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Diffusion tensor imaging (DTI) is highly sensitive to noise and improvement of radiofrequency coil technology represents a straightforward way for augmenting signal-to-noise ratio (SNR) performance in magnetic resonance imaging (MRI) scanners. The aim of this study was to characterize the dependence of DTI measurements of fractional anisotropy (FA) and mean diffusivity (MD) on the choice of head coil, comparing two head coils with different functional designs and sensitivities.Fourteen healthy subjects underwent DTI acquisitions at 1.5 T. Every subject was scanned twice, using a standard quadrature birdcage head coil (coil-A) and an eight-channel array head coil (coil-B). FA and MD maps, estimated using both the linear least squares (LLS) and nonlinear least squares (NLLS) methods, were nonlinearly normalized into a standard space. Then, volumetric regions of interest encompassing typical white and gray matter structures [splenium of the corpus callosum (SCC), internal capsule (IC), cerebral peduncles (CP), middle cerebellar peduncles (MCP), globus pallidus (GP), thalamus (TH), caudate (CA), and putamen (PU)] were analyzed. Significant differences and trends of variation in DTI measurements were assessed by the Wilcoxon test for paired samples with and without Bonferroni correction for multiple comparisons, respectively.The overall SNR of coil-B was 30% higher than that of coil-A. When comparing DTI measurements (coil-B versus coil-A), mean FA values (SCC, IC, and TH), mean MD values (IC, CP, GP, and TH), FA standard deviation (CP, MCP, GP, and CA), and MD standard deviation (IC, CP, TH, and PU) resulted decreased (significant difference, p(cor)0.05, or trend of variation, P(uncor)0.05) in several gray and white matter regions of the human brain. With the exception of CP, the results in terms of revealed significant difference or trend of variation were independent of the method (LLS and NLLS) used for estimating the diffusion tensor.In various gray and white matter structures, the eight-channel array head coil yielded more precise and accurate measurements of DTI derived indices compared to the standard quadrature birdcage head coil.

Background Post-traumatic cerebral infarction (PTCI) is common after traumatic brain injury (TBI). It is unclear what the occurrence of a PTCI is, how it impacts the long-term outcome, and whether it adds incremental prognostic value to established outcome predictors. Methods This was a prospective multicenter cohort study of moderate and severe TBI patients. The primary objective was to evaluate if PTCI was an independent risk factor for the 6-month outcome assessed with the Glasgow Outcome Scale (GOS). We also assessed the PTCI occurrence and if it adds incremental value to the International Mission for Prognosis and Clinical Trial design in TBI (IMPACT) core and extended models. Results We enrolled 143 patients, of whom 47 (32.9%) developed a PTCI. In the multiple ordered logistic regression, PTCI was retained in both the core and extended IMPACT models as an independent predictor of the GOS. The predictive performances increased significantly when PTCI was added to the IMPACT core model (AUC = 0.73, 95% C.I. 0.66–0.82; increased to AUC = 0.79, 95% CI 0.71–0.83, p = 0.0007) and extended model (AUC = 0.74, 95% C.I. 0.65–0.81 increased to AUC = 0.80, 95% C.I. 0.69–0.85; p = 0.00008). Patients with PTCI showed higher ICU mortality and 6-month mortality, whereas hospital mortality did not differ between the two groups. Conclusions PTCI is a common complication in patients suffering from a moderate or severe TBI and is an independent risk factor for long-term disability. The addition of PTCI to the IMPACT core and extended predictive models significantly increased their performance in predicting the GOS. Trial registration The present study was registered in ClinicalTrial.gov with the ID number NCT02430324.

The structural and functional data gathered with Magnetic Resonance Imaging (MRI) techniques about the brain cortical motor damage in Amyotrophic Lateral Sclerosis (ALS) are controversial. In fact some structural MRI studies showed foci of gray matter (GM) atrophy in the precentral gyrus, even in the early stage, while others did not. Most functional MRI (fMRI) studies in ALS reported hyperactivation of extra-primary motor cortices, while contradictory results were obtained on the activation of the primary motor cortex. We aimed to investigate the cortical motor circuitries in ALS patients by a combined structural and functional approach. Twenty patients with definite ALS and 16 healthy subjects underwent a structural examination with acquisition of a 3D T1-weighted sequence and fMRI examination during a maximal force handgrip task executed with the right-hand, the left-hand and with both hands simultaneously. The T1-weighted images were analyzed with Voxel-Based Morphometry (VBM) that showed several clusters of reduced cortical GM in ALS patients compared to controls including the pre and postcentral gyri, the superior, middle and inferior frontal gyri, the supplementary motor area, the superior and inferior parietal cortices and the temporal lobe, bilaterally but more extensive on the right side. In ALS patients a significant hypoactivation of the primary sensory motor cortex and frontal dorsal premotor areas as compared to controls was observed. The hypoactivated areas matched with foci of cortical atrophy demonstrated by VBM. The fMRI analysis also showed an enhanced activation in the ventral premotor frontal areas and in the parietal cortex pertaining to the fronto-parietal motor circuit which paralleled with disease progression rate and matched with cortical regions of atrophy. The hyperactivation of the fronto-parietal circuit was asymmetric and prevalent in the left hemisphere. VBM and fMRI identified structural and functional markers of an extended cortical damage within the motor circuit of ALS patients. The functional changes in non-primary motor cortices pertaining to fronto-parietal circuit suggest an over-recruitment of a pre-existing physiological sensory-motor network. However, the concomitant fronto-parietal cortical atrophy arises the possibility that such a hyper-activation reflects cortical hyper-excitability due to loss of inhibitory inter-neurons.