Childhood-Onset Schizophrenia 

  • Author: Annemarie K Loth, MD; Chief Editor: Caroly Pataki, MD   more...
 
Updated: Feb 7, 2012
 

Background

Childhood-onset schizophrenia is a severe form of psychotic disorder that occurs at age 12 years or younger and is often chronic and persistently debilitating. The definition of childhood schizophrenia has evolved over time and is now believed to be a virulent childhood version of the same disorder exhibited in adolescents and adults. However, in the first 2 editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM), autistic disorder and childhood-onset schizophrenia were not differentiated as distinct disorders; instead, they were listed together as childhood psychoses.

In the third edition of the DSM (DSM-III), autism was listed separately, and childhood-onset schizophrenia was incorporated under the general heading of schizophrenia. According to the fourth edition of the DSM (DSM-IV), the criteria for childhood-onset schizophrenia and adult schizophrenia are synonymous, except for one potential modification for children (ie, in childhood-onset schizophrenia, the failure to meet expected social or academic milestones may be present, rather than a deterioration in functioning).[1] With the text revision of the DSM-IV (DSM-IV-TR), the criterion of social/occupational dysfunction in childhood or adolescent-onset schizophrenia can consist of a failure to achieve an expected level of interpersonal, academic, or occupational achievement.[2]

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Etiology and Pathophysiology

No definite single etiology of schizophrenia has been identified. Most theories accept both genetic and environmental contributions for the causation of childhood-onset schizophrenia.

A review of the data from the Environmental Risk Longitudinal Twin Study of British Children found that childhood psychotic symptoms are familial and heritable. These symptoms are associated with social risk factors; cognitive impairments at age 5 years; home-rearing risk factors; behavioral, emotional, and educational problems at age 5 years; and comorbid conditions such as self-harm. Therefore, childhood psychotic disorders may be a marker of an impaired developmental process.[3]

In addition, compared with the usual onset of schizophrenia in late adolescence or early adulthood, the emergence of earlier-onset schizophrenia during childhood may be due to increased genetic loading for schizophrenia or early central nervous system (CNS) damage due to an environmental factor.

Genetic risk

Several factors suggest a genetic risk. First-degree relatives of children with schizophrenia have a higher prevalence rate of schizophrenia and schizophrenia spectrum disorders.[4]

In the Pittsburgh High-Risk Study, findings among young relatives of schizophrenia patients included the following[5] :

  • High proportions of axis I psychopathology, especially attention deficit hyperactivity disorder (ADHD) and conduct disorder
  • Increased expressed emotion among relatives
  • A trend for more psychopathology in offspring of relatives with high expressed emotion
  • Impaired attention, spatial working memory, and executive functions
  • Increased soft neurologic signs
  • Volume reductions in the amygdala, hippocampus, and superior temporal gyrus
  • Decreased slow-wave sleep

First-degree relatives of individuals with schizophrenia have impairment in ocular smooth pursuit movements similar to that found on examination of patients with schizophrenia. One study found that healthy siblings of patients with childhood-onset schizophrenia had decreased cerebral gray matter in the same pattern as was seen in the patients.[6]

Examination of National Institute of Mental Health patients with onset of schizophrenia before age 13 years revealed a 10% rate of cytogenetic abnormalities.[7] In addition, associations with several schizophrenia-susceptibility genes in adult patient cohorts were replicated in the childhood-onset schizophrenia patients, including DAOA, NRG1, DTNBP1, and GAD1.[8] There was also an excess of novel copy number variants that overlapped or disrupted known genes in patients when compared with the nontransmitted parental “control” chromosomes.[9]

Neurodevelopmental and neurobiologic abnormalities

Several studies have described complications during pregnancy and delivery in adults who subsequently develop schizophrenia. The combination of genetic risk and evidence of acquired damage has suggested a neurodevelopmental theory with early CNS abnormalities that contribute to an increased vulnerability to schizophrenia later in life. An increase in minor dysmorphic features has suggested prenatal-onset problems. An increase in hypoxia-associated complications was demonstrated to increase the odds of developing earlier-onset schizophrenia.

The neurobiologic substrate of persons with childhood-onset schizophrenia has been examined by neuroimaging. As in adults with schizophrenia, the most consistent finding has been enlargement of the lateral ventricles.

