Response inhibition is an important cognitive-control function that allows for already-initiated or habitual behavioral responses to be promptly withheld when needed. A typical paradigm to study this function is the stop-signal task. From this task, the stop-signal response time (SSRT) can be derived, which indexes how rapidly an already-initiated response can be canceled. Typically, SSRTs range around 200 ms, identifying response inhibition as a particularly rapid cognitive-control process. Even so, it has recently been shown that SSRTs can be further accelerated if successful response inhibition is rewarded. Since this earlier study effectively ruled out differential preparatory (proactive) control adjustments, the reward benefits likely relied on boosted reactive control. Yet, given how rapidly such control processes would need to be enhanced, alternative explanations circumventing reactive control are important to consider. We addressed this question with an fMRI study by gauging the overlap of the brain networks associated with reward-related and response-inhibition-related processes in a reward-modulated stop-signal task. In line with the view that reactive control can indeed be boosted swiftly by reward availability, we found that the activity in key brain areas related to response inhibition was enhanced for reward-related stop trials. Furthermore, we observed that this beneficial reward effect was triggered by enhanced connectivity between task-unspecific (reward-related) and task-specific (inhibition-related) areas in the medial prefrontal cortex (mPFC). The present data hence suggest that reward information can be translated very rapidly into behavioral benefits (here, within ~200 ms) through enhanced reactive control, underscoring the immediate responsiveness of such control processes to reward availability in general.

Background: So far, the neural network associated with posttraumatic stress disorder (PTSD) has been suggested to mainly involve the amygdala, hippocampus and medial prefrontal cortex. However, increasing evidence indicates that cortical regions extending beyond this network might also be implicated in the pathophysiology of PTSD. We aimed to investigate PTSD-related structural alterations in some of these regions. Methods: We enrolled highly traumatized refugees with and without (traumatized controls) PTSD and nontraumatized controls in the study. To increase the validity of our results, we combined an automatic cortical parcellation technique and voxel-based morphometry. Results: In all, 39 refugees (20 with and 19 without PTSD) and 13 controls participated in the study. Participants were middle-aged men who were free of psychoactive substances and consumed little to no alcohol. Patients with PTSD (and to a lesser extent traumatized controls) showed reduced volumes in the right inferior parietal cortex, the left rostral middle frontal cortex, the bilateral lateral orbitofrontal cortex and the bilateral isthmus of the cingulate. An influence of cumulative traumatic stress on the isthmus of the cingulate and the lateral orbitofrontal cortex indicated that, at least in these regions, structural alterations might be associated with repeated stress experiences. Voxel-based morphometry analyses produced largely consistent results, but because of a poorer signal-tonoise ratio, conventional statistics did not reach significance. Limitations: Although we controlled for several important confounding variables (e.g., sex, alcohol abuse) with our particular sample, this might limit the generalizibility of our data. Moreover, high comorbidity of PTSD and major depression hinders a definite separation of these conditions in our findings. Finally, the results concerning the lateral orbito frontal cortex should be interpreted with caution, as magnetic resonance imaging acquisition in this region is affected by a general signal loss. Conclusion: Our results indicate that lateral prefrontal, parietal and posterior midline structures are implicated in the pathophysiology of PTSD. As these regions are particularly involved in episodic memory, emotional processing and executive control, this might have important implications for the understanding of PTSD symptoms.PTSD-related alterations in a fronto-parietal brain regions J Psychiatry Neurosci 2011;36(3)

Feature attention operates in a spatially global way, with attended feature values being prioritized for selection outside the focus of attention. Accounts of global feature attention have emphasized feature competition as a determining factor. Here, we use magnetoencephalographic recordings in humans to test whether competition is critical for global feature selection to arise. Subjects performed a color/shape discrimination task in one visual field (VF), while irrelevant color probes were presented in the other unattended VF. Global effects of color attention were assessed by analyzing the response to the probe as a function of whether or not the probe's color was a target-defining color. We find that global color selection involves a sequence of modulations in extrastriate cortex, with an initial phase in higher tier areas (lateral occipital complex) followed by a later phase in lower tier retinotopic areas (V3/V4). Importantly, these modulations appeared with and without color competition in the focus of attention. Moreover, early parts of the modulation emerged for a task-relevant color not even present in the focus of attention. All modulations, however, were eliminated during simple onset-detection of the colored target. These results indicate that global color-based attention depends on target discrimination independent of feature competition in the focus of attention.

Previous studies have shown that in amyotrophic lateral sclerosis (ALS) multiple motor and extra-motor regions display structural and functional alterations. However, their temporal dynamics during disease-progression are unknown. To address this question we employed a longitudinal design assessing motor- and novelty-related brain activity in two fMRI sessions separated by a 3-month interval. In each session, patients and controls executed a Go/NoGo-task, in which additional presentation of novel stimuli served to elicit hippocampal activity. We observed a decline in the patients' movement-related activity during the 3-month interval. Importantly, in comparison to controls, the patients' motor activations were higher during the initial measurement. Thus, the relative decrease seems to reflect a breakdown of compensatory mechanisms due to progressive neural loss within the motor-system. In contrast, the patients' novelty-evoked hippocampal activity increased across 3 months, most likely reflecting the build-up of compensatory processes typically observed at the beginning of lesions. Consistent with a stage-dependent emergence of hippocampal and motor-system lesions, we observed a positive correlation between the ALSFRS-R or MRC-Megascores and the decline in motor activity, but a negative one with the hippocampal activation-increase. Finally, to determine whether the observed functional changes co-occur with structural alterations, we performed voxel-based volumetric analyses on magnetization transfer images in a separate patient cohort studied cross-sectionally at another scanning site. Therein, we observed a close overlap between the structural changes in this cohort, and the functional alterations in the other. Thus, our results provide important insights into the temporal dynamics of functional alterations during disease-progression, and provide support for an anatomical relationship between functional and structural cerebral changes in ALS.