Representational dynamics across multiple timescales in human cortical networks

Human cognition occurs at multiple timescales, including immediate processing of the ongoing experiences and slowly drifting higher-level thoughts. To understand how the brain selects and represents these various types of information to guide behavior, this thesis examined representational content within sensory regions, multiple demand (MD) network, and default mode network (DMN). Chapter 1 provides a background review of the current literature. It begins by reviewing experimental investigations of component visual processes that unfold over time. Next, the MD network is introduced as a collection of frontal and parietal regions involved in implementing cognitive control by assembling the required operations for task-relevant behavior. Finally, the DMN is introduced in the context of temporal processing hierarchies, with focus on its representation of situation models summarizing interactions among entities and the environment. The first experiment, presented in Chapter 2, used EEG/MEG to track multiple component processes of selective attention. Five distinct processing operations with different time-courses were quantified, including representation of visual display properties, target location, target identity, behavioral significance, and finally, possible reactivation of the attentional template. Chapter 3 used fMRI to examine neural representations of task episodes, which are temporally organized sequences of steps that occur within a given context. It was found that MD and visual regions showed sensitivity to the fine structure of the contents within a task. DMN regions showed gradual change throughout the entire task, with increased activation at the offset of the entire episode. Chapter 4 analyzed activation profiles of DMN regions using six diverse tasks to examine their functional convergence during social, episodic, and self-referential thought. Results supported proposals of separate subsystems, yet also suggest integration within the DMN. The final chapter, Chapter 5, provides an extended discussion of theoretical concepts related to the three experiments and proposes possible avenues for further research

Brain structure links trait creativity to openness to experience

Creativity is crucial to the progression of human civilization and has led to important scientific discoveries. Especially, individuals are more likely to have scientific discoveries if they possess certain personality traits of creativity (trait creativity), including imagination, curiosity, challenge and risk-taking. This study used voxel-based morphometry to identify the brain regions underlying individual differences in trait creativity, as measured by the Williams creativity aptitude test, in a large sample (n = 246). We found that creative individuals had higher gray matter volume in the right posterior middle temporal gyrus (pMTG), which might be related to semantic processing during novelty seeking (e.g. novel association, conceptual integration and metaphor understanding). More importantly, although basic personality factors such as openness to experience, extroversion, conscientiousness and agreeableness (as measured by the NEO Personality Inventory) all contributed to trait creativity, only openness to experience mediated the association between the right pMTG volume and trait creativity. Taken together, our results suggest that the basic personality trait of openness might play an important role in shaping an individual’s trait creativity

The not so resting mind: Investigating Neural Activity associated with daydreaming using EEG

A recurring question since the times of classical psychology is concerned with how the human brain gives rise to a variety of experiences despite the lacking of sensory arousal (Antrobus, Singer & Greenberg, 1966). The current study sought to ascertain whether distinct brain activity could be observed across three different visual tasks (Visual, Day-dreaming & N-Back). Areas of interest included both a priori Brodmann areas (in light of previous literature) and post-hoc Brodmann areas – which primarily concern what this investigation found and how it fares with previous academic insight. Using source localization analysis via electroencephalography (EEG), distinct patterns of brain activity were observed across the three tasks. However, the major differences found were shown to be largely dependent on the cognitive-demand of the task – with the N-Back phase eliciting significantly more activity across the majority of Brodmann areas compared to the visual and day-dreaming tasks which, at points, demonstrated very similar patterns of brain activity. These results offer strength to some academic proposals as well as further questioning for others. Finally, these results are weighed in light of what contemporary academia currently proposes and may provide sound reasoning for more integrative measures to reliably assess instances of day-dreaming in a psychological setting

The cognitive neuroscience of visual working memory

Visual working memory allows us to temporarily maintain and manipulate visual information in order to solve a task. The study of the brain mechanisms underlying this function began more than half a century ago, with Scoville and Milner’s (1957) seminal discoveries with amnesic patients. This timely collection of papers brings together diverse perspectives on the cognitive neuroscience of visual working memory from multiple fields that have traditionally been fairly disjointed: human neuroimaging, electrophysiological, behavioural and animal lesion studies, investigating both the developing and the adult brain

Creative conceptual expansion: A combined fMRI replication and extension study to examine individual differences in creativity

