Cortical thickness changes may contribute to early schizophrenia

By Eleanor McDermid, Senior medwireNews Reporter

Altered cortical thickness is related to the severity of positive symptoms in patients with first-episode schizophrenia, but not to the duration of untreated illness, report researchers.

“This finding suggests that widespread cortical deficits occurring in the early stages of schizophrenia may be crucial to the pathogenesis of the disease,” the researchers write in Schizophrenia Bulletin.

Su Lui (West China Hospital of Sichuan University, Chengdu) and co-workers found both decreased and increased cortical thickness at different sites in 128 drug-naïve, first-episode schizophrenia patients who underwent magnetic resonance imaging, relative to 128 mentally healthy controls.

The affected areas included several with a role in managing executive functions that are known to be disturbed in patients with schizophrenia.

Areas with significant decreases included the right dorsolateral prefrontal cortex, left precentral gyrus, left orbitofrontal cortex, and left inferior frontal gyrus pars triangularis. Reduced thickness in these regions correlated with increased severity of symptoms on the Positive and Negative Syndrome Scale, specifically with positive symptoms.

“This finding suggests that reduced cortical thickness, especially in the prefrontal regions, may predispose patients to specific symptoms,” says the team. “Thus, the anatomical deficits in the prefrontal and parietal regions may represent core pathology during the early course of schizophrenia.”

There was significant cortical thickening in the bilateral anterior temporal lobes, the left medial orbitofrontal cortex, and the left cuneus.

Cortical surface area was not different between patients and controls, “suggesting that the alterations in cortical thickness are more pronounced than those in surface area during the early stage of schizophrenia.”

The researchers add that cortical thickness and surface area are thought to be affected by different genetic factors. The two combined comprise cortical volume, so the lack of change in surface area may explain why previous studies found no volume differences between patients and controls.

Cortical thickness was not related to the duration of untreated illness, suggesting “that the cortical deficits in schizophrenia are relatively stable instead of progressing during the early stages of the disease,” contradicting the theory that schizophrenia is a progressive disease.

Lui et al suggest that progressive brain changes seen in other studies may be due to factors such as comorbidities, nonadherence to treatment, or lack of social support. They concede that there may be progressive cortical changes in patients with longer duration of disease, but studying this would be complicated by the confounding effects of treatment.

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