48 research outputs found

    Non-local intracranial cavity extraction

    Get PDF
    [EN] Automatic and accurate methods to estimate normalized regional brain volumes from MRI data are valuable tools which may help to obtain an objective diagnosis and followup of many neurological diseases. To estimate such regional brain volumes, the intracranial cavity volume (ICV) is often used for normalization. However, the high variability of brain shape and size due to normal intersubject variability, normal changes occurring over the lifespan, and abnormal changes due to disease makes the ICV estimation problem challenging. In this paper, we present a new approach to perform ICV extraction based on the use of a library of prelabeled brain images to capture the large variability of brain shapes. To this end, an improved nonlocal label fusion scheme based on BEaST technique is proposed to increase the accuracy of the ICV estimation. The proposed method is compared with recent state-of-the-art methods and the results demonstrate an improved performance both in terms of accuracy and reproducibility while maintaining a reduced computational burden.The authors want to thank the IXI (EPSRC GR/S21533/02) and OASIS (P50 AG05681, P01 AG03991, R01 AG021910, P50 MH071616, U24 RR021382, and R01 MH56584) dataset promoters for making available this valuable resource to the scientific community which surely will boost the research in brain imaging. This work has been supported by the Spanish Grant TIN2011-26727 from Ministerio de Ciencia e Innovacion. This work was funded in part by operating grants ´ from the Canadian Institutes of Health Research, les Fonds de la recherche sante du Quebec, MINDLab UNIK initiative at ´ Aarhus University, funded by the Danish Ministry of Science, Technology and Innovation, Grant agreement no. 09-065250.Manjón Herrera, JV.; Eskildsen, SF.; Coupé, P.; Romero Gómez, JE.; Collins, L.; Robles Viejo, M. (2014). Non-local intracranial cavity extraction. International Journal of Biomedical Imaging. 2014:1-11. https://doi.org/10.1155/2014/820205S111201

    Deep grading for MRI-based differential diagnosis of Alzheimer's disease and Frontotemporal dementia

    Full text link
    Alzheimer's disease and Frontotemporal dementia are common forms of neurodegenerative dementia. Behavioral alterations and cognitive impairments are found in the clinical courses of both diseases and their differential diagnosis is sometimes difficult for physicians. Therefore, an accurate tool dedicated to this diagnostic challenge can be valuable in clinical practice. However, current structural imaging methods mainly focus on the detection of each disease but rarely on their differential diagnosis. In this paper, we propose a deep learning based approach for both problems of disease detection and differential diagnosis. We suggest utilizing two types of biomarkers for this application: structure grading and structure atrophy. First, we propose to train a large ensemble of 3D U-Nets to locally determine the anatomical patterns of healthy people, patients with Alzheimer's disease and patients with Frontotemporal dementia using structural MRI as input. The output of the ensemble is a 2-channel disease's coordinate map able to be transformed into a 3D grading map which is easy to interpret for clinicians. This 2-channel map is coupled with a multi-layer perceptron classifier for different classification tasks. Second, we propose to combine our deep learning framework with a traditional machine learning strategy based on volume to improve the model discriminative capacity and robustness. After both cross-validation and external validation, our experiments based on 3319 MRI demonstrated competitive results of our method compared to the state-of-the-art methods for both disease detection and differential diagnosis

    Lifespan Changes of the Human Brain In Alzheimer's Disease

    Get PDF
