Although it's unclear whether schizophrenia has a single or multiple underlying causes, evidence suggests that it is a neurodevelopmental disease likely involving a genetic predisposition, a prenatal insult to the developing brain and stressful life events. The role of genetics has long been established; the risk of schizophrenia rises from 1 percent with no family history of the illness, to 10 percent if a first degree relative has it, to 50 percent if an identical twin has it. Prenatal insults may include viral infections, such as maternal influenza in the second trimester, starvation, lack of oxygen at birth, and untreated blood type incompatibility. Studies find that children share with adults many of the same abnormal brain structural, physiological and neuropsychological features associated with schizophrenia. The children seem to have more severe cases than adults, with more pronounced neurological abnormalities. This makes childhood onset schizophrenia potentially one of the clearest windows available for research into a still obscure illness process.

For example, unlike most adult-onset patients, children who become psychotic prior to puberty show conspicuous evidence of progressively abnormal brain development. In the first longitudinal brain imaging study of adolescents, magnetic resonance imaging (MRI) scans revealed fluid filled cavities in the middle of the brain enlarging abnormally between ages 14 and 18 in teens with early onset schizophrenia, suggesting a shrinkage in brain tissue volume. These children lost four times as much gray matter, neurons and their branch-like extensions, in their frontal lobes as normally occurs in teens. This gray matter loss engulfs the brain in a progressive wave from back to front over 5 years, beginning in rear structures involved in attention and perception, eventually spreading to frontal areas responsible for organizing, planning, and other "executive" functions impaired in schizophrenia. Since losses in the rear areas are influenced mostly by environmental factors, the researchers suggest that some non-genetic trigger contributes to the onset and initial progression of the illness. The final loss pattern is consistent with that seen in adult schizophrenia. Adult-onset patients' brains may have undergone similar changes when they were teens that went unnoticed because symptoms had not yet emerged, suggest the researchers.

In addition to studies of brain structural abnormalities, researchers are also examining a group of measures associated with genetic risk for schizophrenia. Early onset cases of illness have recently proven crucial in the discovery of genes linked to other genetically complex disorders like breast cancer, Alzheimer's and Crohn's diseases. Hence, children with schizophrenia and their families may play an important role in deciphering schizophrenia's molecular roots. Evidence suggests that the rate of genetically-linked abnormalities is twice as high in children as in adults with the illness. Similarly, schizophrenia spectrum disorders, thought to be genetically-related to schizophrenia, are about twice as prevalent among first-degree relatives of childhood onset patients. In one recent study,11 a third of the families of individuals with childhood onset schizophrenia had at least one first-degree relative with a diagnosis of schizophrenia, or schizotypal or paranoid personality disorder. This profile of psychiatric illness is remarkably similar to that seen in parents of adult onset patients, adding to the likelihood that both forms share common genetic roots. Other anomalies associated with adult schizophrenia, such as abnormal eye movements, are also more common in families of children with the illness.

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