Rationale for Use of Palmitoylethanolamide In Neurological Diseases Associated or Not with Pain
Giovanni Antioco Putzu*
Department of Neurology and Clinical Neurophysiology, Cagliari, Italy
Submission: March 12, 2019; Published: March 20, 2019
*Corresponding author: Giovanni Antioco Putzu, Department of Neurology and Clinical Neurophysiology, Casa di Cura Polispecialistica Sant’Elena, Kinetika Sardegna, Korian Group, Viale Marconi 160, 09045 Quartu S’Elena, Cagliari, Italy
How to cite this article: Giovanni Antioco Putzu. Rationale for Use of Palmitoylethanolamide In Neurological Diseases Associated or Not with Pain. Curr Trends Clin Med Imaging. 2019; 2(5): 555604. DOI: 10.19080/CTCMI.2019.02.555604
Opinion
In the last two decades, nutraceutical products have rapidly grown up all around the world, encountering the favour and consent of a great number of patients. Despite the strong evidences of efficacy of nutraceutical products in many conditions, the Scientific Community is somewhat reluctant yet. We agree that idea a natural substance is not harmful may not always be correct. We can give just a few examples to clarify this concept (curare, atropine and so on). Even Ginko Biloba, generally considered safe, may cause intracerebral hemorrhage in some cases. Obviously, this is not the case of Palmitoylethanolamide (PEA) which safety and absence of side effects have ben confirmed in all studies.
PEA is an endogenous lipid modulator available as a nutraceutical product commercialized in many countries worldwide. Inflammatory cells, such as activated mast cells, play an important role, not only in nerve compression syndromes, but also in more severe inflammatory diseases of Central and Peripheral Nervous Systems. Activated mast cells are one of the sources of pro-inflammatory prostaglandins (PGs) and cytokines. Inflammation and endoneurial edema causes neuropathic pain and nerve damage. Efficacy of PEA on pain has been prooved in numerous indexed papers in Scientific Literature. We also demonstrated in a paper published in Archives of Neurology and Neurosurgery in 2016 the efficacy of PEA on cramps and fatigue in Charcot-Marie-Tooth Neuropathy.
We can individuate other possible rational uses of PEA, in example in the remitting phase of acute Guillain-Barré Syndrome (GBS) or in subacute/chronic GBS. The aim should be to counteract pain and inflammation. Vasculitis of PNS is another condition in which PEA could be administered in association with immunosuppressant drugs during acute phase, alone or in association with other nutraceutical/neurotrophic substances in the healing phase of the disease.
Even in spine surgery PEA may have indications. We are currently using PEA at the dosage of 1200 mg per day 2 weeks prior surgery to prevent ex vacuo medullar edema in decompression of stenosis since many years. We did not observe cases of post-surgical medullar edema anymore (data not published). All the cases of post-surgical medullar edema were observed prior the prophylactical use of PEA. We treated a post-surgical paraparesis with high dosage of PEA (2400 mg per day) in a young female patient. Fortunately, she recovered within a few months. We agree that this is an anecdotal case and more studies must be performed. Bell’s paralysis of VII cranial nerve is another condition in which PEA may be of benefit.
In conclusion, PEA may be a valuable nutraceutical product alone in mild conditions or in association with pharmaceutical conventional drugs (pregabaline, corticosteroids, immunosuppressant) in more severe diseases. Multicentric and double-blind studies have to be performed at larger scale in many of the above cited conditions. We are confident that this will be done in the future and PEA will be available in countries where nowadays this nutraceutical is not commercialized yet.