Advances in cognitive neuroscience offer us new ways to understand the symptoms of mental illness by uniting basic neurochemical and neurophysiological observations with the conscious experiences that characterize these symptoms. Cognitive theories about the positive symptoms of schizophrenia — hallucinations and delusions — have tended to treat perception and belief formation as distinct processes. However, recent advances in computational neuroscience have led us to consider the unusual perceptual experiences of patients and their sometimes bizarre beliefs as part of the same core abnormality — a disturbance in error-dependent updating of inferences and beliefs about the world. We suggest that it is possible to understand these symptoms in terms of a disturbed hierarchical Bayesian framework, without recourse to separate considerations of experience and belief.

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Perceiving is believing: a Bayesian approach to explaining the positive symptoms of schizophrenia

The intricate neuronal circuitry of the cerebellum is thought to encode internal models that reproduce the dynamic properties of body parts. These models are essential for controlling the movement of these body parts: they allow the brain to precisely control the movement without the need for sensory feedback. It is thought that the cerebellum might also encode internal models that reproduce the essential properties of mental representations in the cerebral cortex. This hypothesis suggests a possible mechanism by which intuition and implicit thought might function and explains some of the symptoms that are exhibited by psychiatric patients. This article examines the conceptual bases and experimental evidence for this hypothesis.

Control of mental activities by internal models in the cerebellum

Over the last 2 decades, a large number of neurophysiological and neuroimaging studies of patients with schizophrenia have furnished in vivo evidence for dysconnectivity, ie, abnormal functional integration of brain processes. While the evidence for dysconnectivity in schizophrenia is strong, its etiology, pathophysiological mechanisms, and significance for clinical symptoms are unclear. First, dysconnectivity could result from aberrant wiring of connections during development, from aberrant synaptic plasticity, or from both. Second, it is not clear how schizophrenic symptoms can be understood mechanistically as a consequence of dysconnectivity. Third, if dysconnectivity is the primary pathophysiology, and not just an epiphenomenon, then it should provide a mechanistic explanation for known empirical facts about schizophrenia. This article addresses these 3 issues in the framework of the dysconnection hypothesis. This theory postulates that the core pathology in schizophrenia resides in aberrant N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic plasticity due to abnormal regulation of NMDARs by neuromodulatory transmitters like dopamine, serotonin, or acetylcholine. We argue that this neurobiological mechanism can explain failures of self-monitoring, leading to a mechanistic explanation for first-rank symptoms as pathognomonic features of schizophrenia, and may provide a basis for future diagnostic classifications with physiologically defined patient subgroups. Finally, we test the explanatory power of our theory against a list of empirical facts about schizophrenia.

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Dysconnection in Schizophrenia: From Abnormal Synaptic Plasticity to Failures of Self-monitoring

Cognitive Behavioural Therapy (CBT) has established itself as one of the most effective therapies for treating a wide range of psychological disorders. However, research and treatment in this field typically adopts a DSM driven 'disorder-focused' approach - researchers and clinicians target a specific disorder, try to understand its aetiology and maintenance, and try to develop more effective strategies to treat the disorder. This book proposes an insightful and original approach to understanding these disorders, one that focuses on what they have in common. Instead of examining in isolation, for example, obsessive compulsive disorders, insomnia, schizophrenia, it asks - what do patients with these disorders have in common? It takes each cognitive and behavioural process - attention, memory, reasoning, thought, behaviour, and examines whether it is a transdiagnostic process - i.e., serves to maintain a broad range of psychological disorders. Having shown how these disorders share several important processes, it then describes the practical implications of such an approach to diagnosis and treatment. Importantly it explores why the different psychological disorders can present so differently, despite being maintained by the same cognitive and behavioural processes. It also provides an account of the high rates of comorbidity observed among the different disorders. This book provides a novel review and integration of the empirical literature and gives clinicians and researchers a valuable new theoretical base for assessing and treating psychological disorders. Cognitive Behavioural Therapy (CBT) has established itself as one of the most effective therapies for treating a wide range of psychological disorders. However, research and treatment in this field typically adopts a DSM driven 'disorder-focused' approach - researchers and clinicians target a specific disorder, try to understand its aetiology and maintenance, and try to develop more effective strategies to treat the disorder. This book proposes an insightful and original approach to understanding these disorders, one that focuses on what they have in common. Instead of examining in isolation, for example, obsessive compulsive disorders, insomnia, schizophrenia, it asks - what do patients with these disorders have in common? It takes each cognitive and behavioural process - attention, memory, reasoning, thought, behaviour, and examines whether it is a transdiagnostic process - i.e., serves to maintain a broad range of psychological disorders. Having shown how these disorders share several important processes, it then describes the practical implications of such an approach to diagnosis and treatment. Importantly it explores why the different psychological disorders can present so differently, despite being maintained by the same cognitive and behavioural processes. It also provides an account of the high rates of comorbidity observed among the different disorders. This book provides a novel review and integration of the empirical literature and gives clinicians and researchers a valuable new theoretical base for assessing and treating psychological disorders.

Cognitive Behavioural Processes across Psychological Disorders: A Transdiagnostic Approach to Research and Treatment

http://wexler.free.fr/library/files/blakemore%20(2002)%20abnormalities%20in%20the%20awareness%20of%20action.pdf

Abnormalities in the awareness of action

Background. To test the hypothesis that certain psychotic symptomatology is due to a defect in selfmonitoring, we investigated the ability of groups of psychiatric patients to dierentiate perceptually between self-produced and externally produced tactile stimuli. Methods. Responses to tactile stimulation were assessed in three groups of subjects: schizophrenic patients; patients with bipolar aective disorder or depression; and normal control subjects. Within the psychiatric groups subjects were divided on the basis of the presence or absence of auditory hallucinations and}or passivity experiences. The subjects were asked to rate the perception of a tactile sensation on the palm of their left hand. The tactile stimulation was either self-produced by movement of the subject’s right hand or externally produced by the experimenter. Results. Normal control subjects and those psychiatric patients with neither auditory hallucinations nor passivity phenomena experienced self-produced stimuli as less intense, tickly and pleasant than identical, externally produced tactile stimuli. In contrast, psychiatric patients with these symptoms did not show a decrease in their perceptual ratings for tactile stimuli produced by themselves as compared with those produced by the experimenter. This failure to show a dierence in perception between self-produced and externally produced stimuli appears to relate to the presence of auditory hallucinations and}or passivity experiences rather than to the diagnosis of schizophrenia. Conclusions. We propose that auditory hallucinations and passivity experiences are associated with an abnormality in the self-monitoring mechanism that normally allows us to distinguish selfproduced from externally produced sensations.

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The perception of self-produced sensory stimuli in patients with auditory hallucinations and passivity experiences: evidence for a breakdown in self-monitoring

J. Smith

Papers

The perception of self-produced sensory stimuli in patients with auditory hallucinations and passivity experiences: evidence for a breakdown in self-monitoring