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Review article
peer-reviewed

The Subcortical Confinement Hypothesis: A Neurological Model for Schizotypal Hallucinations



Abstract

Introduction: Different types of hallucinations are symptomatic of different conditions. Schizotypal hallucinations are unique in that they follow existing delusional narrative patterns: they are often bizarre, they are generally multimodal, and they are particularly vivid (the experience of a newsreader abusing you personally over the TV is both visual and aural. Patients who feel and hear silicone chips under their skin suffer from haptic hallucinations as well as aural ones, etc.) Although there are a number of hypotheses for hallucinations, few cogently grapple the sheer bizarreness of the ones experienced in schizotypal psychosis.

Methods: A review-based hypothesis, traversing theory from the molecular level to phenomenological expression as a distinct and recognizable symptomatology.

Conclusion: Hallucinations appear to be caused by a two-fold dysfunction in the mesofrontal dopamine pathway, which is considered here to mediate attention of different types: in the anterior medial frontal lobe, the receptors (largely D1 type) mediate declarative awareness, whereas the receptors in the striatum (largely D2 type) mediate latent awareness of known schemata. In healthy perception, most of the perceptual load is performed by the latter: by the top-down predictive and mimetic engine, with the bottom-up mechanism being used as a secondary tool to bring conscious deliberation to stimuli that fails to match up against expectations. In schizophrenia, the predictive mode is over-stimulated, while the bottom-up feedback mechanism atrophies.

The dysfunctional distribution pattern effectively confines dopamine activity to the striatum, thereby stimulating the structural components of thought and behaviour: well-learned routines, narrative structures, lexica, grammar, schemata, archetypes, and other procedural resources. Meanwhile, the loss of activity in the frontal complex reduces the capacity for declarative awareness and for processing anything that fails to meet expectations. 



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Review article
peer-reviewed

The Subcortical Confinement Hypothesis: A Neurological Model for Schizotypal Hallucinations


Author Information

Jan A. Golembiewski Corresponding Author

Creative Industries, Queensland University of Technology


Ethics Statement and Conflict of Interest Disclosures

Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Acknowledgements

This work was supported by the Schizophrenia Research Institute, utilizing infrastructure funding from NSW Department of Health.


Review article
peer-reviewed

The Subcortical Confinement Hypothesis: A Neurological Model for Schizotypal Hallucinations


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Review article
peer-reviewed

The Subcortical Confinement Hypothesis: A Neurological Model for Schizotypal Hallucinations

Jan A. Golembiewski">Jan A. Golembiewski

  • Author Information
    Jan A. Golembiewski Corresponding Author

    Creative Industries, Queensland University of Technology


    Ethics Statement and Conflict of Interest Disclosures

    Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

    Acknowledgements

    This work was supported by the Schizophrenia Research Institute, utilizing infrastructure funding from NSW Department of Health.


    Article Information

    Published: May 19, 2013

    DOI

    10.7759/cureus.118

    Cite this article as:

    Golembiewski J A (May 19, 2013) The Subcortical Confinement Hypothesis: A Neurological Model for Schizotypal Hallucinations. Cureus 5(5): e118. doi:10.7759/cureus.118

    Publication history

    Received by Cureus: May 05, 2013
    Peer review began: May 08, 2013
    Published: May 19, 2013

    Copyright

    © Copyright 2013
    Golembiewski. This is an open access article distributed under the terms of the Creative Commons Attribution License CC-BY 3.0., which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

    License

    This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Introduction: Different types of hallucinations are symptomatic of different conditions. Schizotypal hallucinations are unique in that they follow existing delusional narrative patterns: they are often bizarre, they are generally multimodal, and they are particularly vivid (the experience of a newsreader abusing you personally over the TV is both visual and aural. Patients who feel and hear silicone chips under their skin suffer from haptic hallucinations as well as aural ones, etc.) Although there are a number of hypotheses for hallucinations, few cogently grapple the sheer bizarreness of the ones experienced in schizotypal psychosis.

Methods: A review-based hypothesis, traversing theory from the molecular level to phenomenological expression as a distinct and recognizable symptomatology.

Conclusion: Hallucinations appear to be caused by a two-fold dysfunction in the mesofrontal dopamine pathway, which is considered here to mediate attention of different types: in the anterior medial frontal lobe, the receptors (largely D1 type) mediate declarative awareness, whereas the receptors in the striatum (largely D2 type) mediate latent awareness of known schemata. In healthy perception, most of the perceptual load is performed by the latter: by the top-down predictive and mimetic engine, with the bottom-up mechanism being used as a secondary tool to bring conscious deliberation to stimuli that fails to match up against expectations. In schizophrenia, the predictive mode is over-stimulated, while the bottom-up feedback mechanism atrophies.

The dysfunctional distribution pattern effectively confines dopamine activity to the striatum, thereby stimulating the structural components of thought and behaviour: well-learned routines, narrative structures, lexica, grammar, schemata, archetypes, and other procedural resources. Meanwhile, the loss of activity in the frontal complex reduces the capacity for declarative awareness and for processing anything that fails to meet expectations. 



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Jan A. Golembiewski, Ph.D., Professor

Creative Industries, Queensland University of Technology

For correspondence:
greenmanarch@gmail.com

Jan A. Golembiewski, Ph.D., Professor

Creative Industries, Queensland University of Technology

For correspondence:
greenmanarch@gmail.com