Although static in adults, the abnormalities in brain morphology evolve during adolescence. The possibility of a neurodegenerative process has been raised but also questioned.[10]

Rapoport et al demonstrated that adolescents with schizophrenia have significantly greater decreases in frontal and temporal gray matter volumes than those observed in healthy age-matched controls (see the images below).[11, 12] The investigators additionally found the children with schizophrenia to have more cortical gray matter loss than children with transient psychosis. Subsequent studies from this group have also shown reduced cerebral volume and gray matter in healthy siblings of patients with childhood-onset schizophrenia.

However, later studies of nonpsychotic siblings of childhood-onset schizophrenia patients have shown a pattern of prefrontal and temporal gray matter deficits during early ages that seem to normalize by the time the subjects reach late adolescence.[13] These results were replicated by Mattai et al, who also showed nonpsychotic siblings of childhood-onset schizophrenia patients have early gray matter deficits that improve over time, suggesting that late adolescence may be a critical time for greatest localization of deficits in probands or normalization in nonpsychotic siblings.[14]

Childhood schizophrenia. Early and late gray matteChildhood schizophrenia. Early and late gray matter deficits in schizophrenia. Areas of gray matter loss, shown in red and yellow, spread from back-to-front (right to left) over 5 years in composite MRI scan data from 12 teens with childhood-onset schizophrenia, beginning at age 14 (left). Red and yellow denotes areas of greater loss. Source: Paul Thompson, MD, UCLA, Laboratory of Neuroimaging. NIMH media file. Childhood schizophrenia. Rate of gray matter loss.Childhood schizophrenia. Rate of gray matter loss. Composite MRI scan data showing areas of gray matter loss over 5 years, comparing 12 normal teens (left) and 12 teens with childhood-onset schizophrenia. Red and yellow denotes areas of greater loss. Front of brain is at left. Source: Paul Thompson, MD, UCLA, Laboratory of Neuroimaging. NIMH media file.

The Edinburgh High-Risk Study suggested that, in high-risk subjects (defined as subjects who had at least 2 close relatives with schizophrenia), the change from vulnerability to psychosis may be preceded by reduction in size and deteriorating function of the temporal lobe.[15]

In a systematic review and meta-analysis of 66 papers comparing brain volume in patients with a first psychotic episode with volume in healthy controls, meta-analysis suggested that the whole brain and hippocampal volume are reduced and that ventricular volume is increased in affected patients relative to healthy controls.[16]

Furthermore, brain magnetic resonance scans obtained in childhood-onset schizophrenia subjects, their nonpsychotic full siblings, and matched health comparison subjects between the ages of 10-29 years that measured the total, left, and right hippocampal volumes showed that childhood-onset schizophrenia patients had a fixed reduction in hippocampal volumes when compared with nonpsychotic siblings and health comparison subjects. In addition, no significant volumetric or trajectory differences were noted between nonpsychotic siblings and healthy comparison subjects. Therefore, decreased hippocampal volume may represent an intermediate disease phenotype.[17]

Greenstein et al reported that cortical thickness loss in childhood-onset schizophrenia appears to localize with age to prefrontal and temporal regions that are seen in patients with adult-onset schizophrenia, regardless of medication.[18] Another study showed that childhood-onset schizophrenia patients who met criteria for remission had thicker gray matter in prefrontal, temporal, and parietal cortices compared with nonremitted patients, suggesting a possible relation of brain plasticity with prognosis.[19]

Cannabis use

Evidence from 6 longitudinal studies in 5 countries showed that regular cannabis use predicts an increased risk of a schizophrenia diagnosis or of reporting symptoms of psychosis.[20]

One study found that 74% of cannabis use disorders subjects had the onset of cannabis use disorder before the onset of positive psychotic symptoms. These subjects were predominately male, younger at study entry, had an earlier age at onset of positive symptoms, less educational attainment, a lower self-socioeconomic status, better premorbid childhood social adjustment, a trend for poorer premorbid childhood academic adjustment, less motor abnormalities, but more severe hallucinations and delusions.

However, in the multivariate analysis only male sex, worse socioeconomic status, better premorbid childhood social adjustment, and more severe positive symptoms at study entry were associated with a lifetime history of cannabis use disorder. The authors concluded that although cannabis use precedes the onset of illness in most patients, no significant association existed between onset of illness and cannabis use disorders that was not accounted for by demographic and clinical variables.[21]

Nevertheless, another study used the Schedule for Affective Disorders and Schizophrenia for School-Age Children (K-SADS) to assess for a possible association between cannabis use, traumatic events, and psychotic symptoms in adolescence. Cannabis use and childhood trauma were significantly associated with a risk of experiencing psychotic symptoms. When cannabis use and childhood trauma occurred within the same patient, the risk for psychotic symptoms increased beyond the risk posed by either factor alone. However, only 14 participants in the study reported experiencing psychotic symptoms. Therefore, these findings must be replicated.[22]