The aims of this fMRI study were two-fold. The first objective of the study was to verify whether the findings associated with a previous fMRI study could be replicated in which a novel event-related experimental design was developed which rendered it possible to investigate the brain basis of creative conceptual expansion. The ability to widen the boundaries of conceptual structures is integral to creative idea generation, which makes conceptual expansion a core component of creative cognition. Creative conceptual expansion led to the engagement of brain regions that are known to be involved in the access, storage and relational integration of conceptual knowledge in the original study. These included the anterior inferior frontal gyrus, the temporal poles and the lateral frontal pole. These findings in relation to the brain basis of creative conceptual expansion were replicated in the current study. The second objective of this study was to evaluate the brain basis of individual differences in creative conceptual expansion. The high creative group relative to the low creative group was shown to exhibit greater activity in regions of the semantic cognition network as well as the salience network during creative conceptual expansion. The findings are discussed from the point of view of classical hypotheses about information processing biases that explain individual differences in creativity including flat associative hierarchies, defocused attention and cognitive disinhibition

Understanding the relationship between chronic pain and emotional disorders

Although frequent coexistence of chronic pain and emotional disorders is well documented, exact mechanisms of comorbidity are not fully understood. The overarching aim of this thesis was to advance our knowledge of the mechanisms that link chronic pain and emotional disorders. Results of the literature review suggest that nosologically different conditions might coexist if they share common transdiagnostic risk factors that predispose individuals to several disorders. Using this transdiagnostic approach, a theoretical model explaining the relationships between different risk factors and how they might contribute to comorbidity between chronic pain and emotional disorders has been developed. According to the proposed model, one of the most fundamental transdiagnostic risk factors associated with both conditions is uncontrollable stress. It does not cause chronic pain or emotional disorders directly but promotes development of other risk factors, such as helplessness, negative affectivity, hypersensitivity to pain, dysregulation of stress response, and cognitive deficits. Importantly, these risk factors are not disorder specific. They equally predispose individuals to depression, anxiety, and chronic pain. Development of a specific disorder is determined by the influence of environmental and biological moderators that transform pre-existing risk factors into specific disorders. Considering that the sequence of pathological processes leading to psychopathology and/or chronic pain starts from the experience of uncontrollable stress, it is important to identify neural mechanisms that could mediate its effects. There is evidence suggesting that the frontal pole comprising of the rostromedial prefrontal cortex (rmPFC) and rostrolateral prefrontal cortex (rlPFC) plays an essential role in evaluation of controllability. Dysfunction of this area may increase the sense of uncontrollability, thereby promoting development of transdiagnostic risk factors. Both subregions of the frontal pole are parts of the neural networks that perform higher-order processing and modulation of nociceptive and emotional reactions. Thus, increased sensitivity to pain and heightened negative affect in patients with chronic pain disorders might be mediated by impaired interaction of the rmPFC and rlPFC with low-level nociceptive and emotional circuits. To test this hypothesis, resting-state functional and effective connectivity of the rmPFC and rlPFC was investigated in two chronic pain conditions: chronic low back pain (CLBP) and osteoarthritis (OA). Functional connectivity (FC) of the rmPFC and rlPFC in CLBP. CLBP patients displayed decreased FC of the rmPFC with retrosplenial cortex (RSC), posterior part of the ventral pallidum (VP), and mediodorsal (MD) thalamus. Diminished interaction with these regions may hinder retrieval of positive episodic memories of control and attribution of positive outcomes to personal actions. This may negatively influence patients’ belief about their ability to cope with stress, increase the sense of perceived uncontrollability. CLBP patients also showed reduced FC of the rmPFC with the medial pulvinar nucleus of the thalamus, midbrain reticular formation, and periaqueductal grey. These structures are parts of the ascending reticular activating system (ARAS) that regulates the level of arousal in the central nervous system. Reduced modulation of the arousal system by the rmPFC may result in development of a hyperarousal state and amplification of nociceptive and emotional responses leading to hyperalgesia and increased negative affectivity. There was no difference in FC of the rlPFC between CLBP patients and healthy controls. Effective connectivity analysis in CLBP. Causal interactions between the rmPFC, stress-related brainstem structures (dorsal raphe nucleus, ventral and dorsal periaqueductal grey), and memory systems (ventral striatum, hippocampus, amygdala) were investigated using the spectral dynamic causal modelling (spDCM). Consistent with the results of the FC analysis in CLBP, the spDCM also found altered interaction between the rmPFC and memory systems. Specifically, patients showed weaker connectivity of the rmPFC with hippocampus and stronger connectivity with the amygdala. Such pattern of connectivity may lead to inaccurate evaluation of the probability of control based on past experiences, overgeneralization and impaired extinction of fears. Patients also demonstrated hyperactivation of the dorsal raphe nucleus, ventral and dorsal periaqueductal grey (parts of the ARAS) that may contribute to hyperalgesia and increased negative affectivity. Functional connectivity of the rmPFC and rlPFC in OA. In this study FC of the rmPFC and rlPFC was compared between patients with shorter duration of OA (7 years), and healthy volunteers. Only patients with longer duration of OA showed increased negative FC of the rmPFC with multiple brainstem nuclei, such as the parabrachial complex, locus coeruleus, dorsal and median raphe nuclei, ventral tegmental area, midbrain reticular formation, and periaqueductal grey, that together comprise the ARAS. Negative FC between the rmPFC and ARAS may reflect increased compensatory inhibition of the activating system by the rmPFC in attempts to suppress pain-induced arousal and negative affect. Despite longer duration of pain, patients did not show signs of hyperalgesia or emotional distress. Perhaps, effective suppression of the brainstem arousal system demonstrated by OA patients was due to preserved connectivity between the rmPFC and memory systems. Both groups of OA patients also showed reduced FC of the rlPFC with the multiple demand network that may contribute to development of another transdiagnostic risk factor, i.e., cognitive deficit. Results of all three studies presented in this thesis suggest that chronic stress may cause development of transdiagnostic risk factors such as negative affectivity and hyperalgesia via hyperactivation of the brainstem arousal system that augments nociceptive and emotional responses. Impaired regulation of the arousal system by the rmPFC, which evaluates controllability of the stress based on previous experiences, may contribute to hyperactivation of the ARAS. Reduced interaction between the rmPFC and memory systems may obstruct retrieval and utilization of positive memories of control, thereby increasing the sense of uncontrollability, facilitating hyperarousal, and contributing to development of transdiagnostic risk factors. In contrast, preserved connectivity between the rmPFC and memory systems may oppose the negative effects of chronic stress and help patients to maintain a belief that they are capable of coping with the stress

