Symptoms and Diagnosis
While schizophrenia sometimes begins as an acute psychotic episode in young adults, it emerges gradually in children, often preceded by developmental disturbances, such as lags in motor and speech/language development. Such problems tend to be associated with more pronounced brain abnormalities. The diagnostic criteria are the same as for adults, except that symptoms appear prior to age 12, instead of in the late teens or early 20s.6 Children with schizophrenia often see or hear things that don't really exist, and harbor paranoid and bizarre beliefs. For example, they may think people are plotting against them or can read their minds. Other symptoms of the disorder include problems paying attention, impaired memory and reasoning, speech impairments, inappropriate, or flattened, expression of emotion, poor social skills, and depressed mood. Such children may laugh at a sad event, make poor eye contact, and show little body language or facial expression.
Misdiagnosis of schizophrenia in children is all too common. It is distinguished from autism by the persistence of hallucinations and delusions for at least 6 months, and a later age of onset7 years or older. Autism is usually diagnosed by age 3.7 Schizophrenia is also distinguished from a type of brief psychosis sometimes seen in affective, personality and dissociative disorders in children. Adolescents with bipolar disorder sometimes have acute onset of manic episodes that may be mistaken for schizophrenia. Children who have been victims of abuse may sometimes claim to hear voices ofor see visions ofthe abuser. Symptoms characteristically pervade the child's life, and are not limited to just certain situations, such as at school. If children show any interest in friendships, even if they fail at maintaining them, it's unlikely that they have schizophrenia.
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 patients. 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 are side effects, including excess weight gain that can increase risk of other health problems. The NIMH is conducting research studies of treatment, testing new experimental medications that may permit reduced doses of antipsychotics (glycine augmentation) or prevent excessive weight gain (aripiprazole). Children with schizophrenia and their families can also benefit from supportive counseling, psychotherapies and social skills training aimed at helping them cope with the illness. They likely require special education and/or other accommodations to succeed in the classroom.
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.6 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,8magnetic 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.9 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.10 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.3 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.
Families of children with schizophrenia who are interested in participating in research are encouraged to fill out the NIMH Childhood-Onset Schizophrenia Survey, to help determine eligibility for studies.
1 US DHHS. Children and mental health (Chapter 3). In: Mental health: a report of the Surgeon General. Rockville, MD: U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Center for Mental Health Services, National Institutes of Health, National Institute of Mental Health, 1999; 123-220. http://www.surgeongeneral.gov/library/mentalhealth/chapter3/sec1.html
2 NIMH Schizophrenia publications. http://www.nimh.nih.gov/publicat/schizmenu.cfm
3 Nicolson R, Rapoport JL. Childhood onset schizophrenia: rare but worth studying. Biological Psychiatry, 1999; 46: 1418-28.
4 Murray CJL, Lopez AD, eds. Summary: The global burden of disease: a comprehensive assessment of mortality and disability from diseases, injuries, and risk factors in 1990 and projected to 2020. Cambridge, MA: Published by the Harvard School of Public Health on behalf of the World Health Organization and the World Bank, Harvard University Press, 1996. http://www.who.int/msa/mnh/ems/dalys/intro.htm
5 American Academy of Child and Adolescent Psychiatry. Practice parameters for the assessment and treatment of children and adolescents with schizophrenia. Journal of the American Academy of Child and Adolescent Psychiatry, 1997; 36(10): 177S-93S.
6 Rapoport JL. Childhood onset of "adult" pathology: clinical and research advances. Washington, DC: American Psychiatric Press, Inc., 2000.
7 American Academy of Child and Adolescent Psychiatry. Practice parameters for the assessment and treatment of children, adolescents and adults with autism and other pervasive developmental disorders. Journal of the American Academy of Child and Adolescent Psychiatry, 1999; 38(12): 32S-54S.
8 Giedd JN, Blumenthal J, Jeffries NO, Castellanos FX, Liu H, Zijdenbos A, Paus T, Evans AC, Rapoport JL. Brain development during childhood and adolescence: a longitudinal MRI study. Nature Neuroscience, 1999; 2(10): 861-3.
9 Rapoport JL, Giedd JN, Blumenthal J, Hamburger S, Jeffries N, Fernandez T, Nicolson R, Bedwell J, Lenane M, Zijdenbos A, Paus T, Evans A. Progressive cortical change during adolescence in childhood-onset schizophrenia: a longitudinal magnetic resonance imaging study. Archives of General Psychiatry, 1999; 56(7): 649-54.
10 Thompson P, Vidal C, Giedd JN, Gochman P, Blumenthal J, Nicolson R, Toga AW, Rapoport JL. Mapping adolescent brain change reveals dynamic wave of accelerated gray matter loss in very early-onset schizophrenia. Proceedings of the National Academy of Sciences, 2001; 98(20): 11650-5.
11 Asarnow RF, Nuechterlein KH, Fogelson D, Subotnik KL, Payne DA, Russell AT, Asamen J, Kuppinger H, Kendler KS. Schizophrenia and schizophrenia-spectrum personality disorders in the first-degree relatives of children with schizophrenia: the UCLA family study. Archives of General Psychiatry, 2001; 58(6): 581-8.