Event-related fMRI is a powerful tool for localising psychological functions to specific brain areas. However, the number of events required to produce stable activation maps is a poorly investigated and understood problem. Huettel and McCarthy [Huettel, S.A., McCarthy, G., 2001. The effects of single-trial averaging upon the spatial extent of fMRI activation. NeuroReport 12, 2411 -2416] have shown that the spatial extent of activation increases monotonically with the number of events in an analysis. In the present paper, this result is replicated and shown to be a consequence of the cross-correlation technique used to determine active voxels and does not hold, for example, for a GLM analysis. Another analysis technique, that does not depend on goodness-of-fit to the data, is also proposed. This technique calculates an impulse response function (IRF) for each voxel, finds the best fitting haemodynamic shape to the IRF and returns an area-under-the-curve (%AUC) activation measure. Using spatial extent as a measure, asymptotic behaviour is evident after as few as 25 events for the %AUC analysis technique in a finger-tapping task with non-overlapping haemodynamic responses and for both the GLM and %AUC techniques in a similar task that allows responses to overlap. The experimental validity of the %AUC technique to identify active brain regions while minimising false positive levels is demonstrated in a group study with 25 participants. D
Visual processing deficits are an integral component of schizophrenia and are sensitive predictors of schizophrenic decompensation in healthy adults. The primate visual system consists of discrete subcortical magnocellular and parvocellular pathways, which project preferentially to dorsal and ventral cortical streams. Subcortical systems show differential stimulus sensitivity, while cortical systems, in turn, can be differentiated using surface potential analysis. The present study examined contributions of subcortical dysfunction to cortical processing deficits using high-density event-related potentials. Event-related potentials were recorded to stimuli biased towards the magnocellular system using low-contrast isolated checks in Experiment 1 and towards the magnocellular or parvocellular system using low versus high spatial frequency (HSF) sinusoidal gratings, respectively, in Experiment 2. The sample consisted of 23 patients with schizophrenia or schizoaffective disorder and 19 non-psychiatric volunteers of similar age. In Experiment 1, a large decrease in the P1 component of the visual event-related potential in response to magnocellular-biased isolated check stimuli was seen in patients compared with controls (F = 13.2, P = 0.001). Patients also showed decreased slope of the contrast response function over the magnocellular-selective contrast range compared with controls (t = 9.2, P = 0.04) indicating decreased signal amplification. In Experiment 2, C1 (F = 8.5, P = 0.007), P1 (F = 33.1, P < 0.001) and N1 (F = 60.8, P < 0.001) were reduced in amplitude to magnocellular-biased low spatial frequency (LSF) stimuli in patients with schizophrenia, but were intact to parvocellular-biased HSF stimuli, regardless of generator location. Source waveforms derived from inverse dipole modelling showed reduced P1 in Experiment 1 and reduced C1, P1 and N1 to LSF stimuli in Experiment 2, consistent with surface waveforms. These results indicate pervasive magnocellular dysfunction at the subcortical level that leads to secondary impairment in activation of cortical visual structures within dorsal and ventral stream visual pathways. Our finding of early visual dysfunction is consistent with and explanatory of classic literature showing subjective complaints of visual distortions and is consistent with early visual processing deficits reported in schizophrenia. Although deficits in visual processing have frequently been construed as resulting from failures of top-down processing, the present findings argue strongly for bottom-up rather than top-down dysfunction at least within the early visual pathway. Deficits in magnocellular processing in this task may reflect more general impairments in neuronal systems functioning, such as deficits in non-linear amplification and may thus represent an organizing principle for predicting neurocognitive dysfunction in schizophrenia.
Several studies have reported reduced cerebral gray matter (GM) volume/density in chronic pain conditions, but there is limited research on plasticity of the human cortex in response to psychological interventions. We investigated GM changes after cognitive behavioral therapy (CBT) in patients with chronic pain. We used voxel based morphometry (VBM) to compare anatomical MRI scans of 13 patients with mixed chronic pain types before and after an 11-week CBT treatment and to 13 healthy control participants. CBT led to significant improvements in clinical measures. Patients did not differ from healthy controls in GM anywhere in the brain. After treatment, patients had increased GM in bilateral dorsolateral prefrontal (DLPFC), posterior parietal (PPC), subgenual anterior cingulate (ACC)/orbitofrontal, and sensorimotor cortices, as well as hippocampus, and reduced GM in supplementary motor area. In most of these areas showing GM increases, GM became significantly higher than in controls. Decreased pain catastrophizing was associated with increased GM in left DLPFC and ventrolateral prefrontal (VLPFC), right PPC, somatosensory cortex, and pregenual ACC. While future studies with additional control groups will be needed to determine the specific roles of CBT on GM and brain function, we propose that increased GM in the PFC and PPC reflects greater top-down control over pain and cognitive reappraisal of pain, and that changes in somatosensory cortices reflect alterations in the perception of noxious signals. Perspective An 11-week CBT intervention for coping with chronic pain resulted in increased gray matter volume in prefrontal and somatosensory brain regions, as well as increased dorsolateral prefrontal volume associated with reduced pain catastrophizing. These results add to mounting evidence that CBT can be a valuable treatment option for chronic pain.
Within the visual modality, it has been shown that attention to a single visual feature of an object such as speed of motion, results in an automatic transfer of attention to other task-irrelevant features (e.g. colour). An extension of this logic might lead one to predict that such mechanisms also operate across sensory systems. But, connectivity patterns between feature modules across sensory systems are thought to be sparser to those within a given sensory system, where interareal connectivity is extensive. It is not clear that transfer of attention between sensory systems will operate as it does within a sensory system. Using high-density electrical mapping of the event-related potential (ERP) in humans, we tested whether attending to objects in one sensory modality resulted in the preferential processing of that object's features within another task-irrelevant sensory modality. Clear evidence for cross-sensory attention effects was seen, such that for multisensory stimuli responses to ignored task-irrelevant information in the auditory and visual domains were selectively enhanced when they were features of the explicitly attended object presented in the attended sensory modality. We conclude that attending to an object within one sensory modality results in coactivation of that object's representations in ignored sensory modalities. The data further suggest that transfer of attention from visual-to-auditory features operates in a fundamentally different manner than transfer from auditory-to-visual features, and indicate that visual-object representations have a greater influence on their auditory counterparts than vice-versa. These data are discussed in terms of 'priming' vs. 'spreading' accounts of attentional transfer.
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