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Visual hallucinations in children with schizophrenia may be due to delayed brain development

Visual hallucinations among children with schizophrenia may be due to delayed development of the inferior longitudinal fasciculus, as results from prospective brain MRI analyses showed genetically influenced and connection-specific developmental abnormalities in the schizophrenia connectome.

“The onset of symptoms [of childhood-onset schizophrenia] typically occurs before puberty, an active period of brain development during which marked changes in white matter organization take place. Studying brain connectivity development longitudinally in patients with [childhood-onset schizophrenia] and their clinically unaffected siblings is therefore of particular interest, as it enables mapping of abnormal changes during key developmental windows and the ability to characterize neural endophenotypes,” study researcher Andrew Zalesky, PhD, of the University of Melbourne and Melbourne Health in Victoria, Australia, and colleagues wrote.

Researchers mapped large-scale corticocortical connectivity from ages 12 to 24 years among 109 patients with childhood-onset schizophrenia, 86 of their unaffected siblings and 102 healthy controls.

Patients with childhood-onset schizophrenia and their unaffected siblings had left-hemisphere occipitotemporal deficits in cortical thickness correlations compared with healthy controls (P < .05).

Deficits among unaffected siblings normalized by mid-adolescence, while patients with childhood-onset schizophrenia did not show evidence of developing cortical thickness correlations between the left temporal lobe and left occipital cortex until early adulthood.

Left-hemisphere occipitotemporal thickness correlations were reduced from age 14 to 18 years among a subgroup of patients with high positive symptoms (P < .05), though patients with low positive symptoms did not have significant deficits.

“In [this], unaffected siblings of patients with childhood-onset schizophrenia showed lower occipitotemporal structural correlations (similar to their relatives with [childhood-onset schizophrenia]) compared with healthy control participants. These correlations increased (were normalized) by mid-adolescence in the unaffected relatives. Patients with [childhood-onset schizophrenia] also normalized with age, albeit with a delay,” Matcheri S. Keshavan, MD, of Beth Israel Deaconess Medical Center and Harvard Medical School, and Tomas Paus, MD, PhD, of the University of Toronto, wrote in an accompanying editorial. “The trajectory of such changes in structural correlations is at least partly heritable but environmental factors are also important. This is especially true for family-based studies of children with severe psychiatric disorders, such as [childhood-onset schizophrenia], and their siblings. Whether driven by genes and/or environment, longitudinal trajectories may be useful biomarkers of familial susceptibility.” – by Amanda Oldt

Disclosure: Zalesky, Keshavan and Paus report no relevant financial disclosures. Please see the full study for a list of all other authors’ relevant financial disclosures.