Research Articles On Paranoid Schizophrenia

Research Articles On Paranoid Schizophrenia-42
A number of potential explanations have been proposed, including that alleles associated with schizophrenia risk confers a fitness advantage in unaffected individuals.

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Although these functions are dissociable, their dysfunction in schizophrenia may reflect an underlying deficit in the ability to represent goal related information in working memory, and to utilize this to direct cognition and behavior.

These impairments have been linked to a number of neuroimaging and neuropathological abnormalities.

A subgroup of persons with schizophrenia present an immune response to gluten different from that found in people with celiac, with elevated levels of certain serum biomarkers of gluten sensitivity such as anti-gliadin Ig G or anti-gliadin Ig A antibodies.

Abnormal dopamine signalling has been implicated in schizophrenia based on the usefulness of medications that effect the dopamine receptor and the observation that dopamine levels are increased during acute psychosis.

However, a large body of evidence suggests that hedonic responses are intact in schizophrenia, Overall, a failure of online maintenance and reward associativity is thought to lead to impairment in the generation of cognition and behavior required to obtain rewards, despite normal hedonic responses.

Both hallucinations and delusions have been suggested to reflect improper encoding of prior expectations, thereby causing expectation to excessively influence sensory perception and the formation of beliefs.Social withdrawal, sloppiness of dress and hygiene, and loss of motivation and judgment are all common in schizophrenia.Distortions of self-experience such as feeling as if one's thoughts or feelings are not really one's own to believing thoughts are being inserted into one's mind, sometimes termed passivity phenomena, are also common.They commonly include flat expressions or little emotion, poverty of speech, inability to experience pleasure, lack of desire to form relationships, and lack of motivation.Negative symptoms appear to contribute more to poor quality of life, functional ability, and the burden on others than positive symptoms do.Reduced NMDA receptor signalling is suggested by multiple lines of evidence.Studies demonstrate reduced NMDA receptor expression and NMDA receptor blockers mimic both schizophrenia symptoms and the physiological abnormalities associated with schizophrenia. The subsets of interneurons that are abnormal in schizophrenia are responsible for the synchronizing of neural ensembles that is necessary during working memory tasks, a process that is electrophysiologically reflected in gamma frequency (30–80 Hz) oscillations.Both working memory tasks and gamma oscillations are impaired in schizophrenia, which may reflect abnormal interneuron functionality.Deficits in executive functions, such as planning, inhibition, and working memory, are pervasive in schizophrenia.The validity of the positive and negative construct has been challenged by factor analysis studies observing a three dimension grouping of symptoms.Different terminology is used, but a dimension for hallucinations, a dimension for disorganization, and a dimension for negative symptoms are usually described.

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