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Dive into the research topics where Adeel Razi is active.

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Featured researches published by Adeel Razi.


NeuroImage | 2014

A DCM for resting state fMRI

K. J. Friston; Joshua Kahan; Bharat B. Biswal; Adeel Razi

This technical note introduces a dynamic causal model (DCM) for resting state fMRI time series based upon observed functional connectivity—as measured by the cross spectra among different brain regions. This DCM is based upon a deterministic model that generates predicted crossed spectra from a biophysically plausible model of coupled neuronal fluctuations in a distributed neuronal network or graph. Effectively, the resulting scheme finds the best effective connectivity among hidden neuronal states that explains the observed functional connectivity among haemodynamic responses. This is because the cross spectra contain all the information about (second order) statistical dependencies among regional dynamics. In this note, we focus on describing the model, its relationship to existing measures of directed and undirected functional connectivity and establishing its face validity using simulations. In subsequent papers, we will evaluate its construct validity in relation to stochastic DCM and its predictive validity in Parkinsons and Huntingtons disease.


IEEE Transactions on Communications | 2012

Secrecy Sum-Rates for Multi-User MIMO Regularized Channel Inversion Precoding

Giovanni Geraci; Malcolm Egan; Jinhong Yuan; Adeel Razi; Iain B. Collings

In this paper, we propose a linear precoder for the downlink of a multi-user MIMO system with multiple users that potentially act as eavesdroppers. The proposed precoder is based on regularized channel inversion (RCI) with a regularization parameter α and power allocation vector chosen in such a way that the achievable secrecy sum-rate is maximized. We consider the worst-case scenario for the multi-user MIMO system, where the transmitter assumes users cooperate to eavesdrop on other users. We derive the achievable secrecy sum-rate and obtain the closed-form expression for the optimal regularization parameter αLS of the precoder using large-system analysis. We show that the RCI precoder with αLS outperforms several other linear precoding schemes, and it achieves a secrecy sum-rate that has same scaling factor as the sum-rate achieved by the optimum RCI precoder without secrecy requirements. We propose a power allocation algorithm to maximize the secrecy sum-rate for fixed α. We then extend our algorithm to maximize the secrecy sum-rate by jointly optimizing α and the power allocation vector. The jointly optimized precoder outperforms RCI with αLS and equal power allocation by up to 20 percent at practical values of the signal-to-noise ratio and for 4 users and 4 transmit antennas.


NeuroImage | 2016

Bayesian model reduction and empirical Bayes for group (DCM) studies.

K. J. Friston; Vladimir Litvak; Ashwini Oswal; Adeel Razi; Klaas E. Stephan; Bernadette C. M. van Wijk; Gabriel Ziegler; Peter Zeidman

This technical note describes some Bayesian procedures for the analysis of group studies that use nonlinear models at the first (within-subject) level – e.g., dynamic causal models – and linear models at subsequent (between-subject) levels. Its focus is on using Bayesian model reduction to finesse the inversion of multiple models of a single dataset or a single (hierarchical or empirical Bayes) model of multiple datasets. These applications of Bayesian model reduction allow one to consider parametric random effects and make inferences about group effects very efficiently (in a few seconds). We provide the relatively straightforward theoretical background to these procedures and illustrate their application using a worked example. This example uses a simulated mismatch negativity study of schizophrenia. We illustrate the robustness of Bayesian model reduction to violations of the (commonly used) Laplace assumption in dynamic causal modelling and show how its recursive application can facilitate both classical and Bayesian inference about group differences. Finally, we consider the application of these empirical Bayesian procedures to classification and prediction.


