Stopping an action in response to an unexpected event requires both that the event is attended to, and that the action is inhibited. Previous neuroimaging investigations of stopping have failed to adequately separate these cognitive elements. Here we used a version of the widely used Stop Signal Task that controls for the attentional capture of stop signals. This allowed us to fractionate the contributions of frontal regions, including the right inferior frontal gyrus and medial frontal cortex, to attentional capture, response inhibition, and error processing. A ventral attentional system, including the right inferior frontal gyrus, has been shown to respond to unexpected stimuli. In line with this evidence, we reasoned that lateral frontal regions support attentional capture, whereas medial frontal regions, including the presupplementary motor area (pre-SMA), actually inhibit the ongoing action. We tested this hypothesis by contrasting the brain networks associated with the presentation of unexpected stimuli against those associated with outright stopping. Functional MRI images were obtained in 26 healthy volunteers. Successful stopping was associated with activation of the right inferior frontal gyrus, as well as the pre-SMA. However, only activation of the pre-SMA differentiated stopping from a high-level baseline that controlled for attentional capture. As expected, unsuccessful attempts at stopping activated the anterior cingulate cortex. In keeping with work in nonhuman primates these findings demonstrate that successful motor inhibition is specifically associated with pre-SMA activation.attention | functional MRI | presupplementary motor area | stop signal task | stopping T he control of voluntary action depends critically upon the ability to inhibit unwanted responses. This process has been extensively studied using the Stop Signal Task (SST) (1). Previous work with this task provides evidence that both medial frontal regions, including the presupplementary motor area (pre-SMA), and more lateral regions, including the right inferior frontal gyrus (IFG; rIFG) and insula (Ins), are involved in stopping. However, the specific contributions of these regions to motor control are unresolved (2-4). Many functional imaging studies have demonstrated activation of right inferior frontal regions during stopping (2, 5-8) and individual differences in response inhibition correlate with the magnitude of the IFG/Ins activation during the SST (5). Activation of medial prefrontal regions are also observed during stopping (2, 5). Pre-SMA activation is correlated with the efficiency of inhibitory processing (2), and work in nonhuman primates supports a role for the medial prefrontal regions in behavioral inhibition (9, 10). Neuropsychological studies provide discrepant results, with correlations between the extent of damage and impairments of inhibitory function reported for both the right lateral and medial frontal regions (3, 4).A limitation of much of the previous neuroimaging literature is that "stop trials" conflate p...

Traumatic brain injury often results in cognitive impairments that limit recovery. The underlying pathophysiology of these impairments is uncertain, which restricts clinical assessment and management. Here, we use magnetic resonance imaging to test the hypotheses that: (i) traumatic brain injury results in abnormalities of functional connectivity within key cognitive networks; (ii) these changes are correlated with cognitive performance; and (iii) functional connectivity within these networks is influenced by underlying changes in structural connectivity produced by diffuse axonal injury. We studied 20 patients in the chronic phase after traumatic brain injury compared with age-matched controls. Network function was investigated in detail using functional magnetic resonance imaging to analyse both regional brain activation, and the interaction of brain regions within a network (functional connectivity). We studied patients during performance of a simple choice-reaction task and at 'rest'. Since functional connectivity reflects underlying structural connectivity, diffusion tensor imaging was used to quantify axonal injury, and test whether structural damage correlated with functional change. The patient group showed typical impairments in information processing and attention, when compared with age-matched controls. Patients were able to perform the task accurately, but showed slow and variable responses. Brain regions activated by the task were similar between the groups, but patients showed greater deactivation within the default mode network, in keeping with an increased cognitive load. A multivariate analysis of 'resting' state functional magnetic resonance imaging was then used to investigate whether changes in network function were present in the absence of explicit task performance. Overall, default mode network functional connectivity was increased in the patient group. Patients with the highest functional connectivity had the least cognitive impairment. In addition, functional connectivity at rest also predicted patterns of brain activation during later performance of the task. As expected, patients showed widespread white matter damage compared with controls. Lower default mode network functional connectivity was seen in those patients with more evidence of diffuse axonal injury within the adjacent corpus callosum. Taken together, our results demonstrate altered patterns of functional connectivity in cognitive networks following injury. The results support a direct relationship between white matter organization within the brain's structural core, functional connectivity within the default mode network and cognitive function following brain injury. They can be explained by two related changes: a compensatory increase in functional connectivity within the default mode network; and a variable degree of structural disconnection that modulates this change in network function.

