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Dive into the research topics where Christopher P. Hess is active.

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Featured researches published by Christopher P. Hess.


Magnetic Resonance in Medicine | 2006

Q-ball reconstruction of multimodal fiber orientations using the spherical harmonic basis.

Christopher P. Hess; Pratik Mukherjee; Eric T. Han; Duan Xu; Daniel B. Vigneron

Diffusion tensor imaging (DTI) accurately delineates white matter pathways when the Gaussian model of diffusion is valid. However, DTI yields erroneous results when diffusion takes on a more complex distribution, as is the case in the brain when fiber tracts cross. High angular resolution diffusion imaging (HARDI) overcomes this limitation of DTI by more fully characterizing the angular dependence of intravoxel diffusion. Among the various HARDI methods that have been proposed, QBI offers advantages such as linearity, model independence, and relatively easy implementation. In this work, reconstruction of the q‐ball orientation distribution function (ODF) is reformulated in terms of spherical harmonic basis functions, yielding an analytic solution with useful properties of a frequency domain representation. The harmonic basis is parsimonious for typical b‐values, which enables the ODF to be synthesized from a relatively small number of noisy measurements and thus brings the technique closer to clinical feasibility from the standpoint of total imaging time. The proposed method is assessed using Monte Carlo computer simulations and compared with conventional q‐ball reconstruction using spherical RBFs. In vivo results from 3T whole‐brain HARDI of adult volunteers are also provided to verify the underlying mathematical theory. Magn Reson Med, 2006.


American Journal of Neuroradiology | 2008

Diffusion Tensor MR Imaging and Fiber Tractography: Theoretic Underpinnings

Pratik Mukherjee; Jeffrey I. Berman; SungWon Chung; Christopher P. Hess; Roland G. Henry

SUMMARY: In this article, the underlying theory of clinical diffusion MR imaging, including diffusion tensor imaging (DTI) and fiber tractography, is reviewed. First, a brief explanation of the basic physics of diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) mapping is provided. This is followed by an overview of the additional information that can be derived from the diffusion tensor, including diffusion anisotropy, color-encoded fiber orientation maps, and 3D fiber tractography. This article provides the requisite background for the second article in this 2-part review to appear next month, which covers the major technical factors that affect image quality in diffusion MR imaging, including the acquisition sequence, magnet field strength, gradient amplitude and slew rate, and multichannel radio-frequency coils and parallel imaging. The emphasis is on optimizing these factors for state-of-the-art DWI and DTI based on the best available evidence in the literature.


American Journal of Neuroradiology | 2008

Diffusion tensor MR imaging and fiber tractography: technical considerations.

Pratik Mukherjee; SungWon Chung; Jeffrey I. Berman; Christopher P. Hess; Roland G. Henry

SUMMARY:This second article of the 2-part review builds on the theoretic background provided by the first article to cover the major technical factors that affect image quality in diffusion imaging, including the acquisition sequence, magnet field strength, gradient amplitude, and slew rate as well as multichannel radio-frequency coils and parallel imaging. The sources of many common diffusion image artifacts are also explored in detail. The emphasis is on optimizing these technical factors for state-of-the-art diffusion-weighted imaging and diffusion tensor imaging (DTI) based on the best available evidence in the literature. An overview of current methods for quantitative analysis of DTI data and fiber tractography in clinical research is also provided.


