MR arthrography of traumatic anterior shoulder lesions showed modest reproducibility and accuracy when evaluated under clinical circumstances.

INTRODUCTION: We examined the reproducibility and accuracy of high-field MRA in traumatic anterior shoulder instability under conditions resembling clinical practice and assessed the influence of observer experience. MATERIALS AND METHODS: Two radiologists with different experience levels evaluated 61 MRAs. Assessment was independent, blinded and non-sequential. For 40 MRAs, surgical reports were available to assess diagnosis accuracy and influence of observer experience. The assessed lesions were cuff lesions, Hill-Sachs lesions, bony and classic Bankart lesions, greater humeral tuberosity fractures, SLAP lesions and joint capsule lesions. Reproducibility was quantified using kappa coefficients. Accuracy was evaluated with sensitivity and specificity rates, positive and negative predictive values. Differences in the percentage of correctly diagnosed MRAs between the radiologists were tested using McNemar's test for paired proportions. RESULTS: Inter-observer k-values ranged from 0.03 for joint capsule lesions to 0.45 for humeral head lesions. The overall kappa was 0.21 (95% CI; 0.12-0.30). We also observed markedly lower sensitivity and specificity rates than those reported in the literature for most lesions. The more experienced radiologist correctly diagnosed 78.9% of all lesions compared to 65.4% for the less experienced radiologist (P < 0.001; McNemar's test). CONCLUSION: MRA-interpretations of traumatic anterior shoulder instability should be regarded with caution in clinical practice. The experience level of radiologists can affect reproducibility and accuracy.

Differentiation between portal-systemic encephalopathy and neurodegenerative disorders in patients with Wilson disease: H-1 MR spectroscopy.

PURPOSE: To investigate the extent to which neurodegeneration and metabolic changes caused by portosystemic shunting occur in Wilson disease. MATERIALS AND METHODS: Twenty-two adult patients with biochemically proved Wilson disease underwent magnetic resonance (MR) imaging, hydrogen-1 MR spectroscopy, neurologic and psychometric testing, and ultrasound evaluation of the liver. In addition, 13 age-matched adult control subjects underwent MR imaging and H-1 MR spectroscopy. For MR spectroscopy, the authors used a single-voxel technique with a repetition time of 2,000 msec and an echo time of 31 msec. The volume of interest included the right and left globi pallidus, which are the most common sites of lesions in Wilson disease. RESULTS: N-acetylaspartate-creatine and choline-creatine ratios were decreased in patients with Wilson disease versus control subjects (P < .001 for N-acetylaspartate-creatine ratio, P < .05 for choline-creatine ratio). Also, patients with Wilson disease and portosystemic shunting had lower myo-inositol-creatine ratios than did patients with Wilson disease and no portosystemic shunting (P < .05). CONCLUSION: Reductions in N-acetylaspartate indicate neuronal loss consistent with the neurodegenerative pattern associated with Wilson disease. In addition, H-1 MR spectroscopy shows metabolic abnormality in the brain, as decreased myoinositol, caused by portosystemic shunting.

Wilson disease: findings at MR imaging and CT of the brain with clinical correlation.

PURPOSE: To describe the spectrum of brain abnormalities in Wilson disease (hepatolenticular degeneration) as depicted at magnetic resonance (MR) imaging and computed tomography (CT) and to relate these findings to neurologic and hepatologic abnormalities. MATERIALS AND METHODS: Fifty patients with Wilson disease participated in the cross-sectional study: Patients underwent cerebral MR imaging (n = 49), CT (n = 44), abdominal duplex ultrasound (US) (n = 46), and neurologic examination (n = 50) within a week. Relative risk and the Fisher exact test were used for statistical analysis. RESULTS: Supratentorial and infratentorial abnormalities in the gray and white matter were found in the pyramidal and extrapyramidal system. In Wilson disease, an abnormal striatum depicted on MR images correlated with pseudoparkinsonian signs, an abnormal dentatothalamic tract correlated with cerebellar signs, and an abnormal pontocerebellar tract correlated with pseudoparkinsonian signs. The presence of portosystemic shunt was strongly associated with abnormality of the globus pallidus. CONCLUSION: MR imaging findings were of some use in the clinical treatment of patients with Wilson disease.

Cranial MR in Wilson disease: abnormal white matter in extrapyramidal and pyramidal tracts.

PURPOSE: To describe abnormal white matter in the brain on MR in Wilson disease and to compare with anatomic location of white matter tracts. METHODS: Forty-six patients with Wilson disease were examined. Axial T1-weighted inversion-recovery, axial T2-weighted spin-echo, and coronal T2*-weighted gradient-echo MR images were performed. Imaging studies were compared with clinical data. RESULTS: Seventeen patients showed abnormalities in the region coinciding with the following white matter tracts: corticospinal tract (24%, n = 11), dentatorubrothalamic tract (24%, n = 11), and pontocerebellar tract (17%, n = 8). CONCLUSION: Abnormal extrapyramidal and pyramidal white matter tracts are part of the neuroimaging spectrum of Wilson disease. No significant correlation was found with neurologic groups and individual white matter tracts affected.

31P magnetic resonance spectroscopy of the liver: correlation with standardized serum, clinical, and histological changes in diffuse liver disease.

The goal of this study was to analyze the possibilities of 31P MR spectroscopy to detect abnormal hepatic histological changes in patients with diffuse liver disease. 31P MR spectroscopy was performed, on a 1.5 T whole-body spectrometer using an image guided localization technique (ISIS), on 38 patients with various diffuse liver diseases, who all underwent histological and serum analysis, and 22 healthy volunteers. Phosphomonoester expressed as a fraction of total phosphorus (PME/P) showed a correlation with abnormal serum aspartate transaminase (AST), histological intralobular degeneration/focal necrosis, portal inflammation, and piecemeal necrosis. We found a lower correlation for PME/P with fibrosis. It was not possible to differentiate between fibrosis and cirrhosis. In summary, 31P MR spectroscopy is a technique to detect intralobular degeneration, inflammation and necrosis and to a less extent fibrosis. No diagnostic value was found with respect to steatosis and cholangitis. Furthermore, 31P MR spectroscopy is a poor method for classifying patients into diagnostic categories.