The emerging biology of delusions

Murray, Graham K.

doi:10.1017/s0033291710000413

Cited by 22 publications

(14 citation statements)

References 69 publications

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“…Consistent with this, we found that reduced connectivity between the midbrain and insula correlated with increased severity of psychotic symptoms. This correlation is also consistent with previous findings indicating that abnormal processing of reinforcers is related to psychotic symptoms such as delusions (Corlett et al, 2007;Heinz and Schlagenhauf, 2010;Murray, 2011;Schlagenhauf et al, 2009).…”

Section: Discussionsupporting

confidence: 93%

Salience network-midbrain dysconnectivity and blunted reward signals in schizophrenia

Gradin¹,

Waiter²,

O'Connor³

et al. 2013

Psychiatry Research: Neuroimaging

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Theories of schizophrenia propose that abnormal functioning of the neural reward system is linked to negative and psychotic symptoms, by disruption of reward processing and promotion of context-independent false associations. Recently, it has been argued that an insula-anterior cingulate cortex (ACC) salience network system enables switching of brain states from the default mode to a task-related activity mode. Abnormal interaction between the insula-ACC system and reward processing regions may help explain abnormal reinforcer processing and symptoms. Here we use functional magnetic resonance imaging to assess the neural correlates of reward processing in schizophrenia. Furthermore, we investigated functional connectivity between the dopaminergic midbrain, a key region for the processing of reinforcers, and other brain regions. In response to rewards, controls activated task related regions (striatum, amygdala/hippocampus and midbrain) and the insula-ACC salience network. Patients similarly activated the insula-ACC salience network system but failed to activate task related regions. Reduced functional connectivity between the midbrain and the insula was found in schizophrenia, with the extent of this abnormality correlating with increased psychotic symptoms. The findings support the notion that reward processing is abnormal in schizophrenia and highlight the potential role of abnormal interactions between the insula-ACC salience network and reward regions.

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Section: Discussionsupporting

confidence: 93%

Salience network-midbrain dysconnectivity and blunted reward signals in schizophrenia

Gradin¹,

Waiter²,

O'Connor³

et al. 2013

Psychiatry Research: Neuroimaging

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“…How paranoia differs in causal factors from anxiety, depression, grandiosity and other related psychological problems remains to be determined [75, 93]. It is notable that the specific neurobiology of delusions and related processing has been neglected [145], while there needs to be a concerted effort to determine the effects at the individual level on psychological processing of known social factors increasing paranoia. Given the clear evidence of advancements in understanding, arguably the greatest focus needs to be on translation into more efficacious treatments and self-management.…”

Section: Reasoningmentioning

confidence: 99%

Advances in understanding and treating persecutory delusions: a review

Freeman

Garety

2014

Soc Psychiatry Psychiatr Epidemiol

298

259

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PurposePersecutory delusions are a central psychotic experience, at the severe end of a paranoia spectrum in the general population. The aim of the review is to provide an introduction to the understanding of persecutory delusions, highlight key putative causal factors that have the potential to be translated into efficacious treatment, and indicate future research directions.MethodsA narrative literature review was undertaken to highlight the main recent areas of empirical study concerning non-clinical and clinical paranoia.ResultsSix main proximal causal factors are identified: a worry thinking style, negative beliefs about the self, interpersonal sensitivity, sleep disturbance, anomalous internal experience, and reasoning biases. Each has plausible mechanistic links to the occurrence of paranoia. These causal factors may be influenced by a number of social circumstances, including adverse events, illicit drug use, and urban environments.ConclusionsThere have been numerous replicated empirical findings leading to a significant advance in the understanding of persecutory delusions, now beginning to be translated into cognitive treatments. The first trials specifically focussed on patients who have persecutory delusions in the context of psychotic diagnoses are occurring. Initial evidence of efficacy is very promising.

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“…Murray [58] modified the two-factor theory in terms of the first factor representing an abnormal perception, thoughts or feelings, and the second factor representing the move from unusual thoughts into delusions. The feeling of unusual perception could lead to different outcomes: if the subject consults a doctor, because he feels something going on, he will probably be assessed as having an ‘at-risk mental state’.…”

Section: The One- and Two-factor Approachmentioning

confidence: 99%

Neurobiological Correlates of Delusion: Beyond the Salience Attribution Hypothesis

et al. 2012

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Dopamine dysfunction is a mainstay of theories aimed to explain the neurobiological correlates of schizophrenia symptoms, particularly positive symptoms such as delusions and passivity phenomena. Based on studies revealing dopamine dysfunction in addiction research, it has been suggested that phasic or chaotic firing of dopaminergic neurons projecting to the (ventral) striatum attribute salience to otherwise irrelevant stimuli and thus contribute to delusional mood and delusion formation. Indeed, several neuroimaging studies revealed that neuronal encoding of usually irrelevant versus relevant stimuli is blunted in unmedicated schizophrenia patients, suggesting that some stimuli that are irrelevant for healthy controls acquire increased salience for psychotic patients. However, salience attribution per se may not suffice to explain anxieties and feelings of threat that often accompany paranoid ideation. Here, we suggest that beyond ventral striatal dysfunction, dopaminergic dysregulation in limbic areas such as the amygdala in interaction with prefrontal and temporal cortex may contribute to the formation of delusions and negative symptoms. Neuroleptic medication, on the other hand, appears to interfere with anticipation of reward in the ventral striatum and can thus contribute to secondary negative symptoms such as apathy and avolition.

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The emerging biology of delusions

Cited by 22 publications

References 69 publications

Salience network-midbrain dysconnectivity and blunted reward signals in schizophrenia

Salience network-midbrain dysconnectivity and blunted reward signals in schizophrenia

Advances in understanding and treating persecutory delusions: a review

Neurobiological Correlates of Delusion: Beyond the Salience Attribution Hypothesis

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