Contributions
Abstract: P1040
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Introduction: Depression occurs often in multiple sclerosis (MS), and its clinical manifestation is very similar to that of patients with major depression disorder (MDD) without MS. From a biological perspective, structural and functional disconnection of limbic and frontal regions is hypothesized to be a key feature. We therefore simultaneously investigated structural and functional changes of the fronto-limbic system in depressed (D) MS patients, non-depressed (nD) MS patients and healthy controls (HCs). Additionally, we explored the effect of depression on cognitive functioning.
Methods: Patients were selected from two different cohorts:
1) 22 moderate-to-severely DMS patients, scoring ≥20 on the Beck Depression Inventory (disease duration 8.2±7.7 years);
2) 21 nDMS patients (disease duration 15.3±8.3 years) and 12 HCs scoring < 8 on the Hospital Anxiety and Depression Scale - Depression (HADS-D).
All subjects underwent magnetic resonance imaging (MRI; 1.5T) and cognitive testing (an equivalent of the brief repeatable battery of neuropsychological tests). Volumes of white matter (WM), grey matter, and WM lesions were obtained. The amygdala, hippocampus, and thalamus were defined as key limbic structures from which the volumes were obtained. Fractional anisotropy (FA) of fronto-limbic tracts and resting-state functional connectivity (FC) between limbic and frontal areas was measured.
Results: Compared to HCs, DMS and nDMS patients performed worse on neuropsychological tests for verbal memory and learning (P< 0.01). Information processing speed was decreased in DMS patients compared to HCs only (P< 0.02). Despite a shorter disease duration of DMS patients (P< 0.01), no differences in cognitive functioning were detected between the patient groups. Both MS groups showed WM and limbic atrophy relative to HCs. Compared to nDMS patients, DMS patients had lower WM volume (P=0.01), lower FA of the uncinate fasciculus (P< 0.01), and decreased FC between the amygdala and frontal regions (P=0.01). These differences were more pronounced in DMS patients with a MDD diagnosis in the past 6 months compared to nDMS patients with a HADS-D < 5
(maximum of HCs; post-hoc analysis).
Conclusion: The present results suggest no effect of depression on cognitive functioning, However, on MRI, DMS patients showed more pronounced (MS) pathology, i.e. structural and functional changes in temporo-frontal regions, suggestive of fronto-limbic disconnection, which is in line with findings in MDD.
Disclosure:
Q. van Geest has nothing to disclose.
R.E. Boeschoten has nothing to disclose.
M.J. Keijzer has nothing to disclose.
M.D. Steenwijk has nothing to disclose.
P.J.W. Pouwels receives research support from the Dutch MS Research Foundation, grant number 14-876.
J.H. Smit has nothing to disclose.
B.M.J. Uitdehaag has received personal compensation for consulting from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche en TEVA.
J.J.G. Geurts is an editor of Multiple Sclerosis Journal, a member of the editorial boards of BMC Neurology, Neurology and Frontiers in Neurology, and serves as a consultant for Biogen and Sanofi-Genzyme.
P. van Oppen has nothing to disclose.
H.E. Hulst receives research support from the Dutch MS Research Foundation, grant number 08-648 and serves as a consultant for Genzyme, Merck-Serono, Teva Pharmaceuticals and Novartis.
Abstract: P1040
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Introduction: Depression occurs often in multiple sclerosis (MS), and its clinical manifestation is very similar to that of patients with major depression disorder (MDD) without MS. From a biological perspective, structural and functional disconnection of limbic and frontal regions is hypothesized to be a key feature. We therefore simultaneously investigated structural and functional changes of the fronto-limbic system in depressed (D) MS patients, non-depressed (nD) MS patients and healthy controls (HCs). Additionally, we explored the effect of depression on cognitive functioning.
Methods: Patients were selected from two different cohorts:
1) 22 moderate-to-severely DMS patients, scoring ≥20 on the Beck Depression Inventory (disease duration 8.2±7.7 years);
2) 21 nDMS patients (disease duration 15.3±8.3 years) and 12 HCs scoring < 8 on the Hospital Anxiety and Depression Scale - Depression (HADS-D).
All subjects underwent magnetic resonance imaging (MRI; 1.5T) and cognitive testing (an equivalent of the brief repeatable battery of neuropsychological tests). Volumes of white matter (WM), grey matter, and WM lesions were obtained. The amygdala, hippocampus, and thalamus were defined as key limbic structures from which the volumes were obtained. Fractional anisotropy (FA) of fronto-limbic tracts and resting-state functional connectivity (FC) between limbic and frontal areas was measured.
Results: Compared to HCs, DMS and nDMS patients performed worse on neuropsychological tests for verbal memory and learning (P< 0.01). Information processing speed was decreased in DMS patients compared to HCs only (P< 0.02). Despite a shorter disease duration of DMS patients (P< 0.01), no differences in cognitive functioning were detected between the patient groups. Both MS groups showed WM and limbic atrophy relative to HCs. Compared to nDMS patients, DMS patients had lower WM volume (P=0.01), lower FA of the uncinate fasciculus (P< 0.01), and decreased FC between the amygdala and frontal regions (P=0.01). These differences were more pronounced in DMS patients with a MDD diagnosis in the past 6 months compared to nDMS patients with a HADS-D < 5
(maximum of HCs; post-hoc analysis).
Conclusion: The present results suggest no effect of depression on cognitive functioning, However, on MRI, DMS patients showed more pronounced (MS) pathology, i.e. structural and functional changes in temporo-frontal regions, suggestive of fronto-limbic disconnection, which is in line with findings in MDD.
Disclosure:
Q. van Geest has nothing to disclose.
R.E. Boeschoten has nothing to disclose.
M.J. Keijzer has nothing to disclose.
M.D. Steenwijk has nothing to disclose.
P.J.W. Pouwels receives research support from the Dutch MS Research Foundation, grant number 14-876.
J.H. Smit has nothing to disclose.
B.M.J. Uitdehaag has received personal compensation for consulting from Biogen Idec, Genzyme, Merck Serono, Novartis, Roche en TEVA.
J.J.G. Geurts is an editor of Multiple Sclerosis Journal, a member of the editorial boards of BMC Neurology, Neurology and Frontiers in Neurology, and serves as a consultant for Biogen and Sanofi-Genzyme.
P. van Oppen has nothing to disclose.
H.E. Hulst receives research support from the Dutch MS Research Foundation, grant number 08-648 and serves as a consultant for Genzyme, Merck-Serono, Teva Pharmaceuticals and Novartis.