Pediatrics | 2009

Consensus Statement on Diagnostic Criteria for PHACE Syndrome

Denise W. Metry; Geoffrey L. Heyer; Christopher P. Hess; Maria C. Garzon; Anita N. Haggstrom; Peter C. Frommelt; Denise Adams; Dawn H. Siegel; Karla Hall; Julie Powell; Ilona J. Frieden; Beth A. Drolet

OBJECTIVES: A subgroup of patients with infantile hemangiomas have associated structural anomalies of the brain, cerebral vasculature, eyes, sternum, and/or aorta in the neurocutaneous disorder known as PHACE syndrome. The diagnosis has been broadly inclusive by using a case definition of a facial hemangioma plus ≥1 extracutaneous features, leading to numerous reports of potential associated disease features, many of uncertain significance. This consensus statement was thus developed to establish diagnostic criteria for PHACE syndrome. METHODS: A multidisciplinary group of specialists with expertise in PHACE syndrome drafted initial diagnostic criteria on the basis of review of published, peer-reviewed medical literature and clinical experience. The group then convened in both executive and general sessions during the PHACE Syndrome Research Conference held in November 2008 for discussion and used a consensus method. All conflicting recommendations were subsequently reconciled via electronic communication and teleconferencing. RESULTS: These criteria were stratified into 2 categories: (1) PHACE syndrome or (2) possible PHACE syndrome. Major and minor criteria were determined for the following organ systems: cerebrovascular, structural brain, cardiovascular, ocular, and ventral/midline. Definite PHACE requires the presence of a characteristic segmental hemangioma or hemangioma >5 cm on the face or scalp plus 1 major criterion or 2 minor criteria. Possible PHACE requires the presence of a hemangioma >5 cm on the face or scalp plus 1 minor criterion. The group recognized that it may be possible to have PHACE syndrome with a hemangioma affecting the neck, chest, or arm only or no cutaneous hemangioma at all. In such cases, fulfillment of additional required criteria would also lead to a possible PHACE diagnosis. CONCLUSIONS: These criteria represent current knowledge and are expected to enhance future assessments of PHACE syndrome. It is understood that modifications are to be expected over time to incorporate new research findings.


Neurology | 2010

Hippocampal CA1 apical neuropil atrophy in mild Alzheimer disease visualized with 7-T MRI

Geoffrey A. Kerchner; Christopher P. Hess; K.E. Hammond-Rosenbluth; Duan Xu; Gil D. Rabinovici; Douglas A.C. Kelley; Daniel B. Vigneron; Sarah J. Nelson; Bruce L. Miller

Objectives: In Alzheimer disease (AD), mounting evidence points to a greater role for synaptic loss than neuronal loss. Supporting this notion, multiple postmortem studies have demonstrated that the hippocampal CA1 apical neuropil is one of the earliest sites of pathology, exhibiting tau aggregates and then atrophy before there is substantial loss of the CA1 pyramidal neurons themselves. In this cross-sectional study, we tested whether tissue loss in the CA1 apical neuropil layer can be observed in vivo in patients with mild AD. Methods: We performed ultra-high-field 7-T MRI on subjects with mild AD (n = 14) and age-matched normal controls (n = 16). With a 2-dimensional T2*-weighted gradient-recalled echo sequence that was easily tolerated by subjects, we obtained cross-sectional slices of the hippocampus at an in-plane resolution of 195 μm. Results: On images revealing the anatomic landmarks of hippocampal subfields and strata, we observed thinning of the CA1 apical neuropil in subjects with mild AD compared to controls. By contrast, the 2 groups exhibited no difference in the thickness of the CA1 cell body layer or of the entire CA1 subfield. Hippocampal volume, measured on a conventional T1-weighted sequence obtained at 3T, also did not differentiate these patients with mild AD from controls. Conclusions: CA1 apical neuropil atrophy is apparent in patients with mild AD. With its superior spatial resolution, 7-T MRI permits in vivo analysis of a very focal, early site of AD pathology.


NeuroImage | 2008

Probabilistic streamline q-ball tractography using the residual bootstrap.

