Alpha oscillations (7–13 Hz) are the dominant rhythm in both the resting and active brain. Accordingly, translational research has provided evidence for the involvement of aberrant alpha activity in the onset of symptomatological features underlying syndromes such as autism, schizophrenia, major depression, and Attention Deficit and Hyperactivity Disorder (ADHD). However, findings on the matter are difficult to reconcile due to the variety of paradigms, analyses, and clinical phenotypes at play, not to mention recent technical and methodological advances in this domain. Herein, we seek to address this issue by reviewing the literature gathered on this topic over the last ten years. For each neuropsychiatric disorder, a dedicated section will be provided, containing a concise account of the current models proposing characteristic alterations of alpha rhythms as a core mechanism to trigger the associated symptomatology, as well as a summary of the most relevant studies and scientific contributions issued throughout the last decade. We conclude with some advice and recommendations that might improve future inquiries within this field.

Perceptual decisions depend on the ability to exploit available sensory information in order to select the most adaptive option from a set of alternatives. Such decisions depend on the perceptual sensitivity of the organism, which is generally accompanied by a corresponding level of certainty about the choice made. Here, by use of corticocortical paired associative transcranial magnetic stimulation protocol (ccPAS) aimed at inducing plastic changes, we shaped perceptual sensitivity and metacognitive ability in a motion discrimination task depending on the targeted network, demonstrating their functional dissociation. Neurostimulation aimed at boosting V5/MT+-to-V1/V2 back-projections enhanced motion sensitivity without impacting metacognition, whereas boosting IPS/LIP-to-V1/V2 back-projections increased metacognitive efficiency without impacting motion sensitivity. This double-dissociation provides causal evidence of distinct networks for perceptual sensitivity and metacognitive ability in humans.

Background and Hypothesis: Humans develop a constellation of different representations of the external environment, even in the face of the same sensory exposure. According to the Bayesian framework, these differentiations could be grounded in a different weight assigned to prior knowledge vs. new external inputs in predictive inference. Since recent advances in computational psychiatry suggest that autism (ASD) and schizophrenia (SSD) lie on the two diametric poles of the same predictive continuum, the adoption of a specific inferential style could be routed by dispositional factors related to autistic and schizotypal traits. However, no studies have directly investigated the role of ASD–SSD dimension in shaping the neuro-behavioral markers underlying perceptual inference. Study Design: We used a probabilistic detection task while simultaneously recording EEG to investigate whether neurobehavioral signatures related to prior processing were diametrically shaped by ASD and SSD traits in the general population (n = 80). Results: We found that the position along the ASD–SSD continuum directed the predictive strategies adopted by the individuals in decision-making. While proximity to the positive schizotypy pole was associated with the adoption of the predictive approach associated to the hyper-weighting of prior knowledge, proximity to ASD pole was related to strategies that favored sensory evidence in decision-making. Conclusions: These findings revealed that the weight assigned to prior knowledge is a marker of the ASD–SSD continuum, potentially useful for identifying individuals at-risk of developing mental disorders and for understanding the mechanisms contributing to the onset of symptoms observed in ASD and SSD clinical forms.

Migraine is among the most common and debilitating neurological disorders typically affecting people of working age. It is characterised by a unilateral, pulsating headache often associated with severe pain. Despite the intensive research, there is still little understanding of the pathophysiology of migraine. At the electrophysiological level, altered oscillatory parameters have been reported within the alpha and gamma bands. At the molecular level, altered glutamate and GABA concentrations have been reported. However, there has been little cross-talk between these lines of research. Thus, the relationship between oscillatory activity and neurotransmitter concentrations remains to be empirically traced. Importantly, how these indices link back to altered sensory processing has to be clearly established as yet. Accordingly, pharmacologic treatments have been mostly symptom-based, and yet sometimes proving ineffective in resolving pain or related issues. This review provides an integrative theoretical framework of excitation–inhibition imbalance for the understanding of current evidence and to address outstanding questions concerning the pathophysiology of migraine. We propose the use of computational modelling for the rigorous formulation of testable hypotheses on mechanisms of homeostatic imbalance and for the development of mechanism-based pharmacological treatments and neurostimulation interventions.