AI Article Synopsis
- Amputation can lead to painful phantom sensations, and current theories suggest the primary somatosensory cortex (S1) may be involved in these sensations.
- Recent findings show that increased brain activity during phantom limb movements correlates with higher levels of phantom pain, offering a new perspective on this phenomenon.
- A computational model developed in this study indicates that strong phantom pain, excessive brain reorganization, and persistent representation may stem from the same issue: heightened activity in pain-sensing neurons that aren't receiving normal input.
Article Abstract
Amputation often leads to painful phantom sensations, whose pathogenesis is still unclear. Supported by experimental findings, an explanatory model has been proposed that identifies maladaptive reorganization of the primary somatosensory cortex (S1) as a cause of phantom pain. However, it was recently found that BOLD activity during voluntary movements of the phantom positively correlates with phantom pain rating, giving rise to a model of persistent representation. In the present study, we develop a physiologically realistic, computational model to resolve the conflicting findings. Simulations yielded that both the amount of reorganization and the level of cortical activity during phantom movements were enhanced in a scenario with strong phantom pain as compared to a scenario with weak phantom pain. These results suggest that phantom pain, maladaptive reorganization, and persistent representation may all be caused by the same underlying mechanism, which is driven by an abnormally enhanced spontaneous activity of deafferented nociceptive channels.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4058874 | PMC |
| http://dx.doi.org/10.1038/srep05298 | DOI Listing |
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