DEFECTIVE INHIBITION OF DREAM EVENT MEMORY FORMATION - A HYPOTHESIZEDMECHANISM IN THE ONSET AND PROGRESSION OF SYMPTOMS OF SCHIZOPHRENIA

Authors
Citation
Ph. Kelly, DEFECTIVE INHIBITION OF DREAM EVENT MEMORY FORMATION - A HYPOTHESIZEDMECHANISM IN THE ONSET AND PROGRESSION OF SYMPTOMS OF SCHIZOPHRENIA, Brain research bulletin, 46(3), 1998, pp. 189-197
Citations number
146
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
03619230
Volume
46
Issue
3
Year of publication
1998
Pages
189 - 197
Database
ISI
SICI code
0361-9230(1998)46:3<189:DIODEM>2.0.ZU;2-G
Abstract
An average person normally spends at least 90 min to 2 h per night dre aming. Nevertheless, memories of dream events are not retrieved while awake unless the person awoke shortly after a dream. It is hypothesize d here that schizophrenic delusions initially arise because a system t hat normally inhibits the formation of memories of dream events is def ective. Therefore, memories of dream events or fragments would be occa sionally made and placed in the normal memory store. The only reason t hat we really know anything happened to us in the past is that we have a memory of it, and having a memory of an event is sufficient to real ly believe it. Therefore, the schizophrenic would believe that the dre am events actually happened, It is proposed that this is the basis of primary delusions. Because memories are represented by strengthened ne ural connections there will be an accumulation of connections that do not correspond to reality. This accumulation may account for other sym ptoms of schizophrenia such as thought disorder, loosening of associat ions, and hallucinations. The brain trying to draw conclusions from se veral memories may be the basis of secondary delusions, Evidence is pr esented for the ideas that primary delusions are due to memories of dr eam events, that a substance, with vasotocin-like bioactivity, is rele ased in the brain during dreaming and inhibits memory formation, that the lateral habenula is a brain area involved in vasotocin actions and is affected by neuroleptics, and that brain mechanisms involved in va sotocin actions show pathological alterations in schizophrenia. (C) 19 98 Elsevier Science Inc.