Ahmed Bahrani

A Novel Noncontact Diffuse Correlation Spectroscopy Device for Assessing Blood Flow in Mastectomy Skin Flaps: A Prospective Study in Patients Undergoing Prosthesis-based Reconstruction

Summary: A new advanced technology, noncontact diffuse correlation spectroscopy, has been recently developed for the measurement of tissue blood flow through analyzing the motions of red blood cells in deep tissues. This technology is portable, inexpensive, and noninvasive, and can measure up to 1.5-cm tissue depth. In this prospective study, the authors aimed to explore the use of this novel device in the prediction of mastectomy skin flap necrosis. The noncontact diffuse correlation spectroscopy device was used to measure mastectomy skin flap flow in patients undergoing mastectomy and immediate implant-based breast reconstruction before and immediately after mastectomy, and after placement of the prosthesis. Patients were tracked for the development of complications, including skin necrosis and the need for further surgery. Nineteen patients were enrolled in the study. Four patients (21 percent) developed skin necrosis, one of which required additional surgery. The difference in relative blood flow levels immediately after mastectomy in patients with or without necrosis was statistically significant, with values of 0.27 ± 0.11 and 0.66 ± 0.22, respectively (p = 0.0005). Relative blood flow measurements immediately after mastectomy show a significant high accuracy in prediction of skin flap necrosis, with an area under the receiver operating characteristic curve of 0.95 (95 percent confidence interval, 0.81 to 1). The noncontact diffuse correlation spectroscopy device is a promising tool that provides objective information regarding mastectomy skin flap viability intraoperatively, allowing surgeons early identification of those compromised and ischemic flaps with the hope of potentially salvaging them. CLINICAL QUESTION/LEVEL OF EVIDENCE: Diagnostic, IV.

White Matter Hyperintensity Associations with Cerebral Blood Flow in Elderly Subjects Stratified by Cerebrovascular Risk

OBJECTIVE This study aims to add clarity to the relationship between deep and periventricular brain white matter hyperintensities (WMHs), cerebral blood flow (CBF), and cerebrovascular risk in older persons. METHODS Deep white matter hyperintensity (dWMH) and periventricular white matter hyperintensity (pWMH) and regional gray matter (GM) and white matter (WM) blood flow from arterial spin labeling were quantified from magnetic resonance imaging scans of 26 cognitively normal elderly subjects stratified by cerebrovascular disease (CVD) risk. Fluid-attenuated inversion recovery images were acquired using a high-resolution 3-dimensional (3-D) sequence that reduced partial volume effects seen with slice-based techniques. RESULTS dWMHs but not pWMHs were increased in patients at high risk of CVD; pWMHs but not dWMHs were associated with decreased regional cortical (GM) blood flow. We also found that blood flow in WM is decreased in regions of both pWMH and dWMH, with a greater degree of decrease in pWMH areas. CONCLUSIONS WMHs are usefully divided into dWMH and pWMH regions because they demonstrate differential effects. 3-D regional WMH volume is a potentially valuable marker for CVD based on associations with cortical CBF and WM CBF.

Global Cerebral Atrophy Detected by Routine Imaging: Relationship with Age, Hippocampal Atrophy, and White Matter Hyperintensities: Risk Factors Contributing to Global Cerebral Atrophy

Interpreting the clinical significance of moderate‐to‐severe global cerebral atrophy (GCA) is a conundrum for many clinicians, who visually interpret brain imaging studies in routine clinical practice. GCA may be attributed to normal aging, Alzheimers disease (AD), or cerebrovascular disease (CVD). Understanding the relationships of GCA with aging, AD, and CVD is important for accurate diagnosis and treatment decisions for cognitive complaints.

ELIMINATING THE SOURCES OF VARIABILITY IN A SEMI-AUTOMATED WMH QUANTIFICATION METHOD

the main hippocampal-PCC white-matter fibre tract connecting the two spectroscopy voxels (Figure 1). Cognitive performance was assessed using the National Alzheimer’s Coordinating Center Neuropsychological Battery, Version 3.0. Relationships between Glu levels, tract FA, and cognitive measurements were assessed. Results: Lower hippocampal Glu levels were observed in MCI compared to NEC (p < 0.05) and as a trend in AD compared to NEC (p 1⁄4 0.07, Figure 2). In the hippocampal-PCC tract, tract FA values were lower in AD compared to NEC and varied along the tract (Figure 3). Hippocampal Glu was positively correlated with average tract FA (r 1⁄4 0.59, p < 0.05) and cognitive measurements including Figure Copy performance (r 1⁄4 0.48, p < 0.05). Figure Copy performance was also positively associated with average tract FA (r 1⁄4 0.48, p < 0.05). PCC Glu levels were not significantly different between groups or related to tract FA or cognitive measurements. Conclusions: H-MRS results in this preliminary study agreed with our previous findings at 4T. Lower FA values in the hippocampal-PCC tract of AD participants indicates less restricted diffusion and may reflect a loss of neuronal density. Lower hippocampal Glu was associated with lower FA and lower cognitive performance, suggesting that hippocampal Glu could be a biomarker of neuronal loss and cognitive performance in AD.

