The neuropsychology of schizophrenia
Abstract
Abstract A model is proposed for integrating the neural and cognitive aspects of the positive symptoms of acute schizophrenia, using evidence from postmortem neuropathology and neurochemistry, clinical and preclinical studies of dopaminergic neurotransmission, anatomical connections between the limbic system and basal ganglia, attentional and other cognitive abnormalities underlying the positive symptoms of schizophrenia, specific animal models of some of these abnormalities, and previous attempts to model the cognitive functions of the septohippocampal system and the motor functions of the basal ganglia. Anatomically, the model emphasises the projections from the septohippocampal system, via the subiculum, and the amygdala to nucleus accumbens, and their interaction with the ascending dopaminergic projection to the accumbens. Psychologically, the model emphasises a failure in acute schizophrenia to integrate stored memories of past regularities of perceptual input with ongoing motor programs in the control of current perception. A number of recent experiments that offer support for the model are briefly described, including anatomical studies of limbic-striatal connections, studies in the rat of the effects of damage to these connections, and of the effects of amphetamine and neuroleptics, on the partial reinforcement extinction effect, latent inhibition and the Kamin blocking effect; and studies of the latter two phenomena in acute and chronic schizophrenics.
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Predictive coding is more generalized than earlier accounts, which tended to localize the pathology to a specific brain area or psychological function.
“One strength of predictive coding is that it is more generalized than earlier accounts, which tended to localize the pathology to a specific brain area or psychological function, e.g. the pathway connecting the subiculum to the nucleus accumbens (43), striatal dopamine release (47, 48), or altered corollary discharge (50).”
From The Predictive Coding Account of Psychosis (2018) · cites this paper as [43]
Perturbed dopamine transmission is related to psychosis through disrupted learning mechanisms, linking psychotic experiences to neurochemistry.
“relating perturbed dopamine transmission to psychosis via disrupted learning mechanisms, [12][13][14] thus linking psychotic experiences to neurochemistry.10”
From Computational psychiatry: a Rosetta Stone linking the brain to mental illness (2014) · cites this paper as [14]
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- Authors
- Gray, J. A., Feldon, J., Rawlins, J. N. P., Hemsley, D. R., & Smith, A. D.
- Affiliations
- Tel Aviv University (IL)
- University of Oxford (GB)
- Venue
- Behavioral and Brain Sciences
- Publisher
- Cambridge University Press (CUP)
- Published
- 1991-03
- Volume
- 14
- Issue
- 1
- Pages
- 1-20
- ISSN
- 0140-525X (ISSN-L)
- 1469-1825
- OpenAlex
- W2039301402
- Cited by
- 1,350
- References
- 6
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 28 · 2023: 5 · 2022: 9 · 2021: 8 · 2020: 12 · 2019: 9 · 2018: 10 · 2017: 20 · 2016: 16 · 2015: 22 · 2014: 28 · 2013: 31 · 2012: 35
- FWCI
- 50.34
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Behavioral and Brain Sciences (publishedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- schizophrenia, positive symptoms, neuropsychology, dopamine signaling, basal ganglia, septo-hippocampal system, nucleus accumbens, amygdala, subiculum, latent inhibition, amphetamine, antipsychotic drugs, memory integration, perceptual control, animal models of schizophrenia
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