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Background and Purpose: This is an observational study to evaluate the safety of magnetic resonance imaging (MRI) to localize subdural grids and depth electrodes in patients with refractory epilepsy using a 1.5 Tesla MR scanner., Methods: We implemented an optimized MRI protocol providing adequate image quality for the assessment of subdural grids and depth electrodes, while minimizing the specific absorption rate (SAR). We reviewed all MRI studies performed in patients with subdural grids and depth electrodes between January 2010 and October 2018. Image quality was graded as acceptable or nonacceptable for the assessment of intracranial device positioning. We reviewed the medical record and any imaging obtained after intracranial implant removal for adverse event or complication occurring during and after the procedure., Results: Ninety-nine patients with refractory epilepsy underwent MRI scans using a magnetization-prepared rapid acquisition of gradient echo sequence and a transmit-receive head coil with depth electrodes and subdural grids in place. Two patients underwent two separate depth electrode implantations for a total of 101 procedures and MRI scans. No clinical adverse events were reported during or immediately after imaging. Image quality was graded as acceptable for 97 MRI scans. Review of follow-up CT and MRI studies after implant removal, available for 70 patients, did not demonstrate unexpected complications in 69 patients., Conclusion: In our experience, a low SAR MRI protocol can be used to safely localize intracranial subdural grids and depth electrode in patients with refractory epilepsy., (© 2021 American Society of Neuroimaging.)

Primary central nervous system posttransplant lymphoproliferative disorder is a rare complication of solid organ transplantation, with increasing incidence in children given a steady rise in pediatric solid organ transplants. Given similar imaging appearance to many opportunistic infections, a high degree of awareness is required for prompt and early diagnosis. We report a case of primary central nervous system posttransplant lymphoproliferative disorder presenting as a single rim enhancing lesion with central restricted diffusion mimicking an intracranial abscess., Competing Interests: The authors declare no conflict of interest., (Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.)

Background and Purpose: Mild cognitive impairment (MCI) is a prevalent disorder, with a subset of patients progressing to dementia each year. Although MCI may be subdivided into amnestic or vascular types as well as into single or multiple cognitive domain involvement, most prior studies using advanced diffusion imaging have not accounted for these categories. The purpose of the current study was to determine if the pattern of diffusion tensor imaging (DTI) and diffusion kurtosis imaging (DKI) metrics in patients with amnestic MCI (aMCI) correlate to specific cognitive domain impairments., Methods: Nineteen consecutive patients with aMCI referred for brain magnetic resonance imaging (MRI) were included. All subjects underwent neurocognitive testing. A z-score was calculated for each domain and a composite of all four domains. Brain MRI included standard structural imaging and diffusion imaging. Volumetric, DTI, and DKI metrics were calculated and statistical analysis was performed with adjustments for multiple measures and comparisons., Results: Statistically significant correlations between diffusion metrics and cognitive z-scores were detected: visuospatial-visuoconstructional z-scores only correlated with alterations in the corpus callosum splenium, executive functioning z-scores with the corpus callosum genu, memory testing z-scores with the left hippocampus, and composite z-scores with the anterior centrum semiovale., Conclusion: Neuroimaging studies of patients with aMCI to date have assumed a population with homogeneous cognitive impairment. Our results demonstrate selective patterns of regional diffusion metric alterations correlate to specific cognitive domain impairments. Future studies should account for this heterogeneity, and this may also be useful for prognostication., (© 2018 by the American Society of Neuroimaging.)

Mutations in the gene encoding the methyl-CpG-binding protein MECP2 are the major cause of Rett syndrome, an autism spectrum disorder mainly affecting young females. MeCP2 is an abundant chromatin-associated protein, but how and when its absence begins to alter brain function is still far from clear. Using a stem cell-based system allowing the synchronous differentiation of neuronal progenitors, we found that in the absence of MeCP2, the size of neuronal nuclei fails to increase at normal rates during differentiation. This is accompanied by a marked decrease in the rate of ribonucleotide incorporation, indicating an early role of MeCP2 in regulating total gene transcription, not restricted to selected mRNAs. We also found that the levels of brain-derived neurotrophic factor (BDNF) were decreased in mutant neurons, while those of the presynaptic protein synaptophysin increased at similar rates in wild-type and mutant neurons. By contrast, nuclear size, transcription rates, and BDNF levels remained unchanged in astrocytes lacking MeCP2. Re-expressing MeCP2 in mutant neurons rescued the nuclear size phenotype as well as BDNF levels. These results reveal a new role of MeCP2 in regulating overall RNA synthesis in neurons during the course of their maturation, in line with recent findings indicating a reduced nucleolar size in neurons of the developing brain of mice lacking Mecp2., (Copyright © 2012 AlphaMed Press.)

