[1]
Gilhus NE, Verschuuren JJ. Myasthenia gravis: subgroup classification and therapeutic strategies. Lancet 2015; 14: 1023-36.
[2]
Sanders DB, Wolfe GI, Benatar M. International consensus guidance for management of myasthenia gravis: executive summary. Neurology 2016; 87(4): 419-25.
[3]
Turkanis SA, Karler R. Changes in neurotransmitter release at a neuromuscular junction of the lobster caused by cannabinoids. Neuropharmacology 1988; 27(7): 737-42.
[4]
Sánchez-Pastor E, Trujillo X, Huerta M, Andrade F. Effects of cannabinoids on synaptic transmission in the frog neuromuscular junction. J Pharmacol Exp Ther 2007; 321(2): 439-45.
[5]
Iannotti FA, Di Marzo V, Petrosino S. Endocannabinoids and endocannabinoid-related mediators: targets, metabolism and role in neurological disorders. Prog Lipid Res 2016; 62: 107-28.
[6]
Turcotte C, Blanchet MR, Laviolette M, Flamand N. The CB2 receptor and its role as a regulator of inflammation. Cell Mol Life Sci 2016; 73(23): 4449-70.
[7]
Petrosino S, Di Marzo V. The pharmacology of palmitoylethanolamide and first data on the therapeutic efficacy of some of its new formulations. Br J Pharmacol 2017; 174(11): 1349-65.
[8]
Hansen HS. Palmitoylethanolamide and other anandamide congeners. Proposed role in the diseased brain. Exp Neurol 2010; 224(1): 48-55.
[9]
Freitag CM, Miller RJ. Peroxisome proliferator-activated receptor agonists modulate neuropathic pain: a link to chemokines? Front Cell Neurosci 2014; 8: 238.
[10]
Skaper SD, Facci L, Fusco M. Palmitoylethanolamide, a naturally occurring disease-modifying agent in neuropathic pain. Inflammopharmacology 2014; 22(2): 79-94.
[11]
Paladini A, Fusco M, Cenacchi T, Schievano C, Piroli A, Varrassi G. Palmitoylethanolamide, a special food for medical purposes, in the treatment of chronic pain: a pooled data meta-analysis. Pain Physician 2016; 19(2): 11-24.
[12]
Skaper SD, Facci L, Barbierato M, et al. N-Palmitoylethanolamine and neuroinflammation: a novel therapeutic strategy of resolution. Mol Neurobiol 2015; 52: 1034-42.
[13]
Palma E, Reyes-Ruiz JM, Lopergolo D, et al. Acetylcholine receptors from human muscle as pharmacological targets for ALS therapy. Proc Natl Acad Sci USA 2016; 113(11): 3060-5.
[14]
Di Marzo V, Melck D, Bisogno T, De Petrocellis L. Endocannabinois: endogenous cannabinoid receptor ligands with neuromodulatory action. Trends Neurosci 1998; 21: 521-8.
[15]
Di Marzo V, Deutsch DG. Biochemistry of the endogenous ligands of cannabinoid receptors. Neurobiol Dis 1998; 5: 386-404.
[16]
Croxford JL, Yamamura T. Cannabinoids and the immune system: potential for the treatment of inflammatory diseases? J Neuroimmunol 2005; 166(1-2): 3-18.
[17]
Salzet M, Breton C, Bisogno T, Di Marzo V. Comparative biology of the endocannabinoid system. Possible role in the immune response. Eur J Biochem 2000; 267: 4917-27.
[18]
Kharraz Y, Guerra J, Mann CJ, Serrano AL, Muñoz-Cánoves P. Macrophage plasticity and the role of inflammation in skeletal muscle repair. Mediators Inflamm 2013; 2013: 491-7.
[19]
Jaretzki A, Barohn RJ, Ernstoff RM. Myasthenia gravis: recommendations for clinical research standards. Task Force of the medical scientific advisory board of the myasthenia gravis foundation of America. Ann Thorac Surg 2000; 70(1): 327-34.
[20]
Bedlack RS, Simel DL, Bosworth H, Samsa G, Tucker-Lipscomb B, Sanders DB. Quantitative myasthenia gravis score: assessment of responsiveness and longitudinal validity. Neurology 2005; 64(11): 1968-70.
[21]
Pavesi G, Cattaneo L, Tinchelli S, Mancia D. Masseteric repetitive nerve stimulation in the diagnosis of myasthenia gravis. Clin Neurophysiol 2011; 112(6): 1064-9.
[22]
Kimura J. Electrodiagnosis in diseases of the nerve and muscle: principles and practice 3rd ed Philadelphia PA: Davis. 1989.
[23]
Orefice NS, Alhouayek M, Carotenuto A. Oral Palmitoylethanolamide treatment is associated with reduced cutaneous adverse effects of Interferon-β1a and circulating proinflammatory cytokines in relapsing-remitting Multiple Sclerosis. Neurotherapeutics 2016; 13(2): 428-38.
[24]
Caltagirone C, Cisari C, Schievano C, et al. Stroke study group Stroke study group. Co-ultramicronized Palmitoylethanolamide/Luteolin in the treatment of cerebral ischemia: from rodent to man. Transl Stroke Res 2016; 7(1): 54-69.
[25]
Brotini S, Schievano C, Guidi L. Ultra-micronized palmitoylethanolamide: an efficacious adjuvant therapy for Parkinson’s disease. CNS Neurol Disord Drug Targets 2017; 16(6): 705-13.
