Increased thalamic N-acetylaspartate in male patients with familial bipolar I disorder.

N-Acetylaspartate (NAA) in the anterior and mediodorsal thalamic regions was measured using proton magnetic resonance spectroscopic imaging (1H-MRSI) in 15 euthymic male patients with familial bipolar I disorder and compared to values in 15 male control subjects to determine if there was evidence for altered neuronal/axonal integrity. MRI tissue segmentation methods were also utilized to obtain tissue-contribution estimates for each MRSI voxel. Relative to the comparison group, the patients with bipolar I disorder demonstrated significantly higher NAA and creatine in both the right and left thalamus. NAA was also significantly higher in the left thalamus compared to the right in both bipolar I patients and controls. There were no group or lateralized differences in the percentages of different tissue types within the MRSI voxels, suggesting that the thalamic NAA and creatine alterations were not an artifact of variations in tissue type percentages in the MRSI voxels. There was also no significant association between NAA or creatine and illness duration. The findings of increased thalamic NAA bilaterally may represent neuronal hypertrophy or hyperplasia, reduced glial cell density, or abnormal synaptic and dendritic pruning. Increased thalamic creatine bilaterally may represent altered cellular energy metabolism and is consistent with prior studies demonstrating changes in thalamic metabolism in mood disorders.

Reduced concentrations of thalamic N-acetylaspartate in male patients with schizophrenia.

OBJECTIVE: The authors measured N-acetylaspartate (a putative neuronal marker) in the right and left thalamus of 17 male patients with schizophrenia using in vivo proton magnetic resonance spectroscopic imaging ((1)H MRSI). METHOD: (1)H MRSI was performed on 17 medicated male patients with schizophrenia and 10 male comparison subjects. Concentrations of N-acetylaspartate, creatine, and choline were determined in the thalamic regions bilaterally. RESULTS: The patients with schizophrenia demonstrated significantly lower concentrations of N-acetylaspartate than the comparison subjects in both the right and left thalamic regions. Right thalamic N-acetylaspartate and left thalamic N-acetylaspartate were significantly correlated in the patients but not in the comparison subjects. There was no association between N-acetylaspartate and duration of illness or medication dose. No group differences or lateralized asymmetries in choline or creatine were noted. CONCLUSIONS: The finding of reduced concentrations of N-acetylaspartate bilaterally suggests neuronal dysfunction and/or loss in both the right and left thalamic regions in male patients with schizophrenia.