NeuroImage | 2015

Construct validation of a DCM for resting state fMRI

Adeel Razi; Joshua Kahan; Geraint Rees; K. J. Friston

Recently, there has been a lot of interest in characterising the connectivity of resting state brain networks. Most of the literature uses functional connectivity to examine these intrinsic brain networks. Functional connectivity has well documented limitations because of its inherent inability to identify causal interactions. Dynamic causal modelling (DCM) is a framework that allows for the identification of the causal (directed) connections among neuronal systems — known as effective connectivity. This technical note addresses the validity of a recently proposed DCM for resting state fMRI – as measured in terms of their complex cross spectral density – referred to as spectral DCM. Spectral DCM differs from (the alternative) stochastic DCM by parameterising neuronal fluctuations using scale free (i.e., power law) forms, rendering the stochastic model of neuronal activity deterministic. Spectral DCM not only furnishes an efficient estimation of model parameters but also enables the detection of group differences in effective connectivity, the form and amplitude of the neuronal fluctuations or both. We compare and contrast spectral and stochastic DCM models with endogenous fluctuations or state noise on hidden states. We used simulated data to first establish the face validity of both schemes and show that they can recover the model (and its parameters) that generated the data. We then used Monte Carlo simulations to assess the accuracy of both schemes in terms of their root mean square error. We also simulated group differences and compared the ability of spectral and stochastic DCMs to identify these differences. We show that spectral DCM was not only more accurate but also more sensitive to group differences. Finally, we performed a comparative evaluation using real resting state fMRI data (from an open access resource) to study the functional integration within default mode network using spectral and stochastic DCMs.


EBioMedicine | 2015

Compensation in Preclinical Huntington's Disease: Evidence From the Track-On HD Study

Stefan Klöppel; Sarah Gregory; Elisa Scheller; Lora Minkova; Adeel Razi; Alexandra Durr; Raymund A.C. Roos; Blair R. Leavitt; Marina Papoutsi; G. Bernhard Landwehrmeyer; Ralf Reilmann; Beth Borowsky; Hans J. Johnson; James A. Mills; G Owen; Julie C. Stout; Rachael I. Scahill; Jeffrey D. Long; Geraint Rees; Sarah J. Tabrizi

Background Cognitive and motor task performance in premanifest Huntingtons disease (HD) gene-carriers is often within normal ranges prior to clinical diagnosis, despite loss of brain volume in regions involved in these tasks. This indicates ongoing compensation, with the brain maintaining function in the presence of neuronal loss. However, thus far, compensatory processes in HD have not been modeled explicitly. Using a new model, which incorporates individual variability related to structural change and behavior, we sought to identify functional correlates of compensation in premanifest-HD gene-carriers. Methods We investigated the modulatory effects of regional brain atrophy, indexed by structural measures of disease load, on the relationship between performance and brain activity (or connectivity) using task-based and resting-state functional MRI. Findings Consistent with compensation, as atrophy increased performance-related activity increased in the right parietal cortex during a working memory task. Similarly, increased functional coupling between the right dorsolateral prefrontal cortex and a left hemisphere network in the resting-state predicted better cognitive performance as atrophy increased. Such patterns were not detectable for the left hemisphere or for motor tasks. Interpretation Our findings provide evidence for active compensatory processes in premanifest-HD for cognitive demands and suggest a higher vulnerability of the left hemisphere to the effects of regional atrophy.


IEEE Transactions on Wireless Communications | 2010

Sum rates, rate allocation, and user scheduling for multi-user MIMO vector perturbation precoding

Adeel Razi; Daniel J. Ryan; Iain B. Collings; Jinhong Yuan

This paper considers the multiuser multiple-input multiple-output (MIMO) broadcast channel. We consider the case where the multiple transmit antennas are used to deliver independent data streams to multiple users via vector perturbation. We derive expressions for the sum rate in terms of the average energy of the precoded vector, and use this to derive a high signal-to-noise ratio (SNR) closed-form upper bound, which we show to be tight via simulation. We also propose a modification to vector perturbation where different rates can be allocated to different users. We conclude that for vector perturbation precoding most of the sum rate gains can be achieved by reducing the rate allocation problem to the user selection problem. We then propose a low-complexity user selection algorithm that attempts to maximize the high-SNR sum rate upper bound. Simulations show that the algorithm outperforms other user selection algorithms of similar complexity.


Brain | 2015

Selective vulnerability of Rich Club brain regions is an organizational principle of structural connectivity loss in Huntington's disease

Peter McColgan; Kiran K. Seunarine; Adeel Razi; James H. Cole; Sarah Gregory; Alexandra Durr; Raymund A.C. Roos; Julie C. Stout; Bernhard Landwehrmeyer; Rachael I. Scahill; Chris A. Clark; Geraint Rees; Sarah J. Tabrizi

Diffuse structural connectivity loss occurs early in Huntington’s disease. However, the organizational principles underlying these changes are unclear. Using whole brain diffusion tractography and graph theoretical analysis, McColgan, Seunarine et al. identify a specific role for highly connected rich club regions as a substrate for structural connectivity loss in Huntington’s disease.


