Neutral images can reinstate pain-related brain activation: Experimental evidence for a memory-based mechanism of pain amplification   January 1st, 2015

Remembering an event reactivates at least part of the cortical and subcortical regions that were engaged during the original experience of that event. This is termed “reinstatement” of brain activity during memory retrieval. German and UK researchers have conducted a fascinating study showing reinstatement of pain-related brain activation during viewing of neural images that had previously been paired with heat pain. 

This experimental study, recently published in Pain journal, exposed healthy pain-free subjects to neutral images (pictures with natural scenes with living – animals like whales and penguins - or non-living objects like dishes and cars) and paired some of them with painful heat stimuli applied to the skin. Brain activation was monitored using functional MRI. Following this first phase, the same healthy volunteers were re-exposed to the same images but this time without painful stimuli. When they were re-exposed to the images that were paired with painful heat, several pain-related brain regions were reinstated, including the bilateral putamen, right operculum, left posterior insula and right thalamus. Reinstatement brain activity correlated with the brain activity observed during the initial heat pain application during viewing of the neutral images. Reinstatement was not observed when the volunteers viewed neutral images that were not previously paired to painful heat pain. 

The learning or memory effect observed here may be an adaptive response to the brain, as it allows recognizing threatening (i.e. painful) situations. In daily life, this protects us from threatening situations and allows us to avoid such (possibly dangerous) situations. However, this adaptive brain response might become maladaptive in chronic pain. The experimental study findings summarized above might explain at least part of the chronic pain problem, where nociceptive pathology has often long subsided and the brain of patients with chronic pain has acquired a protective pain memory. It also explains why pain patients often experience pain flares without obvious (or new) nociceptive input: even neutral events (e.g. doing groceries) that once resulted in pain increases will results in pain increases again when re-exposed to the same event. 

Pain in Motion previously explained that exercise therapy for patients with chronic pain is often hampered by such pain memories, and that therapists may alter pain memories in patients with chronic pain by integrating pain neuroscience education with exercise interventions. The latter includes applying graded exposure in vivo principles during exercise therapy. 

Jo Nijs

2015 Pain in Motion

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