Contributions
Abstract: P1067
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: Recent studies have shown cerebral hypoperfusion in multiple sclerosis (MS). Due to neurovascular coupling, neuronal activity results in increased cerebral blood flow (CBF), regulated by arterioles resistance changes. Vasoreactivity can be estimated with a hemodynamic index such as cerebrovascular reactivity (CVR). CVR changes in MS remain relatively poorly understood, with some studies showing increment, while other showing decrement. Possible causes of CBF alterations include axonal loss and reduced metabolic demand due to neurodegeneration, so grey matter (GM) atrophy should be considered in perfusion studies.
Objective: To investigate if perfusion and CVR are altered in MS and their association with atrophy.
Methods: 24 relapsing-remitting MS patients (median[range] EDSS=1[1-2.5]) and 25 age- and sex-matched Healthy Controls (HC) were imaged using 1.5T MRI. The scanning protocol included pseudo continuous arterial spin labelling (ASL), at normocapnia and hypercapnia (5%CO2), and 3D-T1 weighted images. End-tidal CO2 (etCO2) was measured during ASL acquisitions.
CBF was computed during normocapnia and hypercapnia, then registered to the corresponding 3D-T1 and to MNI space. 3D-T1 tissue segmentation was used for correcting CBF partial volume effects.
CVR was computed as the difference between CBF at hypercapnia and normocapnia, normalized by normocapnia CBF and etCO2 difference. Voxel-based morphometry was used to investigate differences in GM volume between groups. CBF and CVR differences between groups were tested both in the whole GM and in the atrophic areas with voxel-wise statistics. Family wise error corrected p-values< .05 were considered significant.
Results: Areas of GM volume loss for MS vs HC were found in the thalamus, putamen, caudate, and precentral gyrus (all bilateral). No significant CBF changes, but a significant widespread bilateral cortical CVR increase was seen in MS, not co-localized to areas of GM atrophy. CBF/CVR in atrophic regions were not statistically different between groups.
Conclusions: Although CBF at rest was not altered in MS, we found increased CVR in MS as previously shown with transcranial Doppler. Minimal GM atrophy and the absence of reduced CBF could be related to the relatively low disability of the MS cohort, while CVR increase might reflect a compensatory functional mechanism.
Disclosure: This study was in part funded by a grant awarded by the Annette Funicello Research Fundation for Neurological Diseases.
Prof. Danny JJ Wang (UCLA, CA, USA) and Siemens Healthcare S.r.l provided us with the pCASL sequence.
Maria Marcella Laganà has nothing to disclose.
Laura Pelizzari has nothing to disclose.
Niels Bergsland has nothing to disclose.
Laura Mendozzi has nothing to disclose.
Alice Pirastru has nothing to disclose.
Pietro Cecconi has nothing to disclose.
Giuseppe Baselli has nothing to disclose.
Mario Clerici. has nothing to disclose.
Raffaello Nemni has nothing to disclose.
Francesca Baglio has nothing to disclose.
Abstract: P1067
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: Recent studies have shown cerebral hypoperfusion in multiple sclerosis (MS). Due to neurovascular coupling, neuronal activity results in increased cerebral blood flow (CBF), regulated by arterioles resistance changes. Vasoreactivity can be estimated with a hemodynamic index such as cerebrovascular reactivity (CVR). CVR changes in MS remain relatively poorly understood, with some studies showing increment, while other showing decrement. Possible causes of CBF alterations include axonal loss and reduced metabolic demand due to neurodegeneration, so grey matter (GM) atrophy should be considered in perfusion studies.
Objective: To investigate if perfusion and CVR are altered in MS and their association with atrophy.
Methods: 24 relapsing-remitting MS patients (median[range] EDSS=1[1-2.5]) and 25 age- and sex-matched Healthy Controls (HC) were imaged using 1.5T MRI. The scanning protocol included pseudo continuous arterial spin labelling (ASL), at normocapnia and hypercapnia (5%CO2), and 3D-T1 weighted images. End-tidal CO2 (etCO2) was measured during ASL acquisitions.
CBF was computed during normocapnia and hypercapnia, then registered to the corresponding 3D-T1 and to MNI space. 3D-T1 tissue segmentation was used for correcting CBF partial volume effects.
CVR was computed as the difference between CBF at hypercapnia and normocapnia, normalized by normocapnia CBF and etCO2 difference. Voxel-based morphometry was used to investigate differences in GM volume between groups. CBF and CVR differences between groups were tested both in the whole GM and in the atrophic areas with voxel-wise statistics. Family wise error corrected p-values< .05 were considered significant.
Results: Areas of GM volume loss for MS vs HC were found in the thalamus, putamen, caudate, and precentral gyrus (all bilateral). No significant CBF changes, but a significant widespread bilateral cortical CVR increase was seen in MS, not co-localized to areas of GM atrophy. CBF/CVR in atrophic regions were not statistically different between groups.
Conclusions: Although CBF at rest was not altered in MS, we found increased CVR in MS as previously shown with transcranial Doppler. Minimal GM atrophy and the absence of reduced CBF could be related to the relatively low disability of the MS cohort, while CVR increase might reflect a compensatory functional mechanism.
Disclosure: This study was in part funded by a grant awarded by the Annette Funicello Research Fundation for Neurological Diseases.
Prof. Danny JJ Wang (UCLA, CA, USA) and Siemens Healthcare S.r.l provided us with the pCASL sequence.
Maria Marcella Laganà has nothing to disclose.
Laura Pelizzari has nothing to disclose.
Niels Bergsland has nothing to disclose.
Laura Mendozzi has nothing to disclose.
Alice Pirastru has nothing to disclose.
Pietro Cecconi has nothing to disclose.
Giuseppe Baselli has nothing to disclose.
Mario Clerici. has nothing to disclose.
Raffaello Nemni has nothing to disclose.
Francesca Baglio has nothing to disclose.