Cognitive related electrophysiological changes induced by non-invasive cortical electrical stimulation in crack-cocaine addiction.
Prefrontal dysfunction is a hallmark in drug addiction, yet interventions exploring modulation of prefrontal cortex function in drug addiction have not been fully investigated with regard to physiological alterations. We tested the hypothesis that non-invasive prefrontal stimulation would change neural activity in crack-cocaine addiction, investigating the effects of transcranial Direct Current Stimulation (tDCS) of Dorsolateral Prefrontal Cortex (DLPFC) induced cortical excitability modulation on the visual P3 Event Related Potentials (ERP) component under neutral and drug cue exposition in crack-cocaine addicts. Thirteen crack-cocaine users were randomly distributed to receive five applications (once a day, every other day) of bilateral (left cathodal/right anodal) tDCS (20 min, 2 mA, 35 cm2) or sham tDCS over the DLPFC. Brain activity was measured under crack-related or neutral visual-cued ERPs. There were significant differences in P3-related parameters when comparing group of stimulation (active vs. sham tDCS) and number of sessions (single vs. repetitive tDCS). After a single session of tDCS, P3 current intensity in the left DLPFC increased during neutral cues and decreased during crack-related cues. This effect was opposite to what was observed in the sham-tDCS group. In contrast, repetitive tDCS increased current density not only in the DLPFC, but also in a wider array of prefrontal areas, including presumably the frontopolar cortex (FPC) orbitofrontal cortex (OFC) and anterior cingulate cortex (ACC), when subjects were visualizing crack-related cues. Thus, single and repetitive application of tDCS can impact cognitive processing of neutral and especially crack-related visual cues in prefrontal areas, which may be of importance for treatment of crack-cocaine addiction.
Laboratory of Cognitive Sciences and Neuropsychopharmacology, Program of Post-Graduation in Physiological Sciences,Federal University of Espírito Santo,Vitória-ES,Brazil.
Catarine Lima
CL
Conti
Laboratory of Cognitive Sciences and Neuropsychopharmacology, Program of Post-Graduation in Physiological Sciences,Federal University of Espírito Santo,Vitória-ES,Brazil.
Janine Andrade
JA
Moscon
Laboratory of Neuromodulation, Department of Physical Medicine & Rehabilitation and Massachusetts General Hospital, Spauding Rehabilitation Hospital,Harvard Medical School,Boston, MA,USA.
Felipe
F
Fregni
Laboratory of Neuroplasticity, University Medical Center, Clinic for Clinical Neurophysiology,Georg-August-University,Göttingen,Germany.
Michael Andreas
MA
Nitsche
Laboratory of Cognitive Sciences and Neuropsychopharmacology, Program of Post-Graduation in Physiological Sciences,Federal University of Espírito Santo,Vitória-ES,Brazil.
Ester Miyuki
EM
Nakamura-Palacios
D000293:Adolescent; D000328:Adult; D001703:Biophysics; D019970:Cocaine-Related Disorders / Q000150:complications*; D003071:Cognition / Q000502:physiology*; D016578:Crack Cocaine / Q000009:adverse effects*; D003463:Cues; D004569:Electroencephalography; D018913:Event-Related Potentials, P300 / Q000502:physiology; D005260:Female; D006179:Gyrus Cinguli / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D009483:Neuropsychological Tests; D010775:Photic Stimulation; D017397:Prefrontal Cortex / Q000502:physiology*; D065908:Transcranial Direct Current Stimulation / Q000379:methods*; D055815:Young Adult
D016578:Crack Cocaine