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Dynamic Causal Modelling THEORY

Dynamic Causal Modelling THEORY. Hanneke den Ouden Donders Centre for Cognitive Neuroimaging Radboud University Nijmegen Functional Imaging Laboratory (FIL) Wellcome Trust Centre for Neuroimaging University College London. SPM Course FIL, London 22-24 October 2009.

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Dynamic Causal Modelling THEORY

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  1. Dynamic Causal Modelling THEORY Hanneke den Ouden Donders Centre for Cognitive Neuroimaging Radboud University Nijmegen Functional Imaging Laboratory (FIL) Wellcome Trust Centre for Neuroimaging University College London SPM Course FIL, London 22-24 October 2009

  2. Principles of Organisation Functional integration Functional specialization

  3. Overview • Brain connectivity • Dynamic causal models (DCMs) • Basics • Neural model • Hemodynamic model • Parameters & parameter estimation • Inference & Model comparison • Recent extentions to DCM • Planning a DCM compatible study

  4. Structural, functional & effective connectivity • anatomical/structural connectivity= presence of axonal connections • functional connectivity = statistical dependencies between regional time series • effective connectivity = causal (directed) influences between neurons or neuronal populations Sporns 2007, Scholarpedia

  5. For understanding brain function mechanistically, we can use DCM to create models of causal interactions among neuronal populationsto explain regional effects in terms of interregional connectivity

  6. Overview • Brain connectivity • Dynamic causal models (DCMs) • Basics • Neural model • Hemodynamic model • Parameters & parameter estimation • Inference & Model comparison • Recent extentions to DCM • Planning a DCM compatible study

  7. x λ y Basics of DCM: Neuronal and BOLD level • Cognitive system is modelled at its underlying neuronal level (not directly accessible for fMRI). • The modelled neuronal dynamics (x) are transformed into area-specific BOLD signals (y) by a hemodynamicmodel (λ). The aim of DCM is to estimate parameters at the neuronal level such that the modelled and measured BOLD signals are optimally similar.

  8. x3 x1 x2 systemstate input parameters state changes effective connectivity externalinputs DCM: Linear Model u1

  9. Neural State Equation X3 u1 X1 X2 u2 u3 state changes fixed effective connectivity modulatory effective connectivity systemstate input parameters externalinputs DCM: Bilinear Model

  10. x λ y Basics of DCM: Neuronal and BOLD level • Cognitive system is modelled at its underlying neuronal level (not directly accessible for fMRI). • The modelled neuronal dynamics (x) are transformed into area-specific BOLD signals (y) by a hemodynamicmodel (λ).

  11. t The hemodynamic model u stimulus functions • 6 hemodynamic parameters: neural state equation important for model fitting, but of no interest for statistical inference hemodynamic state equations • Computed separately for each area (like the neural parameters) region-specific HRFs! Estimated BOLD response Friston et al. 2000, NeuroImage Stephan et al. 2007, NeuroImage

  12. hemodynamic model X3 λ X1 u1 x y X2 u2 u3 Measured vs Modelled BOLD signal • Recap • The aim of DCM is to estimate • neural parameters {A, B, C} • hemodynamic parameters • such that the modelled (x) and measured (y) BOLD signals are maximally similar.

  13. Overview • Brain connectivity • Dynamic causal models (DCMs) • Basics • Neural model • Hemodynamic model • Parameters & parameter estimation • Inference & Model comparison • Recent extentions to DCM • Planning a DCM compatible study

  14. DCM parameters = rate constants Integration of a first-order linear differential equation gives anexponential function: The coupling parameter adetermines the half life of x(t), and thus describes the speed of the exponential change If AB is 0.10 s-1 this means that, per unit time, the increase in activity in B corresponds to 10% of the activity in A

  15. u1 u 1 u2 u 2 x1 Z 1 x2 Z 2 Example: context-dependent decay stimuli u1 context u2 - + - x1 + + x2 - - Penny, Stephan, Mechelli, Friston NeuroImage (2004)

  16. Estimation: Bayesian framework • Models of • Haemodynamics in a single region • Neuronal interactions • Constraints on • Haemodynamic parameters • Connections likelihood prior posterior Bayesian estimation

  17. Modulatory input (e.g. context/learning/drugs) Driving input (e.g. sensory stim) b12 c1 c2 a12 y y Conceptual overview Neuronal states Parameters are optimised so that the predicted matches the measured BOLD response  But how confident are we in what these parameters tell us? activity x1(t) activity x2(t) BOLD Response

  18. Overview • Brain connectivity • Dynamic causal models (DCMs) • Basics • Neural model • Hemodynamic model • Parameters & parameter estimation • Inference & Model comparison • Recent extentions to DCM • Planning a DCM compatible study

