The partial µ-opioid agonist buprenorphine in autism spectrum disorder: a case report.
Attachment
Autism spectrum disorder
Buprenorphine
Opioid
Social cognition
Journal
Journal of medical case reports
ISSN: 1752-1947
Titre abrégé: J Med Case Rep
Pays: England
ID NLM: 101293382
Informations de publication
Date de publication:
15 Apr 2022
15 Apr 2022
Historique:
received:
06
09
2020
accepted:
11
03
2022
entrez:
15
4
2022
pubmed:
16
4
2022
medline:
19
4
2022
Statut:
epublish
Résumé
There are currently no approved medications for impaired social cognition and function, core symptoms of autism spectrum disorder. We describe marked improvement of these symptoms with long-term low-dose administration of the partial µ-opioid agonist buprenorphine. We discuss these observations in the context of a role for endogenous opioid systems in social attachment, and theories integrating those findings mechanistically with autism spectrum disorder. M, a 43-year-old Caucasian male, is medically healthy. Despite social difficulties since childhood, he completed high school with better-than-average grades, but failed university education. A psychiatric evaluation in his twenties diagnosed attention deficit hyperactivity disorder but also noted symptoms of coexisting autism spectrum disorder. M accidentally came across buprenorphine in his late twenties and experienced progressively improved social functioning on a low daily dosage (0.5-1.0 mg/day), an effect maintained for 15 years. He lived independently and maintained a part-time occupation. After abrupt discontinuation of treatment, his autistic symptoms returned, and function deteriorated. Following evaluation by our team, buprenorphine was resumed, with gradual return to prior level of functioning. An attempt to formally evaluate M both on and off medication was agreed with him and approved by the Swedish Ethics Authority, but medication had to be resumed when the patient worsened following discontinuation. According to the µ-opioid receptor balance model, both excessive and deficient μ-receptor activity may negatively influence social behavior, and accordingly both opioid agonist and opioid antagonist treatment may be able to improve social functioning, depending on an individual's opioid tone before treatment. Our case report is consistent with these hypotheses, and given the extensive unmet medical needs in individuals with autism spectrum disorders, randomized controlled trial appears warranted.
Sections du résumé
BACKGROUND
BACKGROUND
There are currently no approved medications for impaired social cognition and function, core symptoms of autism spectrum disorder. We describe marked improvement of these symptoms with long-term low-dose administration of the partial µ-opioid agonist buprenorphine. We discuss these observations in the context of a role for endogenous opioid systems in social attachment, and theories integrating those findings mechanistically with autism spectrum disorder.
CASE PRESENTATION
METHODS
M, a 43-year-old Caucasian male, is medically healthy. Despite social difficulties since childhood, he completed high school with better-than-average grades, but failed university education. A psychiatric evaluation in his twenties diagnosed attention deficit hyperactivity disorder but also noted symptoms of coexisting autism spectrum disorder. M accidentally came across buprenorphine in his late twenties and experienced progressively improved social functioning on a low daily dosage (0.5-1.0 mg/day), an effect maintained for 15 years. He lived independently and maintained a part-time occupation. After abrupt discontinuation of treatment, his autistic symptoms returned, and function deteriorated. Following evaluation by our team, buprenorphine was resumed, with gradual return to prior level of functioning. An attempt to formally evaluate M both on and off medication was agreed with him and approved by the Swedish Ethics Authority, but medication had to be resumed when the patient worsened following discontinuation.
CONCLUSIONS
CONCLUSIONS
According to the µ-opioid receptor balance model, both excessive and deficient μ-receptor activity may negatively influence social behavior, and accordingly both opioid agonist and opioid antagonist treatment may be able to improve social functioning, depending on an individual's opioid tone before treatment. Our case report is consistent with these hypotheses, and given the extensive unmet medical needs in individuals with autism spectrum disorders, randomized controlled trial appears warranted.
Identifiants
pubmed: 35422015
doi: 10.1186/s13256-022-03384-w
pii: 10.1186/s13256-022-03384-w
pmc: PMC9011926
doi:
Substances chimiques
Analgesics, Opioid
0
Buprenorphine
40D3SCR4GZ
Types de publication
Case Reports
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
152Informations de copyright
© 2022. The Author(s).