    [EN] Brain imaging studies have shown that slow and progressive cerebral atrophy characterized the development of Alzheimer's Disease (AD). Despite a large number of studies dedicated to AD, key questions about the lifespan evolution of AD biomarkers remain open. When does the AD model diverge from the normal aging model? What is the lifespan trajectory of imaging biomarkers for AD? How do the trajectories of biomarkers in AD differ from normal aging? To answer these questions, we proposed an innovative way by inferring brain structure model across the entire lifespan using a massive number of MRI (N = 4329). We compared the normal model based on 2944 control subjects with the pathological model based on 3262 patients (AD + Mild cognitive Impaired subjects) older than 55 years and controls younger than 55 years. Our study provides evidences of early divergence of the AD models from the normal aging trajectory before 40 years for the hippocampus, followed by the lateral ventricles and the amygdala around 40 years. Moreover, our lifespan model reveals the evolution of these biomarkers and suggests close abnormality evolution for the hippocampus and the amygdala, whereas trajectory of ventricular enlargement appears to follow an inverted U-shape. Finally, our models indicate that medial temporal lobe atrophy and ventricular enlargement are two mid-life physiopathological events characterizing AD brain.This work benefited from the support of the project DeepVolBrain of the French National Research Agency (ANR-18-CE45-0013). This study was achieved within the context of the Laboratory of Excellence TRAIL ANR-10-LABX-57 for the BigDataBrain project. Moreover, we thank the Investments for the future Program IdEx Bordeaux (ANR-10-IDEX- 03-02, HL-MRI Project), Cluster of excellence CPU and the CNRS. This study has been also supported by the DPI2017-87743-R grant from the Spanish Ministerio de Economia, Industria y Competitividad. Moreover, this work is based on multiple samples. We wish to thank all investigators of these projects who collected these datasets and made them freely accessible. The C-MIND data used in the preparation of this article were obtained from the C-MIND Data Repository (accessed in Feb 2015) created by the C-MIND study of Normal Brain Development. This is a multisite, longitudinal study of typically developing children from ages newborn through young adulthood conducted by Cincinnati Children's Hospital Medical Center and UCLA and supported by the National Institute of Child Health and Human Development (Contract #s HHSN275200900018C). A listing of the participating sites and a complete listing of the study investigators can be found at https://research.cchmc.org/c-mind. The NDAR data used in the preparation of this manuscript were obtained from the NIH-supported National Database for Autism Research (NDAR). NDAR is a collaborative informatics system created by the National Institutes of Health to provide a national resource to support and accelerate research in autism. The NDAR dataset includes data from the NIH Pediatric MRI Data Repository created by the NIH MRI Study of Normal Brain Development. This is a multisite, longitudinal study of typically developing children from ages newborn through young adulthood conducted by the Brain Development Cooperative Group and supported by the National Institute of Child Health and Human Development, the National Institute on Drug Abuse, the National Institute of Mental Health, and the National Institute of Neurological Disorders and Stroke (Contract #s N01- HD02-3343, N01-MH9-0002, and N01-NS-9-2314, -2315, -2316, -2317, -2319 and -2320). A listing of the participating sites and a complete listing of the study investigators can be found at http://pediatricmri.nih.gov/nihpd/info/participating_centers.html. The ADNI data used in the preparation of this manuscript were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) (National Institutes of Health Grant U01 AG024904). The ADNI is funded by the National Institute on Aging and the National Institute of Biomedical Imaging and Bioengineering and through generous contributions from the following: Abbott, AstraZeneca AB, Bayer Schering Pharma AG, Bristol-Myers Squibb, Eisai Global Clinical Development, Elan