  19. Pitt & Miyung (2002) TICS Model comparison and selection Given competing hypotheses, which model is the best?

  20.  ηθ|y Inference about DCM parameters: Bayesian single subject analysis • The model parameters are distributions that have a mean ηθ|y and covariance Cθ|y. • Use of the cumulative normal distribution to test the probability that a certain parameter is above a chosen threshold γ: Classical frequentist test across Ss • Test summary statistic: mean ηθ|y • One-sample t-test: Parameter > 0? • Paired t-test: parameter 1 > parameter 2? • rmANOVA: e.g. in case of multiple sessions per subject

  21. Neuronal dynamics Haemodynamics State space Model Priors Posterior densities of parameters Bayesian Model inversion fMRI data Model comparison DCM roadmap

  22. Overview • Brain connectivity • Dynamic causal models (DCMs) • Basics • Neural model • Hemodynamic model • Parameters & parameter estimation • Inference & Model comparison • Recent extentions to DCM • Planning a DCM compatible study

  23. Two-state DCM u2 u1 Nonlinear state equation Extensions to DCM • Ext. 2: Nonlinear DCM • Gating of connections by other areas • Ext. 1: two state model • excitatory & inhibitory

  24. Planning a DCM-compatible study • Suitable experimental design: • any design that is suitable for a GLM • preferably multi-factorial (e.g. 2 x 2) • e.g. one factor that varies the driving (sensory) input • and one factor that varies the contextual input • Hypothesis and model: • Define specific a priori hypothesis • Which parameters are relevant to test this hypothesis? • If you want to verify that intended model is suitable to test this hypothesis, then use simulations • Define criteria for inference • What are the alternative models to test?

  25. So, DCM…. • enables one to infer hidden neuronal processes from fMRI data • tries to model the same phenomena as a GLM • explaining experimentally controlled variance in local responses • based on connectivity and its modulation • allows one to test mechanistic hypotheses about observed effects • is informed by anatomical and physiological principles. • uses a Bayesian framework to estimate model parameters • is a generic approach to modeling experimentally perturbed dynamic systems. • provides an observation model for neuroimaging data, e.g. fMRI, M/EEG • DCM is not model or modality specific (Models will change and the method extended to other modalities e.g. ERPs)

  26. Some useful references • The first DCM paper: Dynamic Causal Modelling (2003). Friston et al. NeuroImage 19:1273-1302. • Physiological validation of DCM for fMRI: Identifying neural drivers with functional MRI: an electrophysiological validation (2008). David et al. PLoS Biol. 6 2683–2697 • Hemodynamic model:Comparing hemodynamic models with DCM (2007). Stephan et al. NeuroImage 38:387-401 • Nonlinear DCMs:Nonlinear Dynamic Causal Models for FMRI (2008). Stephan et al. NeuroImage 42:649-662 • Two-state model: Dynamic causal modelling for fMRI: A two-state model (2008). Marreiros et al. NeuroImage 39:269-278 • Group Bayesian model comparison: Bayesian model selection for group studies (2009). Stephan et al. NeuroImage 46:1004-10174 • Watch out for: 10 Simple Rules for DCM, Stephan et al (in prep).

  27. Time to do a DCM!

  28. Dynamic Causal ModellingPRACTICAL Andre Marreiros Hanneke den Ouden Donders Centre for Cognitive Neuroimaging Radboud University Nijmegen Functional Imaging Laboratory (FIL) Wellcome Trust Centre for Neuroimaging University College London SPM Course FIL, London 22-24 October 2009

  29. Attention to Motion in the visual system DCM – Attention to Motion Paradigm • Stimuli 250 radially moving dots at 4.7 degrees/s • Pre-Scanning • 5 x 30s trials with 5 speed changes (reducing to 1%) • Task - detect change in radial velocity • Scanning (no speed changes) • F A F N F A F N S …. • F - fixation • S - observe static dots + photic • N - observe moving dots + motion • A - attend moving dots + attention Parameters • blocks of 10 scans • - 360 scans total • - TR = 3.22 seconds

  30. Attention to Motion in the visual system Paradigm Results SPC V3A V5+ Attention – No attention Büchel & Friston 1997, Cereb. Cortex Büchel et al.1998, Brain • - fixation only • observe static dots + photic  V1 • - observe moving dots + motion  V5 • task on moving dots + attention  V5 + parietal cortex

  31. SPC V1 V5 Photic Attention SPC Photic V1 V5 Motion Motion Attention DCM: comparison of 2 models Model 1attentional modulationof V1→V5: forward Model 2attentional modulationof SPC→V5: backward Bayesian model selection: Which model is optimal?

  32. SPC V1 V5 Photic Attention SPC Photic V1 V5 Motion Motion Attention Attention to Motion in the visual system Paradigm Ingredients for a DCM Specific hypothesis/question Model: based on hypothesis Timeseries: from the SPM Inputs: from design matrix Model 1attentional modulationof V1→V5: forward Model 2attentional modulationof SPC→V5: backward

  33. Attention to Motion in the visual system DCM – GUI basic steps 1 – Extract the time series (from all regions of interest) 2 – Specify the model 3 – Estimate the model 4 – Review the estimated model 5 – Repeat steps 2 and 3 for all models in model space 6 – Compare models

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