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Periodic sensory inputs entrain oscillatory brain activity, reflecting a neural mechanism that might be fundamental to temporal prediction and perception. Most environmental rhythms and patterns in human behavior, such as walking, dancing, and speech do not, however, display strict isochrony but are instead quasi-periodic. Research has shown that neural tracking of speech is driven by modulations of the amplitude envelope, especially via sharp acoustic edges, which serve as prominent temporal landmarks. In the same vein, research on rhythm processing in music supports the notion that perceptual timing precision varies systematically with the sharpness of acoustic onset edges, conceptualized in the beat bin hypothesis. Increased envelope sharpness induces increased precision in localizing a sound in time. Despite this tight relationship between envelope shape and temporal processing, it is currently unknown how the brain uses predictive information about envelope features to optimize temporal perception. With the current EEG study, we show that the predicted sharpness of the amplitude envelope is encoded by pre-target neural activity in the beta band (15–25 Hz), and has an impact on the temporal perception of target sounds. We used probabilistic sound cues in a timing judgment task to inform participants about the sharpness of the amplitude envelope of an upcoming target sound embedded in a beat sequence. The predictive information about the envelope shape modulated task performance and pre-target beta power. Interestingly, these conditional beta-power modulations correlated positively with behavioral performance in the timing judgment task and with perceptual temporal precision in a click-alignment task. This study provides new insight into the neural processes underlying prediction of the sharpness of the amplitude envelope during beat perception, which modulate the temporal perception of sounds. This finding could reflect a process that is involved in temporal prediction, exerting top-down control on neural entrainment via the prediction of acoustic edges in the auditory stream.

Recent theoretical accounts of addiction have acknowledged that addiction to substances and behaviors share inherent similarities (eg, insensitivity to future consequences and self-regulatory deficits). This recognition is corroborated by inquiries into the neurobiological correlates of addiction, which has indicated that different manifestations of addictive pathology share common neural mechanisms. This review of the literature will explore the feasibility of the somatic marker hypothesis as a unifying explanatory framework of the decision-making deficits that are believed to be involved in addiction development and maintenance. The somatic marker hypothesis provides a neuroanatomical and cognitive framework of decision making, which posits that decisional processes are biased toward long-term prospects by emotional marker signals engendered by a neuronal architecture comprising both cortical and subcortical circuits. Addicts display markedly impulsive and compulsive behavioral patterns that might be understood as manifestations of decision-making processes that fail to take into account the long-term consequences of actions. Evidence demonstrates that substance dependence, pathological gambling, and Internet addiction are characterized by structural and functional abnormalities in neural regions, as outlined by the somatic marker hypothesis. Furthermore, both substance dependents and behavioral addicts show similar impairments on a measure of decision making that is sensitive to somatic marker functioning. The decision-making deficits that characterize addiction might exist a priori to addiction development; however, they may be worsened by ingestion of substances with neurotoxic properties. It is concluded that the somatic marker model of addiction contributes a plausible account of the underlying neurobiology of decision-making deficits in addictive disorders that is supported by the current neuroimaging and behavioral evidence. Implications for future research are outlined.

The ability to use predictive information to guide perception and action relies heavily on the prefrontal cortex (PFC), yet the involvement of its subregions in predictive processes remains unclear. Recent perspectives propose that the orbitofrontal cortex (OFC) generates predictions about perceptual events, actions, and their outcomes while the lateral prefrontal cortex (LPFC) is involved in prospective functions, which support predictive processes, such as selective attention, working memory, response preparation or inhibition. To further delineate the roles of these PFC areas in predictive processing, we investigated whether lesions would impair the ability to build predictions of future events and detect deviations from expected regularities. We used an auditory deviance detection task, in which the structural regularities of played tones were controlled at two hierarchical levels by rules defined at a local (i.e., between tones within sequences) and global (i.e., between sequences) level. We have recently shown that OFC lesions affect detecting prediction violations at two hierarchical levels of rule abstraction, i.e., altered MMN and P3a to local and simultaneous local + global prediction violations (https://doi.org/10.7554/eLife.86386). Now, we focus on the task's predictive aspect and present the latest results showing the involvement of PFC subregions in anticipation of deviances informed by implicit predictive information. Behavioral data shows that deviance expectancy induced faster deviance detection in healthy adults (n=22), suggesting that participants track a state space representation of the task and anticipate upcoming deviant sequences. The analysis of EEG data from patients with focal lesions to the OFC (n = 12) or LPFC (n = 10), and SEEG from the same areas in patients with epilepsy (n = 7), revealed interesting differences. Healthy adults (n = 15) showed modulations of the Contingent Negative Variation (CNV) – a marker of anticipatory activity - tracking the expectancy of deviant tone sequences. However, patients with OFC lesions lacked CNV sensitivity to the predictive context, while patients with LPFC lesions showed moderate sensitivity compared to healthy adults. These results were further supported by intracranial recordings, which revealed expectancy modulation of the high-frequency broadband signal from electrodes in OFC and LPFC, with an earlier latency of activity modulation for the OFC and a later one for the LPFC. Altogether, the complementary approach from behavioral, intracerebral EEG, scalp EEG, and causal lesion data provides compelling evidence for the distinct engagement of the two prefrontal areas in predicting future events and signaling deviations.