Traumatic brain injury (TBI) frequently produces impairments of attention in humans.These can result in a failure to maintain consistent goal-directed behavior. A predominantly right-lateralized frontoparietal network is often engaged during attentionally demanding tasks. However, lapses of attention have also been associated with increases in activation within the default mode network (DMN). Here, we study TBI patients with sustained attention impairment, defined on the basis of the consistency of their behavioral performance over time. We show that sustained attention impairments in patients are associated with an increase in DMN activation, particularly within the precuneus and posterior cingulate cortex. Furthermore, the interaction of the precuneus with the rest of the DMN at the start of the task, i.e., its functional connectivity, predicts which patients go on to show impairments of attention. Importantly, this predictive information is present before any behavioral evidence of sustained attention impairment, and the relationship is also found in a subgroup of patients without focal brain damage. TBI often results in diffuse axonal injury, which produces cognitive impairment by disconnecting nodes in distributed brain networks. Using diffusion tensor imaging, we demonstrate that structural disconnection within the DMN also correlates with the level of sustained attention. These results show that abnormalities in DMN function are a sensitive marker of impairments of attention and suggest that changes in connectivity within the DMN are central to the development of attentional impairment after TBI.

The Salience Network (SN) consists of the dorsal anterior cingulate cortex (dACC) and bilateral insulae. The network responds to behaviorally salient events, and an important question is how its nodes interact. One theory is that the dACC provides the earliest cortical signal of behaviorally salient events, such as errors. Alternatively, the anterior right insula (aRI) has been proposed to provide an early cognitive control signal. As these regions frequently coactivate, it has been difficult to disentangle their roles using conventional methods. Here we use dynamic causal modeling and a Bayesian model evidence technique to investigate the causal relationships between nodes in the SN after errors. Thirty-five human subjects performed the Simon task. The task has two conditions (congruent and incongruent) producing two distinct error types. Neural activity associated with errors was investigated using fMRI. Subjects made a total of 1319 congruent and 1617 incongruent errors. Errors resulted in robust activation of the SN. Dynamic causal modeling analyses demonstrated that input into the SN was most likely via the aRI for both error types and that the aRI was the only region intrinsically connected to both other nodes. Only incongruent errors produced behavioral adaptation, and the strength of the connection between the dACC and the left insulae correlated with the extent of this behavioral change. We conclude that the aRI, not the dACC, drives the SN after errors on an attentionally demanding task, and that a change in the effective connectivity of the dACC is associated with behavioral adaptation after errors.

Our results suggest that enhanced activities in right-sided areas observed in recovering aphasia is not the mere consequence of damage to left-sided homologous areas and could reflect the neural correlates of lexical learning also observed in control subjects.

The first objective of the study was to determine whether functional magnetic resonance imaging (fMRI) signal was correlated with motor performance at different stages of poststroke recovery. The second objective was to assess the existence of prognostic factors for recovery in early functional MR images. Eight right-handed patients with pure motor deficit secondary to a first lacunar infarct localized on the pyramidal tract were included. This study concerned moderately impaired patients and recovery of handgrip strength and finger-tapping speed. The fMRI task was a calibrated flexion-extension movement. Ten healthy subjects served as a control group. The intensity of the activation in the "classical" motor network (ipsilesional S1M1, ipsilesional ventral premotor cortex [BA 6], contralesional cerebellum) 20 days after stroke was indicative of the performance (positive correlation). The cluster in M1 was posterior and circumscribed to BA 4p. No area was associated with bad performance (negative correlation). No correlation was found 4 and 12 months after stroke. Prognosis factors were evidenced. The higher early the activation in the ipsilesional M1 (BA 4p), S1, and insula, the better the recovery 1 year after stroke. Although the lesions partly deefferented the primary motor cortex, patients who activated the posterior primary motor cortex early had a better recovery of hand function. This suggests that there is benefit in increasing ipsilesional M1 activity shortly after stroke as a rehabilitative approach in mildly impaired patients.

We have demonstrated that purely passive proprioceptive training applied for 4 weeks is able to modify brain sensorimotor activity after a stroke. This training revealed fMRI change in the ventral premotor and parietal cortices of the contralesional hemisphere, which are secondary sensorimotor areas. Recent studies have demonstrated the crucial role of these areas in severely impaired patients. We propose that increased contralesional activity in secondary sensorimotor areas likely facilitates control of recovered motor function by simple proprioceptive integration in those patients with poor recovery.

Sacral neuromodulation seems to constitute a serious therapeutic option for patients with neurogenic lower urinary tract dysfunction. However, its results depend on the type of the underlying neurologic disease and in particular, whether it may progress or not.