Effects of antidepressant treatment on N-acetyl aspartate and choline levels in the hippocampus and thalami of post-stroke depression patients: A study using 1H magnetic resonance spectroscopy

Abstract

Previous studies in patients with a major depressive disorder show functional abnormalities in the medial frontal cortex. Functional and structural abnormalities in patients with post-stroke depression (PSD) are not well studied. The major goals of this study were to determine the biochemical abnormalities that occur in PSD and to assess the effect of antidepressants in patients with PSD at the biochemical level. We used magnetic resonance imaging to detect structural or functional abnormalities in PSD patients. In a prospective study, we included 30 patients with PSD and 20 age-matched subjects as controls. Magnetic resonance spectroscopy (MRS) of the brain was conducted in all subjects at the beginning of the study. Patients with PSD were treated with the antidepressant paroxetine (20–40 mg/days) for 6 months. After the 6-month period, all PSD subjects underwent MRS again. PSD patients were evaluated with the Hamilton Depression Scale (HAMD) both before and after treatment with the antidepressant. The mean age of the PSD patients was 70.0 ± 4.2 years and that of the controls was 67.2 ± 5.4 years. Before treatment, N-acetyl aspartate/creatine (NAA/Cr) ratios in the bilateral hippocampus and thalami were significantly lower in PSD patients than in controls. Choline/creatine (Cho/Cr) ratios were significantly higher in the bilateral hippocampus and left thalamus in PSD patients than in controls. The Cho/Cr ratios were significantly higher in the left thalamus than in the right in PSD patients. The HAMD scores were significantly correlated with the Cho/Cr ratios in the left and right hippocampus. Compared with PSD patients before antidepressant treatment, the PSD subjects after treatment had significantly higher NAA/Cr ratios in the left hippocampus and bilateral thalami. They had significantly lower Cho/Cr ratios in bilateral hippocampus and left thalamus. Our study suggests that metabolic abnormalities in the hippocampus and thalamus are implicated in PSD. Antidepressants may alter the local metabolic abnormalities in these areas.