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  • 1
    In: Neurology, 2017, Vol.89(5), pp.475-484
    Description: OBJECTIVE:: To detect and quantify lesions of the small-caliber sural nerve (SN) in symptomatic and asymptomatic transthyretin familial amyloid polyneuropathy (TTR-FAP) by high-resolution magnetic resonance neurography (MRN) in correlation with electrophysiologic and histopathologic findings. METHODS:: Twenty-five patients with TTR-FAP, 10 asymptomatic carriers of the mutated transthyretin gene (mutTTR), and 35 age- and sex-matched healthy controls were prospectively included in this cross-sectional case-control study. All participants underwent 3T MRN with high-structural resolution (fat-saturated, T2-weighted, and double-echo sequences). Total imaging time was ≈45 minutes per patient. Manual SN segmentation was performed from its origin at the sciatic nerve bifurcation to the lower leg with subsequent evaluation of quantitative microstructural and morphometric parameters. Additional time needed for postprocessing was ≈1.5 hours per participant. Detailed neurologic and electrophysiologic examinations were conducted in the TTR group. RESULTS:: T2 signal and proton spin density (ρ) reliably differentiated between TTR-FAP (198.0 ± 13.3, 429.6 ± 15.25), mutTTR carriers (137.0 ± 16.9, p = 0.0009; 354.7 ± 21.64, p = 0.0029), and healthy controls (90.0 ± 3.4, 258.2 ± 9.10; p 〈 0.0001). Marked differences between mutTTR carriers and controls were found for T2 signal (p = 0.0065) and ρ (p 〈 0.0001). T2 relaxation time was higher in patients with TTR-FAP only (p = 0.015 vs mutTTR carriers, p = 0.0432 vs controls). SN caliber was higher in patients with TTR-FAP vs controls and in mutTTR carriers vs controls (p 〈 0.0001). Amyloid deposits were histopathologically detectable in 10 of 14 SN specimens. CONCLUSIONS:: SN injury in TTR-FAP is detectable and quantifiable in vivo by MRN even in asymptomatic mutTTR carriers. Differences in SN T2 signal between controls and asymptomatic mutTTR carriers are derived mainly from an increase of ρ, which overcomes typical limitations of established diagnostic methods as a highly sensitive imaging biomarker for early detection of peripheral nerve lesions. CLASSIFICATION OF EVIDENCE:: This study provides Class III evidence that MRN accurately identifies asymptomatic mutTTR carriers.
    Keywords: Adult–Diagnostic Imaging ; Aged–Genetics ; Amyloid Neuropathies, Familial–Pathology ; Case-Control Studies–Genetics ; Cross-Sectional Studies–Diagnostic Imaging ; Disability Evaluation–Injuries ; Early Diagnosis–Pathology ; Female–Pathology ; Heterozygote–Pathology ; Humans–Pathology ; Image Processing, Computer-Assisted–Pathology ; Magnetic Resonance Imaging–Pathology ; Male–Pathology ; Middle Aged–Pathology ; Neural Conduction–Pathology ; Prealbumin–Pathology ; Prodromal Symptoms–Pathology ; Prospective Studies–Pathology ; Sural Nerve–Pathology ; Abridged ; Prealbumin;
    ISSN: 0028-3878
    E-ISSN: 1526632X
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  • 2
    In: Neurology, 2019, Vol.92(24), pp.e2754-e2763
    Description: OBJECTIVE: Imaging necrosis on MRI scans was assessed and compared to outcome measures of the European Organisation for Research and Treatment of Cancer 26101 phase III trial that compared single-agent lomustine with lomustine plus bevacizumab in patients with progressive glioblastoma. METHODS: MRI in this post hoc analysis was available for 359 patients (lomustine = 127, lomustine + bevacizumab = 232). First, imaging necrosis at baseline being formally measurable (〉10 × 10 mm, given 2 slices) was assessed. At weeks 6 and 12 of treatment, it was analyzed whether this necrosis remained stable or increased 〉25% calculated by 2 perpendicular diameters or whether necrosis developed de novo. Univariate and multivariate associations of baseline necrosis with overall survival (OS) and progression-free survival (PFS) were tested by log-rank test. Hazard ratios (HR) with 95% confidence interval were calculated by Cox model. RESULTS: Imaging necrosis at baseline was detected in 191 patients (53.2%) and was associated with worse OS and PFS in univariate, but not in multivariate analysis. Baseline necrosis was predictive for OS in the lomustine-only group (HR 1.46, p = 0.018). At weeks 6 and 12 of treatment, increase of baseline necrosis and de novo necrosis were strongly associated with worse OS and PFS in univariate and multivariate analysis (PFS both p 〈 0.001, OS univariate p 〈 0.001, multivariate p = 0.0046). CONCLUSION: Increase of and new development of imaging necrosis during treatment is a negative prognostic factor for patients with progressive glioblastoma. These data call for consideration of integrating the assessment of imaging necrosis as a separate item into the MRI response assessment criteria.
    ISSN: 0028-3878
    ISSN: 1526632X
    E-ISSN: 1526632X
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