High-dose ethanol intoxication decreases 1/f neural noise or scale-free neural activity in the resting state.

Binge drinking is a frequent phenomenon in many western societies and has been associated with an increased risk of developing alcohol use disorder later in life. Yet, the effects of high-dose alcohol intoxication on neurophysiological processes are still quite poorly understood. This is particularly the case given that neurophysiological brain activity not only contains recurring (oscillatory) patterns of activity, but also a significant fraction of "scale-free" or arrhythmic dynamics referred to as 1/f type activity, pink noise, or 1/f neural noise. Neurobiological considerations suggest that it should be modulated by alcohol intoxication. To investigate this assumption, we collected resting state EEG data from n = 23 healthy young male subjects in a crossover design, where each subject was once tested sober and once tested while intoxicated (mean breath alcohol concentration of 1.1 permille ±0.2). Analyses of the 1/f neural dynamics showed that ethanol intoxication decreased resting state 1/f neural noise, as compared with a sober state. The effects were strongest when the eyes were closed and particularly reliable in the beta frequency band. Given that the dynamics of the beta band have been shown to strongly depend on GABAA receptor neural transmission, this finding nicely aligns with the fact that ethanol increases GABAergic signaling. The study reveals a currently unreported effect of binge drinking on neurophysiological dynamics, which likely revealed a higher sensitivity for ethanol effects than most commonly considered measures of power in neural oscillations. Implications and applicability of these findings are discussed.

The Modulation of Neural Noise Underlies the Effectiveness of Methylphenidate Treatment in Attention-Deficit/Hyperactivity Disorder.

BACKGROUND: Various lines of research suggest that the stability of neural processes is low in attention-deficit/hyperactivity disorder (ADHD). Considering overarching neural principles, this lack of stability relates to increased levels of neural noise. However, no study has directly examined neural noise in ADHD. Likewise, it is unknown whether the modulation of neural noise reflects a mechanistic link as to why methylphenidate (MPH) is effective in treating impulsivity in ADHD. METHODS: We compared neural noise between 29 juvenile patients with ADHD and 32 healthy control subjects and examined the effects of MPH. We examined 1/f neural noise of electroencephalogram data collected while participants performed a response inhibition (Go/NoGo) task. RESULTS: Specific during NoGo trials, children with ADHD showed more neural noise than healthy control subjects. This was especially the case with regard to the theta frequency band, which is very closely related to cognitive control. MPH treatment reduced neural noise in ADHD to the level of healthy control subjects. Correlational analyses showed a direct relationship between decreases in neural noise and increases in behavioral performance. Mechanistically, this can be explained by the MPH-induced increase in dopaminergic neurotransmission that enhances the signal-to-noise ratio in neural networks and thus reduces neural noise. CONCLUSIONS: This study is the first to demonstrate increased (pink) neural noise in patients with ADHD and its reduction through MPH treatment. The study reveals an important mechanistic link as to why MPH is effective in treating impulsivity in ADHD.

On the interrelation of 1/f neural noise and norepinephrine system activity during motor response inhibition.

Several lines of evidence suggest that there is a close interrelation between the degree of noise in neural circuits and the activity of the norepinephrine (NE) system, yet the precise nexus between these aspects is far from being understood during human information processing and cognitive control in particular. We examine this nexus during response inhibition in n = 47 healthy participants. Using high-density EEG recordings, we estimate neural noise by calculating "1/f noise" of those data and integrate these EEG parameters with pupil diameter data as an established indirect index of NE system activity. We show that neural noise is reduced when cognitive control processes to inhibit a prepotent/automated response are exerted. These neural noise variations were confined to the theta frequency band, which has also been shown to play a central role during response inhibition and cognitive control. There were strong positive correlations between the 1/f neural noise parameter and the pupil diameter data within the first 250 ms after the Nogo stimulus presentation at centro-parietal electrode sites. No such correlations were evident during automated responding on Go trials. Source localization analyses using standardized low-resolution brain electromagnetic tomography show that inferior parietal areas are activated in this time period in Nogo trials. The data suggest an interrelation of NE system activity and neural noise within early stages of information processing associated with inferior parietal areas when cognitive control processes are required. The data provide the first direct evidence for the nexus between NE system activity and the modulation of neural noise during inhibitory control in humans. NEW & NOTEWORTHY This is the first study showing that there is a nexus between norepinephrine system activity and the modulation of neural noise or scale-free neural activity during inhibitory control in humans. It does so by integrating pupil diameter data with analysis of EEG neural noise.