Corporation, Genentech, GE Healthcare, GlaxoSmithKline, Innogenetics NV, Johnson & Johnson, Eli Lilly and Co., Medpace, Inc., Merck and Co., Inc., Novartis AG, Pfizer Inc., F. Hoffmann-La Roche, Schering-Plough, Synarc Inc., as well as nonprofit partners, the Alzheimer's Association and Alzheimer's Drug Discovery Foundation, with participation from the U.S. Food and Drug Administration. Private sector contributions to the ADNI are facilitated by the Foundation for the National Institutes of Health (www.fnih.org).Coupé, P.; Manjón Herrera, JV.; Lanuza, E.; Catheline, G. (2019). Lifespan Changes of the Human Brain In Alzheimer's Disease. Scientific Reports. 9:1-12. https://doi.org/10.1038/s41598-019-39809-8S1129Lobo, A. et al. Prevalence of dementia and major subtypes in Europe: a collaborative study of population-based cohorts. Neurology 54, S4 (2000).Barnes, J. et al. Alzheimer’s disease first symptoms are age dependent: evidence from the NACC dataset. Alzheimer’s & dementia 11, 1349–1357 (2015).Jack, C. R. et al. Tracking pathophysiological processes in Alzheimer’s disease: an updated hypothetical model of dynamic biomarkers. The Lancet Neurology 12, 207–216 (2013).Nestor, P. J., Scheltens, P. & Hodges, J. R. Advances in the early detection of Alzheimer’s disease. Nature medicine 10 (2004).Davatzikos, C., Fan, Y., Wu, X., Shen, D. & Resnick, S. M. Detection of prodromal Alzheimer’s disease via pattern classification of magnetic resonance imaging. Neurobiology of aging 29, 514–523 (2008).Bakkour, A., Morris, J. C. & Dickerson, B. C. The cortical signature of prodromal AD Regional thinning predicts mild AD dementia. Neurology 72, 1048–1055 (2009).Chan, D. et al. Change in rates of cerebral atrophy over time in early-onset Alzheimer’s disease: longitudinal MRI study. The Lancet 362, 1121–1122 (2003).Ridha, B. H. et al. Tracking atrophy progression in familial Alzheimer’s disease: a serial MRI study. The Lancet Neurology 5, 828–834 (2006).Sala-Llonch, R., Bartrés-Faz, D. & Junqué, C. Reorganization of brain networks in aging: a review of functional connectivity studies. Frontiers in psychology 6 (2015).Bateman, R. J. et al. Clinical and biomarker changes in dominantly inherited Alzheimer’s disease. New England Journal of Medicine 367, 795–804 (2012).Dickerson, B. et al. Alzheimer-signature MRI biomarker predicts AD dementia in cognitively normal adults. Neurology 76, 1395–1402 (2011).Miller, M. I. et al. The diffeomorphometry of temporal lobe structures in preclinical Alzheimer’s disease. NeuroImage: Clinical 3, 352–360 (2013).Bernard, C. et al. Time course of brain volume changes in the preclinical phase of Alzheimer’s disease. Alzheimer’s & Dementia 10, 143–151. e141 (2014).den Heijer, T. et al. A 10-year follow-up of hippocampal volume on magnetic resonance imaging in early dementia and cognitive decline. Brain 133, 1163–1172 (2010).Coupé, P. et al. Detection of Alzheimer’s disease signature in MR images seven years before conversion to dementia: Toward an early individual prognosis. Hum Brain Mapp 36, 4758–4770, https://doi.org/10.1002/hbm.22926 (2015).Albert, M. et al. Predicting progression from normal cognition to mild cognitive impairment for individuals at 5 years. Brain (2018).Poldrack, R. A. & Gorgolewski, K. J. Making big data open: data sharing in neuroimaging. Nature neuroscience 17, 1510–1517 (2014).Solomon, A. et al. Serum cholesterol changes after midlife and late-life cognition twenty-one-year follow-up study. Neurology 68, 751–756 (2007).Debette, S. et al. Midlife vascular risk factor exposure accelerates structural brain aging and cognitive decline. Neurology 77, 461–468 (2011).Tolppanen, A.