EOS and COS are frequently marked by deficits in cognitive impairment such as deficits in attention or vigilance, memory, and executive functioning. A generalized or global impairment (e.g., subaverage IQ) is also common in this population. Approximately 10-20% of children with schizophrenia have a full-scale IQ of 70 or below.
Because schizophrenia in youth often has an insidious onset, the gradual development of psychotic symptoms in a child with premorbid language delays and social withdrawal can be difficult to recognize. Children may experience less elaborate delusions and hallucinations than adults. Visual hallucinations are more common in children with schizophrenia and should be distinguished from normal fantasy play. Symptoms such as disorganized speech and behavior, which are typically present in schizophrenia, also occur in many other disorders of childhood onset (e.g., autism spectrum disorder and attention-deficit hyperactivity disorder).
Family, twin, and adoption studies support a strong genetic component for schizophrenia. The lifetime risk of developing the illness is 5–20 times higher in first-degree relatives when compared to the general population. Risk factors that include paternal age and in utero exposure to maternal famine have also been hypothesized to contribute to the development of schizophrenia. Early childhood trauma has also been associated with childhood psychotic symptoms. Children who experienced maltreatment by an adult or bullying by peers were found to be at a higher risk for psychotic disorders later in life. Schizophrenia peaks at the age of 15 and this is one of the reasons why many authors see puberty as a risk factor for schizophrenia. Neurobiological changes that occur during the puberty and adolescence can influence more frequent occurrence of schizophrenia during this period of life. These neurobiological changes include progressive ventricular enlargement, reduction in total brain and thalamus volume, changes in temporal lobe structures, reductions in frontal metabolism, volume reduction of the associative cortex and hippocampus, synaptic elimination during adolescent development of the prefrontal cortex, diminishing of cerebral plasticity, and changes in neurotransmission.