Eung Yeop Kim¹, Young Noh², Young-Hee Sung², and Jongho Lee^3
1Radiology, Gachon University Gil Medical Center, Incheon, ., Korea, ²Neurology, Gachon University Gil Medical Center, Incheon, ., Korea, ³Electrical and Computer Engineering, Seoul National University, Seoul, ., Korea

In the early stage of IPD, patients often present asymmetric motor symptoms. We hypothesized that dopaminergic cell loss is observable by the structural change in the region of the nigrosome 1 at 3T MRI. We acquired DAT PET data and 3T MRI data from 24 early-stage IPD patients and correlated the laterality of the imaging results with the patient symptoms. The abnormality involving the nigrosome 1 can be detected at 3T MRI with accuracy of 94.6%. The clinical laterality is in higher concordance with the laterality on nigrosome 1 MRI at 3T than that on dopamine transporter PET.

Stefan Schwarz¹, Olivier Mougin¹, Yue Xing¹, Ania Blazejewska¹, Lesley Martin¹, Nin Bajaj², Dorothee Auer¹, and Penny Gowland^1
1Sir Peter Mansfield Imaging Cetre, University of Nottingham, Nottingham, Nottinghamshire, United Kingdom, ²Division of Neurology, Nottingham University Hospitals NHS Trust, Nottingham, Nottinghamshire, United Kingdom

Nigrosomes 1-5 can be detected at 7T and are less visible in PD patients than in controls. The laterality of loss of the nigrosomes correlates better with disease laterality than DaTscan results for this group. The variation in nigrosome visibility and nigrsome T2*w signal with log(UPDRS) suggests that these measures may provide a quantitative biomarker of PD progression.

Kenji Ito¹, Makoto Sasaki¹, Chigumi Ohtuka², Suguru Yokosawa³, Taisuke Harada¹, Ikuko Uwano¹, Fumio Yamashita¹, Satomi Higuchi¹, and Yasuo Terayama^2
1Division of Ultrahigh Field MRI, Institute for Biomedical Sciences, Iwate Medical University, Yahaba, Iwate, Japan, ²Department of Neurology and Gerontology, Iwate Medical University, Morioka, Iwate, Japan, ³Central Research Laboratory, Hitachi, Ltd., Kokubunji, Tokyo, Japan

The differential diagnosis of early-stage parkinsonisms, such as Parkinson�fs disease, multiple system atrophy, and progressive supranuclear palsy is often difficult. Hence, we investigated whether diffusion kurtosis imaging (DKI) with a quantitative imaging marker, the diffusion magnetic resonance parkinsonism index (dMRPI), can help to differentiate between these disorders. The dMRPI of mean kurtosis (MK) differed significantly among the patients compared to the dMRPI of fractional anisotropy/mean diffusivity, conventional MRPI, and 123I-metaiodobenzylguanidine scintigraphy. The sensitivities and specificities of dMRPI-MK for the differentiations were both over 80%. This quantitative index can therefore contribute to early differential diagnoses of neurodegenerative disorders showing parkinsonism.

Ivana De Lucia¹, An Vo¹, Meggan Mackay², Peter B Kingsley³, Bruce Volpe², Cynthia Aranow², David Eidelberg¹, Betty M Diamond², and Aziz M Ulug^1,4
1Center for Neurosciences, Feinstein Institute for Medical Research, Manhasset, New York, United States, ²Center for Autoimmune Diseases, Feinstein Institute for Medical Research, Manhasset, New York, United States, ³North Shore University Hospital, Manhasset, New York, United States, ⁴Institute of Biomedical Engineering, Bogazici University, Istanbul, Turkey

Neuro psychiatric manifestations of SLE

Freya-Merret Girault¹, Rolf Gruetter^1,2, and Joao M.N. Duarte^1
1LIFMET, EPFL, Lausanne, Vaud, Switzerland, ²Radiology, UNIL and UNIGE, Lausanne and Geneva, Vaud, Switzerland

Insulin signalling deregulation in diabetes deteriorates brain structure and function leading to cognitive deficits. We performed a longitudinal multimodal magnetic resonance imaging (MRI) and spectroscopy (¹H and ¹³C MRS) study in insulin-resistant Goto-Kakizaki and control Wistar rats, as well as behavioural analyses, to elucidate early brain metabolic modifications associated to memory impairment in diabetes. We concluded that altered brain energy metabolism induced neurochemical alterations that were associated with the degree of brain dysfunction, namely impaired memory performance.

