Treatments that help young patients manage their illness have improved significantly in recent decades. As in adults, antipsychotic medications are especially helpful in reducing hallucinations and delusions. The newer-generation "atypical" antipsychotics, such as olanzapine and clozapine, may also help improve motivation and emotional expressiveness in some children. They also have a lower likelihood of producing disorders of movement (including tardive dyskinesia) than the other antipsychotic drugs such as haloperidol. However, even with these newer medications, there can be side effects. One of these potential side effects is excess weight gain, which can increase the risk of other health problems such as diabetes.
Although it is unclear whether schizophrenia has a single cause or multiple underlying causes, evidence suggests that it is a neurodevelopmental disease likely involving:
- A genetic predisposition
- Some form of injury to the developing brain before birth
- 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. The risk jumps to 50 percent if an identical twin has it.
Prenatal injury to the brain may include:
- Viral infections, such as maternal influenza in the second trimester
- Lack of oxygen at birth
- Untreated blood type incompatibility.
Studies find that children with schizophrenia have many of the same abnormal brain structural, physiological, and neuropsychological features found in adults with the condition.
Those with childhood schizophrenia 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 an illness process that is not yet fully understood. For example, unlike most adult-onset patients, children who become psychotic prior to puberty show clear evidence of progressively abnormal brain development.
In the first longitudinal brain imaging study of adolescents, magnetic resonance imaging (MRI) scans showed that the fluid-filled cavities in the middle of the brain (called ventricles) enlarged 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 branchlike extensions, in their frontal lobes as what normally occurs in teens. This gray matter loss engulfs the brain in a progressive wave from the back of the brain to the front over five years. It begins in the rear structures involved in attention and perception, and eventually spreads to the frontal areas responsible for organizing, planning, and other "executive" functions that are impaired in schizophrenia. Since losses in the rear areas are influenced mostly by environmental factors, research suggests 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. Researchers suggest that adult-onset patients' brains may have undergone similar changes when they were teens that went unnoticed because symptoms had not yet emerged.
In addition to studies of structural abnormalities in the brain, researchers are examining a group of measures associated with the genetic risk for schizophrenia. Early-onset cases of illness have recently proved crucial in the discovery of genes linked to other genetically complex disorders, such as:
Hence, children with schizophrenia and their families may play an important role in deciphering the disease's molecular roots. Evidence suggests that the rate of genetically linked abnormalities is twice as high in children versus 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 children with the disorder. In one recent study, a third of the families of individuals with childhood schizophrenia had at least one first-degree relative with a diagnosis of either 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.