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A crucial demand in dual tasks suffering from a capacity limited processing mechanism is task-order scheduling, i.e. the control of the order in which the two component tasks are processed by this limited processing mechanism. The present study aims to test whether the lateral prefrontal cortex (LPFC) is associated with this demand. For this, 15 participants performed a psychological refractory paradigm (PRP) type dual task in an event-related functional magnetic resonance (fMRI) experiment. In detail, two choice reaction tasks, a visual (response with right hand) and an auditory (response with left hand), were presented with a temporal offset of 200 ms, while the participants were required to respond to the tasks in the order of their presentation. Importantly, the presentation order of the tasks changed randomly. Based on previous evidence, we argue that trials in which the present task order changed as compared to the previous trial (differentorder trials) impose higher demands on task coordination than same-order trials do. The analyses showed that cortical areas along the posterior part of the left inferior frontal sulcus as well as the right posterior middle frontal gyrus were more strongly activated in differentorder than in same-order trials, thus supporting the conclusion that one function of the LPFC for dual-task performance is the temporal coordination of two tasks. Furthermore, it is discussed that the present findings favour the active scheduling over the passive queuing hypothesis of dual-task processing.

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The mature mammalian nervous system alters its functional organization in a use-dependent manner. Enhanced stimulation of a body part enlarges its cortical representational zones and may change its topographic order. Little is known about the perceptual and behavioral relevance of these plastic alterations in cortical organization. We used blind Braille readers who use several fingers on each hand and who do so for many hours each day as a model to investigate this issue. Magnetic source imaging indicated that the cortical somatosensory representation of the fingers was frequently topographically disordered in these subjects; in addition, they frequently misperceived which of these fingers was being touched by a light tactile stimulus. In contrast, neither the disordered representation nor mislocalizations were observed in sighted controls. Blind non-teacher Braille readers who used only one finger for reading were not significantly different from the sighted controls. Thus, usedependent cortical reorganization can be associated with functionally relevant changes in the perceptual and behavioral capacities of the individual.

Sleep is ubiquitous in animals and humans, but its function remains to be further determined. The synaptic homeostasis hypothesis of sleep–wake regulation proposes a homeostatic increase in net synaptic strength and cortical excitability along with decreased inducibility of associative synaptic long-term potentiation (LTP) due to saturation after sleep deprivation. Here we use electrophysiological, behavioural and molecular indices to non-invasively study net synaptic strength and LTP-like plasticity in humans after sleep and sleep deprivation. We demonstrate indices of increased net synaptic strength (TMS intensity to elicit a predefined amplitude of motor-evoked potential and EEG theta activity) and decreased LTP-like plasticity (paired associative stimulation induced change in motor-evoked potential and memory formation) after sleep deprivation. Changes in plasma BDNF are identified as a potential mechanism. Our study indicates that sleep recalibrates homeostatic and associative synaptic plasticity, believed to be the neural basis for adaptive behaviour, in humans.

Background: Mild traumatic brain injury (MTBI) can sometimes lead to persistent postconcussion symptoms. One well accepted hypothesis claims that chronic PCS has a neural origin, and is related to neurobehavioral deficits. But the evidence is not conclusive. In the attempt to characterise chronic MTBI consequences, the present experiment used a group comparison design, which contrasted persons (a) with MTBI and PCS, (b) MTBI without PCS, and (c) matched controls. We predicted that participants who have experienced MTBI but show no signs of PCS would perform similar to controls. At the same time, a subgroup of MTBI participants would show PCS symptoms and only these volunteers would have poorer cognitive performance. Thereby, the performance deficits should be most noticeable in participants with highest PCS severity.

Although a proportion of individuals report chronic cognitive difficulties after mild traumatic brain injury (mTBI), results from behavioral testing have been inconsistent. In fact, the variability inherent to the mTBI population may be masking subtle cognitive deficits. We hypothesized that this variability could be reduced by accounting for post-concussion syndrome (PCS) in the sample. Thirty-six participants with mTBI (>1 year post-injury) and 36 non-head injured controls performed information processing speed (Paced Visual Serial Addition Task, PVSAT) and working memory (n-Back) tasks. Both groups were split by PCS diagnosis (4 groups, all n = 18), with categorization of controls based on symptom report. Participants with mTBI and persistent PCS had significantly greater error rates on both the n-Back and PVSAT, at every difficulty level except 0-Back (used as a test of performance validity). There was no difference between any of the other groups. Therefore, a cognitive deficit can be observed in mTBI participants, even 1 year after injury. Correlations between cognitive performance and symptoms were only observed for mTBI participants, with worse performance correlating with lower sleep quality, in addition to a medium effect size association (falling short of statistical significance) with higher PCS symptoms, post-traumatic stress disorder (PTSD), and anxiety. These results suggest that the reduction in cognitive performance is not due to greater symptom report itself, but is associated to some extent with the initial injury. Furthermore, the results validate the utility of our participant grouping, and demonstrate its potential to reduce the variability observed in previous studies.