NeuroImage | 2014

On nodes and modes in resting state fMRI

K. J. Friston; Joshua Kahan; Adeel Razi; Klaas E. Stephan; Olaf Sporns

This paper examines intrinsic brain networks in light of recent developments in the characterisation of resting state fMRI timeseries — and simulations of neuronal fluctuations based upon the connectome. Its particular focus is on patterns or modes of distributed activity that underlie functional connectivity. We first demonstrate that the eigenmodes of functional connectivity – or covariance among regions or nodes – are the same as the eigenmodes of the underlying effective connectivity, provided we limit ourselves to symmetrical connections. This symmetry constraint is motivated by appealing to proximity graphs based upon multidimensional scaling. Crucially, the principal modes of functional connectivity correspond to the dynamically unstable modes of effective connectivity that decay slowly and show long term memory. Technically, these modes have small negative Lyapunov exponents that approach zero from below. Interestingly, the superposition of modes – whose exponents are sampled from a power law distribution – produces classical 1/f (scale free) spectra. We conjecture that the emergence of dynamical instability – that underlies intrinsic brain networks – is inevitable in any system that is separated from external states by a Markov blanket. This conjecture appeals to a free energy formulation of nonequilibrium steady-state dynamics. The common theme that emerges from these theoretical considerations is that endogenous fluctuations are dominated by a small number of dynamically unstable modes. We use this as the basis of a dynamic causal model (DCM) of resting state fluctuations — as measured in terms of their complex cross spectra. In this model, effective connectivity is parameterised in terms of eigenmodes and their Lyapunov exponents — that can also be interpreted as locations in a multidimensional scaling space. Model inversion provides not only estimates of edges or connectivity but also the topography and dimensionality of the underlying scaling space. Here, we focus on conceptual issues with simulated fMRI data and provide an illustrative application using an empirical multi-region timeseries.


NeuroImage | 2017

Dynamic causal modelling revisited

K. J. Friston; Katrin H. Preller; Chris Mathys; Hayriye Cagnan; Jakob Heinzle; Adeel Razi; Peter Zeidman

This paper revisits the dynamic causal modelling of fMRI timeseries by replacing the usual (Taylor) approximation to neuronal dynamics with a neural mass model of the canonical microcircuit. This provides a generative or dynamic causal model of laminar specific responses that can generate haemodynamic and electrophysiological measurements. In principle, this allows the fusion of haemodynamic and (event related or induced) electrophysiological responses. Furthermore, it enables Bayesian model comparison of competing hypotheses about physiologically plausible synaptic effects; for example, does attentional modulation act on superficial or deep pyramidal cells – or both? In this technical note, we describe the resulting dynamic causal model and provide an illustrative application to the attention to visual motion dataset used in previous papers. Our focus here is on how to answer long-standing questions in fMRI; for example, do haemodynamic responses reflect extrinsic (afferent) input from distant cortical regions, or do they reflect intrinsic (recurrent) neuronal activity? To what extent do inhibitory interneurons contribute to neurovascular coupling? What is the relationship between haemodynamic responses and the frequency of induced neuronal activity? This paper does not pretend to answer these questions; rather it shows how they can be addressed using neural mass models of fMRI timeseries.


IEEE Signal Processing Magazine | 2016

The Connected Brain: Causality, models, and intrinsic dynamics

Adeel Razi; K. J. Friston

Recently, there have been several concerted international efforts-the BRAIN Initiative, the European Human Brain Project, and the Human Connectome Project, to name a few-that hope to revolutionize our understanding of the connected brain. During the past two decades, functional neuroimaging has emerged as the predominant technique in systems neuroscience. This is foreshadowed by an ever-increasing number of publications on functional connectivity, causal modeling, connectomics, and multivariate analyses of distributed patterns of brain responses. In this article, we summarize pedagogically the (deep) history of brain mapping. We highlight the theoretical advances made in the (dynamic) causal modeling of brain function, which may have escaped the wider audience of this article, and provide a brief overview of recent developments and interesting clinical applications. We hope that this article engages the signal processing community by showcasing the inherently multidisciplinary nature of this important topic and the intriguing questions that are being addressed.

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K. J. Friston

University College London

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Geraint Rees

University College London

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Sarah J. Tabrizi

UCL Institute of Neurology

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Sarah Gregory

Wellcome Trust Centre for Neuroimaging

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Jinhong Yuan

University of New South Wales

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Peter McColgan

UCL Institute of Neurology

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Kiran K. Seunarine

UCL Institute of Child Health

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