Abstract
The neurodegenerative and neurodevelopmental hypotheses represent the basic etiological framework for the origin of schizophrenia. Additionally, the dopamine hypothesis, adopted more than two decades ago, has repeatedly asserted the position of dopamine as a pathobiochemical substrate through the action of psychostimulants and neuroleptics on the mesolimbic and mesocortical systems, giving insight into the origin of positive and negative schizophrenic symptoms. Meanwhile, cognitive impairments in schizophrenia remain incompletely understood but are thought to be present during all stages of the disease, as well as in the prodromal, interictal and residual phases. On the other hand, observations on the effects of NMDA antagonists, such as ketamine and phencyclidine, reveal that hypoglutamatergic neurotransmission causes not only positive and negative but also cognitive schizophrenic symptoms. This review aims to summarize the different hypotheses about the origin of psychoses and to identify the optimal neuroimaging method that can serve to unite them in an integral etiological framework. We systematically searched Google scholar (with no concern to the date published) to identify studies investigating the etiology of schizophrenia, with a focus on impaired central neurotransmission. The complex interaction between the dopamine and glutamate neurotransmitter systems provides the long-needed etiological concept, which combines the neurodegenerative hypothesis with the hypothesis of impaired neurodevelopment in schizophrenia. Pharmaco-magnetic resonance imaging is a neuroimaging method that can provide a translation of scientific knowledge about the neural networks and the disruptions in and between different brain regions, into clinically applicable and effective therapeutic results in the management of severe psychotic disorders.
Highlights
Psychosis is not a nosological entity, but rather a clinical condition consisting of numerous symptoms that may be a common clinical outcome of a variety of causes
We suggest that the observed task-related hyperactivity of the default mode network (DMN) may be a consequence of the inhibition from the prefrontal cortex (PFC) on the insula, which disrupts its balancing function as a dynamic switch between the anti-correlated DMN and central executive network (CEN)
Schizophrenia and other psychotic disorders affect a huge number of people around the world, destroying the lives of patients, burdening their loved ones and society, and leading to significant and global economic losses
Summary
Psychosis is not a nosological entity, but rather a clinical condition consisting of numerous symptoms that may be a common clinical outcome of a variety of causes. While the concept and definition of psychosis is defined by the core clinical symptoms of delusions, hallucinations, and disorganized thinking, these symptoms are most likely the common final consequences of a variety of different etiopathogenetic pathways, which may all lead to an analogous clinical picture [1]. Schizophrenia is distinguished by a wide range of psychopathological features: positive symptoms (psychotic symptoms: delusions, hallucinations and disorganized behavior), negative symptoms (avolition, alogia, autism, affect flattening, social disengagement, etc.), and cognitive impairment (attention, memory and executive functions deficits) [3]. Negative and cognitive symptoms are often persistent and are correlated with long-term consequences on social function [4]. The first episode of psychosis generally occurs in late adolescence or early adulthood, it is commonly precipitated by a prodromal stage [5] and premorbid cognitive deficits [4]
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