The 40-Hz auditory steady-state response in bipolar disorder: A meta-analysis.

OBJECTIVE: Bipolar disorder is characterized by aberrant neurophysiological responses as measured with electroencephalography (EEG) and magnetoencephalography (MEG), including the 40-Hz auditory steady-state response (ASSR). 40-Hz ASSR deficits are also found in patients with schizophrenia and may represent a transdiagnostic biomarker of neuronal circuit dysfunction. In this systematic review and meta-analysis, we summarize and evaluate the evidence for 40-Hz ASSR deficits in patients with bipolar disorder. METHODS: We identified studies from PubMed, EMBASE, and SCOPUS. We assessed the risk of bias, calculated Hedges' g meta-level effect sizes, and investigated small-study effects using funnel plots and Egger regression. RESULTS: Seven studies, comprising 396 patients with bipolar disorder and 404 healthy controls, were included in the meta-analysis. Studies displayed methodological heterogeneity and an overall high risk of bias. Patients with bipolar disorder showed consistent reductions in 40-Hz ASSR evoked power (Hedges' g = -0.49; 95% confidence intervals [-0.67, -0.31]) and inter-trial phase coherence (ITPC) (Hedges' g = -0.43; 95 %CI [-0.58, -0.29]) compared with healthy controls. CONCLUSIONS: Our meta-analysis provides evidence that 40-Hz ASSRs are reduced in patients with bipolar disorder compared with healthy controls. SIGNIFICANCE: Future large-scale studies are warranted to link 40-Hz ASSR deficits to clinical features and developmental trajectories.

Effective connectivity reveals right-hemisphere dominance in audiospatial perception: implications for models of spatial neglect.

Detecting the location of salient sounds in the environment rests on the brain's ability to use differences in sounds arriving at both ears. Functional neuroimaging studies in humans indicate that the left and right auditory hemispaces are coded asymmetrically, with a rightward attentional bias that reflects spatial attention in vision. Neuropsychological observations in patients with spatial neglect have led to the formulation of two competing models: the orientation bias and right-hemisphere dominance models. The orientation bias model posits a symmetrical mapping between one side of the sensorium and the contralateral hemisphere, with mutual inhibition of the ipsilateral hemisphere. The right-hemisphere dominance model introduces a functional asymmetry in the brain's coding of space: the left hemisphere represents the right side, whereas the right hemisphere represents both sides of the sensorium. We used Dynamic Causal Modeling of effective connectivity and Bayesian model comparison to adjudicate between these alternative network architectures, based on human electroencephalographic data acquired during an auditory location oddball paradigm. Our results support a hemispheric asymmetry in a frontoparietal network that conforms to the right-hemisphere dominance model. We show that, within this frontoparietal network, forward connectivity increases selectively in the hemisphere contralateral to the side of sensory stimulation. We interpret this finding in light of hierarchical predictive coding as a selective increase in attentional gain, which is mediated by feedforward connections that carry precision-weighted prediction errors during perceptual inference. This finding supports the disconnection hypothesis of unilateral neglect and has implications for theories of its etiology.

Cognitive-affective neural plasticity following active-controlled mindfulness intervention.

Mindfulness meditation is a set of attention-based, regulatory, and self-inquiry training regimes. Although the impact of mindfulness training (MT) on self-regulation is well established, the neural mechanisms supporting such plasticity are poorly understood. MT is thought to act through interoceptive salience and attentional control mechanisms, but until now conflicting evidence from behavioral and neural measures renders difficult distinguishing their respective roles. To resolve this question we conducted a fully randomized 6 week longitudinal trial of MT, explicitly controlling for cognitive and treatment effects with an active-control group. We measured behavioral metacognition and whole-brain blood oxygenation level-dependent (BOLD) signals using functional MRI during an affective Stroop task before and after intervention in healthy human subjects. Although both groups improved significantly on a response-inhibition task, only the MT group showed reduced affective Stroop conflict. Moreover, the MT group displayed greater dorsolateral prefrontal cortex responses during executive processing, consistent with increased recruitment of top-down mechanisms to resolve conflict. In contrast, we did not observe overall group-by-time interactions on negative affect-related reaction times or BOLD responses. However, only participants with the greatest amount of MT practice showed improvements in response inhibition and increased recruitment of dorsal anterior cingulate cortex, medial prefrontal cortex, and right anterior insula during negative valence processing. Our findings highlight the importance of active control in MT research, indicate unique neural mechanisms for progressive stages of mindfulness training, and suggest that optimal application of MT may differ depending on context, contrary to a one-size-fits-all approach.

Effect of hypnotic pain modulation on brain activity in patients with temporomandibular disorder pain.

Hypnosis modulates pain perception but the associated brain mechanisms in chronic pain conditions are poorly understood. Brain activity evoked by painful repetitive pin-prick stimulation of the left mental nerve region was investigated with use of fMRI in 19 patients with painful temporomandibular disorders (TMD) during hypnotic hypoalgesia and hyperalgesia and a control condition. Pain intensity and unpleasantness of the painful stimulation was scored on a 0-10 Numerical Rating Scale (NRS). NRS pain and unpleasantness scores during hypnotic hypoalgesia were significantly lower than in the control condition and significantly higher in the hypnotic hyperalgesia condition. In the control condition, painful stimulation caused significant activation of right posterior insula, primary somatosensory cortex (SI), BA21, and BA6, and left BA40 and BA4. Painful stimulation during hypnotic hyperalgesia was associated with increased activity in right posterior insula and BA6 and left BA40 whereas hypnotic hypoalgesia only was associated with activity in right posterior insula. Unexpectedly, direct contrasts between control and hypnotic hyperalgesia conditions revealed significant decreases in S1 during hyperalgesia. Direct contrasts between control and hypnotic hypoalgesia conditions demonstrated significant decreases in right posterior insula and BA21, as well as left BA40 during hypoalgesia. These findings are the first to describe hypnotic modulation of brain activity associated with nociceptive processing in chronic TMD pain patients and demonstrate that hypnotic hypoalgesia is associated with a pronounced suppression of cortical activity and a disconnection between patient-based scores and cortical activity in S1 during hypnotic hyperalgesia.