Understanding the relationship between chronic pain and emotional disorders

Although frequent coexistence of chronic pain and emotional disorders is well documented, exact mechanisms of comorbidity are not fully understood. The overarching aim of this thesis was to advance our knowledge of the mechanisms that link chronic pain and emotional disorders. Results of the literature review suggest that nosologically different conditions might coexist if they share common transdiagnostic risk factors that predispose individuals to several disorders. Using this transdiagnostic approach, a theoretical model explaining the relationships between different risk factors and how they might contribute to comorbidity between chronic pain and emotional disorders has been developed. According to the proposed model, one of the most fundamental transdiagnostic risk factors associated with both conditions is uncontrollable stress. It does not cause chronic pain or emotional disorders directly but promotes development of other risk factors, such as helplessness, negative affectivity, hypersensitivity to pain, dysregulation of stress response, and cognitive deficits. Importantly, these risk factors are not disorder specific. They equally predispose individuals to depression, anxiety, and chronic pain. Development of a specific disorder is determined by the influence of environmental and biological moderators that transform pre-existing risk factors into specific disorders. Considering that the sequence of pathological processes leading to psychopathology and/or chronic pain starts from the experience of uncontrollable stress, it is important to identify neural mechanisms that could mediate its effects. There is evidence suggesting that the frontal pole comprising of the rostromedial prefrontal cortex (rmPFC) and rostrolateral prefrontal cortex (rlPFC) plays an essential role in evaluation of controllability. Dysfunction of this area may increase the sense of uncontrollability, thereby promoting development of transdiagnostic risk factors. Both subregions of the frontal pole are parts of the neural networks that perform higher-order processing and modulation of nociceptive and emotional reactions. Thus, increased sensitivity to pain and heightened negative affect in patients with chronic pain disorders might be mediated by impaired interaction of the rmPFC and rlPFC with low-level nociceptive and emotional circuits. To test this hypothesis, resting-state functional and effective connectivity of the rmPFC and rlPFC was investigated in two chronic pain conditions: chronic low back pain (CLBP) and osteoarthritis (OA). Functional connectivity (FC) of the rmPFC and rlPFC in CLBP. CLBP patients displayed decreased FC of the rmPFC with retrosplenial cortex (RSC), posterior part of the ventral pallidum (VP), and mediodorsal (MD) thalamus. Diminished interaction with these regions may hinder retrieval of positive episodic memories of control and attribution of positive outcomes to personal actions. This may negatively influence patients’ belief about their ability to cope with stress, increase the sense of perceived uncontrollability. CLBP patients also showed reduced FC of the rmPFC with the medial pulvinar nucleus of the thalamus, midbrain reticular formation, and periaqueductal grey. These structures are parts of the ascending reticular activating system (ARAS) that regulates the level of arousal in the central nervous system. Reduced modulation of the arousal system by the rmPFC may result in development of a hyperarousal state and amplification of nociceptive and emotional responses leading to hyperalgesia and increased negative affectivity. There was no difference in FC of the rlPFC between CLBP patients and healthy controls. Effective connectivity analysis in CLBP. Causal interactions between the rmPFC, stress-related brainstem structures (dorsal raphe nucleus, ventral and dorsal periaqueductal grey), and memory systems (ventral striatum, hippocampus, amygdala) were investigated using the spectral dynamic causal modelling (spDCM). Consistent with the results of the FC analysis in CLBP, the spDCM also found altered interaction between the rmPFC and memory systems. Specifically, patients showed weaker connectivity of the rmPFC with hippocampus and stronger connectivity with the amygdala. Such pattern of connectivity may lead to inaccurate evaluation of the probability of control based on past experiences, overgeneralization and impaired extinction of fears. Patients also demonstrated hyperactivation of the dorsal raphe nucleus, ventral and dorsal periaqueductal grey (parts of the ARAS) that may contribute to hyperalgesia and increased negative affectivity. Functional connectivity of the rmPFC and rlPFC in OA. In this study FC of the rmPFC and rlPFC was compared between patients with shorter duration of OA (7 years), and healthy volunteers. Only patients with longer duration of OA showed increased negative FC of the rmPFC with multiple brainstem nuclei, such as the parabrachial complex, locus coeruleus, dorsal and median raphe nuclei, ventral tegmental area, midbrain reticular formation, and periaqueductal grey, that together comprise the ARAS. Negative FC between the rmPFC and ARAS may reflect increased compensatory inhibition of the activating system by the rmPFC in attempts to suppress pain-induced arousal and negative affect. Despite longer duration of pain, patients did not show signs of hyperalgesia or emotional distress. Perhaps, effective suppression of the brainstem arousal system demonstrated by OA patients was due to preserved connectivity between the rmPFC and memory systems. Both groups of OA patients also showed reduced FC of the rlPFC with the multiple demand network that may contribute to development of another transdiagnostic risk factor, i.e., cognitive deficit. Results of all three studies presented in this thesis suggest that chronic stress may cause development of transdiagnostic risk factors such as negative affectivity and hyperalgesia via hyperactivation of the brainstem arousal system that augments nociceptive and emotional responses. Impaired regulation of the arousal system by the rmPFC, which evaluates controllability of the stress based on previous experiences, may contribute to hyperactivation of the ARAS. Reduced interaction between the rmPFC and memory systems may obstruct retrieval and utilization of positive memories of control, thereby increasing the sense of uncontrollability, facilitating hyperarousal, and contributing to development of transdiagnostic risk factors. In contrast, preserved connectivity between the rmPFC and memory systems may oppose the negative effects of chronic stress and help patients to maintain a belief that they are capable of coping with the stress

