Neurophysiological studies in humans employing magneto- and electro- encephalography increasingly suggest that oscillatory rhythmic activity of the brain may be a core mechanism for binding sensory information across space, time, and object features to generate a unified perceptual representation. To distinguish whether oscillatory activity is causally related to binding processes or whether, on the contrary, it is a mere epiphenomenon, one possibility is to employ neuromodulatory techniques such as transcranial alternating current stimulation. tACS has seen a rising interest due to (...) its ability to modulate brain oscillations in a frequency-dependent manner. In the present review, we critically summarize current tACS evidence for a causal role of oscillatory activity in spatial, temporal, and feature binding in the context of visual perception. For temporal binding, the emerging picture supports a causal link with the power and the frequency of occipital alpha rhythms ; however, there is no consistent evidence on the causal role of the phase of occipital tACS. For feature binding, the only study available showed a modulation by occipital alpha tACS. The majority of studies that successfully modulated oscillatory activity and behavioral performance in spatial binding targeted parietal areas, with the main rhythms causally linked being the theta and beta frequency bands. On the other hand, spatio-temporal binding has been directly modulated by parieto-occipital gamma and alpha tACS, suggesting a potential role of cross-frequency coupling when binding across space and time. Nonetheless, negative or partial results have also been observed, suggesting methodological limitations that should be addressed in future research. Overall, the emerging picture seems to support a causal role of brain oscillations in binding processes and, consequently, a certain degree of plasticity for shaping binding mechanisms in visual perception, which, if proved to have long lasting effects, can find applications in different clinical populations. (shrink)

Pain serves the protection of the body. Consequently, noxious stimuli or, more precisely, the thereby induced neurophysiological processes commonly lead to pain perception. Identical noxious stimuli, however, do not always translate into the same pain experience depending on multiple factors. To acknowledge this variability, the distinction between nociception as the neural process elicited by noxious stimuli and pain as subjective multifactorial experience is essential. During longer-lasting experimental pain and chronic pain, nociception and pain can substantially dissociate. Moreover, longer-lasting experimental pain (...) resembles chronic pain regarding certain perceptual features such as prolonged pain duration and intensity fluctuations. Thus, longer-lasting experimental pain offers the opportunity to gain new insights into both the differential neural representation of noxious stimuli and pain and the neuronal mechanisms associated with the state of longer- lasting pain. We applied 10 minutes of painful heat stimulation to the left and right hand of 39 healthy participants while we recorded continuous pain ratings, electroencephalography, and autonomic responses. Data were analyzed in three distinct projects aiming at different aspects of neuronal mechanisms underlying longer-lasting pain. Project 1 assessed whether stimulus intensity as proxy of nociception and pain intensity relate to distinct patterns of oscillatory brain activity. EEG recordings revealed that increases in stimulus intensity were reflected by suppressions of alpha and beta oscillations in sensorimotor areas contralateral to the stimulated hand. In contrast, increases in pain intensity were associated with enhanced gamma oscillations in the medial prefrontal cortex. More importantly, the encoding of stimulus intensity by alpha and beta oscillations in the sensorimotor areas was spatially specific, i.e. depended on the stimulus location, whereas the encoding of pain intensity by gamma oscillations in the medial prefrontal cortex was independent of stimulus location. Thus, prefrontal gamma oscillations might reflect higher- order aspects of noxious stimuli, such as salience, valence, and motivational aspects rather than precise sensory features. Project 2 investigated the relationship between stimulus intensity, pain intensity, autonomic responses, and brain activity. Skin conductance measures, as markers of sympathetic activity, co-varied more closely with stimulus intensity than with pain intensity. Correspondingly, skin conductance measures were related to suppressions of alpha and beta oscillations in the sensorimotor area contralateral to the stimulated hand. These finding suggest that skin conductance measures are in part directly elicited by nociceptive processes and, thus, at least partially independent of perceptual processes during longer-lasting pain. Hence, these observations corroborate concepts of pain in which sensory, motivational, and autonomic processes partially independently contribute to the experience of pain. Finally, project 3 incorporated the systematic and comprehensive assessment of oscillatory brain activity, functional connectivity, and graph- theory based network measures during the state of longer-lasting pain. Longer-lasting pain was associated with suppressions of oscillatory brain activity at alpha frequencies in addition to stronger connectivity at alpha and beta frequencies in sensorimotor areas. Furthermore, sensorimotor areas contralateral to stimulation showed increased connectivity to a common area in the medial prefrontal cortex at alpha frequencies and built a sensorimotor-prefrontal network during longer-lasting pain. This network might be involved in the integration of sensory, cognitive, and motivational-affective information and, consequently, in the translation of a noxious stimulus into a subjective pain experience. All three projects contribute to a better understanding of neuronal mechanisms underlying longer-lasting experimental pain, which serves as an experimental model for chronic pain. Since the treatment of chronic pain has remained insufficient and unsatisfactory, the current results might provide EEG-based targets for urgently needed new treatment approaches, such as non-invasive brain stimulation and neurofeedback. (shrink)