Recurrent, unvarying, and seemingly purposeless patterns of action and cognition are part of normal development, but also feature prominently in several neuropsychiatric conditions. Repetitive stereotyped behaviors can be viewed as exaggerated forms of learned habits and frequently correlate with alterations in motor, limbic, and associative basal ganglia circuits. However, it is still unclear how altered basal ganglia feedback signals actually relate to the phenomenological variability of RSBs. Why do behaviorally overlapping phenomena sometimes require different treatment approaches−for example, sensory shielding strategies (...) versus exposure therapy for autism and obsessive-compulsive disorder, respectively? Certain clues may be found in recent models of basal ganglia function that extend well beyond action selection and motivational control, and have implications for sensorimotor integration, prediction, learning under uncertainty, as well as aesthetic learning. In this paper, we systematically compare three exemplary conditions with basal ganglia involvement, obsessive-compulsive disorder, Parkinson’s disease, and autism spectrum conditions, to gain a new understanding of RSBs. We integrate clinical observations and neuroanatomical and neurophysiological alterations with accounts employing the predictive processing framework. Based on this review, we suggest that basal ganglia feedback plays a central role in preconditioning cortical networks to anticipate self-generated, movement-related perception. In this way, basal ganglia feedback appears ideally situated to adjust the salience of sensory signals through precision weighting of new sensory information, relative to the precision of predictions based on prior generated models. Accordingly, behavioral policies may preferentially rely on new data versus existing knowledge, in a spectrum spanning between novelty and stability. RSBs may then represent compensatory or reactive responses, respectively, at the opposite ends of this spectrum. This view places an important role of aesthetic learning on basal ganglia feedback, may account for observed changes in creativity and aesthetic experience in basal ganglia disorders, is empirically testable, and may inform creative art therapies in conditions characterized by stereotyped behaviors. (shrink)

Adaptive behavior critically depends on performance monitoring, the ability to monitor action outcomes and the need to adapt behavior. PM-related brain activity has been linked to guiding decisions about whether action adaptation is warranted. The present study examined whether PM-related brain activity in a flanker task, as measured by electroencephalography, was associated with adaptive behavior in daily life. Specifically, we were interested in the employment of self-control, operationalized as self-control failures, and measured using ecological momentary assessment. Analyses were conducted using (...) an adaptive elastic net regression to predict SCFs from EEG in a sample of 131 participants. The model was fit using within-subject averaged response-locked EEG activity at each electrode and time point within an epoch surrounding the response. We found that higher amplitudes of the error-related negativity were related to fewer SCFs. This suggests that lower error-related activity may relate to lower recruitment of interventive self-control in daily life. Altered cognitive control processes, like PM, have been proposed as underlying mechanisms for various mental disorders. Understanding how alterations in PM relate to regulatory control might therefore aid in delineating how these alterations contribute to different psychopathologies. (shrink)

Executive dysfunctions, psychopathologies arising from problems in the control and regulation of behavior, can occur as a result of the faulty execution of formal information processing models or as a result of malfunctioning neural mechanisms. The models correspond to the formal descriptions of how signals in the environment must be transformed in order to behave adaptively, and the mechanisms correspond to the signal transformations that nervous systems implement in order to execute those cognitive functions. Mechanisms in the form of repeated (...) patterns of neural dynamics execute information processing models. Two distinct modes of malfunction can occur when neural dynamics execute models of information processing. The processing models describing behavior may fail to be executed correctly by neural mechanisms. Or, the neural mechanisms may malfunction, failing to implement the right computation. As an example of malfunctioning models in executive cognition, purported failures of rule following can be understood as failures to appropriately execute a suite of processing models. As an example of malfunctioning mechanisms of executive cognition, maladaptive behavior resulting from dysfunction in the medial prefrontal cortex (mPFC) can be understood as failures in the signal transformations carried out therein. The purpose of these examples is to illustrate the potential benefits of considering models and mechanisms in the diagnosis and etiology of neuropsychological illness and dysfunction, especially disorders of executive cognition. (shrink)