Nobuhito Abe

Deceiving Others: Distinct Neural Responses of the Prefrontal Cortex and Amygdala in Simple Fabrication and Deception with Social Interactions

Brain mechanisms for telling lies have been investigated recently using neuroimaging techniques such as functional magnetic resonance imaging and positron emission tomography. Although the advent of these techniques has gradually enabled clarification of the functional contributions of the prefrontal cortex in deception with respect to executive function, the specific roles of subregions within the prefrontal cortex and other brain regions responsible for emotional regulation or social interactions during deception are still unclear. Assuming that the processes of falsifying truthful responses and deceiving others are differentially associated with the activities of these regions, we conducted a positron emission tomography experiment with 2 (truth, lie) 2 (honesty, dishonesty) factorial design. The main effect of falsifying the truthful responses revealed increased brain activity of the left dorsolateral and right anterior prefrontal cortices, supporting the interpretation of previous studies that executive functions are related to making untruthful responses. The main effect of deceiving the interrogator showed activations of the ventromedial prefrontal (medial orbitofrontal) cortex and amygdala, adding new evidence that the brain regions assumed to be responsible for emotional processing or social interaction are active during deceptive behavior similar to that in real-life situations. Further analysis revealed that activity of the right anterior prefrontal cortex showed both effects of deception, indicating that this region has a pivotal role in telling lies. Our results provide clear evidence of functionally dissociable roles of the prefrontal subregions and amygdala for human deception.

Neural Correlates of True Memory, False Memory, and Deception

We used functional magnetic resonance imaging (fMRI) to determine whether neural activity can differentiate between true memory, false memory, and deception. Subjects heard a series of semantically related words and were later asked to make a recognition judgment of old words, semantically related nonstudied words (lures for false recognition), and unrelated new words. They were also asked to make a deceptive response to half of the old and unrelated new words. There were 3 main findings. First, consistent with the notion that executive function supports deception, 2 types of deception (pretending to know and pretending not to know) recruited prefrontal activity. Second, consistent with the sensory reactivation hypothesis, the difference between true recognition and false recognition was found in the left temporoparietal regions probably engaged in the encoding of auditorily presented words. Third, the left prefrontal cortex was activated during pretending to know relative to correct rejection and false recognition, whereas the right anterior hippocampus was activated during false recognition relative to correct rejection and pretending to know. These findings indicate that fMRI can detect the difference in brain activity between deception and false memory despite the fact that subjects respond with “I know” to novel events in both processes.

How the Brain Shapes Deception An Integrated Review of the Literature

How do people tell a lie? One useful approach to addressing this question is to elucidate the neural substrates for deception. Recent conceptual and technical advances in functional neuroimaging have enabled exploration of the psychology of deception more precisely in terms of the specific neuroanatomical mechanisms involved. A growing body of evidence suggests that the prefrontal cortex plays a key role in deception, and some researchers have recently emphasized the importance of other brain regions, such as those responsible for emotion and reward. However, it is still unclear how these regions play a role in making effective decisions to tell a lie. To provide a framework for considering this issue, the present article reviews current accomplishments in the study of the neural basis of deception. First, evolutionary and developmental perspectives are provided to better understand how and when people can make use of deception. The ensuing section introduces several findings on pathological lying and its neural correlate. Next, recent findings in the cognitive neuroscience of deception based on functional neuroimaging and loss-of-function studies are summarized, and possible neural mechanisms underlying deception are proposed. Finally, the priority areas of future neuroscience research—human honesty and dishonesty—are discussed.

Changes in brain activation associated with use of a memory strategy: a functional MRI study

It has been confirmed that some kinds of what are called memory strategies dramatically improve the performance of memory recall. However, there has been no direct research to examine changes in brain activity associated with the use of the method of loci within individuals. In the present study, using fMRI, we compared brain activations before and after instruction in the method of loci during both the encoding and recall phases. The resulting behavioral data showed that the use of the method of loci significantly increased scores for memory recall. The imaging data showed that encoding after instruction in the method of loci, relative to encoding before it, was associated with signal increases in the right inferior frontal gyrus, bilateral middle frontal gyrus, left fusiform gyrus, and bilateral lingual gyrus/posterior cingulate gyrus. Comparison of recall after instruction in the method of loci with that before it showed significant activation in the left parahippocampal gyrus/retrosplenial cortex/cingulate gyrus/lingual gyrus, left precuneus, left fusiform gyrus, and right lingual gyrus/cingulate gyrus. The present study demonstrated the changes in brain activation pattern associated with the use of the method of loci; left fusiform and lingual activity was associated with both the encoding and recall phases, bilateral prefrontal activity with the encoding phase, and activity of the posterior part of the parahippocampal gyrus, retrosplenial cortex, and precuneus with the recall phase. These findings suggest that brain networks mediating episodic encoding and retrieval vary with how individuals encode the same stimuli.

The neurobiology of deception: evidence from neuroimaging and loss-of-function studies

Purpose of reviewVisualization of how the brain generates a lie is now possible because of recent conceptual and technical advances in functional neuroimaging; this has led to a rapid increase in studies related to the cognitive neuroscience of deception. The present review summarizes recent work on the neural substrates that underlie human deceptive behavior. Recent findingsFunctional neuroimaging studies in healthy individuals have revealed that the prefrontal cortex plays a predominant role in deception. In addition, recent evidence obtained from loss-of-function studies with neuropsychological investigation and transcranial direct current stimulation has demonstrated the functional contribution of the prefrontal cortex to deception. Other research into the relationship between deception and the brain has focused on the potential use of functional MRI for lie detection, neural correlates of pathological lying, and brain mechanisms underlying inference of deceit by others. SummaryConverging evidence from multiple sources suggests that the prefrontal cortex organizes the processes of inhibiting true responses and making deceptive responses. The neural mechanisms underlying various other aspects of deception are also gradually being delineated, although the findings are diverse, and further study is needed. These studies represent an important step toward a neural explanation of complex human deceptive behavior.

