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Thirty-four joints (19 knees, 15 wrists) of 31 patients suffering from rheumatoid arthritis and related disorders were examined prior to and following intravenous administration of Gadolinium-DTPA (0.1 mmol/kg body weight). T1-weighted spin-echo sequences and the gradient-echo technique FLASH were applied. FLASH scanning was used for the registration of the time-dependent changes of signal intensity following Gd-DTPA. Synovial proliferations exhibited a rapid and marked increase of signal intensity whereas fatty tissue, bone marrow, muscle and synovial effusion demonstrated only minor changes, causing enhanced contrast between synovial pannus and joint effusion or other neighbouring structures. Within the synovial pannus, ratios (absolute signal increase) of 131.3 +/- 53.4% and 122.9 +/- 51.1% were found in T1-weighted spin-echo and in FLASH sequences respectively. The average signal increase gradient of pannus (108.2 +/- 70.6%/min) was significantly (p less than 0.001) different from muscle (13.4 +/- 7.8%/min), fatty tissue (10.2 +/- 8.4%/min), bone marrow (5.5 +/- 7.1%/min), and joint effusion (14.7 +/- 7.8%/min).

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In all three patients, more than 100 liver adenomas revealed no metabolism of the new liver-specific contrast agent in the delayed phase. Because of absent or strongly reduced intracellular uptake of gadoxetic acid in all adenomas during delayed contrast-enhanced series, differentiation of adenomas from dysplastic or malignant lesions was not possible.

Blood-oxygenation-level-dependent (BOLD) contrast in magnetic resonance (MR) imaging of skeletal muscle mainly depends on changes of oxygen saturation in the microcirculation. In recent years, an increasing number of studies have evaluated the clinical relevance of skeletal muscle BOLD MR imaging in vascular diseases, such as peripheral arterial occlusive disease, diabetes mellitus, and chronic compartment syndrome. BOLD imaging combines the advantages of MR imaging, i.e., high spatial resolution, no exposure to ionizing radiation, with functional information of local microvascular perfusion. Due to intrinsic contrast provoked via changes in hemoglobin oxygen saturation, it is a safe and easy applicable procedure on standard whole-body MR devices. Therefore, BOLD MR imaging of skeletal muscle is a potential new diagnostic tool in the clinical evaluation of vascular, inflammatory, and muscular pathologies. Our review focuses on the current evidence concerning the use of BOLD MR imaging of skeletal muscle under pathological conditions and highlights ways for future clinical and scientific applications.

To date there are potential chronology-based but not conclusive reasons to believe that at least some of the gadolinium complexes play a causative role in the pathophysiology of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). Still, the exact pathogenesis and the risk for patients is unclear beside the obvious connection to moderate to severe renal insufficiency. So far, MR imaging with Gd-enhancement was regarded as the safest imaging modality in these patients-the recent development creates tremendous uncertainty in the MR-community. Nevertheless, one should remember that, despite the over 200 cases of NSF and about 100 with proven involvement of Gd 3+ , the vast majority of over 200 million patients exposed to gadolinium since the 1980s have tolerated these agents well. Importantly, NSF is a rare disease and does not appear to occur in patients without renal impairment. Many patients and researchers have undergone MR investigations with Gd exposure in the past. For those, it is essential to know about the safety of the agents at normal renal function. We can hope that pharmacoepidemiological and preclinical studies will allow us to better understand the pathophysiology and role of the various MR contrast agents in the near future.

Three-dimensional MR tomography was used to examine the relationship between symptoms of trigeminal neuralgia and neurovascular compression of the nerve in 18 patients. The intensity of neurovascular interaction was classified according to neuroradiological criteria. We found that a radiologically defined compression or dislocation of the nerve by an artery was always associated with symptoms of trigeminal neuralgia. A simple contact between vessel and nerve, however, was also observed on the asymptomatic sides of 10 out of 18 patients. In 6 of 18 patients, in contrast, trigeminal neuralgia was present in spite of the absence of neurovascular contact. In accordance with a cited study based on autopsy and intraoperative findings, our findings indicate that, in a certain proportion of cases, trigeminal neuralgia may be caused by neurovascular compression alone, whereas in other cases, other pathogenetic factors may be involved to a varying degree or be even exclusively responsible for the development of trigeminal neuralgia. The possible significance of the method for a preoperative estimation of the success of microvascular decompression of the trigeminal nerve is discussed.