This supports the concept of discorrelation, inappropriate timing of information, and deterioration of various parts of the brain due to this.  Unfortunately the model of Correlational Opponent Processing does not immediately suggest procedures for helping.
 
Ron Blue
----- Original Message -----
Sent: Sunday, October 31, 1999 7:40 PM
Subject: Is the 'normal' range of this continuum related to 'paranormal perceptions" ?

 

Acta Psychiatr Scand Suppl 1999;395:80-8

Cortical brain dysfunction in early schizophrenia: secondary
pathogenetic hierarchy of neuroplasticity, psychopathology
and social impairment.

Hemmingsen R, Madsen A, Glenthoj B, Rubin P

Department of Psychiatry E, Bispebjerg Hospital, University of Copenhagen, Denmark.

Schizophrenia has the quality of a 'top-down' disorder with perturbation of self, and malattuned
appraisal of basic experience of the outside world, and of intentionality. There is dissonance
between the faculties of consciousness. The neuronal cortical network displays distributed
activation of the sensory cortices during perception, and retroactivation during recall. This
multimodal organization is sensitive to aberrations of structure and informational content during
the metabolically dynamic phases of expansion and pruning in childhood and adolescence. There
is substantial evidence of deviant function of the cortical network in schizophrenia. This includes
increased neuronal density, reduced prefrontal capacity for activation, impaired fronto-temporal
interaction during language production, defect monitoring of inner speech, activation of
secondary sensory cortices during hallucinations, reduced cortical and thalamic volume, reduced
thalamic activation (filtering) and sensitization of dopaminergic modulation. As a hypothesis the
cortical defects lead to secondary causation of abnormalities at the levels of neuroplasticity,
symptomatology and social competence. Suggestions for empirical testing are presented for the
hypothesis that neocortical defects are primary, thalamic defects secondary and dopaminergic
aberrations tertiary in the schizophrenic process. This testing of hypotheses involves prospective
studies of patient groups at various ages of onset, as well as comparison of neurobiological
measures in remitting vs. treatment-resistant cases.

PMID: 10225336, UI: 99239842
 
 
 
 
 

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