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Rhesus monkeys with neonatal aspiration lesions of the hippocampal formation or the amygdaloid complex were tested on concurrent discrimination learning (24-hr intertrial interval [ITI]) at 3 months, on object recognition memory (delayed nonmatching-to-sample [DNMS]) at 10 months, and retested on both tasks at 6-7 years of age. Neonatal amygdaloid damage mildly impaired acquisition at the 24-hr ITI and the performance test of DNMS at both ages. In contrast, early hippocampal lesions impaired performance only on the longest lists of 10 items in DNMS in adult monkeys. Thus, early amygdala lesions appeared to have resulted in a greater object memory loss than early hippocampal lesions. However, in light of recent findings from lesion studies in adult monkeys, the object memory impairment after early amygdaloid lesions is better accounted for by damage to the entorhinal and perirhinal cortex than by damage to the amygdaloid nuclei.

Three-dimensional multiple object tracking (3D-MOT) is a perceptual-cognitive training system based on a 3D virtual environment. This is the first study to examine the effects of 3D-MOT training on attention, working memory, and visual information processing speed as well as using functional brain imaging on a normative population. Twenty university-aged students were recruited and divided into a training (NT) and nonactive control (CON) group. Cognitive functions were assessed using neuropsychological tests, and correlates of brain functions were assessed using quantitative electroencephalography (qEEG). Results indicate that 10 sessions of 3D-MOT training can enhance attention, visual information processing speed, and working memory, and also leads to quantifiable changes in resting-state neuroelectric brain function.

It has been long established that psychological interventions can markedly alter patients' thinking patterns, beliefs, attitudes, emotional states, and behaviors. Little was known about the neural mechanisms mediating such alterations before the advent of functional neuroimaging techniques. Since the turn of the new millenium, several functional neuroimaging studies have been conducted to tackle this important issue. Some of these studies have explored the neural impact of various forms of psychotherapy in individuals with major depressive disorder. Other neuroimaging studies have investigated the effects of psychological interventions for anxiety disorders. I review these studies in the present article, and discuss the putative neural mechanisms of change in psychotherapy. The findings of these studies suggest that mental and behavioral changes occurring during psychotherapeutic interventions can lead to a normalization of functional brain activity at a global level.

The main objective of this structural magnetic resonance imaging (MRI) study was to investigate, using diffusion tensor imaging, whether a neurofeedback training (NFT) protocol designed to improve sustained attention might induce structural changes in white matter (WM) pathways, purportedly implicated in this cognitive ability. Another goal was to examine whether gray matter (GM) volume (GMV) might be altered following NFT in frontal and parietal cortical areas connected by these WM fiber pathways. Healthy university students were randomly assigned to an experimental group (EXP), a sham group, or a control group. Participants in the EXP group were trained to enhance the amplitude of their β1 waves at F4 and P4. Measures of attentional performance and MRI data were acquired one week before (Time 1) and one week after (Time 2) NFT. Higher scores on visual and auditory sustained attention were noted in the EXP group at Time 2 (relative to Time 1). As for structural MRI data, increased fractional anisotropy was measured in WM pathways implicated in sustained attention, and GMV increases were detected in cerebral structures involved in this type of attention. After 50 years of research in the field of neurofeedback, our study constitutes the first empirical demonstration that NFT can lead to microstructural changes in white and gray matter.

An inability to self-regulate negative emotions appears to play a pivotal role in the genesis of major depressive disorder. This inability may be related to a dysfunction of the neural circuitry underlying emotional self-regulation. This functional magnetic resonance imaging study was conducted to test this hypothesis. Depressed individuals and controls were scanned while they attempted to voluntarily down-regulate sad feelings. The degree of difficulty experienced during down-regulation of sadness was higher in depressed individuals. Furthermore, there was greater activation in the right dorsal anterior cingulate cortex, right anterior temporal pole, right amygdala, and right insula in depressed individuals. These results suggest that emotional dysregulation in major depressive disorder is related to a disturbance in the neural circuitry of emotional self-regulation.

