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Deep learning-based semantic segmentation in neuroimaging currently requires high-resolution scans and extensive annotated datasets, posing significant barriers to clinical applicability. We present a novel synthetic framework for the task of lesion segmentation, extending the capabilities of the established SynthSeg approach to accommodate large heterogeneous pathologies with lesion-specific augmentation strategies. Our method trains deep learning models, demonstrated here with the UNet architecture, using label maps derived from healthy and stroke datasets, facilitating the segmentation of both healthy tissue and pathological lesions without sequence-specific training data. Evaluated against in-domain and out-of-domain (OOD) datasets, our framework demonstrates robust performance, rivaling current methods within the training domain and significantly outperforming them on OOD data. This contribution holds promise for advancing medical imaging analysis in clinical settings, especially for stroke pathology, by enabling reliable segmentation across varied imaging sequences with reduced dependency on large annotated corpora. Code and weights available at https://github.com/liamchalcroft/SynthStroke.

In many scientific disciplines, the features of interest cannot be observed directly, so must instead be inferred from observed behaviour. Latent variable analyses are increasingly employed to systematise these inferences, and Principal Components Analysis (PCA) is perhaps the simplest and most popular of these methods. Here, we examine how the assumptions that we are prepared to entertain, about the latent variable system, mediate the likelihood that PCA-derived components will capture the true sources of variance underlying data. As expected, we find that this likelihood is excellent in the best case, and robust to empirically reasonable levels of measurement noise, but best-case performance is also: (a) not robust to violations of the method's more prominent assumptions, of linearity and orthogonality; and also (b) requires that other subtler assumptions be made, such as that the latent variables should have varying importance, and that weights relating latent variables to observed data have zero mean. Neither variance explained, nor replication in independent samples, could reliably predict which (if any) PCA-derived components will capture true sources of variance in data. We conclude by describing a procedure to fit these inferences more directly to empirical data, and use it to find that components derived via PCA from two different empirical neuropsychological datasets, are less likely to have meaningful referents in the brain than we hoped., Comment: 26 pages, 3 figures, 3 tables

Machine learning offers great potential for automated prediction of post-stroke symptoms and their response to rehabilitation. Major challenges for this endeavour include the very high dimensionality of neuroimaging data, the relatively small size of the datasets available for learning, and how to effectively combine neuroimaging and tabular data (e.g. demographic information and clinical characteristics). This paper evaluates several solutions based on two strategies. The first is to use 2D images that summarise MRI scans. The second is to select key features that improve classification accuracy. Additionally, we introduce the novel approach of training a convolutional neural network (CNN) on images that combine regions-of-interest extracted from MRIs, with symbolic representations of tabular data. We evaluate a series of CNN architectures (both 2D and a 3D) that are trained on different representations of MRI and tabular data, to predict whether a composite measure of post-stroke spoken picture description ability is in the aphasic or non-aphasic range. MRI and tabular data were acquired from 758 English speaking stroke survivors who participated in the PLORAS study. The classification accuracy for a baseline logistic regression was 0.678 for lesion size alone, rising to 0.757 and 0.813 when initial symptom severity and recovery time were successively added. The highest classification accuracy 0.854 was observed when 8 regions-of-interest was extracted from each MRI scan and combined with lesion size, initial severity and recovery time in a 2D Residual Neural Network.Our findings demonstrate how imaging and tabular data can be combined for high post-stroke classification accuracy, even when the dataset is small in machine learning terms. We conclude by proposing how the current models could be improved to achieve even higher levels of accuracy using images from hospital scanners.

Vision transformers are effective deep learning models for vision tasks, including medical image segmentation. However, they lack efficiency and translational invariance, unlike convolutional neural networks (CNNs). To model long-range interactions in 3D brain lesion segmentation, we propose an all-convolutional transformer block variant of the U-Net architecture. We demonstrate that our model provides the greatest compromise in three factors: performance competitive with the state-of-the-art; parameter efficiency of a CNN; and the favourable inductive biases of a transformer. Our public implementation is available at https://github.com/liamchalcroft/MDUNet .

This technical report addresses a pressing issue in the trajectory of the coronavirus outbreak; namely, the rate at which effective immunity is lost following the first wave of the pandemic. This is a crucial epidemiological parameter that speaks to both the consequences of relaxing lockdown and the propensity for a second wave of infections. Using a dynamic causal model of reported cases and deaths from multiple countries, we evaluated the evidence models of progressively longer periods of immunity. The results speak to an effective population immunity of about three months that, under the model, defers any second wave for approximately six months in most countries. This may have implications for the window of opportunity for tracking and tracing, as well as for developing vaccination programmes, and other therapeutic interventions., Comment: 20 pages, 8 figures, 3 tables (technical report)

By equipping a previously reported dynamic causal model of COVID-19 with an isolation state, we modelled the effects of self-isolation consequent on tracking and tracing. Specifically, we included a quarantine or isolation state occupied by people who believe they might be infected but are asymptomatic, and only leave if they test negative. We recovered maximum posteriori estimates of the model parameters using time series of new cases, daily deaths, and tests for the UK. These parameters were used to simulate the trajectory of the outbreak in the UK over an 18-month period. Several clear-cut conclusions emerged from these simulations. For example, under plausible (graded) relaxations of social distancing, a rebound of infections within weeks is unlikely. The emergence of a later second wave depends almost exclusively on the rate at which we lose immunity, inherited from the first wave. There exists no testing strategy that can attenuate mortality rates, other than by deferring or delaying a second wave. A sufficiently powerful tracking and tracing policy--implemented at the time of writing (10th May 2020)--will defer any second wave beyond a time horizon of 18 months. Crucially, this deferment is within current testing capabilities (requiring an efficacy of tracing and tracking of about 20% of asymptomatic infected cases, with less than 50,000 tests per day). These conclusions are based upon a dynamic causal model for which we provide some construct and face validation, using a comparative analysis of the United Kingdom and Germany, supplemented with recent serological studies., Comment: 31 pages, 12 figures, one table. Technical report

