Changes in N‐Acetylaspartate Levels in the Basal Ganglia of Patients with a Schizophrenia‐Like Epileptic Psychosis
Authors: Fujimoto Toshiro , Takano Tetsuya , Takeuchi Kozo , Nakamura Katsumi , Kodama Shinichi , Yatsushiro Kazutaka , Asakura Tetsuhiko , Akimoto Haruo 
Published: August 2009

Purpose: Recently, proton magnetic resonance spectroscopy (1H‐MRS) demonstrated neuronal loss or dysfunction in the epileptogenic focus in temporal lobe epilepsy, and bilateral neuronal abnormalities in the temporal lobes. It is well‐known that a schizophrenia‐like epileptic psychosis is closely related to temporal lobe epilepsy and that the symptoms of a schizophrenia‐like epileptic psychosis are extremely similar to those of schizophrenia. We also reported neuronal dysfunction in the basal ganglia of patients with chronic schizophrenia. The basal ganglia play an important role in neuronal circuitry and receive projections from the temporal cortex. We investigated whether there is neuronal dysfunction in the basal ganglia of patients with a schizophrenia‐like epileptic psychosis, temporal lobe epilepsy, and schizophrenia, by using the 1H MRS. Methods: Nine patients with a schizophrenia‐like epileptic psychosis, seven patients with temporal lobe epilepsy showing no schizophrenia‐like symptoms, 14 patients with positive symptoms of schizophrenia, and 10 control subjects were examined. Using the 1H‐MRS system with 2 Tesla, 1H spectra were acquired from voxels of the left and right basal ganglia with a size of 2.5 × 2.5 × 2.5 cc. The pulse sequence was stimulated echo (STEAM) with TR = 2,000 ms, TE = 60 ms, and acquisition = 400. Peak areas of N‐acetylaspartate (NAA), creatine plus phosphocreatine (Cr), and choline‐containing compounds (Cho) were studied. Results: Mean NAA/Cr ratios in the right basal ganglia were 1.07 (schizophrenia‐like epileptic psychosis), 1.08 (schizophrenia) and 1.I4 (temporal lobe epilepsy), all of which were significantly decreased, compared with those of control subjects (1.41). Mean NANCr ratios in the left basal ganglia were 1.16 (schizophrenia‐like epileptic psychosis), 1.19 (schizophrenia), and 1.24 (temporal lobe epilepsy), all of which were significantly decreased, compared with those of control subjects (1.61). NAA/Cho and NAA/(Cr + Cho) ratios in the right and left basal ganglia were also significantly decreased in patients with a schizophrenia‐like epileptic psychosis, temporal lobe epilepsy, or schizophrenia, compared with those of controls. However, there were no significant differences among the NAA/Cr, NAA/Cho, and NAN (Cr + Cho) ratios in patients with a schizophrenia‐like epileptic psychosis, temporal lobe epilepsy, or schizophrenia. Decreased levels of NAA demonstrated neuronal dysfunction of the basal ganglia in patients with a schizophrenia‐like epileptic psychosis, temporal lobe epilepsy, or schizophrenia, and that neuronal dysfunction in the temporal lobes may cause these changes. These results suggested that neuronal dysfunction of the basal ganglia may reflect disturbances of information processing such as contextual analysis of the environment, and the planning and execution of intelligent behaviors, and may have a close relation with the psychopathological state in a schizophrenia‐like epileptic psychosis and schizophrenia. However, the finding that NAA/Cr ratios were decreased, even in the patients with the complex partial seizures of temporal lobe epilepsy without schizophrenia‐like symptoms, indicated that the effects of the psychopathological state due to neuronal dysfunction in the basal ganglia are complicated. Conclusions: Neuronal dysfunction in the basal ganglia was found in patients with a schizophrenia‐like epileptic psychosis, temporal lobe epilepsy, and schizophrenia.