Jeffrey I. Berman; SungWon Chung; Pratik Mukherjee; Christopher P. Hess; Eric T. Han; Roland G. Henry

Q-ball imaging has the ability to discriminate multiple intravoxel fiber populations within regions of complex white matter architecture. This information can be used for fiber tracking; however, diffusion MR is susceptible to noise and multiple other sources of uncertainty affecting the measured orientation of fiber bundles. The proposed residual bootstrap method utilizes a spherical harmonic representation for high angular resolution diffusion imaging (HARDI) data in order to estimate the uncertainty in multimodal q-ball reconstructions. The accuracy of the q-ball residual bootstrap technique was examined through simulation. The residual bootstrap method was then used in combination with q-ball imaging to construct a probabilistic streamline fiber tracking algorithm. The residual bootstrap q-ball fiber tracking algorithm is capable of following the corticospinal tract and corpus callosum through regions of crossing white matter tracts in the centrum semiovale. This fiber tracking algorithm is an improvement upon prior diffusion tensor methods and the q-ball data can be acquired in a clinically feasible time frame.


PLOS ONE | 2010

Selective Disruption of the Cerebral Neocortex in Alzheimer's Disease

Rahul S. Desikan; Mert R. Sabuncu; Nicholas J. Schmansky; Martin Reuter; Howard Cabral; Christopher P. Hess; Michael W. Weiner; Alessandro Biffi; Christopher D. Anderson; Jonathan Rosand; David H. Salat; Thomas L. Kemper; Anders M. Dale; Reisa A. Sperling; Bruce Fischl

Background Alzheimers disease (AD) and its transitional state mild cognitive impairment (MCI) are characterized by amyloid plaque and tau neurofibrillary tangle (NFT) deposition within the cerebral neocortex and neuronal loss within the hippocampal formation. However, the precise relationship between pathologic changes in neocortical regions and hippocampal atrophy is largely unknown. Methodology/Principal Findings In this study, combining structural MRI scans and automated image analysis tools with reduced cerebrospinal fluid (CSF) Aß levels, a surrogate for intra-cranial amyloid plaques and elevated CSF phosphorylated tau (p-tau) levels, a surrogate for neocortical NFTs, we examined the relationship between the presence of Alzheimers pathology, gray matter thickness of select neocortical regions, and hippocampal volume in cognitively normal older participants and individuals with MCI and AD (n = 724). Amongst all 3 groups, only select heteromodal cortical regions significantly correlated with hippocampal volume. Amongst MCI and AD individuals, gray matter thickness of the entorhinal cortex and inferior temporal gyrus significantly predicted longitudinal hippocampal volume loss in both amyloid positive and p-tau positive individuals. Amongst cognitively normal older adults, thinning only within the medial portion of the orbital frontal cortex significantly differentiated amyloid positive from amyloid negative individuals whereas thinning only within the entorhinal cortex significantly discriminated p-tau positive from p-tau negative individuals. Conclusions/Significance Cortical Aβ and tau pathology affects gray matter thinning within select neocortical regions and potentially contributes to downstream hippocampal degeneration. Neocortical Alzheimers pathology is evident even amongst older asymptomatic individuals suggesting the existence of a preclinical phase of dementia.


American Journal of Neuroradiology | 2010

Cervical and Intracranial Arterial Anomalies in 70 Patients with PHACE Syndrome

Christopher P. Hess; Heather J. Fullerton; Denise W. Metry; Beth A. Drolet; Dawn H. Siegel; Kurtis I. Auguste; Nalin Gupta; Anita N. Haggstrom; Christopher F. Dowd; Ilona J. Frieden; A. J. Barkovich