-M. et al. Midlife and late-life body mass index and late-life dementia: results from a prospective population-based cohort. Journal of Alzheimer’s Disease 38, 201–209 (2014).Coupe, P., Catheline, G., Lanuza, E. & Manjon, J. V. & Alzheimer’s Disease Neuroimaging, I. Towards a unified analysis of brain maturation and aging across the entire lifespan: A MRI analysis. Hum Brain Mapp 38, 5501–5518, https://doi.org/10.1002/hbm.23743 (2017).Villemagne, V. L. et al. Amyloid β deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer’s disease: a prospective cohort study. The Lancet Neurology 12, 357–367 %@1474–4422 (2013).Villemagne, V. L. et al. Longitudinal assessment of Aβ and cognition in aging and Alzheimer disease. Annals of neurology 69, 181–192 (2011).Poulin, S. P. et al. Amygdala atrophy is prominent in early Alzheimer’s disease and relates to symptom severity. Psychiatry Research: Neuroimaging 194, 7–13 (2011).Jack, C. R. et al. Medial temporal atrophy on MRI in normal aging and very mild Alzheimer’s disease. Neurology 49, 786–794 (1997).Apostolova, L. G. et al. Hippocampal atrophy and ventricular enlargement in normal aging, mild cognitive impairment and Alzheimer’s disease. Alzheimer disease and associated disorders 26, 17 (2012).Nestor, S. M. et al. Ventricular enlargement as a possible measure of Alzheimer’s disease progression validated using the Alzheimer’s disease neuroimaging initiative database. Brain 131, 2443–2454 (2008).Petersen, R. C. et al. Alzheimer’s disease Neuroimaging Initiative (ADNI) clinical characterization. Neurology 74, 201–209 (2010).Marcus, D. S. et al. Open Access Series of Imaging Studies (OASIS): cross-sectional MRI data in young, middle aged, nondemented, and demented older adults. Journal of cognitive neuroscience 19, 1498–1507 (2007).Manjon, J. V. & Coupe, P. volBrain: An Online MRI Brain Volumetry System. Front Neuroinform 10, 30, https://doi.org/10.3389/fninf.2016.00030 (2016).Manjon, J. V., Coupe, P., Marti-Bonmati, L., Collins, D. L. & Robles, M. Adaptive non-local means denoising of MR images with spatially varying noise levels. J Magn Reson Imaging 31, 192–203, https://doi.org/10.1002/jmri.22003 (2010).Tustison, N. J. et al. N4ITK: improved N3 bias correction. IEEE Trans Med Imaging 29, 1310–1320, https://doi.org/10.1109/TMI.2010.2046908 (2010).Avants, B. B. et al. A reproducible evaluation of ANTs similarity metric performance in brain image registration. Neuroimage 54, 2033–2044 (2011).Ashburner, J. & Friston, K. J. Unified segmentation. Neuroimage 26, 839–851, https://doi.org/10.1016/j.neuroimage.2005.02.018 (2005).Manjón, J. V., Tohka, J. & Robles, M. Improved estimates of partial volume coefficients from noisy brain MRI using spatial context. Neuroimage 53, 480–490 (2010).Manjon, J. V. et al. Nonlocal intracranial cavity extraction. Int J Biomed Imaging 2014, 820205, https://doi.org/10.1155/2014/820205 (2014).Coupe, P. et al. Patch-based segmentation using expert priors: application to hippocampus and ventricle segmentation. Neuroimage 54, 940–954, https://doi.org/10.1016/j.neuroimage.2010.09.018 (2011).Frisoni, G. B. et al. The EADC-ADNI Harmonized Protocol for manual hippocampal segmentation on magnetic resonance: evidence of validity. Alzheimer’s & Dementia 11, 111–125 (2015).Solow, R. M. A contribution to the theory of economic growth. The quarterly journal of economics 70, 65–94 %@1531–4650 (1956).Coupe, P. et al. Scoring by nonlocal image patch estimator for early detection of Alzheimer’s disease. Neuroimage Clin 1, 141–152, https://doi.org/10.1016/j.nicl.2012.10.002 (2012).Cuingnet, R. et al. Automatic classification of patients with Alzheimer’s disease from structural MRI: a comparison of ten methods using the ADNI database. Neuroimage 56, 766–781, https://doi.org/10.1016/j.neuroimage.2010.06.013 (2011).Eskildsen, S. F. et al. Prediction of Alzheimer’s disease in subjects with mild cognitive impairment from the ADNI cohort using patterns of cortical thinning. Neuroimage 65, 511–521 (2013).Eskildsen, S. F. et al. Structural imaging biomarkers of Alzheimer’s disease: predicting disease progression. Neurobiology of aging 36, S23–S31 (2015).Tong, T. et al. A Novel Grading Biomarker for the Prediction of Conversion From Mild Cognitive Impairment to Alzheimer’s Disease. IEEE Transactions on Biomedical Engineering 64, 155–165 (2017).Wolz, R. et al. Multi-method analysis of MRI images in early diagnostics of Alzheimer’s disease. PLoS One 6, e25446, https://doi.org/10.1371/journal.pone.0025446 (2011).Bron, E. E. et al. Standardized