Epidemiology

The median lifetime morbid risk for schizophrenia is 7.2 per 1000 people.[6] The male-to-female risk ratio is 1.4:1.[7][8]​ The global prevalence of schizophrenia is 23.6 million, although the incidence and prevalence of schizophrenia vary depending on ethnicity and geographic location.[9][10]​​ Patients with schizophrenia have a higher mortality than the general population due to physical illness (e.g., cardiovascular diseases and cancers), accidents, and suicide.[11][12][13][14]

The age of onset peaks around age 20-25 years for males and 25-30 years for females. A smaller second peak of onset occurs in women after the age of 45-50 years.[15][16]​​ More affected people are born in the winter versus the spring or summer seasons.​[17]​​ Additionally, a higher disease incidence has been reported in urban areas and low-income populations when compared with rural and higher-income groups.[7] There is a reported higher incidence in migrant populations, which appears to persist into the second generation.[15][18][19]​​​ While the prevalence of psychotic disorders in the 10- to 18-year-old age group is relatively low at around 0.4%, the prevalence of schizophrenia in 10- to 18-year-olds hospitalised for psychiatric causes is 25%, with an exponential increase throughout the adolescent years.[20]

Cognitive deficits tend to precede the development of schizophrenia, persist for the whole duration of illness, and be closely tied to functional outcomes.[3]

Risk factors

The closer the family relationship to an affected relative, the higher the risk.​[23][24][37]​​ People with an affected first-degree relative (e.g., parent, child, sibling) have an approximate lifetime incidence of 6% to 17% of schizophrenia.[38]​​​

There appears to be a significant increase in the risk of schizophrenia in children of fathers age ≥30 years.[39]

This includes fetal growth retardation, maternal infection, blood group incompatibilities, perinatal hypoxia, and premature delivery.[40]

Heavy marijuana use may increase both the vulnerability to schizophrenia and the likelihood of developing the disorder (odds ratio of around 2.2 to 2.8).[41][42][43][44][45][46][47][48]​​​​​​ A definite causal relationship between cannabis and psychosis has, however, yet to be confirmed.[25]​ Genetic risk factors for schizophrenia also appear to predispose individuals towards illicit drug use.[14]

Cannabis use following onset of first-episode psychosis is associated with an increased risk of relapse and non-adherence with antipsychotic medication. The results of one prospective analysis suggest that up to 36% of the negative effects of continued cannabis use in patients with psychosis are due to a reduction in medication adherence because of cannabis use.[49]

A longitudinal, long-term follow-up cohort study looked at adolescents at ultra-high risk of developing psychosis. Low IQ was the single neurocognitive factor that discriminated the ultra-high risk patients who developed psychosis from those who did not, and from typically developing controls.[50]

Soft neurological signs (minor abnormalities in motor performance on clinical examination: for example, rigidity, gait imbalance, tremor, smooth pursuit eye movement deficit, a sensory integration deficit, and right-left disorientation) are common in people with schizophrenia.[3][51][52]​​ These signs are related to the severity of negative symptoms.[53][54][55]

Evidence suggests a link between psychological stressors and the onset of schizophrenia, and relapses in established cases.[56]

Studies have shown a connection between childhood neglect and abuse and other adverse childhood experiences with an increased risk of schizophrenia in adulthood.[57]

There is a reported higher incidence of schizophrenia in migrant populations, which appears to persist into the second generation.[18][19]

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