自閉症の脳画像研究

Brothers proposed a network of neural regions that comprise the “social brain”, which includes the amygdala, the orbito-frontal cortex, and the superior temporal sulcus and gyrus. Since the psychiatric condition of autism involves deficits in “social intelligence”, it is plausible that autism may be caused by an abnormality of these regions.
We measured chemical metabolites in the left amygdala and the bilateral orbito-frontal cortex, which are the main components of the social brain. We also examined the association between these metabolic findings and social abilities in subjects with autism. The study group included 77 autistic patients and age-matched 31 normal children. Conventional proton magnetic resonance spectra were obtained using the STEAM sequence with parameters of TR＝5 sec and TE＝15 msec by a 1.5-tesla clinical MRI system. We analyzed the concentrations of N-acetylaspartate （NAA）, creatine/phosphocreatine （Cr）, and choline-containing compounds （Cho） using LCModel （Ver.6.1）. The concentrations of NAA in the left amygdala and the bilateral orbito-frontal cortex in autistic patients were significantly decreased compared to those in the control group. In the autistic patients, the NAA concentrations in these regions correlated with their social quotient. These findings suggest the presence of neuronal dysfunction in the amygdala and orbito-frontal cortex in autism.
The amygdala is thought to play a central role in associating sensory cues with their motivational and emotional significance. Schoenbaum et al. proposed models of amygdala-frontal interaction in which motivational and emotional significance, coded by the amygdala, is conveyed to the orbito-frontal cortex for the control of action. Dysfunction in the amygdala and orbito-frontal cortex may contribute to the pathogenesis of autism.