evaluation of algorithms for computer-aided diagnosis of dementia based on structural MRI: the CADDementia challenge. Neuroimage 111, 562–579, https://doi.org/10.1016/j.neuroimage.2015.01.048 (2015).Chaddad, A., Desrosiers, C., Hassan, L. & Tanougast, C. Hippocampus and amygdala radiomic biomarkers for the study of autism spectrum disorder. BMC Neurosci 18, 52, https://doi.org/10.1186/s12868-017-0373-0 (2017).Chaddad, A., Desrosiers, C. & Toews, M. Multi-scale radiomic analysis of sub-cortical regions in MRI related to autism, gender and age. Sci Rep 7, 45639, https://doi.org/10.1038/srep45639 (2017).Apostolova, L. G. et al. Subregional hippocampal atrophy predicts Alzheimer’s dementia in the cognitively normal. Neurobiology of aging 31, 1077–1088 (2010).Younes, L., Albert, M., Miller, M. I. & Team, B. R. Inferring changepoint times of medial temporal lobe morphometric change in preclinical Alzheimer’s disease. NeuroImage: Clinical 5, 178–187 (2014).Braak, H. & Braak, E. Neuropathological stageing of Alzheimer-related changes. Acta neuropathologica 82, 239–259 (1991).Badea, A. et al. The fornix provides multiple biomarkers to characterize circuit disruption in a mouse model of Alzheimer’s disease. NeuroImage 142, 498–511 (2016).Micotti, E. et al. Striatum and entorhinal cortex atrophy in AD mouse models: MRI comprehensive analysis. Neurobiology of aging 36, 776–788 (2015).Whitwell, J. L. et al. MRI correlates of neurofibrillary tangle pathology at autopsy A voxel-based morphometry study. Neurology 71, 743–749 (2008).Iaccarino, L. et al. Local and distant relationships between amyloid, tau and neurodegeneration in Alzheimer’s Disease. NeuroImage: Clinical 17, 452–464 (2018).Das, S. R. et al. Longitudinal and cross-sectional structural magnetic resonance imaging correlates of AV-1451 uptake. Neurobiology of aging 66, 49–58 (2018).Knopman, D. S. et al. Joint associations of β-amyloidosis and cortical thickness with cognition. Neurobiology of aging 65, 121–131 (2018).Doré, V. et al. Cross-sectional and longitudinal analysis of the relationship between Aβ deposition, cortical thickness, and memory in cognitively unimpaired individuals and in Alzheimer disease. JAMA neurology 70, 903–911 (2013).Jack, C. R. et al. A/T/N: an unbiased descriptive classification scheme for Alzheimer disease biomarkers. Neurology 87, 539–547 (2016).Cavedo, E. et al. Local amygdala structural differences with 3T MRI in patients with Alzheimer disease. Neurology 76, 727–733 (2011).Qiu, A., Fennema-Notestine, C., Dale, A. M., Miller, M. I. & Alzheimer’s Disease Neuroimaging, I. Regional shape abnormalities in mild cognitive impairment and Alzheimer’s disease. Neuroimage 45, 656–661 (2009).Lin, T.-W. et al. Neurodegeneration in amygdala precedes hippocampus in the APPswe/PS1dE9 mouse model of Alzheimer’s disease. Current Alzheimer Research 12, 951–963 (2015).Phelps, E. A. Human emotion and memory: interactions of the amygdala and hippocampal complex. Current opinion in neurobiology 14, 198–202 (2004).Kumfor, F. et al. Degradation of emotion processing ability in corticobasal syndrome and Alzheimer’s disease. Brain 137, 3061–3072 (2014).De Olmos, J. S. In The Human Nervous System (Second Edition) Ch. 22, 739–868 (2004).Tabert, M. H. et al. A 10‐item smell identification scale related to risk for Alzheimer’s disease. Annals of neurology 58, 155–160 (2005).Serby, M., Larson, P. & Kalkstein, D. The nature and course of olfactory deficits in Alzheimer’s disease. The American journal of psychiatry 148, 357 (1991).Djordjevic, J., Jones-Gotman, M., De Sousa, K. & Chertkow, H. Olfaction in patients with mild cognitive impairment and Alzheimer’s disease. Neurobiology of aging 29, 693–706 (2008).Price, J. L., Davis, P., Morris, J. & White, D. The distribution of tangles, plaques and related immunohistochemical markers in healthy aging and Alzheimer’s disease. Neurobiology of aging 12, 295–312 (1991).Ohm, T. & Braak, H. Olfactory bulb changes in Alzheimer’s disease. Acta neuropathologica 73, 365–369 (1987).Carmichael, O. T. et al. Cerebral ventricular changes associated with