The brain connectome collects the complex network architectures, looking at both static and dynamic functional connectivity. The former normally requires stationary signals and connections. However, the human brain activity and connections are most likely time dependent and dynamic, and related to ongoing rhythmic activity. We developed an open-source MATLAB toolbox DynamicBC with user-friendly graphical user interfaces, implementing both dynamic functional and effective connectivity for tracking brain dynamics from functional MRI. We provided two strategies for dynamic analysis: (1) the commonly utilized sliding-window analysis and (2) the flexible least squares based time-varying parameter regression strategy. The toolbox also implements multiple functional measures including seed-to-voxel analysis, region of interest (ROI)-to-ROI analysis, and voxel-to-voxel analysis. We describe the principles of the implemented algorithms, and then present representative results from simulations and empirical data applications. We believe that this toolbox will help neuroscientists and neurologists to easily map dynamic brain connectomics.

The hemodynamic response function (HRF) greatly influences the intra- and inter-subject variability of brain activation and connectivity, and might confound the estimation of temporal precedence in connectivity analyses, making its estimation necessary for a correct interpretation of neuroimaging studies. Additionally, the HRF shape itself is a useful local measure. However, most algorithms for HRF estimation are specific for task-related fMRI data, and only a few can be directly applied to resting-state protocols. Here we introduce rsHRF, a Matlab and Python toolbox that implements HRF estimation and deconvolution from the resting-state BOLD signal. We first provide an overview of the main algorithm, practical implementations, and then demonstrate the feasibility and usefulness of rsHRF by validation experiments with a publicly available resting-state fMRI dataset. We also provide tools for statistical analyses and visualization. We believe that this toolbox may significantly contribute to a better analysis and understanding of the components and variability of BOLD signals.

The neurovisceral integration model has shown a key role of the amygdala in neural circuits underlying heart rate variability (HRV) modulation, and suggested that reciprocal connections from amygdala to brain regions centered on the central autonomic network (CAN) are associated with HRV. To provide neuroanatomical evidence for these theoretical perspectives, the current study used covariance analysis of MRI-based gray matter volume (GMV) to map structural covariance network of the amygdala, and then determined whether the interregional structural correlations related to individual differences in HRV. The results showed that covariance patterns of the amygdala encompassed large portions of cortical (e.g., prefrontal, cingulate, and insula) and subcortical (e.g., striatum, hippocampus, and midbrain) regions, lending evidence from structural covariance analysis to the notion that the amygdala was a pivotal node in neural pathways for HRV modulation. Importantly, participants with higher resting HRV showed increased covariance of amygdala to dorsal medial prefrontal cortex and anterior cingulate cortex (dmPFC/dACC) extending into adjacent medial motor regions [i.e., pre-supplementary motor area (pre-SMA)/SMA], demonstrating structural covariance of the prefrontal-amygdala pathways implicated in HRV, and also implying that resting HRV may reflect the function of neural circuits underlying cognitive regulation of emotion as well as facilitation of adaptive behaviors to emotion. Our results, thus, provide anatomical substrates for the neurovisceral integration model that resting HRV may index an integrative neural network which effectively organizes emotional, cognitive, physiological and behavioral responses in the service of goal-directed behavior and adaptability.

Accelerated intermittent Theta Burst Stimulation (aiTBS) has been shown to be an effective antidepressant treatment. Although neurobiological changes shortly after this intervention have been reported, whether aiTBS results in structural brain changes must still be determined. Furthermore, it possible that rapid volumetric changes are driven by factors other than neurotrophic processes. We examined whether possible grey matter volumetric (GMV) increases after aiTBS treatment could be driven by increased brain perfusion, measured by Arterial Spin Labeling (ASL). 46 treatment-resistant depressed patients were randomized to receive 20 sessions of active or sham iTBS applied to the left dorsolateral prefrontal cortex. All sessions were delivered over 4 days at 5 sessions per day (trial registration: http://clinicaltrials.gov/show/NCT01832805). Patients were scanned the day before starting stimulation and three days after aiTBS. There was a significant cluster of increased left hippocampal GMV in the dentate gyrus related to HRSD changes after active aiTBS, but not after sham stimulation. These GMV increases became more pronounced when accounting for changes in cerebral perfusion. Active, but not sham, aiTBS, resulted in acute volumetric changes in parts of the left dentate gyrus, suggesting a connection with adult neurogenesis. Furthermore, taking cerebral perfusion measurements into account impacts on detection of the GMV changes. Whether these hippocampal volumetric changes produced by active aiTBS are necessary for long-term clinical improvement remains to be determined.