Objective: There have been reports that patients with schizophrenia have decreased activity in the prefrontal cortex during emotion processing. However, findings have been confounded by sample nonspecificity and explicit cognitive task interference with emotion processing. We aimed to further investigate this by examining the ventrolateral prefrontal cortex (VLPFC) activation in response to the passive viewing of sad film excerpts.Methods: We presented film excerpts depicting sad and neutral social situations to 25 schizophrenia patients (14 with blunted affect [BA+] and 11 without blunted affect [BA-]) in an implicit perception task to evoke prefronto-limbic activity illustrated by blood oxygenation level–dependent functional magnetic resonance imaging.Results: A random-effects analysis (2-sample ttest) using statistical parametric mapping indicated that BA+ patients differed from BA–patients at a 0.05 level (Pcorrected for multiple comparisons). Consistent with our a priori hypothesis, BA–patients (relative to BA+ patients) showed significant activation in the right VLPFC. An exploratory analysis revealed the following loci of activation: caudate nucleus, VLPFC, middle prefrontal cortex, medial prefrontal cortex, anterior cingulate cortex, and anterior temporal pole in the BA–group; and hippocampus, cerebellum, anterior temporal pole, and midbrain in the BA+ group.Conclusions: We observed not only hypofrontality in the BA+ group but also dysfunctional circuitry distributed throughout the brain. The temporal and midbrain activation seen in the BA+ group may indicate that these brain regions were working harder to compensate for inactivation in other regions. These distributed dysfunctional circuits may form the neural basis of blunted affect through impairment of emotion processing in the brain that prevents it from processing input efficiently and producing output effectively, thereby leading to symptoms such as blunted affect.

Blood-oxygenation-level-dependent (BOLD) brain changes underlying response to quetiapine were examined using passive viewing of emotionally negative stimuli. Twelve DSM-IV schizophrenia patients with blunted affect (BA+) were scanned before and after 22 weeks of quetiapine treatment. Whole-brain, voxel-based methods were used to assess the differential hemodynamic response to quetiapine. In addition, a post hoc comparison to an independent group of 11 schizophrenia patients without blunted affect (BA−) was performed to compare them with BA+ (postquetiapine) in response to emotion processing. A 22-week treatment with quetiapine resulted in significant clinical improvement in the 12 study completers (mean ± SD posttreatment PANSS blunted affect score of 5.50 ± 0.76 at baseline to 2.08 ± 1.00 at end point; t= 7.78, df= 11, P< 0.0001). Treatment response was associated with significant BOLD changes increases in prefrontal cortex activation particularly in the right dorsolateral prefrontal cortex (DLPFC, BA 46) and the right anterior cingulate cortex (ACC, BA 32); and in the left putamen, right anterior temporal pole (ATP), and right amygdala. Conversely, before treatment with quetiapine, the same subjects activated the midbrain bilaterally and the right pons. The post hoc conjunctional analyses demonstrated that BA− subjects activated the left ACC, left insula, left ATP (BA 21), left ATP (BA 38), left amygdala, and right medial prefrontal cortex. Quetiapine seems to affect clinical recovery by modulating the functioning of specific brain regions. Unique BOLD changes in the putamen and DLPFC with quetiapine, in the BA+ postquetiapine, may reflect modality-specific effects. Controlled studies are needed to further assess these preliminary findings.

Neuropsychological research on the neural basis of behaviour generally posits that brain mechanisms will ultimately suffice to explain all psychologically described phenomena. This assumption stems from the idea that the brain is made up entirely of material particles and fields, and that all causal mechanisms relevant to neuroscience can therefore be formulated solely in terms of properties of these elements. Thus, terms having intrinsic mentalistic and/or experiential content (e.g. ‘feeling’, ‘knowing’ and ‘effort’) are not included as primary causal factors. This theoretical restriction is motivated primarily by ideas about the natural world that have been known to be fundamentally incorrect for more than three-quarters of a century. Contemporary basic physical theory differs profoundly from classic physics on the important matter of how the consciousness of human agents enters into the structure of empirical phenomena. The new principles contradict the older idea that local mechanical processes alone can account for the structure of all observed empirical data. Contemporary physical theory brings directly and irreducibly into the overall causal structure certain psychologically described choices made by human agents about how they will act. This key development in basic physical theory is applicable to neuroscience, and it provides neuroscientists and psychologists with an alternative conceptual framework for describing neural processes. Indeed, owing to certain structural features of ion channels critical to synaptic function, contemporary physical theory must in principle be used when analysing human brain dynamics. The new framework, unlike its classic-physics-based predecessor, is erected directly upon, and is compatible with, the prevailing principles of physics. It is able to represent more adequately than classic concepts the neuroplastic mechanisms relevant to the growing number of empirical studies of the capacity of directed attention and mental effort to systematically alter brain function.

