ReviewComputational psychiatry: the brain as a phantastic organ
Introduction
Computational psychiatry uses formal models of brain function to characterise the mechanisms of psychopathology, usually in a way that can be described in computational or mathematical terms. Computational psychiatry has arrived:1, 2, 3 the first international computational psychiatry meeting was held in 2013, and 2014 saw the inception of the Max Planck Society-University College London initiative on computational psychiatry and ageing research—and the first UK computational psychiatry course. Several computational psychiatry units are emerging worldwide.
In this Review, we aim to provide tangible examples of computational psychiatry and to explain how it motivates mechanistic research in systems neuroscience; research that is being, or will soon be, translated into clinical neuroscience. First, we consider the properties a computational formulation must possess to be useful in psychiatry. We focus on active inference or predictive coding as an example (panel). We emphasise the importance of active inference by showing how it contextualises other formal treatments. We conclude with some examples of how theoretical principles can unify apparently disparate aspects of psychiatric disorders. We will consider functional and dissociative symptoms, soft neurological signs in schizophrenia, interoceptive inference and autism, dysconnection models of delusional (false) beliefs, and formal models of interpersonal exchange. We chose these examples to show the breadth of psychopathology that can be understood in terms of one pathology; namely, false inference that can be ascribed to neuromodulatory failures at the synaptic level. This Review is prospective, in that most of the examples we consider relate to the promise of the future—much of the work that substantiates the points we make has yet to be undertaken.
Section snippets
The phantastic organ
Many formal or computational schemes could characterise psychopathology, ranging from parallel distributed processing or neural network theory and dynamical systems theory, to reinforcement learning and game theory. However, these theoretical frameworks do not address the central problem encountered in psychiatry—ie, the production of false beliefs. The problems that concern psychiatrists are, almost universally, abnormal beliefs and their behavioural sequelae (eg, dysmorphophobia, paranoid
Predictive coding and the Bayesian brain
Modern versions of Helmholtz's ideas are now among the most popular explanations for message passing in the brain and are usually portrayed in the setting of the Bayesian brain hypothesis as predictive coding.9, 10, 11, 12 Predictive coding is not a normative or descriptive scheme, it is a process theory with a biologically plausible basis—there is now much circumstantial anatomical and physiological evidence for predictive coding in the brain.12, 13, 14, 15, 16 In this scheme, neuronal
From the Bayesian brain to active inference
If the brain is a generative model of the world, then much of it must be occupied by modelling other people. In other words, individuals spend most of their time predicting the internal (proprioceptive) and external (exteroceptive) consequences of behaviour (both their own and that of others). To fully appreciate the bilateral nature of these predictions, inference can be considered in an embodied context. In this setting, perception can be understood as resolving exteroceptive prediction
Interoceptive inference
Recently, investigators described emotional processing in terms of predictive coding or inference about interoceptive or bodily states.38, 39 In active inference, motor reflexes are driven by proprioceptive prediction errors. Proprioceptive prediction errors compare primary afferents from stretch receptors with proprioceptive predictions that descend to α motor neurons in the spinal-cord and cranial nerve nuclei. This circuit effectively replaces descending motor commands with proprioceptive
Parallel-distributed processing, precision, and the dysconnection hypothesis
Part of the construct validity of active inference is that it leads to, and contexualises other formal approaches. For example, formal models of schizophrenia are often described in terms of neuronal disconnection. There are two versions of the disconnection hypothesis: the first is implied by Wernicke's sejunction hypothesis, which postulates an anatomical disruption or disconnection of association fibres;43 the second postulates abnormalities at the level of synaptic efficacy and plasticity,
Neuromodulation and false inference
We have introduced a computational framework for action and perception, with a special focus on the synaptic mechanisms that might underlie false inference in psychiatric disorders: in brief, the formal constraints implicit in predictive coding mandate modulatory gain control for ascending prediction errors. In an article in 2012, Edwards and colleagues79 illustrates how functional symptoms can be understood as false inference about the causes of abnormal sensations, movements, or their
Conclusion
In this Review, we have discussed how computational psychiatry can use formal models of perceptual inference and learning to provide a mechanistic and functional perspective on psychopathology and its underlying pathophysiology. We focused on inference as the overarching theoretical framework; largely because it can formalise perception and behaviour in terms of probabilistic beliefs. By assuming that the brain engages in some form of active inference, neuronal dynamics and message passing can
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