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In the past two decades, the familiar experience of attention - the emphasis on a particular mental activity so that it "fills the mind" - has been subjected to much scientific inquiry. David LaBerge now provides a systematic view of the attention process as it occurs in everyday perception, thinking, and action. Drawing from a variety of research methods and findings from cognitive psychology, neurobiology, and computer science, he presents a masterful synthesis of what is understood about attentional processing. LaBerge explores how we are able to restrict the input of extraneous and confusing information, or prepare to process a future stimulus, in order to take effective action. As well as describing the pathways in the cortex presumed to be involved in attentional processing, he examines the hypothesis that two subcortical structures, the superior colliculus and the thalamus, contain circuit mechanisms that embody an algorithm of attention. In addition, he takes us through various ways of posing the problem, from an information-processing description of how attention works to a consideration of some of the cognitive and behavioral consequences of the brain's computations, such as desiring, judging, imaging, and remembering. Attentional Processing is a highly sophisticated integration of contributions from several fields of neuroscience. It brings together the latest efforts to solve the puzzle of attention: how it works, how it is modulated, what its benefits are, and how it is expressed in the brain.
Thirty-two participants were tested for both resting electroencephalography (EEG) and neuropsychological function. Eight one-minute trials of resting EEG were recorded from 14 channels referenced to linked ears, which was rederived to an average reference. Neuropsychological tasks included Verbal Fluency, the Tower of London, and Corsi's Recurring Blocks. Asymmetries in EEG alpha activity were correlated with performance on these tasks. Similar patterns were obtained for delta and theta bands. Factor analyses of resting EEG asymmetries over particular regions suggested that asymmetries over anterior scalp regions may be partly independent from those over posterior scalp regions. These results support the notions that resting EEG asymmetries are specified by multiple mechanisms along the rostral/caudal plane, and that these asymmetries predict task performance in a manner consistent with lesion and neuroimaging studies.
Is it really possible to change the structure and function of the brain, and in so doing alter how we think and feel? The answer is a resounding yes. In late 2004, leading Western scientists joined the Dalai Lama at his home in Dharamsala, India, to address this very question–and in the process brought about a revolution in our understanding of the human mind. In this fascinating and far-reaching book, Wall Street Journal science writer Sharon Begley reports on how cutting-edge science and the ancient wisdom of Buddhism have come together to show how we all have the power to literally change our brains by changing our minds. These findings hold exciting implications for personal transformation.For decades, the conventional wisdom of neuroscience held that the hardware of the brain is fixed and immutable–that we are stuck with what we were born with. As Begley shows, however, recent pioneering experiments in neuroplasticity, a new science that investigates whether and how the brain can undergo wholesale change, reveal that the brain is capable not only of altering its structure but also of generating new neurons, even into old age. The brain can adapt, heal, renew itself after trauma, and compensate for disability. Begley documents how this fundamental paradigm shift is transforming both our understanding of the human mind and our approach to deep-seated emotional, cognitive, and behavioral problems. These breakthroughs show that it is possible to reset our happiness meter, regain the use of limbs disabled by stroke, train the mind to break cycles of depression and OCD, and reverse age-related changes in the brain. They also suggest that it is possible to teach and learn compassion, a key step in the Dalai Lama’s quest for a more peaceful world. But as we learn from studies performed on Buddhist monks, an important component in changing the brain is to tap the power of mind and, in particular, focused attention. This is the classic Buddhist practice of mindfulness, a technique that has become popular in the West and that is immediately available to everyone. With her extraordinary gift for making science accessible, meaningful, and compelling, Sharon Begley illuminates a profound shift in our understanding of how the brain and the mind interact. This tremendously hopeful book takes us to the leading edge of a revolution in what it means to be human.
