MR-trackable intramyocardial injection catheter

There is growing interest in delivering cellular agents to infarcted myocardium to prevent postinfarction left ventricular remodeling. MRI can be effectively used to differentiate infarcted from healthy myocardium. MR-guided delivery of cellular agents/therapeutics is appealing because the therapeutics can be precisely targeted to the desired location within the infarct. In this study, a steerable intramyocardial injection catheter that can be actively tracked under MRI was developed and tested. The components of the catheter were arranged to form a loopless RF antenna receiver coil that enabled active tracking. Feasibility studies were performed in canine and porcine myocardial infarction models. Myocardial delayed-enhancement (MDE) imaging identified the infarcted myocardium, and real-time MRI was used to guide left ventricular catheterization from a carotid artery approach. The distal 35 cm of the catheter was seen under MRI with a bright signal at the distal tip of the catheter. The catheter was steered into position, the distal tip was apposed against the infarct, the needle was advanced, and a bolus of MR contrast agent and tissue marker dye was injected intramyocardially, as confirmed by imaging and post-mortem histology. A pilot study involving intramyocardial delivery of magnetically labeled stem cells demonstrated the utility of the active injection catheter system. © 2004 Wiley-Liss, Inc

Brain MRI Findings in Pediatric-Onset Neuromyelitis Optica Spectrum Disorder

BACKGROUND AND PURPOSE: Differentiating pediatric-onset neuromyelitis optica spectrum disorder from acute disseminated encephalomyelitis could be challenging, especially in cases presenting with only brain manifestations. Our purpose was to investigate brain MR imaging features that may help distinguish these 2 entities. MATERIALS AND METHODS: We retrospectively examined initial brain MR imaging studies of 10 patients with pediatric-onset neuromyelitis optica spectrum disorder (female/male ratio, 7:3) and 10 patients with acute disseminated encephalomyelitis (female/male ratio, 2:8). The mean age of the patients was 10.3 ± 5.6 and 8.7 ± 5.3 years, respectively. Brain lesions were evaluated with respect to location, extent, expansion, T1 hypointensity, contrast enhancement/pattern, and diffusion characteristics. The χ2 test (Yates or Fisher exact χ2tests) was used to compare differences between groups. RESULTS: Cerebral subcortical ± juxtacortical and pons ± middle cerebellar peduncle were the most frequent locations involved in both neuromyelitis optica spectrum disorder (n = 5 and 4, respectively) and acute disseminated encephalomyelitis (n = 9 and 7, respectively). Thalamic lesions were more frequent in acute disseminated encephalomyelitis (P = .020) and were detected only in 1 patient with neuromyelitis optica spectrum disorder. None of the patients with neuromyelitis optica spectrum disorder had hypothalamic, internal capsule, or cortical lesions. The internal capsule involvement was found to be significantly different between groups (P = .033). There was no significant difference in terms of extent, expansion, T1 hypointensity, contrast enhancement/pattern, and diffusion characteristics. CONCLUSIONS: Although there is a considerable overlap in brain MR imaging findings, thalamic and internal capsule involvement could be used to differentiate pediatric-onset neuromyelitis optica spectrum disorder from acute disseminated encephalomyelitis.PubMedWo

Mri Predictors Of Recurrence And Outcome After Acute Transverse Myelitis Of Unidentified Etiology

BACKGROUND AND PURPOSE: The early prediction of recurrence after an initial event of transverse myelitis helps to guide preventive treatment and optimize outcomes. Our aim was to identify MR imaging findings predictive of relapse and poor outcome in patients with acute transverse myelitis of unidentified etiology. MATERIALS AND METHODS: Spinal MRIs of 77 patients (mean age, 36.3 +/- 20 years) diagnosed with acute transverse myelitis were evaluated retrospectively. Only the patients for whom an underlying cause of myelitis could not be identified within 3 months of symptom onset were included. Initial spinal MR images of patients were examined in terms of lesion extent, location and distribution, brain stem extension, cord expansion, T1 signal, contrast enhancement, and the presence of bright spotty lesions and the owl's eyes sign. The relapse rates and Kurtzke Expanded Disability Status Scale scores at least 1 year (range, 1-14 years) after a myelitis attack were also recorded. Associations of MR imaging findings with clinical variables were studied with univariate associations and binary log-linear regression. Differences were considered significant for P values < .05. RESULTS: Twenty-seven patients (35.1%) eventually developed recurrent disease. Binary logistic regression revealed 3 main significant predictors of recurrence: cord expansion (OR, 5.30; 95% CI, 1.33-21.11), contrast enhancement (OR, 5.05; 95% CI, 1.25-20.34), and bright spotty lesions (OR, 3.63; 95% CI, 1.06-12.43). None of the imaging variables showed significant correlation with the disability scores. CONCLUSIONS: Cord expansion, contrast enhancement, and the presence of bright spotty lesions could be used as early MR imaging predictors of relapse in patients with acute transverse myelitis of unidentified etiology. Collaborative studies with a larger number of patients are required to validate these findings.WoSScopu

Spinal cord involvement in multiple sclerosis and neuromyelitis optica spectrum disorders

Spinal cord involvement is an important cause of disability in patients with multiple sclerosis or neuromyelitis optica spectrum disorders (NMOSDs). Multiple sclerosis and NMOSDs can be distinguished from other disorders that cause myelopathy by results from laboratory and radiological investigations. However, limitations in the sensitivity and specificity of spinal cord imaging and poor correlation with disability megasures have impeded the understanding of the relationship between spinal cord involvement and clinical manifestations. Nevertheless, studies of the pathological features of multiple sclerosis and NMOSDs have shown that quantitatively different mechanisms lead to differences in clinical course and pattern of accrual of permanent disability in the two dis-orders. Better understanding of these mechanisms is necessary to develop more informative clinical measures, electrophysiological methods, fluid biomarkers, and imaging techniques to detect and monitor spinal cord involvement in the diagnosis and management of patients with multiple sclerosis or NMOSDs, and as outcome measures in clinical trials