[Some questions about the essence of delusions in the light of recent neurobiological findings]

Psychiatr Pol. 2009 Jul-Aug;43(4):403-10.
[Article in Polish]

Abstract

Formation of delusions in the phase of acute psychosis is based on two subsequent processes. The first one is dopamine hyperactivity in mesolimbic neural pathways, the second one is a cognitive process of up-down attribution of meanings of this subjectively perceived state of mind by the higher levels of brain. After the successful antipsychotic treatment, the subjectivity of patients changes. When the state of acute psychosis resolves patients must re-interpret this new emerging subjective experience. These interpretations are often incorrect and bizarre. In most cases they are regarded as delusions (sometimes "chronic delusions"). The question asked in the presented paper is whether they are truly delusions. The essence of delusion must include in the same time an active neurobiological basis of delusion (hyperdopaminergic state) and its cognitive level. It's not clear what is the proper term for the phenomenon when only incorrect or bizarre cognitive convictions are present after successful treatment of psychosis, but without dopaminergic hyperactivity.

Publication types

  • English Abstract
  • Review

MeSH terms

  • Antipsychotic Agents / therapeutic use
  • Delusions / classification*
  • Delusions / diagnosis*
  • Delusions / drug therapy
  • Delusions / metabolism
  • Diagnosis, Differential
  • Dopamine / metabolism
  • Hallucinations / diagnosis
  • Humans
  • Neurobiology
  • Paranoid Disorders / diagnosis
  • Psychotic Disorders / diagnosis

Substances

  • Antipsychotic Agents
  • Dopamine