Pregnant dams were fed a 20% protein diet with caffeine (2 mg/100 g b.wt.), starting on day 9 of gestation. At birth, each dam with 8 assigned pups was fed this diet until weaning, day 22. On day 22, female rats were caged and fed this diet until day 93. Starting on day 93, the caffeine-supplemented diet was replaced with a caffeine-free, 20% protein diet until day 388. Starting on day 31, each animal was placed in a photoactivity cage, and locomotive activity was measured until day 375. On day 388, the animals were killed, and their brains were removed and divided into 7 regions. The weight, DNA, protein and zinc contents, and alkaline phosphatase activity of each region were determined. Locomotive activity of the caffeine-fed group was higher than in the noncaffeine control group. Accumulative activity scores showed 3 subgroups (high, medium, and low) in both groups at day 93. The medium activity subgroup in the caffeine group was greater than the controls from day 72 to day 93. These differences reappeared 5 weeks after cessation of caffeine supplementation and continued until day 375. The differences in activity were minimum in the high and low subgroups. Chronic caffeine intake in early life permanently affected the medium activity subgroup. Furthermore, various regions of the brain were biochemically altered in spite of the feeding of a noncaffeine diet for almost 300 days after caffeine.

Pregnant dams were divided into two subgroups on day 10 of gestation. Half were fed a 20% protein diet and the other half an 8% protein diet. A second group also subdivided was pair-fed with rats of the first group. Their diet was supplemented with caffeine in amount calculated to provide daily doses of 2 mg/100 g body weight. On days 18, 20, and 22 randomly selected dams were injected with 3H-thymidine intraperitoneally and 1.5 h later their fetuses were delivered surgically in order to determine the rate of DNA synthesis along the gestation. The rest of the fetuses were delivered surgically on day 22. Pups' brains were rapidly removed and DNA, RNA, protein and 3H-thymidine uptake were studied. Average body weights of the fetuses in the caffeine-supplemented control group were smaller than those of the noncaffeine group. Effects of caffeine that were similar in both diet groups included a decrease in brain DNA content and concentration and an increase in brain protein content and concentration. However, the percent decrease and increase, respectively, was different depending on the nutritional status. DNA synthesis was not affected by malnutrition or caffeine supplementation on day 18 of gestation. Caffeine's effect on the rate of DNA synthesis was different on day 20 of gestation depending on nutritional status. Caffeine supplementation resulted in a decrease in DNA synthesis in both groups on day 22 of gestation. These data indicate that caffeine intake during pregnancy produces differential effects on fetal rat brain depending on dietary protein content.

At birth, dams with 8 randomly assigned pups were divided into three groups. Dams of group 1 were fed a control diet. Dams of groups 2 and 3 were fed the control diet supplemented with caffeine (1 mg and 2 mg/100 g body weight, respectively). Pups were killed at day 15 and their brains removed. After weighing, brains were analyzed for DNA, protein, cholesterol, zinc and alkaline phosphatase activity. Brain and plasma caffeine levels were also determined on groups 2 and 3. The dams were milked to measure caffeine levels. The brains from the dams were analyzed for the same parameters as the pups. Caffeine levels in group 3 were consistently higher than in group 2. In the pups, body and brain weights were heavier in group 3 than in the controls. Protein and cholesterol concentrations in group 2 were less than either controls or group 3. Alkaline phosphatase activity in group 2 was higher than either controls or group 3. In the dams, DNA concentration in groups 2 and 3 was less than the controls. Protein and cholesterol concentration in group 2 was less than group 3. It was concluded that low levels of caffeine in the maternal diet during lactation could affect various parameters in the newborn brain. These effects were different from those when the dietary caffeine level was doubled. In contrast, the effects of caffeine on brains of the dams were relatively minor.