Abstract
There are many known risk factors for chronic pain conditions, yet the biological underpinnings that link these factors to abnormal processing of painful signals are only just beginning to be explored. This Review will discuss the potential mechanisms that have been proposed to underlie vulnerability and resilience toward developing chronic pain. Particular focus will be given to genetic and epigenetic processes, priming effects on a cellular level, and alterations in brain networks concerned with reward, motivation/learning and descending modulatory control. Although research in this area is still in its infancy, a better understanding of how pain vulnerability emerges has the potential to help identify individuals at risk and may open up new therapeutic avenues.
Original language | English |
---|---|
Pages (from-to) | 192-200 |
Number of pages | 9 |
Journal | Nature Neuroscience |
Volume | 17 |
Issue number | 2 |
Early online date | 28 Jan 2014 |
DOIs | |
Publication status | Published - Feb 2014 |
Keywords
- GENOME-WIDE ASSOCIATION
- IRRITABLE-BOWEL-SYNDROME
- CPG-BINDING PROTEIN-2
- LOW-BACK-PAIN
- NEUROPATHIC PAIN
- DNA METHYLATION
- SPINAL-CORD
- CENTRAL SENSITIZATION
- FIBROMYALGIA PATIENTS
- DIABETIC-NEUROPATHY