Bildgebende Diagnostik von Nervenkompressionssyndromen

Zusammenfassung: Kompressionsbedingte Schädigungen peripherer Nerven können die Ursache hartnäckiger Schmerzen im Bereich des Sprunggelenks und Fußes sein. Eine frühzeitige Diagnose ist entscheidend, um den Patienten der richtigen Therapie zuzuführen und potenzielle Schädigungen zu vermeiden oder zu verringern. Obschon die klinische Untersuchung und die elektrophysiologische Abklärungen die wichtigsten Elemente der Diagnostik peripherer Nervenkompressionssyndrome sind, kann die Bildgebung entscheidend sein, wenn es darum geht, die Höhe des Nervenschadens festzulegen oder die Differenzialdiagnose einzugrenzen. In gewissen Fällen kann durch Bildgebung sogar die Ursache der Nervenkompression gefunden werden. In anderen Fällen ist die Bildgebung wichtig bei der Therapieplanung, insbesondere dann, wenn die Läsion chirurgisch angegangen wird. Magnetresonanztomographie (MRT) und Sonographie ermöglichen eine direkte Visualisierung der Nerven und ihrer umgebenden Strukturen. Knöcherne Läsionen, die zu einem Nervenkompressionssyndrom führen können, werden am besten mittels konventionellem Röntgenbild und/oder Computertomographie (CT) dargestellt. Die Kenntnis der anatomischen Gegebenheiten, Ursachen und klinischen Befunde sowie der Bildbefunde ist für die richtige Diagnose entscheiden

Bildgebende Diagnostik von Nervenkompressionssyndromen

Kompressionsbedingte Schädigungen peripherer Nerven können die Ursache hartnäckiger Schmerzen im Bereich des Sprunggelenks und Fußes sein. Eine frühzeitige Diagnose ist entscheidend, um den Patienten der richtigen Therapie zuzuführen und potenzielle Schädigungen zu vermeiden oder zu verringern. Obschon die klinische Untersuchung und die elektrophysiologische Abklärungen die wichtigsten Elemente der Diagnostik peripherer Nervenkompressionssyndrome sind, kann die Bildgebung entscheidend sein, wenn es darum geht, die Höhe des Nervenschadens festzulegen oder die Differenzialdiagnose einzugrenzen. In gewissen Fällen kann durch Bildgebung sogar die Ursache der Nervenkompression gefunden werden. In anderen Fällen ist die Bildgebung wichtig bei der Therapieplanung, insbesondere dann, wenn die Läsion chirurgisch angegangen wird. Magnetresonanztomographie (MRT) und Sonographie ermöglichen eine direkte Visualisierung der Nerven und ihrer umgebenden Strukturen. Knöcherne Läsionen, die zu einem Nervenkompressionssyndrom führen können, werden am besten mittels konventionellem Röntgenbild und/oder Computertomographie (CT) dargestellt. Die Kenntnis der anatomischen Gegebenheiten, Ursachen und klinischen Befunde sowie der Bildbefunde ist für die richtige Diagnose entscheiden

USPIO-enhanced magnetic resonance imaging of the knee in asymptomatic volunteers

The aim of this study was to compare signal characteristics of the synovium in knees of asymptomatic volunteers before and after intravenous administration of ultrasmall superparamagnetic iron oxide particles (USPIO). Ten knees of 10 asymptomatic volunteers were examined before and 36h after intravenous administration of USPIO on a 1.5-T MR system using T1-weighted spin-echo, T2-weighted fast spin-echo, T2*-weighted gradient-echo (GRE), and short inversion time inversion-recovery sequences. In addition, synovial perfusion was measured using Gd-enhanced GRE imaging during the first imaging session. Images were analyzed qualitatively for any visual changes before and after USPIO administration. Signal-to-noise ratios (SNR) of the synovium were determined on unenhanced and USPIO-enhanced sequences. All MR images were reviewed for presence of any degenerative changes. Qualitative image analysis revealed no visually detectable changes of any knee joint before and after USPIO administration. The SNR values of the synovium on T1w, T2w, and T2*w images before and after USPIO administration showed no significant difference (T1, P = 0.86; T2, P = 0.95; T2*, P = 0.86). None of the volunteers showed any relevant degenerative changes of the knee and synovial perfusion was within normal limits. In knees of asymptomatic volunteers without any relevant degenerative changes and normal synovial perfusion neither visual changes nor changes of SNR values of the synovium can be depicted after USPIO administration. This means that USPIO-enhanced MRI may be used for assessment of knee disorders with increased macrophage activit