Swarupa Kancherla¹, Ed X. Wu², and Kevin C. Chan^1,3
1Department of Ophthalmology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States, ²Department of Electrical and Electronic Engineering, The University of Hong Kong, Pokfulam, Hong Kong, China, ³Department of Bioengineering, Swanson School of Engineering, University of Pittsburgh, Pittsburgh, Pennsylvania, United States

This study used diffusion tensor imaging, manganese-enhanced MRI, and chromium-enhanced MRI to evaluate the structure and physiology of the visual system in experimental diabetes, and elucidate the initial structures compromised in streptozotocin (STZ)-induced type 1 diabetic rats. Our results suggest that STZ-induced type 1 diabetes leads to structural changes of the distal optic nerve before MRI-detectable changes in retina, optic tract, superior colliculus, or lateral geniculate nucleus.

Esmaeil Davoodi Bojd¹, Li Zhang¹, Guangliang Ding¹, Siamak Nejad-Davarani¹, ZhengGang Zhang¹, Lian Li¹, QingJiang Li¹, Michael Chopp¹, and Quan Jiang^1
1Neurology, Henry Ford Health System, Detroit, Michigan, United States

This work demonstrates the first investigation of glymphatic impairment after diabetes in rat using MRI. Gd-DTPA contrast agent is used to monitor the glymphatic pathways by MR imaging. Using an equivalent electrical circuit for the glymphatic system, the clearance rate of CA from the brain is estimated. The results show that the CA remains much longer in diabetic brain than normal one. This means that the CSF moves slower in diabetic rats. The proposed approach can be used to determine quantitatively the effect of treatment after neurological disorder, such as diabetes.

Satish Krishnamurthy¹, Jie Li¹, Yimin Shen², and E Mark Haacke^2
1Department of Neurosurgery, SUNY Upstate Medical University, Syracuse, NY, United States, ²Radiology, Wayne state university, Detroit, MI, United States

We hypothesized that macromolecular transportation is altered in communicating hydrocephalus rats. SWI was used to monitoring iron tagged dextran transportation in rat brains via intraventricular delivery. Fe-Dextran clearance time depended on the dose. Distribution kinetics of Fe-Dextran in cerebral ventricles and parenchyma was clearly different in hydrocephalus rats compared to normal rats. The tracer entering the brain tissue via para-arterial pathways was rapidly cleared and did not build up in the brain parenchyma or vessel wall for normal rats while there was an obvious delay in clearance with a significant increase in Fe-Dextran in the veins for the hydrocephalus rats.

Ian Tagge^1,2, Steven Kohama³, Jim Pollaro¹, Lawrence Sherman³, Dennis Bourdette⁴, Randy Woltjer⁴, Scott Wong³, and William Rooney^1,2
1Advanced Imaging Research Center, Oregon Health & Science University, Portland, Oregon, United States, ²Biomedical Engineering, Oregon Health & Science University, Portland, OR, United States, ³Oregon National Primate Research Center, Oregon Health & Science University, Oregon, United States, ⁴Neurology, Oregon Health & Science University, Portland, Oregon, United States

Dynamic-contrast-enhanced magnetic resonance imaging (DCE-MRI) provides a unique method of quantitatively characterizing neurovascular properties in-vivo. Pharmacokinetic modeling of DCE-MRI data allows quantification of vascular properties, such as BBB permeability, that are sensitive to disease state. Japanese Macaque Encephalomyelitis (JME) is a spontaneous non-human primate analog of human MS. We adopted a short-term longitudinal study design to investigate lesion morphological and microvascular changes in acute JME. Lesions are observed to be fairly stable within approximately 24 hrs, but substantial changes can occur in as few as 3 days. Acute lesions with elevated BBB permeability arise from NABT rapidly (< 7 days).

Michael D. Boska¹, Prasanta K. Dash², Jaclyn Knibbe², Adrian A. Epstein^1,2, Robin High³, Edward Makarov², Harris A. Gelbard⁴, Larisa Poluektova², Howard E. Gendelman², and Santhi Gorantla^2
1Radiology, University of Nebraska Medical Center, Omaha, NE, United States, ²Pharmacology and Experimental Neurosciences, University of Nebraska Medical Center, Omaha, NE, United States, ³College of Public Health, Biostatistics, University of Nebraska Medical Center, Omaha, NE, United States, ⁴5Department of Neurology, Center for Neural Development and Disease, University of Rochester Medical Center, Rochester, NY, United States

Peripheral systemic HIV-1 infection in mice containing a human immune system was studied to determine effects of long term infection on brain metabolism and neuropathology. Cortical reductions of synapses and oligodendrocyte function correlated to alterations in N-acetyl aspartate, creatine, myoinostitol, and glutamate. Alterations in creatine and NAA show the opposing effects of synaptic loss and loss of oligodendrocyte function. These results can be used to address some of the variability in spectroscopic results found in literature reports from HIV-1 infected animals and patients.