Author Of 2 Presentations
P0550 - BOLD signal within and around white matter lesions distinguishes multiple sclerosis and non-specific white matter disease: a 3-dimensional approach (ID 1868)
Abstract
Background
Multiple sclerosis (MS) diagnostic criteria are based upon clinical presentation and presence of white matter hyperintensities on two-dimensional magnetic resonance imaging (MRI) views. Such criteria, however, are prone to false-positive interpretations due to the presence of similar MRI findings in non-specific white-matter disease (NSWMD) states such as migraine and microvascular disease. The coexistence of age-related changes has also been recognized in MS patients, and this comorbidity further poses a diagnostic challenge.
Objectives
To investigate the physiologic profiles within and around MS and NSWMD lesions and their ability to distinguish the two disease states.
Methods
MS and NSWMD patients were scanned on a Philips 3T MRI scanner. A total of 143 MS from 23 patients and 105 NSWMD lesions from 13 patients were identified using three-dimensional (3D) T2- FLAIR images and segmented using geodesic active contouring. A dual-echo functional MRI sequence permitted near-simultaneous measurement of blood-oxygen-level-dependent signal (BOLD) and cerebral blood flow (CBF). BOLD and CBF were calculated within lesions and in 3D concentric layers surrounding each lesion. BOLD slope, an indicator of lesion metabolic capacity was calculated as the change in BOLD from a lesion through its surrounding perimeters.
Results
We observed sequential BOLD signal reductions from the lesion towards the perimeters for MS while no such decreases were observed for NSWMD lesions (p<0.0005). BOLD slope was significantly lower in MS- compared to NSWM-lesions (p=0.0006), suggesting decreased metabolic activity in MS lesions. Furthermore, BOLD signal within and around lesions significantly distinguished MS and NSWMD lesions (p=0.0007).
Conclusions
Alternative approaches beyond the evaluation of structural characteristics are needed to improve the specificity of lesion origin. Our results suggest that this technique shows promise for clinical utility in distinguishing NSWMD or MS disease states and identifying NSWMD lesions occurring in MS patients. In addition, this technique effectively adds to other methods that aim to improve the specificity in identifying the etiology of central nervous system lesions to optimize the quality of medical management provided to the patients we serve.
P0619 - Prefrontal Metabolism Explains Processing Speed Ability in Multiple Sclerosis: A Calibrated fMRI study (ID 1385)
Abstract
Background
Cognitive processing speed deficits are common in multiple sclerosis (MS). Despite this, the exact neural mechanism underlying slowed information processing speed remains unknown. Furthermore, functional magnetic resonance imaging (fMRI) using only blood-oxygen-level-dependent signal may not be sensitive to MS-related metabolic changes affecting processing speed ability. Previous work has shown that cerebral metabolism in motor and visual areas are associated with performance on motor and visual tasks, however, it is unknown if task-based metabolism in the dorso-lateral prefrontal cortex (dlPFC), a region known to be involved in processing speed, is related to the slowed processing speed observed in MS.
Objectives
We aim to assess whether metabolism in the dlPFC, a processing speed region, is associated with MS-related processing speed deficits.
Methods
MS and healthy control (HC) participants who met inclusion criteria were scanned using a 3T MRI scanner with a dualecho calibrated fMRI (cfMRI) sequence which provided nearsimultaneous measures for both cerebral blood flow (CBF) and BOLD signal. During imaging, participants performed a block-design digit-symbol substitution task (DSST) that required the viewing of a digit-symbol pairing key and responding as to whether a probe digit-symbol pair matched the key as fast as they could using button boxes. A hypercapnia gas challenge involving periodic inhalation of room air (4 min) and 5% CO2 (6 min) permitted measures of cerebral metabolic rate of oxygen (CMRO2). Data were preprocessed and average percent signal change from baseline was calculated in each voxel providing BOLD and CBF time series. The anatomical region of interest (ROI) was defined as dlPFC after Freesurfer cortical parcellation. Regression analyses were performed controlling for ROI size to assess whether BOLD, CBF, or CMRO2 could explain variability in processing speed ability.
Results
An independent-samples t-test showed that the MS group had a significantly higher response time (RT) for the DSST (t[50]=3.12, p=.003) compared to HCs. Within the MS group, regression analyses using RT for correct trials as the dependent factor were not significant for BOLD and CBF PSC but was significant for CMRO2 (R2=.170, p=.053) after controlling for number of voxels within the ROI. No regression analyses were significant within the HC group.
Conclusions
Our analyses suggest that metabolism, not BOLD or CBF, in dlPFC, a region known to involved in processing speed, explains MS-related slowed processing speed.