A 2012 study obtained T1-weighted MRIs from adolescents with earlier-onset schizophrenia (EOS), cannabis use disorders (CUD), EOS plus CUD, and healthy controls. In the EOS group and the CUD group, the left superior parietal region had smaller gray matter volumes compared with healthy controls. The combined EOS/CUD group showed similar findings, but no additive effect was found. Nevertheless, the combined EOS/CUD group had smaller gray matter volumes in the left thalamus compared with the CUD and healthy control groups.[23]

Early adolescent cannabis use coupled with a specific genetic vulnerability may be a risk factor for the development of schizophrenia.

Early childhood trauma

As previously stated, early childhood trauma has been correlated with childhood psychotic symptoms.

Specifically, Arsenault et al obtained data from the Environmental Risk longitudinal Twin Study, which interviewed mothers when their children were aged 5, 7, 10, and 12 years on whether the children had experienced maltreatment by an adult, bullying by peers, or involvement in an accident. When the children were aged 12 years, they were asked about bullying experiences and psychotic symptoms. Children who experienced maltreatment by an adult or bullying by peers were more likely to report psychotic symptoms at age 12 years than were children who did not experience maltreatment. The finding of higher risk of psychotic disorders was observed whether these events occurred early in life of later in childhood. In addition, this finding remained significant when sex, socioeconomic deprivation, internalizing or externalizing problems, children’s genetic liability to developing psychosis, and IQ were controlled.[24]

Furthermore a prospective cohort study of 12-year-old children assessed the risk of psychotic symptoms using the Psychosis-like Symptoms Interview. Children who had been victims of bullying at ages 8 and/or 10 years, independent of prior psychopathology, family adversity, or child’s IQ, had a 2-fold increase in risk of psychotic symptoms. The risk increased when victimization was chronic or severe.[25]

Infections

One study also found a link between viral CNS infections and later psychosis. Specifically, a national cohort of children born between 1973-1985 was followed by using Swedish national registers to determine the association between CNS infections at age 0-12 years and admissions for nonaffective psychotic illnesses from the 14th birthday (N=2269). There was a slightly increased risk of nonaffective psychotic illness associated with viral CNS infections, as well as schizophrenia. There was no increased risk in relation to bacterial infections. Exposure to mumps virus or cytomegalovirus were associated with later psychosis.[26] However further research into this correlation is needed.

Neurotransmitters and schizophrenia

Most psychologic, pharmacologic, and neuroimaging studies of childhood-onset schizophrenia have suggested dysfunction in the prefrontal cortex and limbic system. The neurotransmitter implicated in the pathophysiology of schizophrenia is dopamine. Drugs that increase dopaminergic activity may induce a schizophreniform psychosis, and drugs that block postsynaptic D2 receptors help alleviate symptoms of schizophrenia.

Other neurotransmitters may also be involved in the pathophysiology of schizophrenia. Glutamate has been implicated based, in part, on the production of psychotic symptoms by phencyclidine and the presence of N -methyl-D-aspartate (NMDA) receptor dysfunction.[27] Serotonin may be important. The new atypical antipsychotic drugs have prominent serotonergic effects. Preliminary studies suggest gamma-aminobutyric acid (GABA) may be important.

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Epidemiology

Childhood-onset schizophrenia is rare in the United States; in preadolescents, the estimated prevalence is less than 1 case per 10,000 population. The number of new cases significantly increases during late adolescence, reaching an approximate prevalence of 1% for later-onset schizophrenia.

Globally, schizophrenia with an onset later in life appears to have an equal prevalence, with a possible increase in prevalence in urban populations. No studies of prevalence of childhood-onset schizophrenia in underdeveloped countries are available.

Racial, sexual, and age-related differences in incidence

No studies of childhood-onset schizophrenia that allow comparisons based on race or ethnicity are available, nor are studies about the prevalence in underdeveloped nations. The 2006 Aetiology and Ethnicity in Schizophrenia and Other Psychoses Study (AESOP), a large, population-based case-control study conducted over 2 years in 3 study centers in England in adults, reported all psychoses were more common in the black and minority ethnic group compared with the white British group.[28]

Most studies demonstrate an average male-to-female incidence of schizophrenia of 1.5-2:1.

