Short-term ultramicronized palmitoylethanolamide therapy in patients with myasthenia gravis: A pilot study to possible future implications of treatment

Emanuela Onesti, Vittorio Frasca, Marco Ceccanti, Giorgio Tartaglia, Maria Cristina Gori, Chiara Cambieri, Laura Libonati, Eleonora Palma, Maurizio Inghilleri

Research output: Contribution to journalArticlepeer-review

Abstract

Background: The cannabinoid system may be involved in the humoral mechanisms at the neuromuscular junction. Ultramicronized-palmitoylethanolamide (µm-PEA) has recently been shown to reduce the desensitization of Acetylcholine (ACh)-evoked currents in denervated patients modifying the stability of ACh receptor (AChR) function. Objective: To analyze the possible beneficial effects of µm-PEA in patients with myasthenia gravis (MG) on muscular fatigue and neurophysiological changes. Method: The duration of this open pilot study, which included an intra-individual control, was three weeks. Each patient was assigned to a 1-week treatment period with µm-PEA 600 mg twice a day. A neurophysiological examination based on repetitive nerve stimulation (RNS) of the masseteric and the axillary nerves was performed, and the quantitative MG (QMG) score was calculated in 22 MG patients every week in a three-week follow-up period. AChR antibody titer was investigated to analyze a possible immunomodulatory effect of PEA in MG patients. Results: PEA had a significant effect on the QMG score (p=0.03418) and on RNS of the masseteric nerve (p=0.01763), thus indicating that PEA reduces the level of disability and decremental muscle response. Antibody titers did not change significantly after treatment. Conclusion: According to our observations, µm-PEA as an add-on therapy could improve muscular response to fatigue in MG. The possible modulation of AChR currents as a means of eliciting a direct effect from PEA on the conformation of ACh receptors should be investigated. The co-role of cytokines also warrants an analysis. Given the rapidity and reversibility of the response, we suppose that PEA acts directly on AChR, though further studies are needed to confirm this hypothesis.

Original languageEnglish
Pages (from-to)232-238
Number of pages7
JournalCNS and Neurological Disorders - Drug Targets
Volume18
Issue number3
DOIs
Publication statusPublished - Jan 1 2019

Keywords

  • Endocannabinoid system
  • Myasthenia gravis
  • Neurophysiological
  • Palmitoylethanolamide
  • PEA
  • Ultramicronized-PEA

ASJC Scopus subject areas

  • Neuroscience(all)
  • Pharmacology

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