transitions between normal cognitive function, mild cognitive impairment, and dementia. Alzheimer disease and associated disorders 21, 14 (2007).Prince, M., Bryce, R. & Ferri, C. World Alzheimer Report 2011: The benefits of early diagnosis and intervention. (Alzheimer’s Disease International, 2011).De Jong, L. W. et al. Strongly reduced volumes of putamen and thalamus in Alzheimer’s disease: an MRI study. Brain 131, 3277–3285 (2008).Braak, H. & Braak, E. Alzheimer’s disease affects limbic nuclei of the thalamus. Acta neuropathologica 81, 261–268 (1991).Fjell, A. M. et al. Critical ages in the life course of the adult brain: nonlinear subcortical aging. Neurobiol Aging 34, 2239–2247, https://doi.org/10.1016/j.neurobiolaging.2013.04.006 (2013).Fotenos, A. F., Snyder, A. Z., Girton, L. E., Morris, J. C. & Buckner, R. L. Normative estimates of cross-sectional and longitudinal brain volume decline in aging and AD. Neurology 64, 1032–1039 (2005).Fjell, A. M. et al. One-year brain atrophy evident in healthy aging. Journal of Neuroscience 29, 15223–15231 (2009).Jack, C. R. et al. Comparison of different MRI brain atrophy rate measures with clinical disease progression in AD. Neurology 62, 591–600 (2004).Barnes, J. et al. A meta-analysis of hippocampal atrophy rates in Alzheimer’s disease. Neurobiology of aging 30, 1711–1723 (2009).McDonald, C. R. et al. Regional rates of neocortical atrophy from normal aging to early Alzheimer disease. Neurology 73, 457–465 (2009).Sankar, T. et al. Your algorithm might think the hippocampus grows in Alzheimer’s disease: Caveats of longitudinal automated hippocampal volumetry. Human Brain Mapping 38, 2875–2896 (2017).Small, B. J., Fratiglioni, L., Viitanen, M., Winblad, B. & Bäckman, L. The course of cognitive impairment in preclinical Alzheimer disease: three-and 6-year follow-up of a population-based sample. Archives of neurology 57, 839–844 (2000).La Rue, A. & Jarvik, L. F. Cognitive function and prediction of dementia in old age. The International Journal of Aging and Human Development 25, 79–89 (1987).Elias, M. F. et al. The preclinical phase of Alzheimer disease: a 22-year prospective study of the Framingham Cohort. Archives of neurology 57, 808–813 (2000).Snowdon, D. A. et al. Linguistic ability in early life and cognitive function and Alzheimer’s disease in late life: Findings from the Nun Study. Jama 275, 528–532 (1996).Dubois, B. et al. Preclinical Alzheimer’s disease: definition, natural history, and diagnostic criteria. Alzheimer’s & Dementia 12, 292–323 (2016).Krell-Roesch, J. et al. Leisure-Time Physical Activity and the Risk of IncidentDementia: The Mayo Clinic Study of Aging. Journal of Alzheimer’s Disease, 1–7 (2018).Rusanen, M., Kivipelto, M., Quesenberry, C. P., Zhou, J. & Whitmer, R. A. Heavy smoking in midlife and long-term risk of Alzheimer disease and vascular dementia. Archives of internal medicine 171, 333–339 (2011)

    Brain Structure Ages -- A new biomarker for multi-disease classification

    Full text link
    Age is an important variable to describe the expected brain's anatomy status across the normal aging trajectory. The deviation from that normative aging trajectory may provide some insights into neurological diseases. In neuroimaging, predicted brain age is widely used to analyze different diseases. However, using only the brain age gap information (\ie the difference between the chronological age and the estimated age) can be not enough informative for disease classification problems. In this paper, we propose to extend the notion of global brain age by estimating brain structure ages using structural magnetic resonance imaging. To this end, an ensemble of deep learning models is first used to estimate a 3D aging map (\ie voxel-wise age estimation). Then, a 3D segmentation mask is used to obtain the final brain structure ages. This biomarker can be used in several situations. First, it enables to accurately estimate the brain age for the purpose of anomaly detection at the population level. In this situation, our approach outperforms several state-of-the-art methods. Second, brain structure ages can be used to compute the deviation from the normal aging process of each brain structure. This feature can be used in a multi-disease classification task for an accurate differential diagnosis at the subject level. Finally, the brain structure age deviations of individuals can be visualized, providing some insights about brain abnormality and helping clinicians in real medical contexts