This study investigated the effects of imagery on flexibility and the relations among verbal and non-verbal and spontaneous and adaptive flexibility measures. Finally, the effects of brain damage on flexibility and imagery were investigated. Historical and more recent concepts of the cognitive rigidity flexibility dimension were discussed with special emphasis on the effects of brain damage. Forty female and fourteen male volunteer students were tested with verbal and non-verbal flexibility tests. Measures of spontaneous flexibility were the Word Fluency Test and the Five Point Test and measures of adaptive flexibility were the Stroop Test and a newly introduced concept identification test, assessing imagery and interference concepts. Furthermore, a questionnaire to assess individual imagery styles was employed as well as the vocabulary and block design subtests of the WAIS. The results of brain damaged subjects were compared to a matched control group. Furthermore, z-score profiles were prepared to compare the test patterns between the different patient groups. Four dimensions of cognitive flexibility-rigidity were found in healthy subjects. Furthermore it was found that individual imagery styles had little influence on the performance in flexibility tests. A trend was showing that "habitual verbalizers" had no advantage in solving the tests and had in fact more difficulty with the identification of non-verbal concepts. No significant gender effects were found. Brain damaged patients performed significantly more poorly than normal subjects in all flexibility tests. Several test- and subject variables that effect the performance on flexibility tests were discussed. It was concluded that rigidity-flexibility measures represent different dimensions depending on stimulus mode and type of task. It was further concluded that behavioral rigidity-flexibility is not only the function of test variables, but also of various subject variables namely imagery style, intelligence, age, gender and brain damage. In healthy people, the performance on one test was not found to be predictive for the performance on another flexibility test. On the other hand, in brain damaged subjects rigid behavior seems to extend to a wider range of test performance. Finally, different performance patterns were described for different lesion sites in brain damaged.
Many investigators have hypothesized that brain response to cortisol is altered in depression. However, neural activation in response to exogenously manipulated cortisol elevations has not yet been directly examined in depressed humans. Animal research shows that glucocorticoids have robust effects on hippocampal function, and can either enhance or suppress neuroplastic events in the hippocampus depending on a number of factors. We hypothesized that depressed individuals would show 1) altered hippocampal response to exogenous administration of cortisol, and 2) altered effects of cortisol on learning. In a repeated-measures design, 19 unmedicated depressed and 41 healthy individuals completed two fMRI scans. Fifteen mg oral hydrocortisone (i.e., cortisol) or placebo (order randomized and double-blind) was administered 1 h prior to encoding of emotional and neutral words during fMRI scans. Data analysis examined the effects of cortisol administration on 1) brain activation during encoding, and 2) subsequent free recall for words. Cortisol affected subsequent recall performance in depressed but not healthy individuals. We found alterations in hippocampal response to cortisol in depressed women, but not in depressed men (who showed altered response to cortisol in other regions, including subgenual prefrontal cortex). In both depressed men and women, cortisol's effects on hippocampal function were positively correlated with its effects on recall performance assessed days later. Our data provide evidence that in depressed compared to healthy women, cortisol's effects on hippocampal function are altered. Our data also show that in both depressed men and women, cortisol's effects on emotional memory formation and hippocampal function are related.
Individuals who experience early adversity, such as child maltreatment, are at heightened risk for a broad array of social and health difficulties. However, little is known about how this behavioral risk is instantiated in the brain. Here we examine a neurobiological contribution to individual differences in human behavior using methodology appropriate for use with pediatric populations paired with an in-depth measure of social behavior. We show that alterations in the orbitofrontal cortex among individuals who experienced physical abuse are related to social difficulties. These data suggest a biological mechanism linking early social learning to later behavioral outcomes.
BACKGROUND: The broad autism phenotype includes subclinical autistic characteristics found to have a higher prevalence in unaffected family members of individuals with autism. These characteristics primarily affect the social aspects of language, communication, and human interaction. The current research focuses on possible neurobehavioral characteristics associated with the broad autism phenotype. METHODS: We used a face-processing task associated with atypical patterns of gaze fixation and brain function in autism while collecting brain functional magnetic resonance imaging (fMRI) and eye tracking in unaffected siblings of individuals with autism. RESULTS: We found robust differences in gaze fixation and brain function in response to images of human faces in unaffected siblings compared with typically developing control individuals. The siblings' gaze fixations and brain activation patterns during the face processing task were similar to that of the autism group and showed decreased gaze fixation along with diminished fusiform activation compared with the control group. Furthermore, amygdala volume in the siblings was similar to the autism group and was significantly reduced compared with the control group. CONCLUSIONS: Together, these findings provide compelling evidence for differences in social/emotional processing and underlying neural circuitry in siblings of individuals with autism, supporting the notion of unique endophenotypes associated with the broad autism phenotype.
