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Register a new userDiagnosis of Autism Spectrum Disorder by Causal Influence Strength Learned from Resting-State fMRI Data
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Autism spectrum disorder (ASD) is one of the major developmental disorders affecting children. Recently, it has been hypothesized that ASD is associated with atypical brain connectivities. A substantial body of researches use Pearsons correlation coefficients, mutual information, or partial correlation to investigate the differences in brain connectivities between ASD and typical controls from functional Magnetic Resonance Imaging (fMRI). However, correlation or partial correlation does not directly reveal causal influences - the information flow - between brain regions. Comparing to correlation, causality pinpoints the key connectivity characteristics and removes redundant features for diagnosis. In this paper, we propose a two-step method for large-scale and cyclic causal discovery from fMRI. It can identify brain causal structures without doing interventional experiments. The learned causal structure, as well as the causal influence strength, provides us the path and effectiveness of information flow. With the recovered causal influence strength as candidate features, we then perform ASD diagnosis by further doing feature selection and classification. We apply our methods to three datasets from Autism Brain Imaging Data Exchange (ABIDE). From experimental results, it shows that with causal connectivities, the diagnostic accuracy largely improves. A closer examination shows that information flows starting from the superior front gyrus to default mode network and posterior areas are largely reduced. Moreover, all enhanced information flows are from posterior to anterior or in local areas. Overall, it shows that long-range influences have a larger proportion of reductions than local ones, while local influences have a larger proportion of increases than long-range ones. By examining the graph properties of brain causal structure, the group of ASD shows reduced small-worldness.
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What makes a network complex, in addition to its size, is the interconnected interactions between elements, disruption of which inevitably results in dysfunction. Likewise, the brain networks complexity arises from interactions beyond pair connections, as it is simplistic to assume that in complex networks state of a link is independently determined only according to its two constituting nodes. This is particularly of note in genetically complex brain impairments, such as the autism spectrum disorder (ASD). Accordingly, structural balance theory (SBT) affirms that in the real-world signed networks, a link is remarkably influenced by each of its two nodes interactions with the third node within a triadic interrelationship. Thus, it is plausible to ask whether ASD is associated with altered structural balance resulting from atypical triadic interactions. In other words, it is the abnormal interplay of positive and negative interactions that matter in ASD, besides and beyond hypo (hyper) pair connectivity. To address this, we explore triadic interactions in the rs-fMRI network of participants with ASD relative to healthy controls (CON). We demonstrate that balanced triads are overrepresented in the ASD and CON networks while unbalanced triads are underrepresented, providing first-time empirical evidence for the strong notion of structural balance on the brain networks. We further analyze the frequency and energy distribution of triads and suggest an alternative description for the reduced functional integration and segregation in the ASD brain networks. Last but not least, we observe that energy of the salient and the default mode networks are lower in autism, which may be a reflection of the difficulty in flexible behaviors. Altogether, these results highlight the potential value of SBT as a new perspective in functional connectivity studies, especially in neurodevelopmental disorders.
Long-range temporal coherence (LRTC) is quite common to dynamic systems and is fundamental to the system function. LRTC in the brain has been shown to be important to cognition. Assessing LRTC may provide critical information for understanding the potential underpinnings of brain organization, function, and cognition. To facilitate this overarching goal, we provide a method, which is named temporal coherence mapping (TCM), to explicitly quantify LRTC using resting state fMRI. TCM is based on correlation analysis of the transit states of the phase space reconstructed by temporal embedding. A few TCM properties were collected to measure LRTC, including the averaged correlation, anti-correlation, the ratio of correlation and anticorrelation, the mean coherent and incoherent duration, and the ratio between the coherent and incoherent time. TCM was first evaluated with simulations and then with the large Human Connectome Project data. Evaluation results showed that TCM metrics can successfully differentiate signals with different temporal coherence regardless of the parameters used to reconstruct the phase space. In human brain, TCM metrics except the ratio of the coherent/incoherent time showed high test-retest reproducibility; TCM metrics are related to age, sex, and total cognitive scores. In summary, TCM provides a first-of-its-kind tool to assess LRTC and the imbalance between coherence and incoherence; TCM properties are physiologically and cognitively meaningful.
A great improvement to the insight on brain function that we can get from fMRI data can come from effective connectivity analysis, in which the flow of information between even remote brain regions is inferred by the parameters of a predictive dynamical model. As opposed to biologically inspired models, some techniques as Granger causality (GC) are purely data-driven and rely on statistical prediction and temporal precedence. While powerful and widely applicable, this approach could suffer from two main limitations when applied to BOLD fMRI data: confounding effect of hemodynamic response function (HRF) and conditioning to a large number of variables in presence of short time series. For task-related fMRI, neural population dynamics can be captured by modeling signal dynamics with explicit exogenous inputs; for resting-state fMRI on the other hand, the absence of explicit inputs makes this task more difficult, unless relying on some specific prior physiological hypothesis. In order to overcome these issues and to allow a more general approach, here we present a simple and novel blind-deconvolution technique for BOLD-fMRI signal. Coming to the second limitation, a fully multivariate conditioning with short and noisy data leads to computational problems due to overfitting. Furthermore, conceptual issues arise in presence of redundancy. We thus apply partial conditioning to a limited subset of variables in the framework of information theory, as recently proposed. Mixing these two improvements we compare the differences between BOLD and deconvolved BOLD level effective networks and draw some conclusions.
Task-free connectivity analyses have emerged as a powerful tool in functional neuroimaging. Because the cross-correlations that underlie connectivity measures are sensitive to distortion of time-series, here we used a novel dynamic phantom to provide a ground truth for dynamic fidelity between blood oxygen level dependent (BOLD)-like inputs and fMRI outputs. We found that the de facto quality-metric for task-free fMRI, temporal signal to noise ratio (tSNR), correlated inversely with dynamic fidelity; thus, studies optimized for tSNR actually produced time-series that showed the greatest distortion of signal dynamics. Instead, the phantom showed that dynamic fidelity is reasonably approximated by a measure that, unlike tSNR, dissociates signal dynamics from scanner artifact. We then tested this measure, signal fluctuation sensitivity (SFS), against human resting-state data. As predicted by the phantom, SFS--and not tSNR--is associated with enhanced sensitivity to both local and long-range connectivity within the brains default mode network.
The estimation of causal network architectures in the brain is fundamental for understanding cognitive information processes. However, access to the dynamic processes underlying cognition is limited to indirect measurements of the hidden neuronal activity, for instance through fMRI data. Thus, estimating the network structure of the underlying process is challenging. In this article, we embed an adaptive importance sampler called Adaptive Path Integral Smoother (APIS) into the Expectation-Maximization algorithm to obtain point estimates of causal connectivity. We demonstrate on synthetic data that this procedure finds not only the correct network structure but also the direction of effective connections from random initializations of the connectivity matrix. In addition--motivated by contradictory claims in the literature--we examine the effect of the neuronal timescale on the sensitivity of the BOLD signal to changes in the connectivity and on the maximum likelihood solutions of the connectivity. We conclude with two warnings: First, the connectivity estimates under the assumption of slow dynamics can be extremely biased if the data was generated by fast neuronal processes. Second, the faster the time scale, the less sensitive the BOLD signal is to changes in the incoming connections to a node. Hence, connectivity estimation using realistic neural dynamics timescale requires extremely high-quality data and seems infeasible in many practical data sets.
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