AIM: Carpal tunnel syndrome (CTS) is a medical condition in which the median nerve is compressed, leading to discomfort and pain. Palmitoylethanolamide (PEA) is an endogenous fatty acid amide, able to modulate inflammatory cell reactivity and pain. This study deals with the capability of PEA to normalize the electroneurographic alterations associated with moderate CTS. METHODS:Patients displaying moderate CTS were enrolled and daily PEA (600 mg or 1 200 mg/die) was administered for 30 days. Control group received no treatment. RESULTS:PEA treatment significantly improved the CTS-induced reduction of median nerve latency time (P<0.0004); PEA effect was dose-dependent. Tinel's sign presence and symptoms of discomfort were also reduced. CONCLUSION: Although further studies are needed to better characterize PEA effect, the present report represents the first evidence on the improvement of distal motor latency elicited by PEA in patients with moderate CTS. The data support the hypothesis of protection against inflammatory and neuropathic pain by PEA.
RCT Entities:
AIM: Carpal tunnel syndrome (CTS) is a medical condition in which the median nerve is compressed, leading to discomfort and pain. Palmitoylethanolamide (PEA) is an endogenous fatty acid amide, able to modulate inflammatory cell reactivity and pain. This study deals with the capability of PEA to normalize the electroneurographic alterations associated with moderate CTS. METHODS:Patients displaying moderate CTS were enrolled and daily PEA (600 mg or 1 200 mg/die) was administered for 30 days. Control group received no treatment. RESULTS:PEA treatment significantly improved the CTS-induced reduction of median nerve latency time (P<0.0004); PEA effect was dose-dependent. Tinel's sign presence and symptoms of discomfort were also reduced. CONCLUSION: Although further studies are needed to better characterize PEA effect, the present report represents the first evidence on the improvement of distal motor latency elicited by PEA in patients with moderate CTS. The data support the hypothesis of protection against inflammatory and neuropathic pain by PEA.
Authors: Stephen D Skaper; Laura Facci; Mariella Fusco; Maria Federica Della Valle; Morena Zusso; Barbara Costa; Pietro Giusti Journal: Inflammopharmacology Date: 2013-11-01 Impact factor: 4.473