18 September 2009

Why papercuts hurt so damn much

During my bimonthly rereading of Price's Psychological Mechanisms of Pain and Analgesia, I ran across this in the middle of a discussion of the relationship between tissue damage and pain intensity:

the rate of tissue damage is a direct function of protein in activation that, in turn, is a function of temperature. However, the amount of tissue damage is a function of both skin temperature and duration of stimulation. Since heat-induced pain depends only on the temperature attained by the cells of the skin and on duration of stimulation, pain intensity follows the rate of tissue damage and not its total amount. One consequence of this phenomenon is that some extensive wounds may be less painful than slight wounds. Pain from tissues that have suddenly become inflamed, such as a toothache, is an example." [Page 11; italics original]

A role for glial cell-targeting treatments for pain?

The Psychology of Pain blog links to an interesting new study from CU-Boulder. I don't want to steal too much of his post, so here's a tease:
Under normal circumstances glial cells are thought to be like housekeepers, said Watkins. They essentially clean up debris and provide support for neurons.

But, like Gremlins, they have a nasty side too
[the researchers] believe they have figured out how morphine affects glial cells and neurons. 'We've found that different receptors are involved in how morphine suppresses pain through its actions on neurons versus how morphine activates glial cells,' Watkins said. 'What this means is that you should be able to separate the suppressive effects of morphine -- its pain-reducing effects through its action on neurons -- from all of its bad effects when it excites glial cells.'

(Via Psychology of Pain.)