Contributions of Human Prefrontal Cortex to the Recogitation of Thought

Human beings have a unique ability to not only verbally articulate past and present experiences, as well as potential future ones, but also evaluate the mental representations of such things. Some evaluations do little good, in that they poorly reflect facts, create needless emotional distress, and contribute to the obstruction of personal goals, whereas some evaluations are the converse: They are grounded in logic, empiricism, and pragmatism and, therefore, are functional rather than dysfunctional. The aim of non-pharmacological mental health interventions is to revise dysfunctional thoughts into more adaptive, healthier ones; however, the neurocognitive mechanisms driving cognitive change have hitherto remained unclear. Therefore, this thesis examines the role of the prefrontal cortex (PFC) in this aspect of human higher cognition using the relatively new method of functional near-infrared spectroscopy (fNIRS). Chapter 1 advances recogitation as the mental ability on which cognitive restructuring largely depends, concluding that, as a cognitive task, it is a form of open-ended human problem-solving that uses metacognitive and reasoning faculties. Because these faculties share similar executive resources, Chapter 2 discusses the systems in the brain involved in controlled information processing, specifically the nature of executive functions and their neural bases. Chapter 3 builds on these ideas to propose an information-processing model of recogitation, which predicts the roles of different subsystems localized within the PFC and elsewhere in the context of emotion regulation. This chapter also highlights several theoretical and empirical challenges to investigating this neurocognitive theory and proposes some solutions, such as to use experimental designs that are more ecologically valid. Chapter 4 focuses on a neuroimaging method that is best suited to investigating questions of spatial localization in ecological experiments, namely functional near-infrared spectroscopy (fNIRS). Chapter 5 then demonstrates a novel approach to investigating the neural bases of interpersonal interactions in clinical settings using fNIRS. Chapter 6 explores physical activity as a ‘bottom-up’ approach to upregulating the PFC, in that it might help clinical populations with executive deficits to regulate their mental health from the ‘top-down’. Chapter 7 addresses some of the methodological issues of investigating clinical interactions and physical activity in more naturalistic settings by assessing an approach to recovering functional events from observed brain data. Chapter 8 draws several conclusions about the role of the PFC in improving psychological as well as physiological well-being, particularly that rostral PFC is inextricably involved in the cognitive effort to modulate dysfunctional thoughts, and proposes some important future directions for ecological research in cognitive neuroscience; for example, psychotherapy is perhaps too physically stagnant, so integrating exercise into treatment environments might boost the effectiveness of intervention strategies