1,987 publications from this institution
Cognitive models indicate that there are multiple ways of completing the same task. This implicit degeneracy cannot be revealed by functional imaging studies of normal subjects if more than one of the sufficient neural systems is activated. Nor can it be detected by neuropsychological studies of patients because their performance might not be impaired when only one degenerate system is damaged. We propose that degenerate sets of sufficient neural systems can only be identified by an iterative approach that integrates the lesion-deficit model and functional imaging studies of normal and neurologically damaged subjects.
Normal ageing is associated with a decline in episodic memory, and neuroimaging studies in older adults have shown reduced activity in prefrontal cortex and other regions critical for memory function in the young. However, older adults also activate additional regions, suggesting a degree of functional reorganisation that has been attributed variously to detrimental and adaptive changes. Evaluation of these competing hypotheses depends critically upon inferences about the relative location and distribution of activity that are not well supported by current univariate or multivariate analyses. Here, we employed a recently developed model-based multivariate 'decoding' approach (Friston et al., 2008) to re-analyse a rich episodic encoding dataset and examine directly how the patterns of activity change in ageing. We assessed which spatial activity patterns, within lateral prefrontal cortex, best predict successful memory formation. Bayesian model comparison showed that the older adults had more distributed and bilateral (fragmented) predictive patterns of activity in anterior inferior frontal gyrus and middle frontal gyrus. With this direct multivariate test for changes in patterns of activity, we replicate and extend earlier findings of reduced prefrontal lateralisation in ageing. These findings extend conclusions based on conventional analyses, and support the notion that ageing alters the spatial deployment of neuronal activity, to render it less spatially coherent and regionally specific. This greater distribution of activity in older adults was also linked to poorer individual memory performance, suggesting that it reflects neural ageing, rather than adaptive compensatory responses.
This chapter is about modeling-distributed brain responses and, in particular, the functional integration among neuronal systems. Inferences about the functional organization of the brain rest on models of how measurements of evoked responses are caused. These models can be quite diverse, ranging from conceptual models of functional anatomy to mathematical models of neuronal and hemodynamics. The aim of this chapter is to introduce dynamic causal models. These models can be regarded as generalizations of the simple models employed in conventional analyses of regionally specific brain responses. In what follows, we will start with anatomical models of functional brain architectures, which motivate some of the basic principles of neuroimaging. We then review briefly statistical models (e.g., the general linear model) used for making classical and Bayesian inferences about where neuronal responses are expressed. By incorporating biophysical constraints, these basic models can be finessed and, in a dynamic setting, rendered causal. This allows us to infer how interactions among brain regions are mediated. This chapter focuses on causal models for distributed responses measured with fMRI and electroencephalography. The latter is based on neural-mass models and affords mechanistic inferences about how evoked responses are caused, at the level of neuronal subpopulations and the coupling among them.
Abstract Cognitive processes such as decision-making, working memory, and motor planning operate across a hierarchy of timescales, manifesting as rapid neural transients alongside slower physiological mechanisms like short-term plasticity. Conventional Dynamic Causal Modelling (DCM) limits our ability to study these dynamics by assuming stationary parameters, whilst recent time-varying approaches often rely on segmenting data into epochs. This segmentation artificially resets neural states between windows, fundamentally obscuring the continuous hysteresis essential to sequential processing. To address this limitation, we introduce DCM for Sequential Responses (DCM-SR), a generative framework that embeds parameter evolution directly within the first-level model whilst employing a continuous state-space formulation that removes the requirement for epoching. This approach generalises non-stationarity to all neural mass parameters, including synaptic gains and time constants, modelling them as piecewise smooth trajectories that evolve alongside continuous neural states. Consequently, the model explicitly captures two distinct forms of temporal memory: transient history dependence, where responses are shaped by the carryover effect of recent perturbations, and path dependence, where the system’s trajectory through parameter space determines its responsiveness. The framework accommodates both exogenous, stimulus-locked transitions and endogenous, autonomous state changes, permitting inference on both external perturbations and internal drivers of network evolution. Simulations establish the model’s face validity, demonstrating robust parameter recovery and conservative model selection that accurately discriminates between genuine parameter evolution and spurious complexity. We applied the framework to empirical data from an auditory go/no-go task, modelling a full sequence of cognitive phases from initial cue processing and anticipation through to motor preparation and execution. This analysis established construct validity by resolving the biophysical generators of the contingent negative variation, attributing this slow potential to sustained thalamocortical drive and deep-layer hyperpolarisation rather than superficial-layer activity. Furthermore, the model captured trial-specific modulations of the hyperdirect pathway during motor inhibition, tracking the dynamic interplay between prefrontal executive control and basal ganglia gating. DCM-SR offers the first principled approach to decomposing compound signals such as slow cortical potentials into evolving synaptic mechanisms and continuous state trajectories, and provides a necessary bridge for investigating the biophysical implementation of extended cognitive phenomena including evidence accumulation and physiological hysteresis.
This chapter is about modelling-distributed brain responses and, in particular, the functional integration among neuronal systems. Inferences about the functional organisation of the brain rest on models of how measurements of evoked responses are caused. These models can be quite diverse, ranging from conceptual models of functional anatomy to mathematical models of neuronal and haemodynamics. The aim of this chapter is to introduce dynamic causal models. These models can be regarded as generalisations of the simple models employed in conventional analyses of regionally specific brain responses. In what follows, we will start with anatomical models of functional brain architectures, which motivate some of the basic principles of neuroimaging. We then review briefly statistical models (e.g., the general linear model) used for making classical and Bayesian inferences about where neuronal responses are expressed. By incorporating biophysical constraints, these basic models can be finessed and, in a dynamic setting, rendered causal. This allows us to infer how interactions among brain regions are mediated. This chapter focuses on causal models for distributed responses measured with fMRI and electroencephalography. The latter is based on neural-mass models and affords mechanistic inferences about how evoked responses are caused, at the level of neuronal sub-populations and the coupling among them.
Neural data presented in figures 3,4,s3-5 in Kaplan & Friston (2019) PLoS Biology
Understanding the neural substrates of depression is crucial for diagnosis and treatment. Here, we review recent studies of functional and effective connectivity in depression, in terms of functional integration in the brain. Findings from these studies, including our own, point to the involvement of at least four networks in patients with depression. Elevated connectivity of a ventral limbic affective network appears to be associated with excessive negative mood (dysphoria) in the patients; decreased connectivity of a frontal-striatal reward network has been suggested to account for loss of interest, motivation, and pleasure (anhedonia); enhanced default mode network connectivity seems to be associated with depressive rumination; and diminished connectivity of a dorsal cognitive control network is thought to underlie cognitive deficits especially ineffective top-down control of negative thoughts and emotions in depressed patients. Moreover, the restoration of connectivity of these networks-and corresponding symptom improvement-following antidepressant treatment (including medication, psychotherapy, and brain stimulation techniques) serves as evidence for the crucial role of these networks in the pathophysiology of depression.