INTRODUCTION: Major depressive disorder (MDD) is characterized by cognitive biases in attention, memory and language use. Language use biases often parallel depression symptoms, and contain over-representations of both negative emotive and death words as well as low levels of positive emotive words. This study further explores cognitive biases in depression by comparing the effect of current depression status to cumulative depression history on an elaborated verbal recall of emotional photographs. METHODS: Following a negative mood induction, fifty-two individuals (42 women) with partially-remitted depression viewed - then recalled and verbally described - slides from the International Affective Picture System (IAPS). Descriptions were transcribed and frequency of depression-related word use (positive emotion, negative emotion, sex, ingestion and death) was analyzed using the Linguistic Inquiry and Word Count program (LIWC). RESULTS: Contrary to expectations and previous findings, current depression status did not affect word use in any categories of interest. However, individuals with more than 5 years of previous depression used fewer words related to positive emotion (t(50) = 2.10, p = .04, (d = 0.57)), and sex (t(48) = 2.50, p = .013 (d = 0.81)), and there was also a trend for these individuals to use fewer ingestion words (t(50) = 1.95, p = .057 (d = 0.58)), suggesting a deficit in appetitive processing. CONCLUSIONS: Our findings suggest that depression duration affects appetitive information processing and that appetitive word use may be a behavioral marker for duration related brain changes which may be used to inform treatment.
A leading researcher in brain dysfunction and a "Wall Street Journal" science writer demonstrate that the human mind is an independent entity that can shape and control the physical brain.
Objective: ADHD is a childhood-onset psychiatric condition that often continues into adulthood. Stimulant medications are the mainstay of treatment; however, additional approaches are frequently desired. In recent years, mindfulness meditation has been proposed to improve attention, reduce stress, and improve mood. This study tests the feasibility of an 8-week mindfulness training program for adults and adolescents with ADHD. Method: Twenty-four adults and eight adolescents with ADHD enrolled in a feasibility study of an 8-week mindfulness training program. Results: The majority of participants completed the training and reported high satisfaction with the training. Pre—post improvements in self-reported ADHD symptoms and test performance on tasks measuring attention and cognitive inhibition were noted. Improvements in anxiety and depressive symptoms were also observed. Conclusion: Mindfulness training is a feasible intervention in a subset of ADHD adults and adolescents and may improve behavioral and neurocognitive impairments. A controlled clinical study is warranted. (J. of Att. Dis. 2008; 11(6) 737-746)
Ironically, in spite of the label "affective disorders", research on affective disorders has little to say about just what is disordered about emotion in these illnesses. One major purpose of this Special Issue is to begin to raise this question as a legitimate domain of inquiry in studies of emotion and psychopathology. Historically, the literature on emotion in normal subjects has proceeded almost entirely independently of studies of emotion-related psychopathology. And, studies on psychopathology make virtually no reference to basic research on emotion in normals. Major advances have occurred in our understanding of the neural substrates of these affective processes. Their application to the study of disordered emotion in affective and anxiety disorders is comparatively recent. A goal of this Special Issue is to foster increased integration between research on the neural mechanisms underlying normal emotion and disordered emotion in depression and anxiety-related illnesses. It features exemplars of the best research at many levels, from animal studies of the detailed circuitry subserving fear and anxiety, to human studies of cognitive abnormalities in subjects with affective and anxiety disorders. It also highlights a myriad array of methods for making inferences about affective processes, ranging from the biological to the behavioral, and from the molecular to the molar. A central concept that figures prominently in this collection of articles is the importance of individual differences in different components of affective processes. The study of the brain circuitry that underlies such differences in affective style offers great promise in providing a biologically plausible way of parsing the affect domain and developing a theoretically compelling taxonomy of mechanisms that give rise to vulnerability to affective and anxiety disorders.
Differences between dyslexics and controls in the unimanual and bimanual conditions of the peg placement section of the Purdue Pegboard Test were examined. Twenty-three disabled and twenty-three normal readers were studied. The groups were carefully screened on a neuropsychological battery. The disabled readers were comprised of a relatively homogeneous language-disordered subgroup exhibiting deficits in naming. Significant Group X Condition interactions were obtained for both raw and percentile scores and indicated that disabled readers performed worse than controls in the unimanual compared to bimanual conditions. The dyslexics performed particularly poorly compared with controls on the left hand condition. The implications of these data for hypotheses which argue for left hemisphere dysfunction, as well as those which posit interhemispheric transfer deficits in reading disabled children, are discussed.
