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Anterior Visual Pathway (aVP) damage may be linked to diverse inflammatory, degenerative and/or vascular conditions. Currently however, a standardized methodological framework for extracting MRI biomarkers of the aVP is not available. We used high-resolution, 3-D MRI data to generate a probabilistic anatomical atlas of the normal aVP and its intraorbital (iOrb), intracanalicular (iCan), intracranial (iCran), optic chiasm (OC), and tract (OT) subdivisions. We acquired 0.6 mm 3 steady-state free-precession images from 24 healthy participants using a 3 T scanner. aVP masks were obtained by manual segmentation of each aVP subdivision. Mask straightening and normalization with cross-sectional area (CSA) preservation were obtained using scripts developed in-house. A probabilistic atlas (“aVP-24”) was generated by averaging left and right sides of all subjects. Leave-one-out cross-validation with respect to interindividual variability was performed employing the Dice Similarity Index (DSI). Spatially normalized representations of the aVP subdivisions were generated. Overlapping CSA values before and after normalization demonstrate preservation of the aVP cross-section. Volume, length, CSA, and ellipticity index ( ε ) biometrics were extracted. The aVP-24 morphology followed previous descriptions from the gross anatomy. Atlas spatial validation DSI scores of 0.85 in 50% and 0.77 in 95% of participants indicated good generalizability across the subjects. The proposed MRI standardization framework allows for previously unavailable, geometrically unbiased biometric data of the entire aVP and provides the base for future spatial-resolved, group-level investigations.

Nigrostriatal dopaminergic degeneration in alpha-synucleinopathies is indirectly reflected by low dopamine transporter (DaT) uptake through [123I]FP-CIT-SPECT. Bulk magnetic susceptibility ( ) in the substantia nigra, from MRI-based quantitative susceptibility mapping (QSM), is a potential biomarker of nigrostriatal degeneration, however, QSM cannot disentangle paramagnetic (e.g. iron) and diamagnetic (e.g. myelin) sources. Using the susceptibility source-separation technique DECOMPOSE, paramagnetic component susceptibility (PCS) and diamagnetic component susceptibility (DCS) were studied in prodromal and overt alpha-synucleinopathies, and their relationships with DaT-SPECT specific binding ratio (SBR) and clinical scores. 78 participants were included (23 controls, 30 prodromal and 25 overt alpha-synucleinopathies). Prodromal patients were subdivided into groups with positive or negative DaT-SPECT (SBR Z-scores below or above -1, respectively). Correlations of putamen and caudate SBR Z-scores with PCS and DCS in the substantia nigra, putamen, and caudate were investigated. Increased PCS was observed in the substantia nigra of prodromal alpha-synucleinopathy patients with positive DaT-SPECT compared to controls and prodromal patients with negative DaT-SPECT. SBR Z-scores in the putamen correlated with increased PCS in the substantia nigra and reduced |DCS| in the putamen, which may reflect dopaminergic degeneration ascribable to iron accumulation and nigrostriatal neuron axonal loss, respectively.

Objective This study aims to investigate the association between specific imaging parameters, namely, the Evans index (EI) and ventricular volume (VV), and the variation in gait speed observed in patients with idiopathic normal pressure hydrocephalus (iNPH) before and after cerebrospinal fluid (CSF) removal/lumbar drain (LD). Furthermore, it seeks to identify which imaging parameters are the most reliable predictors for significant improvements in gait speed post procedure. Methods In this retrospective analysis, the study measured the gait speed of 35 patients diagnosed with idiopathic normal pressure hydrocephalus (iNPH) before and after they underwent CSF removal. Before lumbar drain (LD), brain images were segmented to calculate the Evans index and ventricular volume. The study explored the relationship between these imaging parameters (the Evans index and ventricular volume) and the improvement in gait speed following CSF removal. Patients were divided into two categories based on the degree of improvement in gait speed, and we compared the imaging parameters between these groups. Receiver operating characteristic (ROC) curve analysis was employed to determine the optimal imaging parameter thresholds predictive of gait speed enhancement. Finally, the study assessed the predictive accuracy of these thresholds for identifying patients likely to experience improved gait speed post-LD. Results Following CSF removal/lumbar drain, the participants significantly improved in gait speed, as indicated by a paired sample t-test (p-value = 0.0017). A moderate positive correlation was observed between the imaging parameters (EI and VV) and the improvement in gait speed post-LD. Significant differences were detected between the two patient groups regarding EI, VV, and a composite score (statistical test value = 3.1, 2.8, and 2.9, respectively; p-value < 0.01). Receiver operating characteristic (ROC) curve analysis identified the optimal thresholds for the EI and VV to be 0.39 and 110.78 cm³, respectively. The classification based on these thresholds yielded significant associations between patients displaying favorable imaging parameters and those demonstrating improved gait speed post-LD, with chi-square (χ²) values of 8.5 and 7.1, respectively, and p-values < 0.01. Furthermore, these imaging parameter thresholds had a 74% accuracy rate in predicting patients who would improve post-LD. Conclusion The study demonstrates that ventricle volume and the Evans index can significantly predict gait speed improvement after lumbar drain (LD) in patients with iNPH.

Neurodegeneration with brain iron accumulation (NBIA) comprises various rare clinical entities with brain iron overload as a common feature. Magnetic resonance imaging (MRI) allows diagnosis of this condition, and genetic molecular testing can confirm the diagnosis to better understand the intracellular damage mechanism involved. NBIA groups disorders include: pantothenate kinase-associated neurodegeneration (PKAN), mutations in the gene encoding pantothenate kinase 2 (PANK2); neuroferritinopathy, mutations in the calcium-independent phospholipase A2 gene (PLA2G6); aceruloplasminemia; and other subtypes with no specific clinical or MRI specific patterns identified. There is no causal therapy, and only symptom treatments are available for this condition. Promising strategies include the use of deferiprone (DFP), an orally administered bidentate iron chelator with the ability to pass through the blood–brain barrier. This is a prospective study analysis with a mean follow-up time of 5.5 ± 2.3 years (min–max: 2.4–9.6 years) to define DFP (15 mg/kg bid)’s efficacy and safety in the continuous treatment of 10 NBIA patients through clinical and neuroradiological evaluation. Our results show the progressive decrease in the cerebral accumulation of iron evaluated by MRI and a substantial stability of the overall clinical neurological picture without a significant correlation between clinical and radiological findings. Complete ferrochelation throughout the day appears to be of fundamental importance considering that oxidative damage is generated, above, all by non-transferrin-bound iron (NTBI); thus, we hypothesize that a (TID) administration regimen of DFP might better apply its chelating properties over 24 h with the aim to also obtain clinical improvement beyond the neuroradiological improvement.