In a new review article (2013) Dr Skraper regfers to PEA as a Broad-Acting Anti-inflammatory and Neuroprotective Lipid Mediator. He discusses all data related to PEA over the last decade and concludes:
The capacity of PEA to modulate the protective responses of animals during inflammation and pain led to the hypothesis that endogenous PEA may be a component of the complex homeostatic system controlling the basal threshold of both inflammation and pain. The production of PEA during inflammatory conditions supports this role, and emerging data that selective inhibition of PEA degradation is antiinflammatory provides more direct evidence for the involvement of PEA in the control of pain and inflammation. As an endogenous compound, PEA has no adverse effects at pharmacological doses, while possessing a double therapeutic effect (i.e., anti-inflammatory and anti-nociceptive).
His final summary is:
PEA, its analogues, and agents that inhibit specifically its degradation are likely to result in the development of new therapeutic strategies for the treatment of pathological conditions where neuroinflammation is a factor
Source: Skaper SD, Facci L, Giusti P. Glia and Mast Cells as Targets for Palmitoylethanolamide, an Anti-inflammatory and Neuroprotective Lipid Mediator. Mol Neurobiol. 2013 Jun 28.