This experiment was designed to test whether reading disabled boys differ from matched controls on behavioral measures of interhemispheric transfer time (IHTT). Specifically, we proposed that language-disordered reading disabled children who had deficits in naming would show either faster or slower IHTTs compared with controls. From an initial group of 118 right-handed males, we selected a group of 25 disabled and 25 normal readers, matched on age. All subjects had to obtain a full scale IQ of 90 or above, a PIQ score of 85 or above, and a scaled score of 7 or above on the Block Design Subtest of the WISC-R. After meeting additional criteria for group assignment, manual reaction time (RT) measures of IHTT were obtained in response to simple visual and tactile stimuli during two laboratory testing sessions. Half the trials were conducted with the hands in an uncrossed orientation and half with the hands crossed in order to examine the effects of spatial compatibility on estimates of IHTT. The results revealed no overall group differences in IHTT for any of the conditions. However, correlations between IHTT measures and indices of cognitive performance indicated that faster IHTTs were significantly correlated with poorer performance on measures of reading and language function in the dyslexic group. These data are discussed within the context of a model of interhemispheric transfer deficits in disabled readers.
Depression has been associated with dysfunctional executive functions and abnormal activity within the anterior cingulate cortex (ACC), a region critically involved in action regulation. Prior research invites the possibility that executive deficits in depression may arise from abnormal responses to negative feedback or errors, but the underlying neural substrates remain unknown. We hypothesized that abnormal reactions to error would be associated with dysfunctional rostral ACC activity, a region previously implicated in error detection and evaluation of the emotional significance of events. To test this hypothesis, subjects with low and high Beck Depression Inventory (BDI) scores performed an Eriksen Flanker task. To assess whether tonic activity within the rostral ACC predicted post-error adjustments, 128-channel resting EEG data were collected before the task and analyzed with low-resolution electromagnetic tomography (LORETA) using a region-of-interest approach. High BDI subjects were uniquely characterized by significantly lower accuracy after incorrect than correct trials. Mirroring the behavioral findings, high BDI subjects had significantly reduced pretask gamma (36.5-44 Hz) current density within the affective (rostral; BA24, BA25, BA32) but not cognitive (dorsal; BA24', BA32') ACC subdivision. For low, but not high, BDI subjects pretask gamma within the affective ACC subdivision predicted post-error adjustments even after controlling for activity within the cognitive ACC subdivision. Abnormal responses to errors may thus arise due to lower activity within regions subserving affective and/or motivational responses to salient cues. Because rostral ACC regions have been implicated in treatment response in depression, our findings provide initial insight into putative mechanisms fostering treatment response.
Facial expressions of pain are an important part of the pain response, signaling distress to others and eliciting social support. To evaluate how voluntary modulation of this response contributes to the pain experience, 29 subjects were exposed to thermal stimulation while making standardized pain, control, or relaxed faces. Dependent measures were self-reported negative effect (valence and arousal) as well as the intensity of nociceptive stimulation required to reach a given subjective level of pain. No direct social feedback was given by the experimenter. Although the amount of nociceptive stimulation did not differ across face conditions, subjects reported more negative effects in response to painful stimulation while holding the pain face. Subsequent analyses suggested the effects were not due to preexisting differences in the difficulty or unpleasantness of making the pain face. These results suggest that voluntary pain expressions have no positively reinforcing (pain attenuating) qualities, at least in the absence of external contingencies such as social reinforcement, and that such expressions may indeed be associated with higher levels of negative affect in response to similar nociceptive input. PERSPECTIVE: This study demonstrates that making a standardized pain face increases negative affect in response to nociceptive stimulation, even in the absence of social feedback. This suggests that exaggerated facial displays of pain, although often socially reinforced, may also have unintended aversive consequences.
Dynamic adjustments in cognitive control are well documented in conflict tasks, wherein competition from irrelevant stimulus attributes intensifies selection demands and leads to subsequent performance benefits. The current study investigated whether mnemonic demands, in a working memory (WM) task, can drive similar online control modifications. Demand levels (high vs. low) of WM maintenance (memory load of 2 items vs. 1 item) and delay-spanning distractor interference (confusable vs. not confusable with memoranda) were manipulated using a factorial design during a WM delayed-recognition task. Performance was best subsequent to trials in which both maintenance and distractor interference demands were high, followed by trials with high demand in either of these 2 control domains, and worst following trials with low demand in both domains. These results suggest that dynamic adjustments in cognitive control are not triggered exclusively by conflict-specific contexts but are also triggered by WM demands, revealing a putative mechanism by which this system configures itself for successful task performance.