    Hierarchical multi-atlas label fusion with multi-scale feature representation and label-specific patch partition

    Get PDF
    Multi-atlas patch-based label fusion methods have been successfully used to improve segmentation accuracy in many important medical image analysis applications. In general, to achieve label fusion a single target image is first registered to several atlas images, after registration a label is assigned to each target point in the target image by determining the similarity between the underlying target image patch (centered at the target point) and the aligned image patch in each atlas image. To achieve the highest level of accuracy during the label fusion process it’s critical the chosen patch similarity measurement accurately captures the tissue/shape appearance of the anatomical structure. One major limitation of existing state-of-the-art label fusion methods is that they often apply a fixed size image patch throughout the entire label fusion procedure. Doing so may severely affect the fidelity of the patch similarity measurement, which in turn may not adequately capture complex tissue appearance patterns expressed by the anatomical structure. To address this limitation, we advance state-of-the-art by adding three new label fusion contributions: First, each image patch now characterized by a multi-scale feature representation that encodes both local and semi-local image information. Doing so will increase the accuracy of the patch-based similarity measurement. Second, to limit the possibility of the patch-based similarity measurement being wrongly guided by the presence of multiple anatomical structures in the same image patch, each atlas image patch is further partitioned into a set of label-specific partial image patches according to the existing labels. Since image information has now been semantically divided into different patterns, these new label-specific atlas patches make the label fusion process more specific and flexible. Lastly, in order to correct target points that are mislabeled during label fusion, a hierarchically approach is used to improve the label fusion results. In particular, a coarse-to-fine iterative label fusion approach is used that gradually reduces the patch size. To evaluate the accuracy of our label fusion approach, the proposed method was used to segment the hippocampus in the ADNI dataset and 7.0 tesla MR images, sub-cortical regions in LONI LBPA40 dataset, mid-brain regions in SATA dataset from MICCAI 2013 segmentation challenge, and a set of key internal gray matter structures in IXI dataset. In all experiments, the segmentation results of the proposed hierarchical label fusion method with multi-scale feature representations and label-specific atlas patches are more accurate than several well-known state-of-the-art label fusion methods

    Optical imaging and spectroscopy for the study of the human brain: status report

    Full text link
    This report is the second part of a comprehensive two-part series aimed at reviewing an extensive and diverse toolkit of novel methods to explore brain health and function. While the first report focused on neurophotonic tools mostly applicable to animal studies, here, we highlight optical spectroscopy and imaging methods relevant to noninvasive human brain studies. We outline current state-of-the-art technologies and software advances, explore the most recent impact of these technologies on neuroscience and clinical applications, identify the areas where innovation is needed, and provide an outlook for the future directions. Keywords: DCS; NIRS; diffuse optics; functional neuroscience; optical imaging; optical spectroscop
    corecore