Contributions
Abstract: P616
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 24 Neuropsychology
Objective: To assess the course of cognitive function of MS patients from a single centre and the relationship to clinical disability and MRI metrics.
Patients and methods: 116 patients with MS who had undergone clinical and cognitive assessment up to ten years ago were invited to attend a cognitive follow-up testing in 2016. Disability was measured using the Expanded Disability Status Scale (EDSS). Cognition (verbal learning and memory, visuospatial learning and memory, processing speed, attention, verbal fluency) was assessed by the “Brief Repeatable Battery of Neuropsychological Tests”. T2-lesion load, normalized brain, thalamic and hippocampal volume were assessed at baseline and follow-up at the same 3T magnet.
Results: 30 MS patients (26% of the baseline cohort) consented to follow-up cognitive assessment after a mean follow-up of seven years (1.6 SD; range 4-10 years; 17 female, 56.7%; 5 clinically isolated syndrome, 22 relapsing-remitting MS, 3 secondary-progressive MS at baseline). Their mean age at baseline was 37 years (10 SD). At baseline, half of these patients had a cognitive deficit in at least one domain and 13% (N=4) showed deficits in at least 3 domains (defined by 1.5 SDs below standardized mean). Processing speed was the most affected domain (47%). Despite a significant increase in the median EDSS (2.0 vs. 3.3, p< 0.05), patients did not change regarding their cognitive function in any domain. Mean T2-lesion load did not significantly increase. Annualized mean percent brain volume change was -0.35%. Higher lesion load and lower brain volume at baseline correlated with higher EDSS scores at baseline (r=0.37 /-0.58, respectively) and worse cognitive function at baseline and follow-up. Lower thalamic or hippocampal volume correlated with worse cognitive function at baseline and follow-up.
Conclusions: In this small cohort of MS patients we found no evidence of further cognitive deterioration over 7 years of follow-up despite a high prevalence of cognitive deficits at baseline. Interestingly this was paralleled by MRI changes likely not exceeding normal ageing although overall disability as measured with the EDSS deteriorated. This discrepancy needs further exploration.
Disclosure:
Daniela Pinter receives funding from the Austrian Science fund (T 690- B23) and has received funding for travel from Merck.
Franz Fazekas serves on scientific advisory boards for Bayer Schering Pharma, Biogen Idec, Merck Serono, Novartis, D-Pharm Ltd., and Teva Pharmaceutical Industries Ltd./sanofi-aventis; serves on the editorial boards of Cerebrovascular Diseases, Multiple Sclerosis, the Polish Journal of Neurology and Neurosurgery, Stroke, and the Swiss Archives of Neurology and Psychiatry; and has received speaker honoraria from Biogen Idec, Bayer Schering Pharma, Merck Serono, and sanofi-aventis.
Anna Damulina reports no disclosures.
Lukas Pirpamer reports no disclosures.
Alexander Pichler reports no disclosures.
Michael Khalil has received funding for travel and speaker honoraria from Bayer Schering Pharma, Novartis, Genzyme, Merck, Shire, Biogen Idec and Teva Pharmaceutical Industries.
Stefan Ropele reports no disclosures.
Siegrid Fuchs serves on scientific advisory boards and / or has received speaker honoraria from Biogen Idec, Merck, Novartis; Roche, TEVA Pharmaceutical Industries and Sanofi-Aventis.
Christian Enzinger received funding for traveling and speaker honoraria from Biogen Idec, Bayer Schering Pharma, Merck Serono, Novartis, Genzyme and Teva Pharmaceutical Industries Ltd./sanofi-aventis, Shire; received research support from Merck Serono, Biogen Idec, and Teva Pharmaceutical Industries Ltd./sanofi-aventis; and serves on scientific advisory boards for Bayer Schering Pharma, Biogen Idec, Merck Serono, Novartis, Genzyme, Roche, and Teva Pharmaceutical Industries Ltd./sanofi- Aventis.