[26]
Esposito E, Paterniti I, Mazzon E, et al. Effects of palmitoylethanolamide on release of mast cell peptidases and neurotrophic factors after spinal cord injury. Brain Behav Immun 2011; 25(6): 1099-112.
[27]
D’Agostino G, Russo R, Avagliano C, Cristiano C, Meli R, Calignano A. Palmitoylethanolamide protects against the amyloid-β25-35-induced learning and memory impairment in mice, an experimental model of Alzheimer disease. Neuropsychopharmacology 2012; 37(7): 1784-92.
[28]
Costa B, Comelli F, Bettoni I, Colleoni M, Giagnoni G. The endogenous fatty acid amide, palmitoylethanolamide, has anti-allodynic and anti-hyperalgesic effects in a murine model of neuropathic pain: involvement of CB(1), TRPV1 and PPARgamma receptors and neurotrophic factors. Pain 2008; 139(3): 541-50.
[29]
De Filippis D, Luongo L, Cipriano M, et al. Palmitoylethanolamide reduces granuloma-induced hyperalgesia by modulation of mast cell activation in rats. Mol Pain 2011; 7: 3.
[30]
Di Cesare Mannelli L, D’Agostino G, Pacini A, et al. Palmitoylethanolamide is a disease-modifying agent in peripheral neuropathy: pain relief and neuroprotection share a PPAR-alpha-mediated mechanism. Mediators Inflamm 2013; 328797.
[31]
Bettoni I, Comelli F, Colombo A, Bonfanti P, Costa B. Non-neuronal cell modulation relieves neuropathic pain: efficacy of the endogenous lipid palmitoylethanolamide. CNS Neurol Disord Drug Targets 2013; 12(1): 34-44.
[32]
Impellizzeri D, Bruschetta G, Cordaro M, et al. Micronized/ultramicronized palmitoylethanolamide displays superior oral efficacy compared to nonmicronized palmitoylethanolamide in a rat model of inflammatory pain. J Neuroinflammation 2014; 11: 136.
[33]
Facci L, Dal Toso R, Romanello S, Buriani A, Skaper SD, Leon A. Mast cells express a peripheral cannabinoid receptor with differential sensitivity to anandamide and palmitoylethanolamide. Proc Natl Acad Sci USA 1995; 92(8): 3376-80.
[34]
Paterniti I, Cordaro M, Campolo M, et al. Neuroprotection by association of palmitoylethanolamide with luteolin in experimental Alzheimer’s disease models: the control of neuroinflammation. CNS Neurol Disord Drug Targets 2014; 13(9): 1530-41.
[35]
Petrosino S, Schiano Moriello A, Cerrato S. The anti-inflammatory mediator palmitoylethanolamide enhances the levels of 2-arachidonoyl-glycerol and potentiates its actions at TRPV1 cation channels. Br J Pharmacol 2016; 173(7): 1154-62.
[36]
Vacondio F, Bassi M, Silva C. Amino acid derivatives as Palmitoylethanolamide prodrugs: synthesis, in vitro metabolism and in vivo plasma profile in rats. PLoS One 2015; 10(6): e0128699.
[37]
Clemente S. Amyotrophic lateral sclerosis treatment with ultramicronized palmitoylethanolamide: a case report. CNS Neurol Disord Drug Targets 2012; 11(7): 933-6.
[38]
Colón-Sáez JO, Yakel JL. The α7 nicotinic acetylcholine receptor function in hippocampal neurons is regulated by the lipid composition of the plasma membrane. J Physiol 2011; 589(Pt 13): 3163-74.
[39]
Trujillo X, Sánchez-Pastor E, Andrade F, Huerta M. Presence and colocalization of type-1 cannabinoid receptors with Acetylcholine receptors in the motor end-plate of twitch skeletal muscle fibers in the frog. J Membr Biol 2014; 247(11): 1199-205.
[40]
Stella N. Cannabinoid and cannabinoid-like receptors in microglia, astrocytes, and astrocytomas. Glia 2010; 58(9): 1017-30.
[41]
Silveira PE, Silveira NA, Morini Vde C, Kushmerick C, Naves LA. Opposing effect of cannabinoids and vanilloids on evoked quantal release at the frog neuromuscular junction. Neurosci Lett 2010; 473(2): 97-101.
[42]
Newman Z, Malik P, Wu TY, Ochoa C, Watsa N, Lindgren C. Endocannabinoids mediate muscarine-induced synaptic depression at the vertebrate neuromuscular junction. Eur J Neurosci 2007; 25(6): 1619-30.
[43]
Uzawa A, Kawaguchi N, Himuro K, Kanai T, Kuwabara S. Serum cytokine and chemokine profiles in patients with myasthenia gravis. Clin Exp Immunol 2014; 176: 232-7.
[44]
Roche JC, Capablo JL, Larrad L, et al. Increased serum interleukin-17 levels in patients with myasthenia gravis. Muscle Nerve 2011; 44(2): 278-80.
[45]
Yilmaz V, Oflazer P, Aysal F, et al. B cells produce less IL-10, IL-6 and TNF-α in myasthenia gravis. Autoimmunit 2015; 48: 201-7.
[46]
Oh S, Eslami N, Nishihira T, Sarala PK. Electrophysiological and clinical correlation in myasthenia gravis. Ann Neurol 1982; 12: 348-54.
39
1