ECTRIMS eLearning

Comparison of cortical perfusion between relapse-remitting multiple sclerosis patients and healthy controls measured using arterial spin labelling MRI
Author(s): ,
R.A Oliver
Affiliations:
Brain and Mind Centre, Sydney Neuroimaging Analysis Centre;Medical School, University of Sydney, Sydney, NSW, Australia
,
L Ly
Affiliations:
Brain and Mind Centre, Sydney Neuroimaging Analysis Centre
,
H Beadnall
Affiliations:
Medical School, University of Sydney, Sydney, NSW, Australia
,
C Wang
Affiliations:
Brain and Mind Centre, Sydney Neuroimaging Analysis Centre;Medical School, University of Sydney, Sydney, NSW, Australia
,
T Hardy
Affiliations:
Medical School, University of Sydney, Sydney, NSW, Australia
M.H Barnett
Affiliations:
Brain and Mind Centre, Sydney Neuroimaging Analysis Centre;Medical School, University of Sydney, Sydney, NSW, Australia
ECTRIMS Learn. Oliver R. 09/14/16; 145537; EP1441
Ruth A. Oliver
Ruth A. Oliver
Contributions
Abstract

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.

By clicking “Accept Terms & all Cookies” or by continuing to browse, you agree to the storing of third-party cookies on your device to enhance your user experience and agree to the user terms and conditions of this learning management system (LMS).

Cookie Settings
Accept Terms & all Cookies