Findings of category-specific impairments have suggested that human semantic memory may be organized around a living/nonliving dichotomy. In order to assess implicit memory performance for living and nonliving concepts, one group of neurologically intact individuals participated in a cross-form conceptual priming paradigm. In Block 1, pictures primed words while in Block 2 words were used to prime pictures. Across all phases of the experiment, subjects decided whether items represented something which was living or nonliving, and response times were recorded. Results revealed greater priming for living concepts across both blocks. Greater priming for living concepts may have occurred because of increased or prolonged conceptual activation of these concepts. Results are discussed in the context of theoretical accounts of the category-specific impairments observed in brain-damaged populations. (JINS, 2003, 9, 796–805.)

The question of whether distinct or similar neural substrates underlie primary emotions has not been resolved yet. To address this issue, we used fMRI to scan professional actors during self-induced states of sadness and happiness. Results demonstrated that, relative to an emotionally Neutral state, both the Sad and the Happy states were associated with significant loci of activation, bilaterally, in the orbitofrontal cortex, and in the left medial prefrontal cortex, left ventrolateral prefrontal cortex, left anterior temporal pole, and right pons. These loci of activation were localized distinctly within these regions, that is, in different sub-regions. These results suggest that sadness and happiness may be associated with similar brain regions but distinct sub-regions and neural circuits.

Various lines of evidence indicate that men generally experience greater sexual arousal (SA) to erotic stimuli than women. Yet, little is known regarding the neurobiological processes underlying such a gender difference. To investigate this issue, functional magnetic resonance imaging was used to compare the neural correlates of SA in 20 male and 20 female subjects. Brain activity was measured while male and female subjects were viewing erotic film excerpts. Results showed that the level of perceived SA was significantly higher in male than in female subjects. When compared to viewing emotionally neutral film excerpts, viewing erotic film excerpts was associated, for both genders, with bilateral blood oxygen level dependant (BOLD) signal increases in the anterior cingulate, medial prefrontal, orbitofrontal, insular, and occipitotemporal cortices, as well as in the amygdala and the ventral striatum. Only for the group of male subjects was there evidence of a significant activation of the thalamus and hypothalamus, a sexually dimorphic area of the brain known to play a pivotal role in physiological arousal and sexual behavior. When directly compared between genders, hypothalamic activation was found to be significantly greater in male subjects. Furthermore, for male subjects only, the magnitude of hypothalamic activation was positively correlated with reported levels of SA. These findings reveal the existence of similarities and dissimilarities in the way the brain of both genders responds to erotic stimuli. They further suggest that the greater SA generally experienced by men, when viewing erotica, may be related to the functional gender difference found here with respect to the hypothalamus. Hum. Brain Mapping 16:1–13, 2002. © 2002 Wiley‐Liss, Inc.

Animal studies and observations of neglect patients suggest that the posterior parietal cortex is part of a system that codes egocentred space. Few studies show the existence of areas involved in the representation of egocentred space in healthy humans. We investigated with fMRI and a conjunction protocol, the overlap of activity between optokinetic stimulation and a task of midline computation. Results showed that the right posterior parietal and frontal cortices were involved in both tasks (p<0.0001). The evidence presented in this study provides the neuroanatomical substrate involved in the recovery of neglect during vestibular stimulation. This last point is of clinical interest for the rehabilitation of hemineglect.

AN important issue regarding the neural basis of major depression is whether the functional brain changes associated with the affect disturbance seen in this syndrome are similar to those that accompany transient sadness in normal subjects. To address this question, we carried out an fMRI study using an emotional activation paradigm. Brain activity associated with passive viewing of an emotionally laden film clip aimed at inducing a transient state of sadness was contrasted with that associated with passive viewing of an emotionally neutral film clip in patients suffering from unipolar depression and in normal control subjects. Results showed that transient sadness produced significant activation in the medial and inferior prefrontal cortices, the middle temporal cortex, the cerebellum and the caudate in both depressed and normal subjects. They also revealed that passive viewing of the emotionally laden film clip produced a significantly greater activation in the left medial prefrontal cortex and in the right cingulate gyrus in depressed patients than in normal control subjects. These findings suggest that these two cortical regions might be part of a neural network implicated in the pathophysiology of major depression. Taken together, these results strongly support the view that activation paradigms represent an extremely useful and powerful way of delineating the functional anatomy of the various symptoms that characterize major depression.

