The authors report a case of a 40-year-old man presenting with chronic pelvic pain due to pudendal nerve entrapment, successfully treated with our body-own analgesic palmitoylethanolamide (PEA). Their hypothesis of its mechanism of action in this ailment is:

PEA may induce relief of neuropathic pain through an action upon receptors located on the nociceptive pathway as well as a more direct action on mast cells via an ALIA (autocoid local injury antagonism) mechanism. ^[1]

They conclude stating that: the present case suggests that PEA could be a valuable pharmacological alternative to the most common drugs (anti-epileptics and antidepressants) used in the treatment of neuropathic pain. 

Autacoid local inflammation antagonism" (ALIA) 

ALIA stands for "autacoid local inflammation antagonism" (ALIA), the above inserted term injury is not totally correct. The Nobelprice winnar professor Rita Levi Montalcini wrote about this topic:

Evidence is provided here supporting the existence of a novel autacoid mechanism negatively modulating mast cell behaviour in response to noxious stimuli in vivo; hence, the denomination "autacoid local inflammation antagonism" (ALIA).

In particular, as lipid amides of the N-acylethanolamine type have been reported to accumulate in tissues in degenerative inflammatory conditions, we examined whether these N-acylated lipids could exert regulatory effects on mast cell activation in vivo.

The results reported show that both long- and short-chain N-acylethanolamines, when systemically administered, are effective in reducing mast cell degranulation induced by local injection of substance P in the ear pinna of developing rats. These and other data suggest that the endogenous production of N-acylethanolamines may constitute a local autocrine/paracrine response for the negative feedback control of mast cell responses to various activating signals. Such a process may be of physio-pathological relevance in the regulation of functional neuro-immune-mast cell interactions..^[2] 

PEA is such an endogenous mediator whose levels are increased following neuroinflammatory or neuropathic conditions in both animals and humans, possibly to exert a local anti-inflammatory and analgesic action.^[3]  

PEA is registered in some European countries as food for medical purposes under the tradename Normast®, and in the Netherlands as a foodsupplement distributed by Ergomax. 

December 2010, Jan M. Keppel Hesselink, MD, PhD

Revised version January 2011, revision July 2011

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