Obsessive compulsive disorder (OCD) is characterized by intrusive thoughts and repetitive ritualistic behaviors and has been associated with diverse functional brain abnormalities. We sought to synthesize current evidence from functional magnetic resonance imaging (fMRI) studies and examine their alignment to pathogenetic models of OCD. Following systematic review, we identified 54 task-fMRI studies published in the last decade comparing adults with OCD (n = 1186) to healthy adults (n = 1159) using tasks of affective and non-affective cognition. We used voxel-based quantitative meta-analytic methods to combine primary data on anatomical coordinates of case-control differences, separately for affective and non-affective tasks. We found that functional abnormalities in OCD cluster within cortico-striatal thalamic circuits. Within these circuits, the abnormalities identified showed significant dependence on the affective or non-affective nature of the tasks employed as circuit probes. In studies using affective tasks, patients overactivated regions involved in salience, arousal and habitual responding (anterior cingulate cortex, insula, caudate head and putamen) and underactivated regions implicated in cognitive and behavioral control (medial prefrontal cortex, posterior caudate). In studies using non-affective cognitive tasks, patients overactivated regions involved in self-referential processing (precuneus, posterior cingulate cortex) and underactivated subcortical regions that support goal-directed cognition and motor control (pallidum, ventral anterior thalamus, posterior caudate). The overall pattern suggests that OCD-related brain dysfunction involves increased affective and self-referential processing, enhanced habitual responding and blunted cognitive control.

Positron emission tomography is one of the most important techniques of functional imaging in psychiatry. This paper gives a synopsis of the findings in mood disorders: determination of brain glucose metabolism, cerebral blood flow and receptor studies. Investigation in a resting state as well as after activation are discussed.

Although findings are somewhat discrepant hypometabolism, and/or hypoperfusion, most often in frontal and limbic areas are frequently described. Further research is needed, and standardization of the methodology would be most wellcome.

A magnetoencephalogram (MEG) is the registration of the magnetic field in points near the head. Because MEG's are weak fields, they have to be measured by means of superconducting sensors. The electric active population of neurons can be computed from the distribution of the magnetic field at a certain instant of time. This is called the inverse problem. In order to solve this probem, both the generators and the head have to be modelled. Usually, a patch of active neurons is modelled as a current dipole. Commonly, the head is described by three compartments, representing the brain, the skull and the scalp. The compartments may have the shape of spheres or they may have a realistic shape. Integration of EEG and MEG with MRI leads to a technique for functional imaging of the brain with a time resolution of one millisecond and a spatial resolution of one centimetre. Clinical applications are the non-invasive localization of an epileptic focus or the presurgical mapping of the sensorimotor cortex.

This review discusses the contributions of functional imaging (fMRI/PET) to our understanding of how semantic concepts are represented and processed in the human brain. The sensory-motor theory of semantic memory suggests that semantic processing relies on reactivation of sensory-motor representations that were involved in perception and action. More specifically, it attributes an apparent category-specific (e.g. tool vs. animals) organization of semantics to anatomical segregation for different semantic features (e.g. action vs. visual). Within this framework, we will review functional imaging evidence that semantic processing of tools and actions may rely on activations within the visuo-motor system.

In June 2011 a two-day expert meeting “The Ageing Brain” took place in Amsterdam, The Netherlands. The main aim was to discuss the available preclinical and clinical data on Ginkgo biloba special extract EGb 761® in the context of current developments in the diagnosis and treatment of age-related cognitive decline and Alzheimer's disease. 19 dementia experts covering the disciplines bio- and neurochemistry, gerontology, neurology, pharmacology, and psychiatry from Australia, Asia, Europe and North America reviewed available preclinical and clinical data for EGb 761® and identified core topics for future research. Based on a wide range of preclinical effects demonstrated for Ginkgo biloba, EGb 761® can be conceptualized as a multi-target compound with activity on distinct pathophysiological pathways in Alzheimer's disease (AD) and age-related cognitive decline. While symptomatic efficacy in dementia and mild cognitive impairment (MCI) has been demonstrated, interpretation of data from dementia prevention trials is complicated by important methodological issues. Bridging pre-clinical research and clinical research as well as deciding on suitable study designs for future trials with EGb 761® remain important questions. The participants of the “Ageing Brain” meeting on Ginkgo biloba special extract EGb 761® concluded that there is plenty of promising data, both pre-clinical and clinical, to consider future research with the compound targeting cognitive impairment in old age as a worthwhile activity.

The idea of reserve against brain damage stems from the repeated observation that there does not appear to be a direct relationship between the degree of brain pathology or brain damage and the clinical manifestation of that damage. This paper attempts to develop a coherent theoretical account of reserve. One convenient subdivision of reserve models revolves around whether they envision reserve as a passive process, such as in brain reserve or threshold, or see the brain as actively attempting to cope with or compensate for pathology, as in cognitive reserve. Cognitive reserve may be based on more efficient utilization of brain networks or of enhanced ability to recruit alternate brain networks as needed. A distinction is suggested between reserve, the ability to optimize or maximize normal performance, and compensation, an attempt to maximize performance in the face of brain damage by using brain structures or networks not engaged when the brain is not damaged. Epidemiologic and imaging data that help to develop and support the concept of reserve are presented. (JINS, 2002, 8, 448–460.)

Category-specific impairments of object recognition and naming are among the most intriguing disorders in neuropsychology, affecting the retrieval of knowledge about either living or nonliving things. They can give us insight into the nature of our representations of objects: Have we evolved different neural systems for recognizing different categories of object? What kinds of knowledge are important for recognizing particular objects? How does visual similarity within a category influence object recognition and representation? What is the nature of our semantic knowledge about different objects? We review the evidence on category-specific impairments, arguing that deficits even for one class of object (e.g., living things) cannot be accounted for in terms of a single information processing disorder across all patients; problems arise at contrasting loci in different patients. The same apparent pattern of impairment can be produced by damage to different loci. According to a new processing framework for object recognition and naming, the hierarchical interactive theory (HIT), we have a hierarchy of highly interactive stored representations. HIT explains the variety of patients in terms of (1) lesions at different levels of processing and (2) different forms of stored knowledge used both for particular tasks and for particular categories of object.

We present evidence disputing the hypothesis that memories are processed or consolidated in REM sleep. A review of REM deprivation (REMD) studies in animals shows these reports to be about equally divided in showing that REMD does, or does not, disrupt learning/memory. The studies supporting a relationship between REM sleep and memory have been strongly criticized for the confounding effects of very stressful REM deprivation techniques. The three major classes of antidepressant drugs, monoamine oxidase inhibitors (MAOIs), tricyclic antidepressants (TCAs), and selective serotonin reuptake inhibitors (SSRIs), profoundly suppress REM sleep. The MAOIs virtually abolish REM sleep, and the TCAs and SSRIs have been shown to produce immediate (40–85%) and sustained (30–50%) reductions in REM sleep. Despite marked suppression of REM sleep, these classes of antidepressants on the whole do not disrupt learning/memory. There have been a few reports of patients who have survived bilateral lesions of the pons with few lingering complications. Although these lesions essentially abolished REM sleep, the patients reportedly led normal lives. Recent functional imaging studies in humans have revealed patterns of brain activity in REM sleep that are consistent with dream processes but not with memory consolidation. We propose that the primary function of REM sleep is to provide periodic endogenous stimulation to the brain which serves to maintain requisite levels of central nervous system (CNS) activity throughout sleep. REM is the mechanism used by the brain to promote recovery from sleep. We believe that the cumulative evidence indicates that REM sleep serves no role in the processing or consolidation of memory.