The "Peeking" Effect in Supervised Feature Selection on Diffusion Tensor Imaging Data

We read with great interest the article by Haller et al[1][1] in the February 2013 issue of the American Journal of Neuroradiology . The authors used whole-brain diffusion tensor imaging–derived fractional anisotropy (FA) data, skeletonized through use of the standard tract-based spatia

Fractal Analysis of MRI Data at 7 T: How Much Complex Is the Cerebral Cortex?

The human brain is a highly complex structure, which can be only partially described by conventional metrics derived from magnetic resonance imaging (MRI), such as volume, cortical thickness, and gyrification index. In the last years, the fractal dimension (FD) - a useful quantitative index of fractal geometry - has proven to well express the morphological complexity of the cerebral cortex. However, this complexity is likely higher than that we can observe using MRI scanners with 1.5 T or 3 T field strength. Ultrahigh-field MRI (UHF-MRI) improves imaging of smaller anatomical brain structures by exploring down to a submillimetric spatial resolution with higher signal-to-noise and contrast-to-noise ratios. Accordingly, we hypothesized that UHF-MRI might reveal a higher level of the structural complexity of the cerebral cortex. In this study, using an improved box-counting algorithm, we estimated the FD of the cerebral cortex in six public or private T1-weighted MRI datasets of young healthy subjects (for a total of 87 subjects), acquired at different field strengths (1.5 T, 3 T, and 7 T). Our results showed, for the first time, that MRI-derived FD values of the cerebral cortex imaged at 7 T were significantly higher than those observed at lower field strengths. UHF-MRI provides an anatomical definition not achievable at lower field strengths and can improve unveiling the real structural complexity of the human brain

Regional Distribution and Clinical Correlates of White Matter Structural Damage in Huntington Disease: A Tract-Based Spatial Statistics Study

BACKGROUND AND PURPOSE: HD entails damage of the WM. Our aim was to explore in vivo the regional volume and microstructure of the brain WM in HD and to correlate such findings with clinical status of the patients. MATERIALS AND METHODS: Fifteen HD gene carriers in different clinical stages of the disease and 15 healthy controls were studied with T1-weighted images for VBM and DTI for TBSS. Maps of FA, MD, and λ∥ and λ⊥ were reconstructed. RESULTS: Compared with controls, in addition to neostriatum and cortical GM volume loss, individuals with HD showed volume loss in the genu of the internal capsule and subcortical frontal WM bilaterally, the right splenium of the corpus callosum, and the left corona radiata. TBSS revealed symmetrically decreased FA in the corpus callosum, fornix, external/extreme capsule, inferior fronto-occipital fasciculus, and inferior longitudinal fasciculus. Areas of increased MD were more extensive and included arciform fibers of the cerebral hemispheres and cerebral peduncles. Increase of the λ∥ and a comparatively more pronounced increase of the λ⊥ underlay the decreased FA of the WM in HD. Areas of WM atrophy, decreased FA, and increased MD correlated with the severity of the motor and cognitive dysfunction, whereas only the areas with increased MD correlated with disease duration. CONCLUSIONS: Microstructural damage accompanies volume decrease of the WM in HD and is correlated with the clinical deficits and disease duration. MR imaging−based measures could be considered as a biomarker of neurodegeneration in HD gene carriers

Mouse tracking to explore motor inhibition processes in go/no-go and stop signal tasks

Response inhibition relies on both proactive and reactive mechanisms that exert a synergic control on goal-directed actions. It is typically evaluated by the go/no-go (GNG) and the stop signal task (SST) with response recording based on the key-press method. However, the analysis of discrete variables (i.e., present or absent responses) registered by key-press could be insufficient to capture dynamic aspects of inhibitory control. Trying to overcome this limitation, in the present study we used a mouse tracking procedure to characterize movement profiles related to proactive and reactive inhibition. A total of fifty-three participants performed a cued GNG and an SST. The cued GNG mainly involves proactive control whereas the reactive component is mainly engaged in the SST. We evaluated the velocity profile from mouse trajectories both for responses obtained in the Go conditions and for inhibitory failures. Movements were classified as one-shot when no corrections were observed. Multi-peaked velocity profiles were classified as non-one-shot. A higher proportion of one-shot movements was found in the SST compared to the cued GNG when subjects failed to inhibit responses. This result suggests that proactive control may be responsible for unsmooth profiles in inhibition failures, supporting a differentiation between these tasks

magnetization transfer imaging demonstrates a distributed pattern of microstructural changes of the cerebral cortex in amyotrophic lateral sclerosis

BACKGROUND AND PURPOSE: To date, damage of the cerebral cortex neurons in ALS was investigated by using conventional MR imaging and proton MR spectroscopy. We explored the capability of MTI to map the microstructural changes in cerebral motor and extramotor cortices of patients with ALS. MATERIALS AND METHODS: Twenty patients with ALS and 17 age-matched healthy controls were enrolled. A high-resolution 3D SPGR sequence with and without MT saturation pulses was obtained on a 1.5T scanner to compute MTR values. Using the FMRIB Software Library tools, we automatically computed the MTR of the cerebral cortex GM in 48 regions of the entire cerebral cortex derived from the standard Harvard-Oxford cortical atlas. RESULTS: The MTR values were significantly lower in patients with ALS than in healthy controls in the primary motor cortex (precentral gyrus), nonprimary motor areas (superior and middle frontal gyri and superior parietal lobe), and some extramotor areas (frontal pole, planum temporale, and planum polare). No correlation was found between regional MTR values and the severity of clinical deficits or disease duration. CONCLUSIONS: MTI analysis can detect the distributed pattern of microstructural changes of the GM in the cerebral cortex of patients with ALS with involvement of both the motor and extramotor areas

Brain structural damage in Friedreich's ataxia.

ABSTRACT Objective: Neuropathological descriptions of the brain in Friedreich’s ataxia (FRDA) were obtained before avail- ability of the current molecular genetic tests for this disease. Voxel-based morphometry (VBM) enables an unbiased whole-brain quantitative analysis of differences in gray matter (GM) and white matter (WM) volume. Methods: Using VBM, we assessed the brain structural damage in 22 patients with genetically confirmed FRDA and 25 healthy controls. The results were correlated with the disease duration and the severity of the patients’ clinical deficits—evaluated using the International Cerebellar Ataxia Rating Scale and Inherited Ataxia Clinical Rating Scale. Results: In patients with FRDA, VBM showed a symmetrical volume loss in dorsal medulla, infero-medial portions of the cerebellar hemispheres, the rostral vermis and in the dentate region. No volume loss in cerebral hemispheres was observed. The atrophy of the cerebel- lum and medulla correlated with the severity of the clinical deficit and disease duration. Conclusions: In patients with FRDA, significant GM and WM loss was observed only in the cerebellum and dorsal medulla. These structural changes correlate with the severity of the clinical deficit and disease duration