Patients with chronic hepatitis C virus (HCV) infection frequently report fatigue, lassitude, depression, and a perceived inability to function effectively. Several studies have shown that patients exhibit low quality-of-life scores that are independent of disease severity. We therefore considered whether HCV infection has a direct effect on the central nervous system, resulting in cognitive and cerebral metabolite abnormalities. Twenty-seven viremic patients with biopsy-proven mild hepatitis due to HCV and 16 patients with cleared HCV were tested with a computer-based cognitive assessment battery and also completed depression, fatigue, and quality-of-life questionnaires. The HCV-infected patients were impaired on more cognitive tasks than the HCV-cleared group ( C hronic hepatitis C (HCV) infection is estimated to affect 170 million people worldwide 1 and constitutes a major public health problem. It causes a fluctuating chronic hepatitis that may progress to cirrhosis and hepatocellular carcinoma. Attempts to understand the natural history of this infection have largely focused on the viral and host factors that predict progression of liver pathology from necroinflammation and fibrosis to cirrhosis and hepatocellular carcinoma. Consequently, the decision to treat patients is normally based on an assessment of these factors, including staging of disease with a liver biopsy, 2 rather than on particular symptoms. There is, however, emerging literature suggesting that, even in the absence of clinically significant liver disease, chronic HCV infection causes a substantial reduction in quality of life 3 that improves following successful antiviral treatment. 4 These findings are in agreement with the clinical observation that patients with chronic HCV infection frequently report fatigue, lassitude, depression, and a perceived inability to function effectively. 5,6 The etiology of these symptoms is unknown. The symptoms do not appear to be associated with the degree of hepatitis, the presence of autoimmune disorders 5 or cirrhosis, 3 a history of intravenous drug usage (IVDU), 3 or the level of circulating cytokines. 7 We have previously reported cerebral metabolite abnormalities in patients with histologically proven mild HCV infection using proton magnetic resonance spectroscopy ( 1 H MRS). 8 These abnormalities are similar to the 1 H MRS changes reported in cerebral human immunodeficiency virus (HIV) infection in both cognitively impaired 9,10 and asymptomatic individuals. 11 In this study, we address the hypothesis that HCV infection can result in cerebral dysfunction, which may underlie both the neuropsychological symptoms and the 1 H MRS abnormalities described. We used a cognitive assessment battery to determine whether cognitive impairment exists in patients with histologically defined mild chronic HCV infection and 1 H MRS to determine whether cerebral metabolite abnormalities are associated with impaired cognitive function.

Diffuse white matter abnormalities and post-hemorrhagic ventricular dilation are common at term and seem to correlate with reduced developmental quotients. Early lesions, except for cerebellar hemorrhage and major destructive lesions, do not show clear relationships with outcomes.

BackgroundWe postulated that during ontogenesis cortical surface area and cerebral volume are related by a scaling law whose exponent gives a quantitative measure of cortical development. We used this approach to investigate the hypothesis that premature termination of the intrauterine environment by preterm birth reduces cortical development in a dose-dependent manner, providing a neural substrate for functional impairment.Methods and FindingsWe analyzed 274 magnetic resonance images that recorded brain growth from 23 to 48 wk of gestation in 113 extremely preterm infants born at 22 to 29 wk of gestation, 63 of whom underwent neurodevelopmental assessment at a median age of 2 y. Cortical surface area was related to cerebral volume by a scaling law with an exponent of 1.29 (95% confidence interval, 1.25–1.33), which was proportional to later neurodevelopmental impairment. Increasing prematurity and male gender were associated with a lower scaling exponent (p < 0.0001) independent of intrauterine or postnatal somatic growth.ConclusionsHuman brain growth obeys an allometric scaling relation that is disrupted by preterm birth in a dose-dependent, sexually dimorphic fashion that directly parallels the incidence of neurodevelopmental impairments in preterm infants. This result focuses attention on brain growth and cortical development during the weeks following preterm delivery as a neural substrate for neurodevelopmental impairment after premature delivery.

Interest in muscle MRI has been largely stimulated in the last few years by the recognition of an increasing number of genetic defects in the field of inherited neuromuscular disorders. Muscle ultrasound (US) and computed tomography (CT) have been used to detect the presence of muscle involvement in patients affected by these disorders, but until recently the use of muscle MRI has been, with a few exceptions, limited to detecting inflammatory forms. The aim of this review is to illustrate how muscle MRI, in combination with clinical evaluation, can contribute to the selection of appropriate genetic tests and more generally in the differential diagnosis of genetically distinct forms of neuromuscular disorders. Possible future applications of muscle MRI are also discussed.

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This study provides objective evidence that DEHSI represents diffuse white matter abnormality.

Thalamocortical connections are: essential for brain function, established early in development, and significantly impaired following preterm birth. Impaired cognitive abilities in preterm infants may be related to disruptions in thalamocortical connectivity. The aim of this study was to test the hypothesis: thalamocortical connectivity in the preterm brain at term-equivalent is correlated with cognitive performance in early childhood. We examined 57 infants who were born <35 weeks gestational age (GA) and had no evidence of focal abnormality on magnetic resonance imaging (MRI). Infants underwent diffusion MRI at term and cognitive performance at 2 years was assessed using the Bayley III scales of Infant and Toddler development. Cognitive scores at 2 years were correlated with structural connectivity between the thalamus and extensive cortical regions at term. Mean thalamocortical connectivity across the whole cortex explained 11% of the variance in cognitive scores at 2 years. The inclusion of GA at birth and parental socioeconomic group in the model explained 30% of the variance in subsequent cognitive performance. Identifying impairments in thalamocortical connectivity as early as term equivalent can help identify those infants at risk of subsequent cognitive delay and may be useful to assess efficacy of potential treatments at an early age.