Front Psychiatry. 2016 Aug 08;7:133. doi: 10.3389/fpsyt.2016.00133. eCollection 2016.
Bilateral Transcranial Magnetic Stimulation of the Prefrontal Cortex Reduces Cocaine Intake: A Pilot Study.
Frontiers in psychiatry
Corinna Bolloni, Riccardo Panella, Mariano Pedetti, Anna Grazia Frascella, Cristiana Gambelunghe, Tommaso Piccoli, Giuseppe Maniaci, Anna Brancato, Carla Cannizzaro, Marco Diana
Affiliations
Affiliations
- Department of Experimental Biomedicine and Clinical Neuroscience, University of Palermo , Palermo , Italy.
- Laboratory of Cognitive Neuroscience 'G. Minardi', University of Sassari , Sassari , Italy.
- Ser.T, 'Health's House n.1', A.S.L. No. 1 Umbria , Perugia , Italy.
- Legal Medicine, Forensic Science and Sports Medicine Section, Department of Surgical and Biomedical Science, University of Perugia , Perugia , Italy.
- Department of Health Promotion and Maternal Care 'G. D'Alessandro' University of Palermo , Palermo , Italy.
- Laboratory of Cognitive Neuroscience 'G. Minardi', Department of Chemistry and Pharmacy, University of Sassari , Sassari , Italy.
PMID: 27551268
PMCID: PMC4976094 DOI: 10.3389/fpsyt.2016.00133
Abstract
BACKGROUND: Chronic cocaine consumption is associated with a decrease in mesolimbic dopamine transmission that maintains drug intake. transcranial magnetic stimulation (TMS) is gaining reliability, a useful therapeutic tool in drug addiction, since it can modulate cortico-limbic activity resulting in reduction of drug craving.
AIMS: In the present study, we investigated the therapeutic effect of bilateral TMS of prefrontal cortex (PFC) in reducing cocaine intake, in a sample of treatment-seeking patients with current cocaine use disorder (DSM-V).
METHODS: Ten cocaine addicts (DSM-V) were randomly assigned to the active or sham stimulation protocol in a double-blind experimental design. Twelve repetitive TMS (rTMS) sessions were administered three times a week for 4 weeks at 100% of motor threshold, over bilateral PFC. Cocaine intake (ng/mg) was assessed by hair analysis at baseline (before treatment, T0), after 1 month (end of treatment, T1), 3 (T2), and 6 (T3) months later. All subjects received psychological support weekly.
RESULTS: The two-way ANOVA for repeated measures did not show a significant effect of the interaction between time and treatment (F 4,32 = 0.35; p = 0.87). Despite that result indicated no difference in the effect of the two conditions (active vs. sham) along time, a decreasing trend in cocaine consumption in active TMS group (F 3,23 = 3.42; p = 0.04) vs. sham (F 3,15 = 1.88; p = 0.20) was observed when we performed exploratory analysis with time as factor. Indeed, Post hoc comparisons showed a significant reduction in the amount of cocaine detected from the onset to 3 months later (T0-T2; p = 0.02) and to the end of treatment (T0-T3; p = 0.01) in addicts from the active group.
CONCLUSION: Bilateral rTMS of PFC at 10 Hz did not show a significant effect on cocaine intake compared to sham. However, a long-term reduction on cocaine intake in active TMS-treated patients was observed when we considered the time as factor. Further studies are required to confirm these encouraging but preliminary findings, in order to consolidate rTMS as a valid tool to treat cocaine addiction.
Keywords: PFC; cocaine use disorder; dopamine; rTMS
References
- Curr Pharm Des. 2010;16(19):2159-18 - PubMed
- Addiction. 2010 Jan;105(1):49-55 - PubMed
- Neuroreport. 2007 Feb 12;18(3):289-92 - PubMed
- Clin Neurophysiol. 2005 Apr;116(4):775-9 - PubMed
- Int J Addict. 1992 Jan;27(1):51-69 - PubMed
- Neurosci Biobehav Rev. 2010 Mar;34(4):559-74 - PubMed
- J Toxicol Clin Toxicol. 2001;39(4):361-6 - PubMed
- Electroencephalogr Clin Neurophysiol. 1998 Jan;108(1):1-16 - PubMed
- Forensic Sci Int. 2009 Aug 10;189(1-3):24-7 - PubMed
- Eur J Pharmacol. 1992 Oct 20;221(2-3):227-34 - PubMed
- Clin Neurophysiol. 2009 Dec;120(12):2008-39 - PubMed
- Drug Alcohol Depend. 2007 Jan 5;86(1):91-4 - PubMed
- J Appl Toxicol. 2005 May-Jun;25(3):205-11 - PubMed
- Clin Neurophysiol. 2014 Feb;125(2):336-43 - PubMed
- Neuron. 2005 Jan 20;45(2):201-6 - PubMed
- Nat Neurosci. 2005 Nov;8(11):1442-4 - PubMed
- Nat Rev Neurosci. 2011 Oct 20;12(11):652-69 - PubMed
- Int Rev Neurobiol. 2005;63:101-54 - PubMed
- Forensic Sci Int. 2005 Nov 25;154(2-3):96-8 - PubMed
- Ann N Y Acad Sci. 2014 Oct;1327:79-93 - PubMed
- Neuropsychopharmacology. 2010 Jan;35(1):217-38 - PubMed
- Brain Stimul. 2009 Oct;2(4):188-200 - PubMed
- Am J Psychiatry. 2007 Apr;164(4):622-9 - PubMed
- Eur Neuropsychopharmacol. 2016 Jan;26(1):37-44 - PubMed
- Forensic Sci Int. 1995 Jan 5;70(1-3):63-76 - PubMed
- Nature. 1997 Apr 24;386(6627):830-3 - PubMed
- Neuropsychopharmacology. 2012 Jan;37(1):163-77 - PubMed
- Forensic Sci Int. 2012 May 10;218(1-3):20-4 - PubMed
- Biol Psychiatry. 2014 Nov 1;76(9):742-9 - PubMed
- Am J Addict. 2008 Jul-Aug;17(4):345-6 - PubMed
- J Neurosci. 2001 Aug 1;21(15):RC157 - PubMed
- Subst Use Misuse. 2013 Aug 7;:null - PubMed
- J Clin Neurophysiol. 2007 Feb;24(1):31-8 - PubMed
- Front Psychiatry. 2011 Nov 29;2:64 - PubMed
- Addiction. 2009 Apr;104(4):653-60 - PubMed
- Front Psychiatry. 2013 Jun 03;4:40 - PubMed
- Nat Med. 2012 Apr 05;18(4):502-3 - PubMed
- Neuropsychopharmacology. 2008 Sep;33(10):2517-23 - PubMed
- World Psychiatry. 2015 Feb;14(1):64-73 - PubMed
- Lancet. 1985 May 11;1(8437):1106-7 - PubMed
- N Engl J Med. 2016 Jan 28;374(4):363-71 - PubMed
- Can J Physiol Pharmacol. 2015 Apr;93(4):283-90 - PubMed
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