Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Email this article to a Colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My Articles & Searches Download to citation manager Citing Articles via HighWire Citing Articles via Google Scholar Articles by Hoffman, R. E. Articles by McGlashan, T. H. Search for Related Content PubMed Citation Articles by Hoffman, R. E. Articles by McGlashan, T. H. Schizophrenia Spectrum Disorders Other Research Techniques Neurodevelopment

Synaptic Elimination, Neurodevelopment, and the Mechanism of Hallucinated "Voices" in Schizophrenia

OBJECTIVE: After peaking during childhood, synaptic density in the human frontal cortex declines by 30%–40% during adolescence because of progressive elimination of synaptic connections. The characteristic age at onset of schizophrenia—late adolescence and early adulthood—suggests that the disorder could arise from irregularities involving this neurodevelopmental process. METHOD: A computer simulation of a speech perception neural network was developed. Connections within the working memory component of the network were eliminated on the basis of a "Darwinian rule" in order to model loss of synapses. As a comparison, neuronal cell death, also postulated as being linked to both neurodevelopment and schizophrenia, was simulated. The authors determined whether these alterations at low levels could enhance perceptual capacity and at high levels produce spontaneous speech percepts that simulate hallucinated speech or "voices." RESULTS: Eliminating up to 65% of working memory connections improved perceptual ability; beyond that point, network performance declined and speech hallucinations emerged. Simulating excitotoxic neuronal loss at low levels also improved network performance, but in excess it did not produce hallucinations. CONCLUSIONS: The model demonstrates perceptual advantages of selective synaptic elimination as well as selective neuronal loss, suggesting a functional explanation for these aspects of neurodevelopment. The model predicts that psychosis arises from a pathological extension of one of these neurodevelopmental trends, namely, synaptic elimination. (Am J Psychiatry 1997; 154:1683–1689)

This article has been cited by other articles:

				D. R Hemsley The Schizophrenic Experience: Taken Out of Context? Schizophr Bull, January 1, 2005; 31(1): 43 - 53. [Abstract] [Full Text] [PDF]

				P. J. SIEKMEIER and R. E. HOFFMAN Enhanced semantic priming in schizophrenia: a computer model based on excessive pruning of local connections in association cortex The British Journal of Psychiatry, April 1, 2002; 180(4): 345 - 350. [Abstract] [Full Text] [PDF]

				T. H. McGlashan and R. E. Hoffman Schizophrenia as a Disorder of Developmentally Reduced Synaptic Connectivity Arch Gen Psychiatry, July 1, 2000; 57(7): 637 - 648. [Abstract] [Full Text] [PDF]

				R. E. Hoffman, J. Rapaport, C. M. Mazure, and D. M. Quinlan Selective Speech Perception Alterations in Schizophrenic Patients Reporting Hallucinated "Voices" Am J Psychiatry, March 1, 1999; 156(3): 393 - 399. [Abstract] [Full Text]

				Can Computer Simulations Model Psychotic Processes? Journal Watch Psychiatry, February 1, 1998; 1998(201): 13 - 13. [Full Text]

Get information about faster international access.

Privacy Policy

Copyright © 1997 American Psychiatric Association. All rights reserved.

Home | Search | Current Issue | Past Issues | Subscribe | All APPI Journals | Help | Contact Us