections of the chronic pain state, cannot be determined from the present study.
Thus, the present findings of decreased theta connectivity between the insula and the DMN may reflect persistent pain encoding associated with the chronic pain state of FM.
Synovial membrane inflammation is the most commonly presenting finding during hip arthroscopy, and may have a role in the pain state.
In normal animals, peripheral nerve injury produces a persistent, neuropathic pain state in which pain is exaggerated and can be produced by nonpainful stimuli.