The contested and contingent outcomes of Thatcherism in the UK

The death of Margaret Thatcher in April 2013 sparked a range of discussions and debates about the significance of her period in office and the political project to which she gave her name: Thatcherism. This article argues that Thatcherism is best understood as a symbolically important part of the emergence of first-phase neoliberalism. It engages with contemporary debates about Thatcherism among Marxist commentators and suggests that several apparently divergent positions can help us now reach a more useful analysis of Thatcherism’s short- and long-term outcomes for British political economy. The outcomes identified include: an initial crisis in the neoliberal project in the UK; the transformation of the party political system to be reflective of the politics of neoliberalism, rather than its contestation; long-term attempts at the inculcation of the neoliberal individual; de-industrialisation and financial sector dependence; and a fractured and partially unconscious working class. In all long-term outcomes, the contribution of Thatcherism is best understood as partial and largely negative, in that it cleared the way for a longer-term and more constructive attempt to embed neoliberal political economy. The paper concludes by suggesting that this analysis can inform current debates on the left of British politics about how to oppose and challenge the imposition of neoliberal discipline today

Sirolimus and kidney growth in autosomal dominant polycystic kidney disease

BACKGROUND: In autosomal dominant polycystic kidney disease (ADPKD), aberrant activation of the mammalian target of rapamycin (mTOR) pathway is associated with progressive kidney enlargement. The drug sirolimus suppresses mTOR signaling. METHODS: In this 18-month, open-label, randomized, controlled trial, we sought to determine whether sirolimus halts the growth in kidney volume among patients with ADPKD. We randomly assigned 100 patients between the ages of 18 and 40 years to receive either sirolimus (target dose, 2 mg daily) or standard care. All patients had an estimated creatinine clearance of at least 70 ml per minute. Serial magnetic resonance imaging was performed to measure the volume of polycystic kidneys. The primary outcome was total kidney volume at 18 months on blinded assessment. Secondary outcomes were the glomerular filtration rate and urinary albumin excretion rate at 18 months. RESULTS: At randomization, the median total kidney volume was 907 cm(3) (interquartile range, 577 to 1330) in the sirolimus group and 1003 cm(3) (interquartile range, 574 to 1422) in the control group. The median increase over the 18-month period was 99 cm(3) (interquartile range, 43 to 173) in the sirolimus group and 97 cm(3) (interquartile range, 37 to 181) in the control group. At 18 months, the median total kidney volume in the sirolimus group was 102% of that in the control group (95% confidence interval, 99 to 105; P=0.26). The glomerular filtration rate did not differ significantly between the two groups; however, the urinary albumin excretion rate was higher in the sirolimus group. CONCLUSIONS: In adults with ADPKD and early chronic kidney disease, 18 months of treatment with sirolimus did not halt polycystic kidney growth. (ClinicalTrials.gov number, NCT00346918.

Safety and tolerability of sirolimus treatment in patients with autosomal dominant polycystic kidney disease

Background. We initiated a randomized controlled clinical trial to assess the effect of sirolimus on disease progression in patients affected by autosomal dominant polycystic kidney disease (ADPKD). Here we report the preliminary safety results of the first 6 months of treatment. Method. A total of 25 patients were randomized to sirolimus 2 mg/day and 25 patients to no treatment except standard care. Treatment adherence was monitored electronically. At baseline and at Month 6, laboratory parameters were analysed and the urinary protein profile in 24-h urine collections was determined. Results. Both treatment groups were well balanced for age, sex and renal function. In 94.1 ± 11.4% of the study days, patients in the sirolimus group were exposed to the drug when assuming a therapeutic efficacy duration of 30 h. At Month 6, the mean sirolimus dose and trough level were 1.28 ± 0.71 mg/day and 3.8 ± 1.9 μg/l, respectively. Glomerular (albumin, transferrin, IgG) and tubular (retinol-binding protein, α1-microglobulin) protein excretion remained unchanged. Glomerular filtration rate also did not change significantly. Haematological parameters were similar in both groups, except for a mild reduction of the mean corpuscular volume of erythrocytes in patients receiving sirolimus. Lipid levels were similar in both groups. Adverse events were transient and mild, and no grade 3 or 4 events occurred. The incidence of infections was similar in the sirolimus group (80%) and the standard group (88%). The most common gastrointestinal adverse events were mucositis (72% in the sirolimus group versus 16% in the standard group, P = 0.0001) and diarrhoea (36% in the sirolimus versus 20% in the standard group, P = 0.345). Conclusion. Treatment of ADPKD patients with sirolimus with a dose of 1-2 mg/day is safe and does not cause proteinuria or impairment of GFR. Treatment adherence was excellent. (ClinicalTrials.gov number, NCT00346918.