J Intensive Care Med. 2025 Nov 24:8850666251393943. Revista: 10.1177/08850666251393943. Online ahead of print.

Although the brain itself lacks nociceptors and cannot directly perceive pain, it can generate chronic pain following injuries such as traumatic brain injury (TBI) or ischemic stroke. This phenomenon arises from disruptions in neural connectivity that distort the interpretation of sensory input. According to Bayes’ Rule, the brain combines current sensory input with prior experiences to formulate response predictions. When this process is disrupted by TBI, chronic pain may emerge. This review identified 60 relevant studies through systematic keyword searches, with inclusion based on content relevance following abstract screening. The literature underscores the brain’s adaptive processes in interpreting sensory stimuli. Disruptions to this adaptability-such as those caused by neuroinflammation, cytokine activation, or cellular injury-may contribute to persistent pain states. TBI-associated chronic pain is often classified as neuropathic and may arise from peripheral or central nerve damage, inflammation-induced injury, or impaired central processing. Pain resulting from central misinterpretation, as described by Bayesian models, frequently falls outside traditional inflammatory or neuropathic patterns and may not correspond with known dermatomal distributions, complicating diagnosis and treatment.

PubMed:41284709 | Revista:10.1177/08850666251393943