'Moderate global aphasia': A generalized decline of language processing caused by glioma surgery but not stroke.

Unlike stroke, neurosurgical removal of left-hemisphere gliomas acts upon a reorganized language network and involves brain areas rarely damaged by stroke. We addressed whether this causes the profiles of neurosurgery- and stroke-induced language impairments to be distinct. K-means clustering of language assessment data (neurosurgery cohort: N = 88, stroke cohort: N = 95) identified similar profiles in both cohorts. But critically, a cluster of individuals with specific phonological deficits was only evident in the stroke but not in the neurosurgery cohort. Thus, phonological deficits are less clearly distinguished from other language deficits after glioma surgery compared to stroke. Furthermore, the correlations between language production and comprehension scores at different linguistic levels were more extensive in the neurosurgery than in the stroke cohort. Our findings suggest that neurosurgery-induced language impairments do not correspond to those caused by stroke, but rather manifest as a 'moderate global aphasia' - a generalized decline of language processing abilities.

Serum albumin, total bilirubin, and patient age are independent confounders of hepatobiliary-phase gadoxetate parenchymal liver enhancement.

PURPOSE: To identify independent confounding variables of gadoxetate-enhanced hepatobiliary-phase liver MRI using multiple regression analysis. MATERIALS AND METHODS: The institutional review board generally approved retrospective analyses and all patients provided written informed consent. One hundred ten patients who underwent a standardized 3.0-T gadoxetate-enhanced liver MRI between November 2008 and June 2013 were retrospectively reviewed. The gadoxetate liver enhancement normalized to enhancement in the erector spinae muscle (relative signal enhancement, SE) was related to biochemical laboratory parameters and descriptive patient characteristics (patient age, body mass index) using non-parametric univariate correlation analysis followed by a multiple linear regression model. RESULTS: Using univariate statistics, relative SE was inversely correlated with patient age, ALP, AST, total bilirubin, gamma-glutamyltransferase, INR, model of end-stage liver disease score, and proportionally with albumin and hemoglobin (all p < 0.01). In a multiple regression analysis, total bilirubin (p = 0.001), serum albumin (p = 0.016), and patient age (p = 0.018) were independently correlated with relative liver SE (n = 110). CONCLUSION: A multiple regression analysis showed that high total bilirubin, low serum albumin, or advanced age was associated with low hepatobiliary-phase gadoxetate parenchymal liver enhancement. In these patients, the lower contrast-to-noise ratio might impair diagnostic evaluation of non-enhancing liver lesions (e.g., HCC, liver metastasis). KEY POINTS: • A multiple regression analysis identified independent confounding variables of hepatobiliary-phase gadoxetate liver enhancement. • High bilirubin, low albumin, or advanced age was associated with low enhancement. • Diagnostic evaluation might be hampered in these patients.

Age dependence of spleen- and muscle-corrected hepatic signal enhancement on hepatobiliary phase gadoxetate MRI.

OBJECTIVES: To identify correlations of signal enhancements (SE) and SE normalized to reference tissues of the spleen, kidney, liver, musculus erector spinae (MES) and ductus hepatocholedochus (DHC) on hepatobiliary phase gadoxetate-enhanced MRI with patient age in non-cirrhotic patients. METHODS: A heterogeneous cohort of 131 patients with different clinical backgrounds underwent a standardized 3.0-T gadoxetate-enhanced liver MRI between November 2008 and June 2013. After exclusion of cirrhotic patients, a cohort of 75 patients with no diagnosed diffuse liver disease was selected. The ratio of signal intensity 20 min post- to pre-contrast administration (SE) in the spleen, kidney, liver, MES and DHC, and the SE of the kidney, liver and DHC normalized to the reference tissues spleen or MES were compared to patient age. RESULTS: Patient age was inversely correlated with the liver SE normalized to the spleen and MES SE (both p < 0.001) and proportionally with the SE of the spleen (p = 0.043), the MES (p = 0.030) and the kidney (p = 0.022). No significant correlations were observed for the DHC (p = 0.347) and liver SE (p = 0.606). CONCLUSION: The age dependence of hepatic SE normalized to the enhancement in the spleen and MES calls for a cautious interpretation of these quantification methods. KEY POINTS: • Patient age was inversely correlated with spleen- and MES-corrected liver rSE (p < 0.001). • Patient age was correlated with spleen (p = 0.043) and MES SE (p = 0.030). • Patient age may confound quantitative liver function assessment using gadoxetate-enhanced liver MRI.

Magnetic resonance imaging identifies early effects of sunitinib treatment in human melanoma xenografts.

BACKGROUND: Antiangiogenic treatment may change the tumor microenvironment and hence influence the effect of conventional therapies. The potential of diffusion weighted magnetic resonance imaging (DW-MRI) and dynamic contrast enhanced MRI (DCE-MRI) in assessing microenvironmental effects of sunitinib treatment was investigated in this preclinical study. METHODS: Sunitinib-treated and untreated A-07 tumors were subjected to DW-MRI and DCE-MRI, and parametric images of ADC and Ktrans were produced. Microvascular density, hypoxic fraction, and necrotic fraction were assessed from immunohistochemical preparations, and tumor interstitial fluid pressure (IFP) was assessed with probe measurement. RESULTS: Sunitinib-treated tumors showed reduced microvascular density, increased hypoxic fraction, increased necrotic fraction, increased ADC, and reduced Ktrans, but did not differ from untreated tumors in growth rate and IFP. CONCLUSIONS: Sunitinib treatment affected the tumor microenvironment without affecting tumor size. DW-MRI and DCE-MRI were sensitive to the sunitinib-induced changes in the tumor microenvironment.