Definition of Chronic Pain
Pain is considered chronic when it persists for longer than 3 to 6 months beyond the acute onset and resolution of the initial insult or injury. 1
Temporal Criteria
The 3-6 month threshold represents the standard definition across multiple clinical contexts:
Most recent guidelines from the AGA (2024) specifically define abdominal pain as chronic when it has persisted 3-6 months past acute onset and resolution of the insult (such as surgery for stricture or resolution of obstruction). 1
The HIVMA/IDSA guidelines (2017) similarly define chronic pain as pain lasting longer than 3-6 months, persisting beyond the typical period of direct tissue injury and repair. 1
The IASP classification for ICD-11 defines chronic pain as pain that persists or recurs for more than 3 months. 2
Key Distinguishing Features Beyond Duration
Chronic pain differs fundamentally from acute pain in several critical ways:
Independence from peripheral stimuli: Chronic pain is experienced irrespective of the presence, intensity, or duration of peripheral stimuli arising from the affected area. 1
Central nervous system changes: Chronic pain involves substantial functional and structural changes (plasticity) in the central nervous system, including upregulation of nociception at every level of the nervous system, alterations in the "pain matrix" on functional imaging, and changes in sympathetic nervous system activation and hormonal regulation. 1
Episodic and fluctuating nature: Chronic pain can be episodic and fluctuating, related to biological, psychological, and social triggers rather than ongoing tissue damage. 1
Clinical Recognition Challenges
A common pitfall is waiting too long to recognize the transition from acute to chronic pain, particularly in conditions with relapsing-remitting patterns:
In inflammatory bowel disease, knowing when acute pain has converted to chronic pain is often difficult due to the relapsing and remitting nature of inflammation and lack of clarity as to when the peripheral "cause" of pain is resolved. 1
Animal models demonstrate that inflammation-induced hyperalgesia often outlasts actual inflammation, yet providers are often reluctant to intervene for pain symptoms before a certain "recovery time" has passed. 1
Patients cannot consciously distinguish between ongoing injury versus upregulation of the sensory system where nociceptive signals continue in the absence of actual injury. 1
Pathophysiological Mechanisms
Central sensitization is the hallmark mechanism that distinguishes chronic from acute pain:
Central sensitization can occur at the spinal cord, brainstem, and cortical levels, with alterations in descending tonic pain modulation of spinal cord excitability. 1
Patients may exhibit allodynia (innocuous stimuli perceived as painful) or hyperalgesia (exaggerated response to noxious stimuli) even when the original tissue injury has resolved. 1
The peripheral factors that initiated pain become different from the central factors that maintain and amplify it (such as fear of pain or re-injury). 1