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Penn State College of Medicine
Same diagnostic criteria apply to children, adolescents, and adults
Based on characteristic symptoms, deficits in adaptive functioning, and
duration of six months
of childhood schizophrenia is less than 1/10,000 births
educated and professionally successful families
have low-average to average range of intelligence
of behavior before a formal diagnosis: attention/conduct
problems, earlier patterns of inhibition, withdrawal and sensitivity
is rarely observed before age 5
children have auditory hallucinations; 50% have delusional beliefs
observed with additional conditions such as: conduct disorder, learning disabilities, mental retardation,
prognosis if onset before age 10 with above personality difficulties
Since 1990 there has been an ongoing study of childhood onset
schizophrenia (COS) of 49 patients at the National Institute of Mental Health
(NIMH) which most of the following findings are based on.
before a Formal Diagnosis is made6: based
on 49 treatment refractory patients at NIMH (patients that did not respond to
conventional therapy currently available for schizophrenia)
either failed a grade or required placement in special education
poor neuropsychological functioning in attention, working memory and executive
function (i.e. making and carrying out appropriate decisions on a day to day
were more striking than those in adult patients which indicates a more severe
early disruption of brain development in COS – also indicates greater
familial vulnerability (possibly a greater likihood of a genetic component to
rate of spectrum personality disorders (schizoaffective, schizotypal,
paranoid) 45% had at least one relative with a disorder
schizophrenia in relatives (1.8%) vs. control group (0.5%)
of patients with family members with spectrum disorders had prediagnosis
language abnormalities which was more striking than adult patients
study doesn’t show an increase in obstetrical complications in COS vs.
adults patients (though there have been studies that have found a link between
obstetrical complications and schizophrenia in general)
association of socioeconomic status, psychological trauma with an earlier age
at UCLA of Finnish patients showed an increase in early onset schizophrenia
with perinatal hypoxia (each event increased the risk 2 fold)2
correlation has been shown b/w onset of puberty and onset of psychosis4
study found several chromosomal abnormalities in patients such as:
Turner’s Syndrome (female patients with one X chromosome),
translocation of chromosomes 1 and 7 and Velocardiofacial syndrome (deletion
of 22q11) – findings were more striking than adult patients
association found with ApoE4, HLA or trinucleotide repeats3,7 (which
are protein and genetic abnormalities found in diseases like Alzheimer’s and
Huntington’s Disease respectively)
syndrome (VCFS) found in 6.4% of COS patients vs 0.025% of general population,
and 2.0% of adult schizophrenic patients – causes craniofacial malformation,
cardiac abnormalities, and developmental problems
with both COS and VCFS found to have increased neurodevelopmental impairment11
Smooth Pursuit Eye Movements and P50 sensory gating
COS patients had qualitatively poor eye tracking
relatives noted to have poor eye tracking vs. 5% of controls
also noted to have an increased rate of anticipatory saccades6
of Colorado study demonstrated the bilineal inheritance (inheritance from both
parents) of both anticipatory saccades and P50 auditory evoked responses10
COS had both parents with elevated anticipatory saccades vs 0% of adult onset
COS also had both parents with diminished suppression of P50 auditory evoked
responses (responded equally to both sounds) vs 13% of adult onset patients
responses are linked to a7
nicotinic receptor gene locus on chromosome 15q14
smooth pursuit eye movements are on chromosome 6
findings continue to highlight to possibility of multiple genetic
abnormalities in COS children.
in lateral ventricular volume with decreased cerebellar volume and midsagittal
decrease in adolescence related to decreased ability of patients to learn new
24 patients, 12.5% were found to have enlarged cavum septi pellucidi
(> 6 cm) which were more severe than patients with adult onset
(relates to the area of the brain in charge of emotion and memory)
suggest more severe brain abnormalities and an earlier onset of sx8
noted to have smaller than normal amounts of regional N-acetylaspartate (NAA)
(a neurotransmitter in the brain) in the hippocampus and dorsolateral
correlation with volume losses or length of illness
noted to have a decreased volume of the following areas during adolescence
(age 13-18): 10.9% in frontal
gray matter, 8.5% in parietal gray matter, 7% in temporal gray matter (unique
to COS – controls have an increase in temporal lobe)9
had a decrease of 2.6% in frontal and 4.1% in parietal
had a mean onset of psychosis at 10.3 years so the decreases were not a
coincides with MRI findings of adult patients
study also showed that the adolescent changes tend to level off in adulthood5
that since the hippocampal volume has been noted to be related to stress if
the decrease in the size of the hippocampus during adolescence is related to
the stress of the illness vs. the direct effects of schizophrenia on the body
1. Bertolino, et al: Common pattern of cortical pathology in childhood-onset and adult-onset schizophrenia as identified by proton magnetic resonance spectroscopic imaging. American Journal of Psychiatry 1998; 155:1376-1383.
et al: Fetal hypoxia linked to
early onset schizophrenia. American
Journal of Psychiatry 2000; 157:801-807.
et al: Apolipoprotein E alleles
in childhood-onset schizophrenia. American
Journal of Medical Genetics 1999; 88:211-213.
et al: Pubertal development and
onset of psychosis in childhood onset schizophrenia. Psychiatry Research 1997; 70:1-7.
et al: Childhood-onset
schizophrenia: Progressive brain
changes during adolescence. Biological
Psychiatry 1999; 46:892-898.
et al: Childhood-onset
schizophrenia: Rare but worth
studying. Biological Psychiatry
et al: Lessons from
childhood-onset schizophrenia. Brain
Research Reviews 2000; 31:147-156.
et al: Frequency and severity of
enlarged cavum septi pellucidi in childhood-onset schizophrenia. American Journal of Psychiatry 1998; 155:1074-1079.
et al: Progressive cortical
change during adolescence in childhood-onset schizophrenia: A longitudinal magnetic resonance imaging study.
Archives of General Psychiatry 1999; 56:649-654.
et al: Evidence for bilineal
inheritance of physiological indicators of risk in childhood-onset
schizophrenia. American Journal
of Medical Genetics 1999; 88:188-199.
et al: Velocardiofacial syndrome
in childhood-onset schizophrenia. Journal
of the American Academy of Child and Adolescent Psychiatry 1999; 38:1536-1543.
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Revised: January 20, 2008 .