In a child younger than 13 years, the onset of schizophrenia is rare and is generally insidious, carrying a worse prognosis. Onset of the disorder in the adolescent years is more common and may have an acute or insidious onset. In general, the earlier the onset of schizophrenia, the poorer the outcome.

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Prognosis

The prognosis for childhood-onset schizophrenia and adolescent-onset schizophrenia is worse than that observed in adult-onset schizophrenia. As adults, these children experience the following:

  • Fewer close social relationships
  • Less academic achievement
  • More unemployment
  • Less capacity for independent living

Patients with an onset before adolescence and those with an insidious onset appear to have a worse response to medication and a worse prognosis.

An increased risk of death from suicide is present in patients with schizophrenia. In large follow-up studies of childhood-onset schizophrenia, the mortality rate from suicide is 5-11%. In follow-up studies, more than 50% of children with schizophrenia have persistent severe impairment in social skills and limitations in academic and occupational achievement. Approximately 10% of adults with schizophrenia commit suicide.

Violence is also a potential problem, particularly for the adolescent with paranoid ideation. Other complications arise from poor self-care, impulsivity leading to injury or sexually acquired diseases, and substance abuse.

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Patient Education

Psychoeducation is essential for families of children with schizophrenia. They need to be educated about the causes, symptoms, natural history, therapy, adverse effects of medication, and complications of childhood-onset schizophrenia.

Families must also know the warning signs of impending relapse. High levels of expressed emotion have been associated with an increased risk of relapse in adults with schizophrenia and can possibly contribute to problems in children with schizophrenia.

Once children with schizophrenia are in remission, teach them to self-monitor for signs of possible relapse. Inform these children about possible adverse effects of medication.

For patient education information, see Mental Health and Behavior Center, as well as Schizophrenia.

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Contributor Information and Disclosures
Author

Annemarie K Loth, MD  Fellow in Child and Adolescent Psychiatry, Indiana University School of Medicine

Annemarie K Loth, MD is a member of the following medical societies: American Psychiatric Association and Indiana Psychiatric Society

Disclosure: Nothing to disclose.

Coauthor(s)

David W Dunn, MD  Program Director, Child and Adolescent Psychiatry, Professor, Departments of Psychiatry and Neurology, Indiana University School of Medicine

David W Dunn, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, American Academy of Neurology, American Epilepsy Society, American Psychiatric Association, and Child Neurology Society

Disclosure: Lilly Grant/research funds Other; GlaxoSmithKline Grant/research funds Other; Supernus Grant/research funds Other

Chief Editor

Caroly Pataki, MD  Professor of Clinical Psychiatry and Behavioral Sciences, Department of Psychiatry, Division Chair, Child and Adolescent Psychiatry, Keck School of Medicine of the University of Southern California

Caroly Pataki, MD is a member of the following medical societies: American Academy of Child and Adolescent Psychiatry, New York Academy of Sciences, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Additional Contributors

Angelo P Giardino, MD, PhD Clinical Associate Professor, Department of Pediatrics, Baylor College of Medicine; Medical Director, Texas Children's Health Plan, Inc

Angelo P Giardino, MD, PhD is a member of the following medical societies: Academic Pediatric Association, American Academy of Pediatrics, American Professional Society on the Abuse of Children, Harris County Medical Society, Helfer Society, and International Society for Prevention of Child Abuse and Neglect

Disclosure: Bayer Honoraria Review panel membership; Pfizer Grant/research funds Independent contractor; MedImmune Honoraria Review panel membership

Raj K Kalapatapu, MD Fellow, Addiction Psychiatry, Columbia University College of Physicians and Surgeons

Raj K Kalapatapu, MD is a member of the following medical societies: American Academy of Addiction Psychiatry, American Academy of Child and Adolescent Psychiatry, American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Childhood schizophrenia. Early and late gray matter deficits in schizophrenia. Areas of gray matter loss, shown in red and yellow, spread from back-to-front (right to left) over 5 years in composite MRI scan data from 12 teens with childhood-onset schizophrenia, beginning at age 14 (left). Red and yellow denotes areas of greater loss. Source: Paul Thompson, MD, UCLA, Laboratory of Neuroimaging. NIMH media file.
Childhood schizophrenia. Rate of gray matter loss. Composite MRI scan data showing areas of gray matter loss over 5 years, comparing 12 normal teens (left) and 12 teens with childhood-onset schizophrenia. Red and yellow denotes areas of greater loss. Front of brain is at left. Source: Paul Thompson, MD, UCLA, Laboratory of Neuroimaging. NIMH media file.
 
 
 
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