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.
To minimize the developmental disruption associated with schizophrenia, much work has recently been done to identify and treat the prodromal (pre-onset) phase of the disorder, which has been detected up to 30 months before the onset of symptoms.
Children who go on to develop schizophrenia may also demonstrate decreased intelligence, decreased motor development (reaching milestones such as walking slowly), isolated play preference, social anxiety, and poor school performance.
A number of potential explanations have been proposed, including that alleles associated with schizophrenia risk confers a fitness advantage in unaffected individuals.
Maternal nutritional deficiencies, such as those observed during a famine, as well as maternal obesity have also been identified as possible risk factors for schizophrenia.
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.
Both maternal stress and infection have been demonstrated to alter fetal neurodevelopment through pro-inflammatory proteins such as IL-8 and TNF.
It has been hypothesized that in some people, development of schizophrenia is related to intestinal tract dysfunction such as seen with non-celiac gluten sensitivity or abnormalities in the intestinal flora.