Association between reduced white matter integrity in the corpus callosum and serotonin transporter gene DNA methylation in medication-naive patients with major depressive disorder.

Previous evidence suggests that the serotonin transporter gene (SLC6A4) is associated with the structure of brain regions that are critically involved in dysfunctional limbic-cortical network activity associated with major depressive disorder (MDD). Diffusion tensor imaging (DTI) and tract-based spatial statistics were used to investigate changes in white matter integrity in patients with MDD compared with healthy controls. A possible association between structural alterations in white matter tracts and DNA methylation of the SLC6A4 promoter region was also assessed. Thirty-five medication-naive patients with MDD (mean age: 40.34, male/female: 10/25) and age, gender and education level matched 49 healthy controls (mean age: 41.12, male/female: 15/34) underwent DTI. SLC6A4 DNA methylation was also measured at five CpG sites of the promoter region, and the cell type used was whole-blood DNA. Patients with MDD had significantly lower fractional anisotropy (FA) values for the genu of the corpus callosum and body of the corpus callosum than that in healthy controls (family-wise error corrected, P<0.01). Significant inverse correlations were observed between SLC6A4 DNA methylation and FA (CpG3, Pearson's correlation: r=-0.493, P=0.003) and axial diffusivity (CpG3, Pearson's correlation: r=-0.478, P=0.004) values of the body of the corpus callosum in patients with MDD. These results contribute to evidence indicating an association between epigenetic gene regulation and structural brain alterations in depression. Moreover, we believe this is the first report of a correlation between DNA methylation of the SLC6A4 promoter region and white matter integrity in patients with MDD.

Atypical diffusion-restricted lesion in 5-Fluorouracil encephalopathy.

Central nervous system toxicity of 5-FU could show various manifestations, such as decreased alertness, disorientation, and agitation. It is generally accepted that lesions of 5-FU encephalopathy are mainly in the deep cerebral white matter and corpus callosum on MR imaging. Here we describe a case of 5-FU encephalopathy in gastric cancer with an atypical reversible diffusion-restricted lesion on MR imaging, showing bilateral basal ganglia, thalami, and parasagittal frontal cortex involvement on diffusion and T2-weighted imaging.

Correlation between CT and diffusion-weighted imaging of acute cerebral ischemia in a rat model.

BACKGROUND AND PURPOSE: The quantitative temporal relationship between changes in CT attenuation, ADC value, and DWI signal intensity of acute ischemic tissue has not yet been determined in an animal model. This study was performed to determine the temporal relationship between CT attenuation, ADC value, and DWI signal intensity in acute cerebral ischemia. MATERIALS AND METHODS: CT and DWI were performed at 1, 3, 5, 7, and 9 hours after left MCA occlusion in 11 rats. Mean values for CT attenuation, ADC, and DWI signal intensity were determined for the ischemic hemisphere and contralateral normal hemisphere. Temporal changes in each mean value and the relationship between CT attenuation and ADC value and DWI signal intensity were evaluated. RESULTS: The decrease of CT attenuation and the increase of DWI signal intensity occurred gradually after MCA occlusion, while ADC value decreased rapidly at 1 hour. Although correlation was significant between time and rCT or rDWI (P<.01, respectively), no correlation between time and rADC was found (P=.33). There was a significant linear correlation between rCT and rDWI (r=0.497, P<.01), but no significant correlation between rCT and rADC (P=.509) was found. CONCLUSIONS: The temporal change in CT attenuation was different from that in ADC value with no significant linear correlation between CT attenuation and ADC value for acute cerebral ischemia. However, rCT and rDWI showed a modest correlation.

MR imaging of metronidazole-induced encephalopathy: lesion distribution and diffusion-weighted imaging findings.

BACKGROUND AND PURPOSE: MR imaging features of metronidazole-induced encephalopathy (MIE) have not been fully established. This study was undertaken to determine the topographic distributions and diffusion-weighted imaging (DWI) findings of MIE. MATERIALS AND METHODS: We retrospectively evaluated the initial MR images (n = 7), including DWI (n = 5), and follow-up MR images (n = 4) after drug discontinuation in 7 patents with clinically diagnosed MIE. The topographic distributions of lesions were evaluated on MR images, and DWI signal intensities and apparent diffusion coefficient (ADC) values of the lesions were assessed. RESULTS: MR images demonstrated bilateral symmetric T2 hyperintense lesions in the cerebellar dentate nucleus (n = 7), midbrain (n = 7), dorsal pons (n = 6), medulla (n = 4), corpus callosum (n = 4), and cerebral white matter (n = 1). Brain stem lesions involved the following: tectum (n = 5), tegmentum (n = 4), red nucleus (n = 3) of the midbrain, vestibular nucleus (n = 6), and a focal tegmental lesion involving the superior olivary nucleus (n = 6) and abducens nucleus (n = 4) of the pons and vestibular nucleus (n = 4) and inferior olivary nucleus (n = 1) of the medulla. DWI (n = 5) showed isointensity or hyperintensity of lesions, and the decreased ADC value was found only in the corpus callosum lesions (n = 2). All detected lesions were completely reversible at follow-up except for the single corpus callosum lesion with an initial low ADC value. CONCLUSION: Brain lesions were typically located at the cerebellar dentate nucleus, midbrain, dorsal pons, medulla, and splenium of the corpus callosum. According to DWI, most of the lesions in MIE probably corresponded to areas of vasogenic edema, whereas only some of them, located in the corpus callosum, corresponded to cytotoxic edema.