Trial measurement of movement-related cortical dynamics using electroencephalography and diffuse correlation spectroscopy

To better characterize movement-related neurophysiological change, the authors propose to measure not only neural activity through the electroencephalogram (EEG) but also cerebral blood flow (CBF) using a new technology, near-infrared diffuse correlation spectroscopy (DCS). A preliminary trial is described, in which EEG, DCS, and exerted force were simultaneously recorded during a cue-triggered hand grip task. Eight channels of EEG were acquired from frontal, central, and occipital regions, and DCS signals were collected from locations over frontal and motor cortex. Event-related desynchronization (ERD) was observed at the onset of hand movement and lasted until movement ceased. EEG from the motor area showed a significant ERD in the 8–13 Hz mu band (p<0.001). Mean CBF increased during the task by 6.8 % (p<0.001) in the motor location and by 4.5 % (p<0.001) in the frontal location, respectively. These preliminary observations suggest that a combination of electrical and optical measurements may provide a more complete characterization of brain dynamics related to movement. A broader study is required to explore the potential benefit of these combined measurements when used as command signals for brain-computer interfaces.

CEREBROVASCULAR DISEASE AND ALZHEIMER’S DISEASE, BUT NOT AGING, ARE ASSOCIATED WITH MODERATE TO SEVERE GLOBAL CEREBRAL ATROPHY SEEN ON CLINICAL BRAIN IMAGING STUDIES

only (Table 3). There were no group differences in baseline cognitive performance; however, Stages 1 and 2 exhibited steeper memory decline compared to Stage 0 (Figure 1). Only Stage 2 exhibited steeper executive functioning decline (p < .01; Figure 2). The tau+ only group did not differ significantly from Stage 0 on 6 of 7 measures. Baseline age moderated the relationship between biomarker group and time; older age at study entry was associated with steeper rates of decline for Stage 1 only. Conclusions:In this latemiddle-aged cohort, abnormality in both Ab and tau was associated with decline across memory and executive functioning domains, whereas Ab+

CLINICAL IMAGING, COGNITIVE, AND GENETIC RISK PROFILES IN INCIDENT MCI FOR THE PREDICTION OF LONG-TERM NEUROPATHOLOGICAL OUTCOMES AT AUTOPSY

Background:The neuropathological substrates of incident mild cognitive impairment (MCI) are heterogeneous, even when MCI subtypes are classified according to up-to-date clinical criteria. The present study investigates the predictive accuracy of brain imaging, cognitive test profiles, and ApoE status, in relation to autopsy-confirmed neuropathological outcomes focusing on Alzheimer’s (AD) and cerebrovascular disease (CVD).Methods:Clinical cognitive test profiles, brain imaging, and ApoE genotypewere available on 105 participants from a community based sample with incident MCI. Demographic, semi-quantitative imaging (Fazekas scale for CVD and Scheltens score for medial temporal lobe atrophy as a surrogate for AD), cognitive profile by domain (memory, attention/executive, language), and ApoE genotype at time of incident MCI were evaluated in relation to eventual neuropathological outcomes in 34 subjects with subsequent autopsy that included analysis of AD and CVD features (mean time from MCI diagnosis to death 4.1 years, range 0-14 years).Results:There were no baseline differences between subjects with and without AD or CVD neuropathological changes for demographic, ApoE, or imaging variables, with the exception of increased global cerebral atrophy (p<0.05) and white matter hyperintensities (p<0.001) for the subjects with neuropathological CVD diagnoses. Only ApoE e4 status (65% correct classification; p<0.05) or the presence of any one imaging, cognitive, ApoE genotype risk (71% correct classification; p<0.01) predicted AD pathology at autopsy. Imaging evidence of CVD at the time of MCI diagnosis (79% correct classification; p<0.005) or the presence of any one imaging, cognitive, or ApoE genotype risk (76% correct classification; p<0.05) predicted CVD pathology at autopsy. Conclusions: Genetic risk and clinical imaging outperformed cognitive test profiles at first diagnosis of MCI in the prediction of the eventual neuropathological outcome. These results suggest that utilization of routine clinical tests, covered by most third party payers, as biomarkers for the prediction of long term outcomes in MCI is feasible.