Recent anatomical brain magnetic resonance imaging (MRI) studies show
a striking postpsychotic progressive loss of cortical gray matter (GM) in
patients with childhood-onset schizophrenia (COS), which appears greater than
that seen for adult patients. However, the diagnostic specificity and the
relationship of these changes to drug treatment and cognitive functioning
remain unclear. We performed a comparative prospective brain MRI study in
patients with COS and pediatric patients with transient psychosis with behavior
problems (psychosis not otherwise specified) provisionally considered multidimensionally
impaired (MDI). We hypothesized that cortical GM loss would occur in patients
with COS but not in adolescents with atypical psychoses.
Anatomical brain MRI was performed at baseline and follow-up in 19 patients
in the MDI group (mean [SD] age of 13.3 [3.1] years); in 23 patients with
COS matched for age, sex, IQ score, and drug treatment (mean [SD] age of 13.9
[2.5] years); and 38 healthy control subjects matched for age and sex (mean
[SD] age of 13.3 [3.1] years). The mean (SD) follow-up was 2.5 (0.8) years.
Volumes of the cerebrum and total and regional GM were obtained by using automated
analysis, and percent change in volume across time was calculated. One-way
analyses of variance with post hoc Tukey Honestly Significantly Different
comparisons were performed to examine group differences in the percent change
in GM across follow-up.
The COS group had significantly greater total, frontal, temporal, and
parietal GM loss than did the MDI or healthy control groups; analysis of variance
post hoc P values ranged from .03 to .001. The MDI
and control groups did not differ significantly from each other.
The cortical GM volume loss in COS appears diagnostically specific;
it was not seen in children and adolescents with atypical psychosis. Because
both patient groups had similar early developmental patterns, cognitive functioning,
medications, and hospitalizations, this progressive loss appears to be intrinsic
to COS. An ongoing neurodevelopmental process and/or brain response specific
to the illness could account for these changes.