Posterior Cingulate Gyrus Metabolic Changes in Chronic Schizophrenia with Generalized Cognitive Deficits

N-Methyl-d-aspartate (NMDA) receptor antagonists are known to induce schizophrenia-like psychotic symptoms & cognitive deficits in humans, & have been shown to cause neuronal damage in the posterior cingulate gyrus (PCG) of rodents. Patients with chronic schizophrenia exhibit generalized cognitive deficits, but it remains unclear whether or not the PCG is related to their cognitive dysfunction. To determine what biochemical changes may occur in the PCG of patients with chronic schizophrenia, & to ascertain whether or not such abnormalities may be related to the incidence of cognitive deficits, we obtained cognitive scores & proton magnetic resonance spectra (MRS) from the PCG & the left & right medial temporal lobes (MTL) of 19 patients with schizophrenia & 18 age- & sex-matched normal healthy controls. Compared to the normal controls, the patients with chronic schizophrenia showed significantly worse cognitive performance on verbal & visual memory tests, verbal fluency tests, & the Trail Making Test. The ratio of N-acetylaspartate to creatine & phosphocreatine (NAA/Cr) in the PCG of the patients was significantly lower than that of the controls. Moreover, the NAA/Cr in the PCG of the healthy controls exhibited age-related decline, whereas in the patients with schizophrenia, the corresponding values were consistently low, regardless of age. These findings are thus in accord with current speculation about neuronal dysfunction in the PCG based on the NMDA hypofunction hypothesis regarding the pathophysiology of chronic schizophrenia. Tables, Figures, References. [Copyright 2005 Elsevier Ltd.]