Is Rest Really Rest? Resting-State Functional Connectivity During Rest and Motor Task Paradigms.

Numerous studies have identified several large-scale networks within the brain of healthy individuals, some of which have been attributed to ongoing mental activity during the wakeful resting state. While engaged during specific resting-state functional magnetic resonance imaging (fMRI) paradigms, it remains unclear as to whether traditional block-design simple movement fMRI experiments significantly influence these mode networks or other areas. Using blood-oxygen level-dependent fMRI, we characterized the pattern of functional connectivity in healthy subjects during a resting-state paradigm and compared this with the same resting-state analysis performed on motor task data residual time courses after regressing out the task paradigm. Using seed-voxel analysis to define the default mode network, the executive control network (ECN), and sensorimotor, auditory, and visual networks, the resting-state analysis of the residual time courses demonstrated reduced functional connectivity in the motor network and reduced connectivity between the insula and the ECN compared with the standard resting-state data sets. Overall, performance of simple self-directed motor tasks does little to change the resting-state functional connectivity across the brain, especially in nonmotor areas. This would suggest that previously acquired fMRI studies incorporating simple block-design motor tasks could be mined retrospectively for assessment of the resting-state connectivity.

Vascular steal explains early paradoxical blood oxygen level-dependent cerebrovascular response in brain regions with delayed arterial transit times.

INTRODUCTION: Blood oxygen level-dependent (BOLD) magnetic resonance imaging (MRI) during manipulation of inhaled carbon dioxide (CO2) can be used to measure cerebrovascular reactivity (CVR) and map regions of exhausted cerebrovascular reserve. These regions exhibit a reduced or negative BOLD response to inhaled CO2. In this study, we sought to clarify the mechanism behind the negative BOLD response by investigating its time delay (TD). Dynamic susceptibility contrast (DSC) MRI with the injection of a contrast agent was used as the gold standard in order to provide measurement of the blood arrival time to which CVR TD could be compared. We hypothesize that if negative BOLD responses are the result of a steal phenomenon, they should be synchronized with positive BOLD responses from healthy brain tissue, even though the blood arrival time would be delayed. METHODS: On a 3-tesla MRI system, BOLD CVR and DSC images were collected in a group of 19 patients with steno-occlusive cerebrovascular disease. For each patient, we generated a CVR magnitude map by regressing the BOLD signal with the end-tidal partial pressure of CO2 (PETCO2), and a CVR TD map by extracting the time of maximum cross-correlation between the BOLD signal and PETCO2. In addition, a blood arrival time map was generated by fitting the DSC signal with a gamma variate function. ROI masks corresponding to varying degrees of reactivity were constructed. Within these masks, the mean CVR magnitude, CVR TD and DSC blood arrival time were extracted and averaged over the 19 patients. CVR magnitude and CVR TD were then plotted against DSC blood arrival time. RESULTS: The results show that CVR magnitude is highly correlated to DSC blood arrival time. As expected, the most compromised tissues with the longest blood arrival time have the lowest (most negative) CVR magnitude. However, CVR TD shows a noncontinuous relationship with DSC blood arrival time. CVR TD is well correlated to DSC blood arrival time (p < 0.0001) for tissue of positive reactivity, but fails to maintain this trend for tissue of negative reactivity. Regions with negative reactivity have similar CVR TD than healthy regions. CONCLUSION: These results support the hypothesis that negative reactivity is the result of a steal phenomenon, lowering the BOLD signal as soon as healthier parts of the brain start to react and augment their blood flow. BOLD CVR MRI is capable of identifying this steal distribution, which has particular diagnostic significance as it represents an actual reduction in flow to already compromised tissue.

White matter brain and trigeminal nerve abnormalities in temporomandibular disorder.

Temporomandibular disorder (TMD) is a prevalent chronic pain disorder that remains poorly understood. Recent imaging studies reported functional and gray matter abnormalities in brain areas implicated in sensorimotor, modulatory, and cognitive function in TMD, but it is not known whether there are white matter (WM) abnormalities along the trigeminal nerve (CNV) or in the brain. Here, we used diffusion tensor imaging, and found that, compared to healthy controls, TMD patients had 1) lower fractional anisotropy (FA) in both CNVs; 2) a negative correlation between FA of the right CNV and pain duration; and 3) diffuse abnormalities in the microstructure of WM tracts related to sensory, motor, cognitive, and pain functions, with a highly significant focal abnormality in the corpus callosum. Using probabilistic tractography, we found that the corpus callosum in patients had a higher connection probability to the frontal pole, and a lower connection probability to the dorsolateral prefrontal cortex, compared to controls. Finally, we found that 1) FA in tracts adjacent to the ventrolateral prefrontal cortex and tracts coursing through the thalamus negatively correlated with pain intensity; 2) FA in the internal capsule negatively correlated with pain intensity and unpleasantness; and 3) decreases in brain FA were associated with increases in mean diffusivity and radial diffusivity, markers of inflammation and oedema. These data provide novel evidence for CNV microstructural abnormalities that may be caused by increased nociceptive activity, accompanied by abnormalities along central WM pathways in TMD.

Absence of localized grey matter volume changes in the motor cortex following spinal cord injury.

The consequences of spinal cord injury (SCI) have considerable effects on motor function, typically resulting in functional impairment. Pathological changes have been studied at the site of trauma, rostrocaudally within the cord, and in the periphery. Few studies, however, have investigated the consequences of SCI at the cortical level. Magnetic resonance imaging (MRI) was used to explore the morphological changes in the grey and white matter within the primary motor (M1) cortex of individuals with cervical SCI. The "precentral knob," a landmark of M1 cortex dedicated to hand function, was selected for regionally specific measurements of change. Thirty-one hemispheres of SCI subjects and 28 hemispheres of control subjects were compared using a manual measurement after the images were segmented into grey matter, white matter, and cerebral spinal fluid (CSF). No significant differences in grey matter area measured at the precentral knob were found with the manual approach. An automated voxel-based morphometric analysis was also performed and demonstrated no significant differences in grey or white matter volume within an M1 region of interest. These data suggest that there is no gross anatomical change within M1 following cervical SCI. Our previously reported findings of reorganization of cortical motor output maps following SCI therefore likely result from changes in functional organization rather than anatomical changes.