
Contributions
Abstract: EP1441
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - Imaging
Introduction: Arterial Spin Labelling (ASL) is a noninvasive MRI technique that permits a quantitative assessment of cerebral function, but few studies exist in MS. It is hypothesized that low GM perfusion in MS could reflect decreased metabolism secondary to neuronal loss or dysfunction, with a predilection for progressive forms of MS. Increased white matter (WM) perfusion may indicate increased metabolic activity due to inflammation1. Cortical perfusion is impaired even in early MS and is detectable prior to the development of cortical volume loss2, which suggest ASL measurements may be a biomarker of reversible neuronal dysfunction prior to substantive tissue loss. This work is part of an ongoing study of cortical function and structure in 30 patients with RRMS commencing disease modifying therapy with dimethyl fumarate (Tecfidera).
Methods: 6 RRMS patients (5F, 1M aged 24-56Y, mean=43.5Y), 6 controls (5F, 1M aged 26-40Y, mean=32.5Y) were imaged on a 3T scanner with 8 ch head coil. Acquisitions: T2 FLAIR (TE/TR=162/8000ms, TI= 2181ms, resolution = 0.47x0.47x0.6 mm3 , IR-SPGR (TE/TR=2.8/7.1 ms, TI=450 ms, FA=12°, resolution = 0.47x0.47x0.7 mm3), ASL pCASL labeling with 8-arm 3D stack-of-spirals read-out (inflow time=1525 ms, bolus length=1525 ms, resolution=1.88x1.88x5 mm3). The ASL images were partial volume corrected using a combined deblurring and linear regression algorithm to separate voxels into GM and WM CBF. ROIs were created using Freesurfer.
Results: The GM perfusion was higher in the patient group for each cortical region. Controls: frontal: 79.9±8.4, central: 70.0±6.3, parietal: 67.3±6.9, temporal: 66.1± 5.3, occipital: 64.9±6.5, deep GM: 60.4±3.0. Patients: frontal: 81.5±13.0, central: 80.1±10.9, parietal: 74.7±8.8, temporal: 71.4±11.3, occipital: 72.0± 11.2, deep GM: 67.2±11.6. The WM was lower for patients, 34.2±7.6 versus 35.3±1.8.
(All units: ml/100g/min). Difference between 2 groups was significant, p=0.03.
Discussion: Diffusely increased cortical and deep GM perfusion could indicate compensatory metabolic change, or a primary pathogenic event, in patients with RRMS3.
Conclusion: Our results are discordant with previous studies that indicate reduced GM perfusion in RRMS, potentially reflecting dynamic changes in GM perfusion and metabolism in early disease. Exploration of this hypothesis in a larger, longitudinal cohort will follow.
References:
1. Rashid JNNP 2004
2. Debernard JNNP 2014
3. Peruzzo J Cere Blood Flow Metab 2013 Mar 33(3)
Disclosure:
Ruth Oliver: nothing to disclose
Linda Ly: nothing to disclose
Heidi Beadnall: nothing to disclose
Chenyu Wang: nothing to disclose
Todd Hardy: nothing to disclose
Michael Barnett has received institutional support for research activities, speaking and consulting from Biogen, Genzyme, Novartis, Teva and Roche; and travel support from Novartis and Biogen.
This study receives funding from Biogen.
Abstract: EP1441
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - Imaging
Introduction: Arterial Spin Labelling (ASL) is a noninvasive MRI technique that permits a quantitative assessment of cerebral function, but few studies exist in MS. It is hypothesized that low GM perfusion in MS could reflect decreased metabolism secondary to neuronal loss or dysfunction, with a predilection for progressive forms of MS. Increased white matter (WM) perfusion may indicate increased metabolic activity due to inflammation1. Cortical perfusion is impaired even in early MS and is detectable prior to the development of cortical volume loss2, which suggest ASL measurements may be a biomarker of reversible neuronal dysfunction prior to substantive tissue loss. This work is part of an ongoing study of cortical function and structure in 30 patients with RRMS commencing disease modifying therapy with dimethyl fumarate (Tecfidera).
Methods: 6 RRMS patients (5F, 1M aged 24-56Y, mean=43.5Y), 6 controls (5F, 1M aged 26-40Y, mean=32.5Y) were imaged on a 3T scanner with 8 ch head coil. Acquisitions: T2 FLAIR (TE/TR=162/8000ms, TI= 2181ms, resolution = 0.47x0.47x0.6 mm3 , IR-SPGR (TE/TR=2.8/7.1 ms, TI=450 ms, FA=12°, resolution = 0.47x0.47x0.7 mm3), ASL pCASL labeling with 8-arm 3D stack-of-spirals read-out (inflow time=1525 ms, bolus length=1525 ms, resolution=1.88x1.88x5 mm3). The ASL images were partial volume corrected using a combined deblurring and linear regression algorithm to separate voxels into GM and WM CBF. ROIs were created using Freesurfer.
Results: The GM perfusion was higher in the patient group for each cortical region. Controls: frontal: 79.9±8.4, central: 70.0±6.3, parietal: 67.3±6.9, temporal: 66.1± 5.3, occipital: 64.9±6.5, deep GM: 60.4±3.0. Patients: frontal: 81.5±13.0, central: 80.1±10.9, parietal: 74.7±8.8, temporal: 71.4±11.3, occipital: 72.0± 11.2, deep GM: 67.2±11.6. The WM was lower for patients, 34.2±7.6 versus 35.3±1.8.
(All units: ml/100g/min). Difference between 2 groups was significant, p=0.03.
Discussion: Diffusely increased cortical and deep GM perfusion could indicate compensatory metabolic change, or a primary pathogenic event, in patients with RRMS3.
Conclusion: Our results are discordant with previous studies that indicate reduced GM perfusion in RRMS, potentially reflecting dynamic changes in GM perfusion and metabolism in early disease. Exploration of this hypothesis in a larger, longitudinal cohort will follow.
References:
1. Rashid JNNP 2004
2. Debernard JNNP 2014
3. Peruzzo J Cere Blood Flow Metab 2013 Mar 33(3)
Disclosure:
Ruth Oliver: nothing to disclose
Linda Ly: nothing to disclose
Heidi Beadnall: nothing to disclose
Chenyu Wang: nothing to disclose
Todd Hardy: nothing to disclose
Michael Barnett has received institutional support for research activities, speaking and consulting from Biogen, Genzyme, Novartis, Teva and Roche; and travel support from Novartis and Biogen.
This study receives funding from Biogen.