Abstract: P616
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 24 Neuropsychology
Objective: To assess the course of cognitive function of MS patients from a single centre and the relationship to clinical disability and MRI metrics.
Patients and methods: 116 patients with MS who had undergone clinical and cognitive assessment up to ten years ago were invited to attend a cognitive follow-up testing in 2016. Disability was measured using the Expanded Disability Status Scale (EDSS). Cognition (verbal learning and memory, visuospatial learning and memory, processing speed, attention, verbal fluency) was assessed by the “Brief Repeatable Battery of Neuropsychological Tests”. T2-lesion load, normalized brain, thalamic and hippocampal volume were assessed at baseline and follow-up at the same 3T magnet.
Results: 30 MS patients (26% of the baseline cohort) consented to follow-up cognitive assessment after a mean follow-up of seven years (1.6 SD; range 4-10 years; 17 female, 56.7%; 5 clinically isolated syndrome, 22 relapsing-remitting MS, 3 secondary-progressive MS at baseline). Their mean age at baseline was 37 years (10 SD). At baseline, half of these patients had a cognitive deficit in at least one domain and 13% (N=4) showed deficits in at least 3 domains (defined by 1.5 SDs below standardized mean). Processing speed was the most affected domain (47%). Despite a significant increase in the median EDSS (2.0 vs. 3.3, p< 0.05), patients did not change regarding their cognitive function in any domain. Mean T2-lesion load did not significantly increase. Annualized mean percent brain volume change was -0.35%. Higher lesion load and lower brain volume at baseline correlated with higher EDSS scores at baseline (r=0.37 /-0.58, respectively) and worse cognitive function at baseline and follow-up. Lower thalamic or hippocampal volume correlated with worse cognitive function at baseline and follow-up.
Conclusions: In this small cohort of MS patients we found no evidence of further cognitive deterioration over 7 years of follow-up despite a high prevalence of cognitive deficits at baseline. Interestingly this was paralleled by MRI changes likely not exceeding normal ageing although overall disability as measured with the EDSS deteriorated. This discrepancy needs further exploration.
Disclosure:
Daniela Pinter receives funding from the Austrian Science fund (T 690- B23) and has received funding for travel from Merck.
Franz Fazekas serves on scientific advisory boards for Bayer Schering Pharma, Biogen Idec, Merck Serono, Novartis, D-Pharm Ltd., and Teva Pharmaceutical Industries Ltd./sanofi-aventis; serves on the editorial boards of Cerebrovascular Diseases, Multiple Sclerosis, the Polish Journal of Neurology and Neurosurgery, Stroke, and the Swiss Archives of Neurology and Psychiatry; and has received speaker honoraria from Biogen Idec, Bayer Schering Pharma, Merck Serono, and sanofi-aventis.
Anna Damulina reports no disclosures.
Lukas Pirpamer reports no disclosures.
Alexander Pichler reports no disclosures.
Michael Khalil has received funding for travel and speaker honoraria from Bayer Schering Pharma, Novartis, Genzyme, Merck, Shire, Biogen Idec and Teva Pharmaceutical Industries.
Stefan Ropele reports no disclosures.
Siegrid Fuchs serves on scientific advisory boards and / or has received speaker honoraria from Biogen Idec, Merck, Novartis; Roche, TEVA Pharmaceutical Industries and Sanofi-Aventis.
Christian Enzinger received funding for traveling and speaker honoraria from Biogen Idec, Bayer Schering Pharma, Merck Serono, Novartis, Genzyme and Teva Pharmaceutical Industries Ltd./sanofi-aventis, Shire; received research support from Merck Serono, Biogen Idec, and Teva Pharmaceutical Industries Ltd./sanofi-aventis; and serves on scientific advisory boards for Bayer Schering Pharma, Biogen Idec, Merck Serono, Novartis, Genzyme, Roche, and Teva Pharmaceutical Industries Ltd./sanofi- Aventis.