We recently described a dynamic causal model of a COVID-19 outbreak within a single region. Here, we combine several of these (epidemic) models to create a (pandemic) model of viral spread among regions. Our focus is on a second wave of new cases that may result from loss of immunity--and the exchange of people between regions--and how mortality rates can be ameliorated under different strategic responses. In particular, we consider hard or soft social distancing strategies predicated on national (Federal) or regional (State) estimates of the prevalence of infection in the population. The modelling is demonstrated using timeseries of new cases and deaths from the United States to estimate the parameters of a factorial (compartmental) epidemiological model of each State and, crucially, coupling between States. Using Bayesian model reduction, we identify the effective connectivity between States that best explains the initial phases of the outbreak in the United States. Using the ensuing posterior parameter estimates, we then evaluate the likely outcomes of different policies in terms of mortality, working days lost due to lockdown and demands upon critical care. The provisional results of this modelling suggest that social distancing and loss of immunity are the two key factors that underwrite a return to endemic equilibrium., Comment: Technical report: 35 pages, 14 figures, 1 table

This technical report describes a dynamic causal model of the spread of coronavirus through a population. The model is based upon ensemble or population dynamics that generate outcomes, like new cases and deaths over time. The purpose of this model is to quantify the uncertainty that attends predictions of relevant outcomes. By assuming suitable conditional dependencies, one can model the effects of interventions (e.g., social distancing) and differences among populations (e.g., herd immunity) to predict what might happen in different circumstances. Technically, this model leverages state-of-the-art variational (Bayesian) model inversion and comparison procedures, originally developed to characterise the responses of neuronal ensembles to perturbations. Here, this modelling is applied to epidemiological populations to illustrate the kind of inferences that are supported and how the model per se can be optimised given timeseries data. Although the purpose of this paper is to describe a modelling protocol, the results illustrate some interesting perspectives on the current pandemic; for example, the nonlinear effects of herd immunity that speak to a self-organised mitigation process., Comment: Technical report: 40 pages, 13 figures and 2 tables

Dynamic Causal Modelling (DCM) is the predominant method for inferring effective connectivity from neuroimaging data. In the 15 years since its introduction, the neural models and statistical routines in DCM have developed in parallel, driven by the needs of researchers in cognitive and clinical neuroscience. In this tutorial, we step through an exemplar fMRI analysis in detail, reviewing the current implementation of DCM and demonstrating recent developments in group-level connectivity analysis. In the first part of the tutorial (current paper), we focus on issues specific to DCM for fMRI, unpacking the relevant theory and highlighting practical considerations. In particular, we clarify the assumptions (i.e., priors) used in DCM for fMRI and how to interpret the model parameters. This tutorial is accompanied by all the necessary data and instructions to reproduce the analyses using the SPM software. In the second part (in a companion paper), we move from subject-level to group-level modelling using the Parametric Empirical Bayes framework, and illustrate how to test for commonalities and differences in effective connectivity across subjects, based on imaging data from any modality.

This tutorial provides a worked example of using Dynamic Causal Modelling (DCM) and Parametric Empirical Bayes (PEB) to characterise inter-subject variability in neural circuitry (effective connectivity). This involves specifying a hierarchical model with two or more levels. At the first level, state space models (DCMs) are used to infer the effective connectivity that best explains a subject's neuroimaging timeseries (e.g. fMRI, MEG, EEG). Subject-specific connectivity parameters are then taken to the group level, where they are modelled using a General Linear Model (GLM) that partitions between-subject variability into designed effects and additive random effects. The ensuing (Bayesian) hierarchical model conveys both the estimated connection strengths and their uncertainty (i.e., posterior covariance) from the subject to the group level; enabling hypotheses to be tested about the commonalities and differences across subjects. This approach can also finesse parameter estimation at the subject level, by using the group-level parameters as empirical priors. We walk through this approach in detail, using data from a published fMRI experiment that characterised individual differences in hemispheric lateralization in a semantic processing task. The preliminary subject specific DCM analysis is covered in detail in a companion paper. This tutorial is accompanied by the example dataset and step-by-step instructions to reproduce the analyses.

One third of stroke survivors have language difficulties. Emerging evidence suggests that their likelihood of recovery depends mainly on the damage to language centers. Thus previous research for predicting language recovery post-stroke has focused on identifying damaged regions of the brain. In this paper, we introduce a novel method where we only make use of stitched 2-dimensional cross-sections of raw MRI scans in a deep convolutional neural network setup to predict language recovery post-stroke. Our results show: a) the proposed model that only uses MRI scans has comparable performance to models that are dependent on lesion specific information; b) the features learned by our model are complementary to the lesion specific information and the combination of both appear to outperform previously reported results in similar settings. We further analyse the CNN model for understanding regions in brain that are responsible for arriving at these predictions using gradient based saliency maps. Our findings are in line with previous lesion studies., Comment: Machine Learning for Health (ML4H) Workshop at NeurIPS 2018 arXiv:1811.07216