Alzheimer's disease detection through whole-brain 3D-CNN MRI

The projected burden of dementia by Alzheimer's disease (AD) represents a looming healthcare crisis as the population of most countries grows older. Although there is currently no cure, it is possible to treat symptoms of dementia. Early diagnosis is paramount to the development and success of interventions, and neuroimaging represents one of the most promising areas for early detection of AD. We aimed to deploy advanced deep learning methods to determine whether they can extract useful AD biomarkers from structural magnetic resonance imaging (sMRI) and classify brain images into AD, mild cognitive impairment (MCI), and cognitively normal (CN) groups. We tailored and trained Convolutional Neural Networks (CNNs) on sMRIs of the brain from datasets available in online databases. Our proposed method, ADNet, was evaluated on the CADDementia challenge and outperformed several approaches in the prior art. The method's configuration with machine-learning domain adaptation, ADNet-DA, reached 52.3% accuracy. Contributions of our study include devising a deep learning system that is entirely automatic and comparatively fast, presenting competitive results without using any patient's domain-specific knowledge about the disease. We were able to implement an end-to-end CNN system to classify subjects into AD, MCI, or CN groups, reflecting the identification of distinctive elements in brain images. In this context, our system represents a promising tool in finding biomarkers to help with the diagnosis of AD and, eventually, many other diseasesCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQCOORDENAÇÃO DE APERFEIÇOAMENTO DE PESSOAL DE NÍVEL SUPERIOR - CAPESFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP304497/2018-5; 304497/2018-5Não tem2017/12646-

Many names and a single disease: the plurality of the sensory neuronopathies

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Selective sensory deafferentation induces structural and functional brain plasticity

Sensory-motor integration models have been proposed aiming to explain how the brain uses sensory information to guide and check the planning and execution of movements. Sensory neuronopathy (SN) is a peculiar disease characterized by exclusive, severe and widespread sensory loss. It is a valuable condition to investigate how sensory deafferentation impacts brain organization. We thus recruited patients with clinical and electrophysiological criteria for SN to perform structural and functional MRI analyses. We investigated volumetric changes in gray matter (GM) using anatomical images; the microstructure of WM within segmented regions of interest (ROI), via diffusion images; and brain activation related to a finger tapping task. All significant results were related to the long disease duration subgroup of patients. Structural analysis showed hypertrophy of the caudate nucleus, whereas the diffusion study identified reduction of fractional anisotropy values in ROIs located around the thalamus and the striatum. We also found differences regarding finger-tapping activation in the posterior parietal regions and in the medial areas of the cerebellum. Our results stress the role of the caudate nucleus over the other basal ganglia in the sensory-motor integration models, and suggest an inhibitory function of a recently discovered tract between the thalamus and the striatum. Overall, our findings confirm plasticity in the adult brain and open new avenues to design neurorehabilitation strategies. Keywords: Sensory-motor integration, MRI, Sensory neuronopathy, Deafferentation, Plasticit

Brain connectivity and functional recovery in patients with ischemic stroke

BACKGROUND: Brain mapping studies have demonstrated that functional poststroke brain reorganization is associated with recovery of motor function. Nonetheless, the specific mechanisms associated with functional reorganization leading to motor recovery are still partly unknown. In this study, we performed a cross-sectional evaluation of poststroke subjects with the following goals: (1) To assess intra-and interhemispheric functional brain activation patterns associated with motor function in poststroke patients with variable degrees of recovery; (2) to investigate the involvement of other nonmotor functional networks in relationship with recovery. METHODS: We studied 59 individuals: 13 patients with function Rankin > 1 and Barthel < 100; 19 patients with preserved function with Rankin 0-1 and Barthel = 100; and 27 healthy controls. All subjects underwent structural and functional magnetic resonance imaging (3T Philips Achieva, Holland) using the same protocol (TR = 2 seconds, TE = 30 ms, FOV = 240 x 240 x 117, slice = 39). Resting state functional connectivity was used by in-house software, based on SPM12. Among patients with and without preserved function, the functional connectivity between the primary motor region (M1) and the contralateral hemisphere was increased compared with controls. Nonetheless, only patients with decreased function exhibited decreased functional connectivity between executive control, sensorimotor and visuospatial networks. CONCLUSION: Functional recovery after stroke is associated with preserved functional connectivity of motor to nonmotor networks2716570FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP2013/07559-

Derek Denny-Brown: the man behind the ganglia

ABSTRACT The authors present an historical review about the main contributions of Professor Derek Denny-Brown to neurology. Some of his achievements include the first description of sensory neuronopathies, and some of the essential textbooks on the function and anatomy of the basal ganglia. In 2016, on the 35th anniversary of his death, modern neurologists are still strongly influenced by his legacy

Multimodal MRI-Based Study in Patients with <i>SPG4</i> Mutations

<div><p>Mutations in the <i>SPG4</i> gene (SPG4-HSP) are the most frequent cause of hereditary spastic paraplegia, but the extent of the neurodegeneration related to the disease is not yet known. Therefore, our objective is to identify regions of the central nervous system damaged in patients with SPG4-HSP using a multi-modal neuroimaging approach. In addition, we aimed to identify possible clinical correlates of such damage. Eleven patients (mean age 46.0 ± 15.0 years, 8 men) with molecular confirmation of hereditary spastic paraplegia, and 23 matched healthy controls (mean age 51.4 ± 14.1years, 17 men) underwent MRI scans in a 3T scanner. We used 3D T1 images to perform volumetric measurements of the brain and spinal cord. We then performed tract-based spatial statistics and tractography analyses of diffusion tensor images to assess microstructural integrity of white matter tracts. Disease severity was quantified with the Spastic Paraplegia Rating Scale. Correlations were then carried out between MRI metrics and clinical data. Volumetric analyses did not identify macroscopic abnormalities in the brain of hereditary spastic paraplegia patients. In contrast, we found extensive fractional anisotropy reduction in the corticospinal tracts, cingulate gyri and splenium of the corpus callosum. Spinal cord morphometry identified atrophy without flattening in the group of patients with hereditary spastic paraplegia. Fractional anisotropy of the corpus callosum and pyramidal tracts did correlate with disease severity. Hereditary spastic paraplegia is characterized by relative sparing of the cortical mantle and remarkable damage to the distal portions of the corticospinal tracts, extending into the spinal cord.</p></div

Characterization of the Cohort.

<p>Clinical and genetic data of patients with SPG4-HSP.</p><p>Characterization of the Cohort.</p

Neuroimaging findings according to <i>SPG4</i> mutation subtypes.

<p>Group analysis based on genetic features, Nonsense/Frameshift mutation vs Missense mutation.</p><p>Neuroimaging findings according to <i>SPG4</i> mutation subtypes.</p

Tractography Results.

<p>Results of automatic tractography for the corticospinal tracts in patients and controls.</p><p>Tractography Results.</p

TBSS analyses showing microstructural damage in SPG4-HSP.

<p>TBSS results showing areas of reduced FA and increased MD, RD and AD in patients with SPG4 mutations after comparison with age and sex matched controls. Areas with reduced FA and increased MD, RD and AD are shown in yellow-red and represent cluster based values (p<0.05, corrected). Results are shown on the MNI152 1 mm template.</p