Rhythmic auditory cues shape neural network recruitment in Parkinson's disease during repetitive motor behavior.

It is well established clinically that rhythmic auditory cues can improve gait and other motor behaviors in Parkinson's disease (PD) and other disorders. However, the neural systems underlying this therapeutic effect are largely unknown. To investigate this question we scanned people with PD and age-matched healthy controls using functional magnetic resonance imaging (fMRI). All subjects performed a rhythmic motor behavior (right hand finger tapping) with and without simultaneous auditory rhythmic cues at two different speeds (1 and 4 Hz). We used spatial independent component analysis (ICA) and regression to identify task-related functional connectivity networks and assessed differences between groups in intra- and inter-network connectivity. Overall, the control group showed greater intra-network connectivity in perceptual and motor related networks during motor tapping both with and without rhythmic cues. The PD group showed greater inter-network connectivity between the auditory network and the executive control network, and between the executive control network and the motor/cerebellar network associated with the motor task performance. We interpret our results as indicating that the temporal rhythmic auditory information may assist compensatory mechanisms through network-level effects, reflected in increased interaction between auditory and executive networks that in turn modulate activity in cortico-cerebellar networks.

Smokers exhibit biased neural processing of smoking and affective images.

OBJECTIVE: There has been growing interest in the role that implicit processing of drug cues can play in motivating drug use behavior. However, the extent to which drug cue processing biases relate to the processing biases exhibited to other types of evocative stimuli is largely unknown. The goal of the present study was to determine how the implicit cognitive processing of smoking cues relates to the processing of affective cues using a novel paradigm. METHOD: Smokers (n = 50) and nonsmokers (n = 38) completed a picture-viewing task, in which participants were presented with a series of smoking, pleasant, unpleasant, and neutral images while engaging in a distractor task designed to direct controlled resources away from conscious processing of image content. Electroencephalogram recordings were obtained throughout the task for extraction of event-related potentials (ERPs). RESULTS: Smokers exhibited differential processing of smoking cues across 3 different ERP indices compared with nonsmokers. Comparable effects were found for pleasant cues on 2 of these indices. Late cognitive processing of smoking and pleasant cues was associated with nicotine dependence and cigarette use. CONCLUSIONS: Results suggest that cognitive biases may extend across classes of stimuli among smokers. This raises important questions about the fundamental meaning of cognitive biases, and suggests the need to consider generalized cognitive biases in theories of drug use behavior and interventions based on cognitive bias modification. (PsycINFO Database Record

Nicotine-induced cortical activation among nonsmokers with moderation by trait cognitive control.

RATIONALE: Considerable research suggests that nicotine enhances cognitive control-related processes (e.g., attention, memory) among nicotine-deprived smokers, both in terms of behavior and neural indices (e.g., ERP, slow-wave EEG). Nicotine may also increase cognitive control among nonsmokers, and this may vary as a function of trait cognitive control. It is important to examine the effects of nicotine on cognitive control-related processes among nonsmokers as these effects may provide a path for the initiation of smoking. OBJECTIVES: The objectives of the study were to examine in nonsmokers (1) the effect of nicotine on resting cortical activity, an indirect measure of cognitive control, and (2) trait cognitive control as a moderator of nicotine-induced cortical activity changes. METHOD: Eighty participants were given placebo and 7-mg nicotine patches in separate sessions for this counter-balanced, double-blind, within-subject study. Resting cortical activity was measured with EEG for a 3-min period with eyes opened. RESULTS: Average alpha-1 band power density values in frontal and central regions were lower during the nicotine versus placebo condition, which provides evidence of nicotine-induced cortical activation. Furthermore, those with lower self-reported cognitive control exhibited greater nicotine-induced reductions in alpha-1 power density values. CONCLUSIONS: These individual differences in nicotine-induced cortical activation are consistent with a model of nicotine self-medication whereby individuals with lower cognitive control may find smoking more reinforcing via amelioration of related cognitive deficits.

7 mg nicotine patch fails to enhance P300 neural indices of cognitive control among nonsmokers.

Nicotine administration facilitates and nicotine deprivation reduces cognitive control in smokers. Importantly, nicotine effects on cognition may reinforce smoking behavior, especially among individuals who have cognitive deficits. The target P300 (P3b) and distracter P300 (P3a) are well-validated electrocortical markers of attention- and memory-related cognitive control processes. Nicotine deprivation has been shown to reduce P3b/P3a amplitudes. The current study sought to examine the direct effects of nicotine on P3b/P3a amplitudes among nonsmokers. It was hypothesized that nicotine would increase P3b and P3a amplitudes, and that individuals lower on trait cognitive control would show greater nicotine-induced increases. 78 nonsmokers attended two separate experimental sessions, during which they performed the P3b/P3a evoking 3-stimulus oddball task following nicotine (7-mg) or placebo patch administration. Nicotine did not enhance P3b or P3a amplitudes, nor did trait cognitive control moderate the influence of nicotine on these indices. Nicotine-induced changes in P3 amplitudes may be limited to nicotine deprivation and/or nonsmokers may be fundamentally different with respect to the influence of nicotine on P3b/P3a indices of cognitive control. Directions for future research that may further examine the effects of nicotine on P3b/P3a independent of withdrawal reversal are discussed.

Nicotine deprivation influences P300 markers of cognitive control.

Studies suggest that reduced cognitive control due to nicotine withdrawal may have a critical role in promoting tobacco use. The P3 family of event-related brain potential (ERP) components is thought to serve as markers of cognitive control processes. Unfortunately, existing research that examines the effects of nicotine deprivation on P3 amplitude has been marred by small sample sizes and other design limitations. The present study sought to determine the effects of nicotine deprivation on P3b and P3a amplitudes, which index task relevant target detection and orienting responses to novelty, respectively. A secondary aim was to examine self-reported trait cognitive control as a moderator of nicotine deprivation-induced reductions in P3b and P3a amplitudes. In all, 121 nicotine-dependent smokers attended two experimental sessions following 12-h smoking/nicotine deprivation. In a counterbalanced manner, participants smoked nicotine cigarettes during one session and placebo cigarettes during the other session. Findings indicated that nicotine deprivation reduced P3b amplitude (p<0.00001) during a three-stimulus oddball task independent of trait cognitive control. In contrast, nicotine deprivation reduced P3a only among participants who scored lower on measures of trait cognitive control. Implications for conceptualizing risk for nicotine dependence, and its treatment, are discussed.