At the Third International Congress on Neuropathic Pain, Athens, Greece, May 27 – 30, 2010 A. Biasiotta, S. et al presented a poster which demonstrated a clinical relevant and electrophysiological measurable effect from a rather unknown compound, in some European countries registered as food for medical purposes, a body own molecule, palmitoylethanolamide (PEA, Normast©).

Palmitoylethanolamide in neuropathic pain 

In the introduction they refered to the fact that recent studies suggest that inflammation and mast cell activity play a crucial role inthe pathophysiology of neuropathic pain. Palmitoylethanolamide is a body-own molecule, which, based on in vivo findings, inhibits mast cell activity, in addition to various relevant other mechanisms of action, such as its high affinity to the TRPV1 and PPAR-gamma receptors. ^[1]

The researchers assessed the efficacy and safety ofpalmitoylethanolamide in painful neuropathy. Thirty drug naïve patients with painful neuropathy were included and treated with 600 mg palmitoylethanolamide/day.

They clinically investigated sensory disturbances and pain, using the 11-point Lickert numerical rating scale in 20 patients before and after treatment with palmitoylethanolamide. Furthermore they investigated non-nociceptive fibre function by nerve conduction study and nociceptive fibre function by laser evoked potentials.

Both neuropathic pain and positive sensory symptoms significantly improved after treatment (P < 0.01), and clear trends in amplitude changes of suraland ulnar sensory nerve action potential and foot and hand LEPs were documented(P < 0.06).

Their preliminary findings suggest that palmitoylethanolamide may improve nerve function and reduce neuropathic pain.^[2]

In our clinic we treated many patients with PEA and we could also duplicate these findings: for instance in one of our CIAP patients the neuropathic pain decreased significantly and the nerve velocity increased by 15 m/sec.

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

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