Epidemiology
The median lifetime morbid risk for schizophrenia is 7.2 per 1000 people.[2] The male-to-female risk ratio is 1.4:1.[3][4] The global prevalence of schizophrenia is 23.6 million.[5] It appears that the incidence and prevalence of schizophrenia vary depending on race and geographic location.[6] Patients with schizophrenia have a higher mortality than the general population due to physical illness (e.g., cardiovascular diseases and cancers), accidents, and suicide.[7][8][9]
The age of onset is usually <25 years for males and <35 years for females. It has been reported that more affected people are born in the winter versus the spring or summer seasons, but these data are controversial.[10][11] Additionally, a higher disease incidence has been reported in urban areas and low-income populations when compared with rural and higher-income groups.[3] The incidence and prevalence appears to have increased over time.[12] There is a reported higher incidence in migrant populations, which appears to persist into the second generation.[13][14] While the prevalence of psychotic disorders in 10- to 18-year-olds is relatively low at around 0.4%, the prevalence of schizophrenia in 10- to 18-year-olds hospitalized for psychiatric causes is 25%, with an exponential increase throughout the adolescent years.[15] A second peak of psychosis onset occurs in women after the age of 45.[16]
Cognitive deficits tend to precede the development of schizophrenia, persist for the whole duration of illness, and be closely tied to functional outcomes.[1]
Risk factors
There appears to be a significant increase in the risk of schizophrenia in children of fathers age ≥30 years.[34]
Including fetal growth retardation, maternal infection, blood group incompatibilities, perinatal hypoxia, and preterm delivery.[35]
Heavy marijuana use may increase a person's vulnerability to schizophrenia and their likelihood of developing the disorder (odds ratio of approximately 2.2 to 2.8).[36][37][38][39][40][41][42][43] However, a causal relationship between cannabis and psychosis has not been identified.[21] Genetic risk factors for schizophrenia also appear to predispose individuals toward drug use.[44] Cannabis use following onset of first episode psychosis is associated with an increased risk of relapse and nonadherence 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.[45]
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.[46]
Soft neurologic signs (minor abnormalities in motor performance on clinical examination; for example, rigidity, gait imbalance, tremor) have been identified in individuals at ultra-high risk for psychosis. These signs also correlate with an increase over time in the severity of negative symptoms.[47][48][49]
Evidence suggests a link between psychological stressors and the onset of schizophrenia.[50]
Studies have shown a connection between childhood psychological trauma and an increased risk of schizophrenia in adulthood.[51]
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