Brain loss in Childhood Onset Schizophrenia (COS)
> 1/14/2006 8:30:58 PM

The following elegant study published in the Archives of General Psychiatry by Christine N. Vidal, PhD et al allows us to have better insight into the brain pathology which affects children afflicted with Schizophrenia.

“In this study of the brains of children who develop Childhood-onset schizophrenia (COS)—in which psychotic symptoms occur by age 12 years—is a very rare form of the disorder that is neurobiologically continuous with the later-onset disorder. Adolescents with schizophrenia have a similar clinical presentation, with more severe premorbid symptoms and poorer prognosis. The authors selected twelve subjects with childhood-onset schizophrenia, 12 healthy controls, and 9 medication- and IQ-matched subjects with psychosis not otherwise specified. Three-dimensional (3D) (2562 x 124 resolution) T1-weighted fast spoiled gradient echo magnetic resonance (MR) imaging volumes were acquired from all 33 subjects. All images were acquired on the same 1.5-T scanner (Signa; General Electric Co, Milwaukee, Wis) at the National Institutes of Health Clinical Center, Bethesda, Md.

The authors discuss the possible explanation for the loss of grey matter in these patients. “The neuropathology of schizophrenia is unclear, and the cellular correlate of this cortical atrophy is unknown. Selemon and Goldman-Rakic suggested that decreased cortical volume in schizophrenia represents a reduction in neuropil and neuronal size, rather than overt neuronal loss. The emphasis on neuronal changes, rather than changes in other cell types, is supported by MR spectroscopic studies that repeatedly report frontal and temporal reductions in N-acetylaspartate, a metabolite that is relatively specific to neurons. Some postmortem studies report increased cell packing density in Brodmann areas 9 and 10 of schizophrenic patients, reflecting a decrease in the amount of neuropil. Some studies report a similar effect in Brodmann area 32, which is considered part of the cingulofrontal transition cortex, or the medial prefrontal cortex. In Golgi-stained material, Broadbelt et al found a significant decrease in the number of both primary (29%) and secondary (46%) basilar dendrites on layer V pyramidal neurons and similar, but less severe, reductions in layer III. Any such decrease in cingulate and frontal dendritic fields or the associated synaptic surface area might cause or exacerbate impairments in information processing. An opposing hypothesis, also consistent with our data, is that derailed cortical myelination may contribute to the apparent regression of gray matter in MR imaging data. Changes in white matter tracts and functional connectivity may also ensue if there are aberrant cellular changes in the cortical regions they connect.”

Whatever the explanation for this loss of grey matter in the brains of these patients it is abundantly clear that there are serious anatomical changes occurring in the brains of schizophrenics. The unraveling of this mystery is even more perplexing when you consider that it may be the neuropil which is being progressively lost. The potential to understand what neurohumoral agents are mediating this cerebral loss will become greater if researchers can determine the specific reason for this brain volume loss and what types of brain cells are being affected.

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