http://hdl.handle.net/10027/7314 Tue, 18 Jun 2013 05:46:48 GMT 2013-06-18T05:46:48Z http://hdl.handle.net/10027/8438 Etiologies of Chronic Anterior Uveitis at a Tertiary Referral Center over 35 years. Birnbaum, Andrea D.; Little, Deborah M.; Tessler, Howard H.; Goldstein, Debra A. Post print version of article may differ from published version. © 2011 Informa Healthcare. The definitive version is available through Informa Healthcare at DOI: 10.3109/09273948.2010.519852 Fri, 01 Jul 2011 05:00:00 GMT http://hdl.handle.net/10027/8438 2011-07-01T05:00:00Z http://hdl.handle.net/10027/8224 Anatomical Correlates of Age Related Working Memory Declines Schulze, Evan T.; Geary, Elizabeth K.; Susmaras, Teresa M.; Paliga, James T.; Maki, Pauline M.; Little, Deborah M. Aging studies consistently show a relationship between decreased gray matter volume and decreased performance on working memory tasks. Few aging studies have investigated white matter changes in relation to functional brain changes during working memory tasks. Twenty-five younger and 25 older adults underwent anatomical magnetic resonance imaging (MRI) scans to measure gray matter volume, diffusion tensor imaging (DTI) to measure fractional anisotropy (FA) as a measure of white matter integrity, and functional magnetic resonance imaging (fMRI) while performing a working memory task. Significant increases in activation (fMRI) were seen in the left dorsal and ventral lateral prefrontal cortex with increased working memory load and with increased age (older showing greater bilateral activation). Partial correlational analyses revealed that even after controlling for age, frontal FA correlated significantly with fMRI activation during performance on the working memory task. These findings highlight the importance of white matter integrity in working memory performance associated with normal aging. Copyright © 2011 Evan T. Schulze et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. doi:10.4061/2011/606871 Mon, 01 Aug 2011 05:00:00 GMT http://hdl.handle.net/10027/8224 2011-08-01T05:00:00Z http://hdl.handle.net/10027/7783 Detection of Intracranial In-Stent Restenosis Using Quantitative Magnetic Resonance Angiography Amin-Hanjani, Sepideh; Alaraj, Ali; Calderon-Arnulphi, Mateo; Aletich, Victor A.; Thulborn, Keith R.; Charbel, Fady T. BACKGROUND AND PURPOSE: In-stent restenosis (ISR) after angioplasty/stenting for intracranial stenosis has been reported in up to 25% to 30% of patients. Detection and monitoring of ISR relies primarily on serial catheter angiography, because noninvasive imaging methods are typically hampered by stent-related artifact. We examined the value of serial vessel flow measurements using quantitative magnetic resonance angiography (QMRA) in detection of ISR. Material and METHODS: Records of patients undergoing stenting for intracranial symptomatic stenosis >50% between 2005 and 2009 were retrospectively reviewed. Angiographic images were graded by a blinded neurointerventionalist for stenosis pretreatment, immediately after treatment, and during follow-up. Flow in the affected vessel measured by QMRA was recorded; > 25% reduction in flow was considered indicative of an adverse change. Clinical data regarding neurological outcome were also collected. RESULTS: Twenty-eight patients underwent stenting during the time interval studied. Of these, 12 patients (mean age, 55.5 years; 8 female) had contemporaneous angiography and QMRA and were analyzed. Median follow-up was 9 months. Six patients (50%) demonstrated angiographic restenosis 2 to 12 months after treatment; all had an analogous decrease in flow in the vessel of interest. Of 3 patients with more severe flow decrement (> 50%), 2 experienced stroke. None of the patients without angiographic ISR demonstrated a flow decrease on QMRA. CONCLUSIONS: In this preliminary series, flow decrease on QMRA is highly predictive of angiographic ISR. Additionally, the degree of flow decrement correlates with symptomatic ISR. QMRA may provide a useful noninvasive tool for serial monitoring after intracranial stenting. The original version of this publication is available through the American Heart Association (www.ahajournals.org) at DOI: 10.1161/STROKEAHA.110.594739. Fri, 01 Oct 2010 05:00:00 GMT http://hdl.handle.net/10027/7783 2010-10-01T05:00:00Z http://hdl.handle.net/10027/7688 Combined Measures of Movement and Force Variability Distinguish Parkinson's Disease from Essential Tremor Poon, Cynthia; Robichaud, Julie A.; Corcos, Daniel M.; Goldman, Jennifer G.; Vaillancourt, David E. Objective: To examine whether behavioral and electrophysiological measures of motor performance accurately differentiate Parkinson’s disease (PD) and essential tremor (ET). Methods: Twenty-four patients (12 PD; 12 ET) performed isometric force, ballistic movements, and tremor tasks. Receiver operating characteristic (ROC) analyses were conducted on all dependent measures that were significantly different between the two patient groups. Results: Patients with PD were more impaired on measures of movement deceleration than ET. Patients with ET were more impaired on measures of force variability than PD. ROC analyses revealed that sensitivity and specificity were excellent when combining measures during the isometric force task (torque rise time and force variability; 92% sensitivity and 92% specificity; AUC = 0.97). When combining measures across the force and movement tasks, the ROC analysis revealed improved sensitivity and specificity (force variability and peak deceleration; 92% sensitivity and 100% specificity; AUC = 0.99). Conclusions: Combining measures of force variability and movement deceleration accurately differentiate patients with PD from those with ET with high sensitivity and specificity. Significance: If validated in a larger sample, these measures can serve as markers to confirm the diagnosis of PD or ET and thus, enhance decision making for appropriate treatments for patients with these respective diseases. NOTICE: this is the author’s version of a work that was accepted for publication in Clinical Neurophysiology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Clinical Neurophysiology, [(May 12, 2011)] DOI: 10.1016/j.clinph.2011.04.014. The original publication is available at www.elsevier.com. Thu, 12 May 2011 05:00:00 GMT http://hdl.handle.net/10027/7688 2011-05-12T05:00:00Z