White matter involvement in idiopathic normal pressure hydrocephalus: a voxel-based diffusion tensor imaging study

The aim of this study was to characterise the white matter damage involved in idiopathic normal pressure hydrocephalus (INPH) using diffusion tensor imaging (DTI) and the relationship between this damage and clinical presentation. Twenty patients with INPH, 20 patients with Alzheimer’s disease and 20 patients with idiopathic Parkinson’s disease (as disease control groups) were enrolled in this study. Mean diffusivity (MD) and fractional anisotropy (FA) were determined using DTI, and these measures were analysed to compare the INPH group with the control groups and with certain clinical correlates. On average, the supratentorial white matter presented higher MD and lower FA in the INPH group than in the control groups. In the INPH group, the mean hemispheric FA correlated with some of the clinical measures, whereas the mean hemispheric MD did not. On a voxel-based statistical map, white matter involvement with high MD was localised to the periventricular regions, and white matter involvement with low FA was localised to the corpus callosum and the subcortical regions. The total scores on the Frontal Assessment Battery were correlated with the FA in the frontal and parietal subcortical white matter, and an index of gait disturbance was correlated with the FA in the anterior limb of the left internal capsule and under the left supplementary motor area. DTI revealed the presence of white matter involvement in INPH. Whereas white matter regions with high MD were not related to symptom manifestation, those with low FA were related to motor and cognitive dysfunction in INPH.

Memory repression: Brain mechanisms underlying dissociative amnesia

Dissociative amnesia usually follows a stressful event and cannot be attributable to explicit brain damage. It is thought to reflect a reversible deficit in memory retrieval probably due to memory repression. However, the neural mechanisms underlying this condition are not clear. We used fMRI to investigate neural activity associated with memory retrieval in two patients with dissociative amnesia. For each patient, three categories of face photographs and three categories of peoples names corresponding to the photographs were prepared: those of “recognizable” high school friends who were acquainted with and recognizable to the patients, those of “unrecognizable” colleagues who were actually acquainted with but unrecognizable to the patients due to their memory impairments, and “control” distracters who were unacquainted with the patients. During fMRI, the patients were visually presented with these stimuli and asked to indicate whether they were personally acquainted with them. In the comparison of the unrecognizable condition with the recognizable condition, we found increased activity in the pFC and decreased activity in the hippocampus in both patients. After treatment for retrograde amnesia, the altered pattern of brain activation disappeared in one patient whose retrograde memories were recovered, whereas it remained unchanged in the other patient whose retrograde memories were not recovered. Our findings provide direct evidence that memory repression in dissociative amnesia is associated with an altered pattern of neural activity, and they suggest the possibility that the pFC has an important role in inhibiting the activity of the hippocampus in memory repression.

The role of the dorsolateral prefrontal cortex in deception when remembering neutral and emotional events

We used functional magnetic resonance imaging (fMRI) to investigate the neural correlates of deception while remembering neutral events and emotional events. Before fMRI, subjects were presented with a series of neutral and emotional pictures and were asked to rate each picture for arousal. During fMRI, subjects were presented with the studied and nonstudied pictures and were asked to make an honest recognition judgment in response to half of the pictures and a dishonest response to the remaining half. We found that deception pertaining to the memory of neutral pictures was associated with increased activity in the bilateral dorsolateral prefrontal cortex, the left ventrolateral prefrontal cortex, and the left orbitofrontal cortex. We also found that deception while remembering emotional pictures was associated with increased activity in the bilateral dorsolateral prefrontal cortex. An overlapping activation between the two types of deception was found in the bilateral dorsolateral prefrontal cortex. Our results indicate that the dorsolateral prefrontal cortex is associated with the executive aspects of deception, regardless of the emotional valence of memory content.

Do parkinsonian patients have trouble telling lies? The neurobiological basis of deceptive behaviour

Parkinsons disease is a common neurodegenerative disorder with both motor symptoms and cognitive deficits such as executive dysfunction. Over the past 100 years, a growing body of literature has suggested that patients with Parkinsons disease have characteristic personality traits such as industriousness, seriousness and inflexibility. They have also been described as ‘honest’, indicating that they have a tendency not to deceive others. However, these personality traits may actually be associated with dysfunction of specific brain regions affected by the disease. In the present study, we show that patients with Parkinsons disease are indeed ‘honest’, and that this personality trait might be derived from dysfunction of the prefrontal cortex. Using a novel cognitive task, we confirmed that patients with Parkinsons disease (n = 32) had difficulty making deceptive responses relative to healthy controls (n = 20). Also, using resting-state 18F-fluorodeoxyglucose PET, we showed that this difficulty was significantly correlated with prefrontal hypometabolism. Our results are the first to demonstrate that the ostensible honesty found in patients with Parkinsons disease has a neurobiological basis, and they provide direct neuropsychological evidence of the brain mechanisms crucial for human deceptive behaviour.

A 12-Week Physical and Cognitive Exercise Program Can Improve Cognitive Function and Neural Efficiency in Community-Dwelling Older Adults: A Randomized Controlled Trial

To investigate whether a 12‐week physical and cognitive exercise program can improve cognitive function and brain activation efficiency in community‐dwelling older adults.