BACKGROUND AND PURPOSE: Cerebral and cervical arterial abnormalities are the most common non-cutaneous anomaly in PHACE syndrome, but the location and type of arterial lesions that occur have not been systematically assessed in a large cohort. Our aim was to characterize the phenotypic spectrum of arteriopathy, assess the frequency with which different arteries are involved, and evaluate spatial relationships between arteriopathy, brain structural lesions, and hemangiomas in PHACE syndrome. MATERIALS AND METHODS: Intracranial MRA and/or CTA images from 70 children and accompanying brain MR images in 59 patients with arteriopathy and PHACE syndrome were reviewed to identify the type and location of arterial lesions and brain abnormalities. Five categories of arteriopathy were identified and used for classification: dysgenesis, narrowing, nonvisualization, primitive embryonic carotid-vertebrobasilar connections, and anomalous arterial course or origin. Univariate logistic regression analyses were performed to test for associations between arteriopathy location, hemangiomas, and brain abnormalities. RESULTS: By study design, all patients had arterial abnormalities, and 57% had >1 form of arteriopathy. Dysgenesis was the most common abnormality (56%), followed by anomalous course and/or origin (47%), narrowing (39%), and nonvisualization (20%). Primitive embryonic carotid-vertebrobasilar connections were present in 20% of children. Hemangiomas were ipsilateral to arteriopathy in all but 1 case. The frontotemporal and/or mandibular facial segments were involved in 97% of cases, but no other specific associations between arteriopathy location and hemangioma sites were detected. All cases with posterior fossa anomalies had either ICA anomalies or persistent embryonic carotid-basilar connections. CONCLUSIONS: The arteriopathy of PHACE syndrome commonly involves the ICA and its embryonic branches, ipsilateral to the cutaneous hemangioma, with dysgenesis and abnormal arterial course the most commonly noted abnormalities. Brain abnormalities are also typically ipsilateral.


Journal of Magnetic Resonance Imaging | 2007

Intracranial time-of-flight MR angiography at 7T with comparison to 3T.

Cornelius von Morze; Duan Xu; Derk D. Purcell; Christopher P. Hess; Pratik Mukherjee; David Saloner; Douglas A.C. Kelley; Daniel B. Vigneron

To establish the feasibility of intracranial time‐of‐flight (TOF) MR angiography (MRA) at 7T using phased array coils and to compare its performance to 3T.


Neurobiology of Aging | 2010

Automated MRI measures predict progression to Alzheimer's disease

Rahul S. Desikan; Howard Cabral; Fabio Settecase; Christopher P. Hess; William P. Dillon; Christine M. Glastonbury; Michael W. Weiner; Nicholas J. Schmansky; David H. Salat; Bruce Fischl

The prediction of individuals with mild cognitive impairment (MCI) destined to develop Alzheimers disease (AD) is of increasing clinical importance. In this study, using baseline T1-weighted MRI scans of 324 MCI individuals from two cohorts and automated software tools, we employed factor analyses and Cox proportional hazards models to identify a set of neuroanatomic measures that best predicted the time to progress from MCI to AD. For comparison, cerebrospinal fluid (CSF) assessments of cellular pathology and positron emission tomography (PET) measures of metabolic activity were additionally examined. By 3 years follow-up, 60 MCI individuals from the first cohort and 58 MCI individuals from the second cohort had progressed to a diagnosis of AD. Cox models on the first cohort demonstrated significant effects for the medial temporal factor [Hazards Ratio (HR) = 0.43{95% confidence interval (CI), 0.32-0.55}, p < 0.0001], the fronto-parietoccipital factor [HR = 0.59{95% CI, 0.48-0.80}, p < 0.001], and the lateral temporal factor [HR = 0.67 {95% CI, 0.52-0.87}, p < 0.01]. When applied to the second cohort, these Cox models showed significant effects for the medial temporal factor [HR = 0.44 {0.32-0.61}, p < 0.001] and lateral temporal factor [HR = 0.49 {0.38-0.62}, p < 0.001]. In a combined Cox model, consisting of individual CSF, PET, and MRI measures that best predicted disease progression, only the medial temporal factor [HR = 0.53 {95% CI, 0.34-0.81}, p < 0.001] demonstrated a significant effect. These findings illustrate that automated MRI measures of the medial temporal cortex accurately and reliably predict time to disease progression, outperform cellular and metabolic measures as predictors of clinical decline, and can potentially serve as a predictive marker for AD.

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Duan Xu

University of California

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Anders M. Dale

University of California

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Celeste M. Karch

Washington University in St. Louis

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