Tinnitus is an auditory phantom percept with a tone, hissing, or buzzing sound in the absence of any objective physical sound source. Persons with tinnitus engage in a number of health behaviors to manage tinnitus. This can go from prescription medication, masking devices, behavioral training techniques to cortical implants. Potentially less adaptive methods of coping with tinnitus, such as the use of alcohol, are poorly studied. The purpose of this study was to further explore the neurobiological mechanism of tinnitus improvement by the use of alcohol. We observed differences in the alpha, beta and gamma frequency band when comparing resting-state EEG before and after alcohol intake. More precisely increased synchronized alpha1 activity was found in the posterior cingulate cortex and decreased synchronized alpha2 activity was demonstrated in orbitofrontal cortex, ventrolateral prefrontal cortex and subcallosal anterior cingulate cortex after alcohol intake. Increased synchronized activity was found in a region between the pregenual and dorsal anterior cingulate cortex and the left insula for beta and decreased activity in the precuneus after alcohol intake. For the gamma frequency band decreased synchronized activity in the precuneus and the posterior cingulate cortex was demonstrated after alcohol intake. Region of interest analyses in auditory cortices and parahippocampal area revealed however no differences in the different frequency bands before and after alcohol consumption.