A major methodological limitation arising in the experimental study of implicit memory is that tasks that are characterized as implicit memory tests can be seriously contaminated by the use of covert explicit memory strategies. Given the evidence indicating that brief presentation of words (below the awareness threshold of subjects) can produce semantic priming, we wondered whether rapid visual presentation of primed words might provide an avenue to produce word priming without explicit memory contamination. Normal subjects were tested for word priming on a speeded category membership decision task. Explicit or implicit encoding procedures were used in four different experiments. Results demonstrated that brief presentation of words can indeed offer a means of producing word priming in absence of explicit recognition or recall of the primed words presented during the study phase. They also showed that such priming is equivalent in degree to the priming measured when using either a conventional implicit memory design or an explicit encoding procedure prior to the study of the primes.

THE present study was aimed at determining whether early hippocampal damage alters the development of normal social interactions. Results showed that, at 2 months of age, animals with neonatal hippocampal lesions presented minor disturbances in initiation of social interactions. These subtle changes in behavior were less evident at 6 months, although at this age, the operated animals displayed more withdrawals in response to an increase in aggressive responses from their unoperated peers. Finally, in adulthood, the amount of time spent by the operated monkeys in social contacts with their normal peers was markedly less than that in normal dyads. Only in adulthood did the operated animals exhibit more locomotor Stereotypies than normal controls. This finding suggest that the hippocampal formation may directly or indirectly affect the maintenance of social bounds in primates.

THE apparent preservation of word priming effects in amnesia has been interpreted as supporting the view that implicit memory depends on brain systems that are independent of mesial temporal lobe structures which are in part responsible for explicit memory disorders. Nevertheless, a number of studies have demonstrated word priming deficits in amnesic patients relatively to normal subjects, suggesting that such structures may also be involved in implicit memory. To determine whether one such structure, the hippocampal formation, is a component of the brain system subserving word priming, a 3-D PET study was carried out in 13 normal individuals. Encoding was carried out using the brief multiple presentation technique, a procedure that allows one to effectively circumvent contamination of implicit memory tasks by explicit memory strategies. Results revealed that word priming was indeed associated with an activation of the right hippocampal formation. This finding of an hippocampal involvement in word priming calls into question the notion of absolute dissociability between the brain systems underlying performance on various explicit and implicit memory tasks.

Objective: To review the mounting evidence implicating early hippocampal dysfunction in the pathogenesis and the pathophysiology of schizophrenia. An account is made of recent neurodevelopmental hypotheses indicating how an early dysfunction of the hippocampal region disrupts maturational events in brain systems connected to that structure, thus inducing dysfunctional connectional development. Finally, an animal model is presented.Method: Socioemotional behaviour of monkeys(Macaca mulatta) with selective neonatal hippocampal lesions was assessed by analyzing their interactions with their age-matched controls at 2 months, 6 months, and 5 to 8 years of age and by comparing the social interactions at each age with those of normal controls paired together.Results: At 2 months of age, monkeys with neonatal hippocampal lesions presented minor disturbances in initiation of social interactions. These subtle changes of behaviour were less evident at 6 months, although by that age, the operated monkeys displayed more withdrawals in response to an increase in aggressive responses from their unoperated peers. In adulthood, the amount of time spent by the hippocampectomized monkeys in social contacts with their normal peers decreased markedly. In addition, operated monkeys exhibited more locomotor stereotypies than normal controls.Conclusion: These experimental findings indicate that the time-course and nature of the behavioural disturbances resulting from early trauma to the hippocampal region have some similarities with the clinical symptoms of schizophrenic patients and the typical time-course of the disease.

A letter to the editor is presented in response to an article on the cultural war over the brain which is claimed to represent non-materialist neuroscience in the October 25, 2008 issue.