Search

We propose a computational neurology of movement based on the convergence of theoretical neurobiology and clinical neurology. A significant development in the former is the idea that we can frame brain function as a process of (active) inference, in which the nervous system makes predictions about its sensory data. These predictions depend upon an implicit predictive (generative) model used by the brain. This means neural dynamics can be framed as generating actions to ensure sensations are consistent with these predictions-and adjusting predictions when they are not. We illustrate the significance of this formulation for clinical neurology by simulating a clinical examination of the motor system using an upper limb coordination task. Specifically, we show how tendon reflexes emerge naturally under the right kind of generative model. Through simulated perturbations, pertaining to prior probabilities of this model's variables, we illustrate the emergence of hyperreflexia and pendular reflexes, reminiscent of neurological lesions in the corticospinal tract and cerebellum. We then turn to the computational lesions causing hypokinesia and deficits of coordination. This in silico lesion-deficit analysis provides an opportunity to revisit classic neurological dichotomies (e.g. pyramidal versus extrapyramidal systems) from the perspective of modern approaches to theoretical neurobiology-and our understanding of the neurocomputational architecture of movement control based on first principles. [ABSTRACT FROM AUTHOR]

To infer the causes of its sensations, the brain must call on a generative (predictive) model. This necessitates passing local messages between populations of neurons to update beliefs about hidden variables in the world beyond its sensory samples. It also entails inferences about how we will act. Active inference is a principled framework that frames perception and action as approximate Bayesian inference. This has been successful in accounting for a wide range of physiological and behavioral phenomena. Recently, a process theory has emerged that attempts to relate inferences to their neurobiological substrates. In this paper, we review and develop the anatomical aspects of this process theory. We argue that the form of the generative models required for inference constrains the way in which brain regions connect to one another. Specifically, neuronal populations representing beliefs about a variable must receive input from populations representing the Markov blanket of that variable. We illustrate this idea in four different domains: perception, planning, attention, and movement. In doing so, we attempt to show how appealing to generative models enables us to account for anatomical brain architectures. Ultimately, committing to an anatomical theory of inference ensures we can form empirical hypotheses that can be tested using neuroimaging, neuropsychological, and electrophysiological experiments. [ABSTRACT FROM AUTHOR]

In recent years, the "planning as inference" paradigm has become central to the study of behaviour. The advance offered by this is the formalisation of motivation as a prior belief about "how I am going to act". This paper provides an overview of the factors that contribute to this prior. These are rooted in optimal experimental design, information theory, and statistical decision making. We unpack how these factors imply a functional architecture for motivated behaviour. This raises an important question: how can we put this architecture to work in the service of understanding observed neurobiological structure? To answer this question, we draw from established techniques in experimental studies of behaviour. Typically, these examine the influence of perturbations of the nervous system—which include pathological insults or optogenetic manipulations—to see their influence on behaviour. Here, we argue that the message passing that emerges from inferring what to do can be similarly perturbed. If a given perturbation elicits the same behaviours as a focal brain lesion, this provides a functional interpretation of empirical findings and an anatomical grounding for theoretical results. We highlight examples of this approach that influence different sorts of goal-directed behaviour, active learning, and decision making. Finally, we summarise their implications for the neuroanatomy of inferring what to do (and what not to). [ABSTRACT FROM AUTHOR]

Perceptual awareness depends upon the way in which we engage with our sensorium. This notion is central to active inference, a theoretical framework that treats perception and action as inferential processes. This variational perspective on cognition formalizes the notion of perception as hypothesis testing and treats actions as experiments that are designed (in part) to gather evidence for or against alternative hypotheses. The common treatment of perception and action affords a useful interpretation of certain perceptual phenomena whose active component is often not acknowledged. In this article, we start by considering Troxler fading – the dissipation of a peripheral percept during maintenance of fixation, and its recovery during free (saccadic) exploration. This offers an important example of the failure to maintain a percept without actively interrogating a visual scene. We argue that this may be understood in terms of the accumulation of uncertainty about a hypothesized stimulus when free exploration is disrupted by experimental instructions or pathology. Once we take this view, we can generalize the idea of using bodily (oculomotor) action to resolve uncertainty to include the use of mental (attentional) actions for the same purpose. This affords a useful way to think about binocular rivalry paradigms, in which perceptual changes need not be associated with an overt movement. [ABSTRACT FROM AUTHOR]

How do we navigate a deeply structured world? Why are you reading this sentence first – and did you actually look at the fifth word? This review offers some answers by appealing to active inference based on deep temporal models. It builds on previous formulations of active inference to simulate behavioural and electrophysiological responses under hierarchical generative models of state transitions. Inverting these models corresponds to sequential inference, such that the state at any hierarchical level entails a sequence of transitions in the level below. The deep temporal aspect of these models means that evidence is accumulated over nested time scales, enabling inferences about narratives (i.e., temporal scenes). We illustrate this behaviour with Bayesian belief updating – and neuronal process theories – to simulate the epistemic foraging seen in reading. These simulations reproduce perisaccadic delay period activity and local field potentials seen empirically. Finally, we exploit the deep structure of these models to simulate responses to local (e.g., font type) and global (e.g., semantic) violations; reproducing mismatch negativity and P300 responses respectively. [ABSTRACT FROM AUTHOR]

How do we navigate a deeply structured world? Why are you reading this sentence first – and did you actually look at the fifth word? This review offers some answers by appealing to active inference based on deep temporal models. It builds on previous formulations of active inference to simulate behavioural and electrophysiological responses under hierarchical generative models of state transitions. Inverting these models corresponds to sequential inference, such that the state at any hierarchical level entails a sequence of transitions in the level below. The deep temporal aspect of these models means that evidence is accumulated over nested time scales, enabling inferences about narratives (i.e., temporal scenes). We illustrate this behaviour with Bayesian belief updating – and neuronal process theories – to simulate the epistemic foraging seen in reading. These simulations reproduce perisaccadic delay period activity and local field potentials seen empirically. Finally, we exploit the deep structure of these models to simulate responses to local (e.g., font type) and global (e.g., semantic) violations; reproducing mismatch negativity and P300 responses respectively. [ABSTRACT FROM AUTHOR]

Delusions are, by popular definition, false beliefs that are held with certainty and resistant to contradictory evidence. They seem at odds with the notion that the brain at least approximates Bayesian inference. This is especially the case in schizophrenia, a disorder thought to relate to decreased - rather than increased - certainty in the brain's model of the world. We use an active inference Markov decision process model (a Bayes-optimal decision-making agent) to perform a simple task involving social and non-social inferences. We show that even moderate changes in some model parameters - decreasing confidence in sensory input and increasing confidence in states implied by its own (especially habitual) actions - can lead to delusions as defined above. Incorporating affect in the model increases delusions, specifically in the social domain. The model also reproduces some classic psychological effects, including choice-induced preference change, and an optimism bias in inferences about oneself. A key observation is that no change in a single parameter is both necessary and sufficient for delusions; rather, delusions arise due to conditional dependencies that create 'basins of attraction' which trap Bayesian beliefs. Simulating the effects of antidopaminergic antipsychotics - by reducing the model's confidence in its actions - demonstrates that the model can escape from these attractors, through this synthetic pharmacotherapy. [ABSTRACT FROM AUTHOR]