Références
Psychoneuroendocrinology. 2016 Jan;63:43-9
pubmed: 26409030
J Formos Med Assoc. 2014 Nov;113(11):839-49
pubmed: 25294100
Autism. 2018 Aug;22(6):703-711
pubmed: 28666391
Neurosci Biobehav Rev. 1980 Winter;4(4):473-87
pubmed: 6258111
J Am Acad Child Adolesc Psychiatry. 2008 Aug;47(8):921-9
pubmed: 18645422
Alcohol Clin Exp Res. 2002 Feb;26(2):272-9
pubmed: 11964568
Am J Ment Retard. 2006 May;111(3):199-215
pubmed: 16597187
Psychoneuroendocrinology. 2018 May;91:123-131
pubmed: 29550675
Psychoneuroendocrinology. 2015 Mar;53:10-5
pubmed: 25569708
J Autism Dev Disord. 2017 Sep;47(9):2703-2709
pubmed: 28589494
Neuropsychopharmacology. 2014 Aug;39(9):2049-60
pubmed: 24619243
Lancet Psychiatry. 2016 Aug;3(8):760-773
pubmed: 27475769
Elife. 2018 Nov 16;7:
pubmed: 30444488
J Autism Dev Disord. 2012 Aug;42(8):1592-605
pubmed: 22068820
Addiction. 1993 Jun;88(6):791-804
pubmed: 8329970
Br J Psychiatry. 2016 Dec;209(6):498-503
pubmed: 27388569
Br J Pharmacol. 2018 Jul;175(14):2750-2769
pubmed: 28369738
Cochrane Database Syst Rev. 2013 Aug 20;(8):CD004677
pubmed: 23959778
J Neurosci. 2011 Apr 27;31(17):6362-70
pubmed: 21525276
Neuropsychol Rev. 2008 Dec;18(4):320-38
pubmed: 18956239
J Intellect Disabil Res. 2015 Apr;59(4):293-306
pubmed: 24589346
P T. 2015 Jun;40(6):389-97
pubmed: 26045648
J Child Psychol Psychiatry. 2017 Apr;58(4):439-469
pubmed: 27709604
Int J Neuropsychopharmacol. 2018 Feb 1;21(2):120-127
pubmed: 29025085
Mol Psychiatry. 2014 Jul;19(7):746-7
pubmed: 24514570
Nat Rev Dis Primers. 2020 Jan 16;6(1):5
pubmed: 31949163
Depress Anxiety. 2015 Jul;32(7):527-38
pubmed: 26010478
Drug Alcohol Depend. 2013 Oct 1;132(3):587-96
pubmed: 23660242
Neuropsychopharmacology. 2011 Oct;36(11):2200-10
pubmed: 21734650
Drug Alcohol Depend. 2014 Nov 1;144:1-11
pubmed: 25179217
J Subst Abuse Treat. 2007 Jun;32(4):357-69
pubmed: 17481459
J Autism Dev Disord. 2015 Jun;45(6):1766-73
pubmed: 25475364
Br J Psychiatry. 2016 Mar;208(3):232-8
pubmed: 26541693
Soc Cogn Affect Neurosci. 2016 Dec;11(12):1902-1909
pubmed: 27531386
Eur Psychiatry. 1998;13(1):26-34
pubmed: 19698595
Soc Sci Med. 2021 Dec;291:114497
pubmed: 34710820
Proc Natl Acad Sci U S A. 2008 Apr 1;105(13):5277-81
pubmed: 18378897
J Autism Dev Disord. 2007 Jul;37(6):1155-65
pubmed: 17066307
Appl Health Econ Health Policy. 2017 Apr;15(2):127-137
pubmed: 28194657
Science. 2004 Jun 25;304(5679):1983-6
pubmed: 15218152
Acta Psychiatr Scand. 2017 Jan;135(1):8-28
pubmed: 27624381
J Gen Intern Med. 2001 Sep;16(9):606-13
pubmed: 11556941
Lancet. 2006 Jul 15;368(9531):210-5
pubmed: 16844490
Res Dev Disabil. 2011 Sep-Oct;32(5):1910-7
pubmed: 21515028