Negative Correlation between Brain Glutathione Level and Negative Symptoms in Schizophrenia: A 3T 1H-MRS Study

BACKGROUND: Glutathione (GSH), a major intracellular antioxidant, plays a role in NMDA receptor-mediated neurotransmission, which is involved in the pathophysiology of schizophrenia. In the present study, we aimed to investigate whether GSH levels are altered in the posterior medial frontal cortex of schizophrenic patients. Furthermore, we examined correlations between GSH levels and clinical variables in patients. METHODS AND FINDINGS: Twenty schizophrenia patients and 16 age- and gender-matched normal controls were enrolled to examine the levels of GSH in the posterior medial frontal cortex by using 3T SIGNA EXCITE (1)H-MRS with the spectral editing technique, MEGA-PRESS. Clinical variables of patients were assessed by the Global Assessment of Functioning (GAF), Scale for the Assessment of Negative Symptoms (SANS), Brief Psychiatric Rating Scale (BPRS), Drug-Induced Extra-Pyramidal Symptoms Scale (DIEPSS), and five cognitive performance tests (Word Fluency Test, Stroop Test, Trail Making Test, Wisconsin Card Sorting Test and Digit Span Distractibility Test). Levels of GSH in the posterior medial frontal cortex of schizophrenic patients were not different from those of normal controls. However, we found a significant negative correlation between GSH levels and the severity of negative symptoms (SANS total score and negative symptom subscore on BPRS) in patients. There were no correlations between brain GSH levels and scores on any cognitive performance test except Trail Making Test part A. CONCLUSION: These results suggest that GSH levels in the posterior medial frontal cortex may be related to negative symptoms in schizophrenic patients. Therefore, agents that increase GSH levels in the brain could be potential therapeutic drugs for negative symptoms in schizophrenia

The changing MR imaging appearance of polymicrogyria: a consequence of myelination.

BACKGROUND AND PURPOSE: During the review of MR studies of multiple patients with polymicrogyria (PMG), it was noted that the patterns of cortical abnormality differed significantly among affected patients. In particular, the cortex appeared very thin in some patients, but was thick in others. The purpose of the present study was to attempt to clarify the cause of the different imaging appearances. METHODS: T1- and T2-weighted images obtained in 17 patients (age range, 3 days to 43 years) with PMG diagnosed on the basis of imaging characteristics were retrospectively reviewed. One patient was examined four times over a period of 21 months. Particular attention was paid to the thickness and signal intensity of the cortex and underlying white matter and how these features varied with maturation of the cortex and white matter. RESULTS: T2-weighted images revealed two patterns of PMG. Pattern 1 showed small, fine, and undulating cortex with normal thickness (3-4 mm) in seven patients, all younger than 12 months; and pattern 2, a bumpy cortex that appeared abnormally thick (6-8 mm) and had an irregular cortical-white matter junction in seven patients older than 18 months. Both patterns were observed in four patients between 15 months and 2 years of age (ie, pattern 1 in the anterior frontal region and pattern 2 in the posterior frontal, parietal, or perisylvian regions). A layer of T2 prolongation (2-3 mm) was recognized between pattern 1 PMG and underlying myelinated white matter in four patients 11 months to 2 years of age. T1-weighted images showed either poor differentiation of the cortex and underlying white matter or pattern 2. Serial MR imaging in one patient depicted longitudinal changes of the PMG from pattern 1 to pattern 2. CONCLUSION: These findings suggest that the two appearances (thin and thick) of the cortex seen in PMG likely represent the same process, with the apparent difference being the result of myelination in subcortical and intracortical fibers that cause a change of the appearance and apparent thickness of PMG on T2-weighted images

Influenza-Associated Encephalitis/Encephalopathy with a Reversible Lesion in the Splenium of the Corpus Callosum:A Case Report and Literature Review

We report the cases of two patients with influenza-associated encephalitis/encephalopathy(IAEE)who presented with mild CNS manifestations and complete recovery within a few days.Initial MR imaging at days 4 and 5 revealed a lesion in the central portion of the splenium of the corpus callosum with a reduced apparent diffusion coefficient (ADC) value, which completely resolved on follow-up studies at day 10. We postulate two possible mechanisms for decreased ADC; namely, intramyelinic edema and an inflammatory infiltrate

Central Tegmental Tract Involvement in an Infant with 6-Pyruvoyltetrahydropterin Synthetase Deficiency

SUMMARY: We report the case of an asymptomatic 2-month-old infant with 6-pyruvoyltetrahydropterin synthetase deficiency detected through a neonatal phenylketonuria screening program. MR imaging revealed symmetrical lesions in the central tegmental tract with reduced diffusion, which resolved after treatment. A possible explanation for these lesions is intramyelinic edema resulting from brain insults in utero

Brain MR imaging in neonatal hyperammonemic encephalopathy resulting from proximal urea cycle disorders.

We present brain MR images in three patients with neonatal-onset hyperammonemic encephalopathy resulting from urea-cycle disorders (two sisters with deficiency of the carbamyl phosphate synthetase I reaction step and one boy with an ornithine transcarbamylase deficiency). MR imaging revealed almost identical findings of injury to the bilateral lentiform nuclei and the deep sulci of the insular and perirolandic regions; to our knowledge, this pattern has not been previously reported. We hypothesize that these lesions presumably reflect the distribution of brain injury due to hypoperfusion secondary to hyperammonemia and hyperglutaminemia in the neonatal period