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Descending inhibitory noxious control. Don’t bite your lip – stand on your opposite toe

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Descending modulation, descending inhibition, descending noxious inhibitory control, descending inhibitory noxious control etc etc etc, are used interchangeably and I wish they weren’t. A recent article in PAIN has looked specifically at DNIC – you can work out which term it acronymises (I just made that word up).  Before I give you a very quick run-down of that paper, I will first point out why I think we shouldn’t just use these words as though they mean the same thing.  Descending modulation – my gold medallist – means that projections from ABOVE the spinal cord modulate activity of the spinal nociceptors in the dorsal horn. Descending inhibition is the inhibitory influence and descending facilitation is the, believe it or not, facilitatory influence. DNIC and DINC mean the same thing – DNIC preferred worldwide, but DINC, is preferred in Australia because we can then say “Fair Dinc”, but both terms actually mean ‘the analgesic effect of one painful stimulus on another’.  I reckon the terms are misleading and unhelpful because they define modulation of pain, not necessarily modulation of nociception.

This paper in PAIN, by Ruth Defrin and mates at Tel Aviv University, investigates the effect of distance between the two painful stimuli on the degree to which one inhibits the other.  They got two hot probes and put one on the front of the left wrist. They then put the second hot probe on one of three other points – 5 cm away on the the same wrist, 30 cm away on the same shoulder, at an identical location on the opposite wrist or on the opposite leg.  The main result was that the further away the second probe was from the first one, the bigger the analgesic effect on the first one. In fact, when the second probe was only 5 cm away, it increased pain cause by the first probe. This is called spatial summation.  There were some interesting secondary results – attention toward EITHER stimulus, made the first one hurt less.  These results tell me that the main mechanism is more likely to be in the brain’s processing of the noxious input.  Although the animal studies on this stuff implicate brain stem neurons that modulate high-level (convergent) spinal neurons, the best data, as far as I can tell, implicate the usual cortical suspects – L1, insula, pre-frontal and cingulate cortices. This tells me that it is not JUST about nociception.

In conclusion, I have one beef and one take-home message: My beef is that I reckon DINC was called DINC by people who thought if it modulates pain it must be by modulating nociception. I would predict if the main mechanism was at the dorsal horn, or even the thalamus, it would not have its greatest effect when the second stimulus is on the opposite foot and it would not be so easily modulated by cognitive factors. Happy to be debated on this point of course.  My take-home message is that if you have a sore finger, it would seem more sensible to stand on your toe than bite your lip.

ResearchBlogging.org

Defrin R, Tsedek I, Lugasi I, Moriles I, & Urca G (2010). The interactions between spatial summation and DNIC: effect of the distance between two painful stimuli and attentional factors on pain perception. Pain, 151 (2), 489-95 PMID: 20822850

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