The aim of our study was to visualize developing vessel occlusion in focal cerebral ischemia in vivo. Cortical photothrombosis (PT) was induced in rats, which in addition received superparamagnetic iron oxide (SPIO) particles intravenously. When SPIO particles were applied simultaneously during illumination of the brain for induction of PT, animals showed a markedly hypointense cortical lesion on T2-weighted (T2-w) magnetic-resonance images (MRI). At 3 h after PT, this hypointense area was surrounded by a small hyperintense rim. At 48 h after PT the hyperintense rim had further extended, whereas the hypointense lesion core did not change in size or signal. On histological sections areas of signal loss on T2-w MRI corresponded to local accumulation of iron particles, which were trapped within vessel thrombi. When SPIO particles were applied at 2 h after PT, the lesion appeared hyperintense on T2-w MRI, but was surrounded by a small hypointense rim indicating ongoing vessel occlusion at its outer margins. In contrast, delayed SPIO application at 24 h after completion of PT produced a merely hyperintense cortical lesion on T2-w MRI. Correspondingly, no iron deposits were seen on tissue sections. In conclusion, early SPIO-enhanced MRI provides a reliable in vivo tool to delineate areas of developing vessel occlusion in experimental cerebral ischemia and identifies vessel thrombosis as one mechanism of secondary infarct growth in the PT paradigm. This new imaging technique may aid to evaluate antithrombotic treatment strategies in the future.
Nerve injury represents a major cause of disability. In the peripheral nervous system, nerves have the capacity to regrow but within weeks after injury, it is impossible to clarify whether proper regeneration is under way or is failing. In this experimental study, we report on a novel tool to assess nerve outgrowth in vivo. After systemic application, the novel gadolinium-based magnetic resonance (MR) contrast agent Gadofluorine M (Gf) selectively accumulated and persisted in nerve fibers undergoing Wallerian degeneration causing bright contrast on T1-weighted MR images. Gf enhancement on MR imaging was present already at 48 hours within the entire nerve segments undergoing Wallerian degeneration, and subsequently disappeared from proximal to distal parts in parallel to regrowth of nerve fibers. Most importantly, Gf enhancement persisted in nonregenerating, permanently transected nerves. Our novel Gf-based MR imaging methodology holds promise for clinical use to bridge the diagnostic gap between nerve injury and completed nerve regeneration, and to determine the necessity for neurolysis and engraftment if spontaneous regeneration is not successful.
Prediction of endoleaks with absolute certainty remains elusive. The single correlating risk factor identified from the data was patency of four or more lumbar arteries visualized preoperatively at CT.
Coil fracture represents a serious device-related complication during coil embolisation of intracranial aneurysms. If the coil cannot be retrieved completely, the loose end floating in the parent vessel can prolapse into the distal part of the vessel and may cause occlusion and brain infarction. We present a new technique in which the loose end of the fractured coil is fixed with a stent at the proximal parent vessel wall. Herniation of the loose coil end to the distal part of the vessel with potential vessel occlusion is therefore prevented. This procedure was technically feasible in all cases and no clinical complications were encountered. We suggest this new technique as a treatment option in cases of fractured coils.
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