Contributions
Abstract: 58
Type: Oral
Abstract Category: Clinical aspects of MS - 8 Clinical assessment tools
Background: Upper extremity (UE) dysfunction is present in up to 80% of patients with multiple sclerosis (MS) and occurs early in the disease. Importantly, subtle but meaningful UE deficits are often overlooked during routine clinical exam and on crude measures such as the expanded disability status scale (EDSS). While UE impairment is common in early MS, UE disability metrics in this population are lacking, and little is known about the contributions of specific anatomical structures to UE impairment. Disease topography, particularly cervical cord pathology, can contribute to disability accrual. We set out to determine which anatomical structures predict UE function, as measured by a composite Upper Extremity Score (UES), in early MS patients.
Methods: 105 patients with early MS (87) or CIS (18)(68 women;< 5 years diagnosed) completed 4 UE function tasks: Nine Hole Peg Test, Grooved Pegboard, Electronic Finger Tapping Test, and Grip Strength (hand dynamometer). Tasks were completed with dominant and non-dominant hands and then averaged. Outliers were winsorized. Z-scores were computed for each task and averaged into the composite UES. 3D brain and cervical spine MRIs were acquired at 3T. FreeSurfer was used to derive normalized volumes of total cerebrum, cerebral grey, cerebral white, total cerebellum, cerebellar grey, cerebellar white, thalamus, caudate, putamen, pallidum, hippocampus, amydgala, and accumbens. Cord lesion count was quantified. Stepwise regression (entry p=.05, removal p=.10, controlled for age, sex, body size) predicted UE z-score with all MRI predictors.
Results: The total model accounted for 38.0% of the variance in the UES (F[7,97]=8.48, p< .001), with poorer performance independently predicted by higher cervical lesion count (rp=-.294, p=.003) and lower normalized thalamic (rp=.326, p=.001), cerebellar (rp=.289, p=.004), and putaminal (rp=.216, p=.032) volumes. A second round of analysis was done controlling for cerebellar and pyramidal functional system scores (FSS), but the results remained unchanged.
Conclusion: In our population of early MS/CIS patients, the UES was independently predicted by cervical cord lesion count and thalamic, cerebellar, and putaminal volumes. Furthermore, the relationship between the UES and these predictors remained independent of cerebellar and pyramidal FSS, demonstrating that our composite metric identified disease burden that cannot be captured with routine clinical evaluation.
Disclosure:
Asaff Harel has received consulting fees from Teva pharmaceuticals.
Stephen Krieger has received compensation for consulting and advisory board work with Acorda Therapeutics Inc.; Bayer; Biogen; EMD Serono (Merck & Co., Inc.); Genentech; Genzyme; Mallinckrodt; Novartis; and Teva Pharmaceutical Industries Ltd. and has given non-promotional lectures with Biogen.
Oluwasheyi Ayeni has no relevant disclosures.
Rachel Brandstadter has no relevant disclosures.
Christina Lewis has no relevant disclosures.
Aaron Miller has received research support from BiogenIdec, Genzyme/sanofi, Mallinckrodt (Questcor), Novartis, Roche /Genentech, MedDay; consulting fees from Accordant Health Services (Caremark), Acorda, Adamas, Alkermes, Biogen Idec, Celgene, EMD Serono ( Merck Serono), Genzyme/Sanofi, Mallinckrodt (Questcor), Mapi-Pharma, Novartis, Roche/Genentech; and speaking fees from Biogen Idec (unbranded disease awareness programs only) and Genentech/Roche (unbranded programs only).
Gabrielle Pelle has no relevant disclosures.
Fred Lublin has received research support from Biogen Idec; Novartis Pharmaceuticals Corp; Teva Neuroscience, Inc.; Genzyme; Sanofi; Celgene; Transparency Life Sciences; NIH; NMSS, consulting fees from Bayer HealthCare Pharmaceuticals; Biogen Idec; EMD Serono, Inc.; Novartis; Teva Neuroscience; Actelion; Sanofi/Genzyme; Acorda; Questcor/Malinckrodt; Roche/Genentech; MedImmune; Osmotica; Xenoport, Receptos/Celgene; Forward Pharma; Akros; TG Therapeutics; Abbvie; Toyama; Amgen; Medday; Atara Biotherapeutics; Polypharma, speaking fees from Genentech (non-promotional); Genzyme (non-promotional), and has been co-chief editor of Multiple Sclerosis and Related Disorders.
James Sumowski has no relevant disclosures.
Abstract: 58
Type: Oral
Abstract Category: Clinical aspects of MS - 8 Clinical assessment tools
Background: Upper extremity (UE) dysfunction is present in up to 80% of patients with multiple sclerosis (MS) and occurs early in the disease. Importantly, subtle but meaningful UE deficits are often overlooked during routine clinical exam and on crude measures such as the expanded disability status scale (EDSS). While UE impairment is common in early MS, UE disability metrics in this population are lacking, and little is known about the contributions of specific anatomical structures to UE impairment. Disease topography, particularly cervical cord pathology, can contribute to disability accrual. We set out to determine which anatomical structures predict UE function, as measured by a composite Upper Extremity Score (UES), in early MS patients.
Methods: 105 patients with early MS (87) or CIS (18)(68 women;< 5 years diagnosed) completed 4 UE function tasks: Nine Hole Peg Test, Grooved Pegboard, Electronic Finger Tapping Test, and Grip Strength (hand dynamometer). Tasks were completed with dominant and non-dominant hands and then averaged. Outliers were winsorized. Z-scores were computed for each task and averaged into the composite UES. 3D brain and cervical spine MRIs were acquired at 3T. FreeSurfer was used to derive normalized volumes of total cerebrum, cerebral grey, cerebral white, total cerebellum, cerebellar grey, cerebellar white, thalamus, caudate, putamen, pallidum, hippocampus, amydgala, and accumbens. Cord lesion count was quantified. Stepwise regression (entry p=.05, removal p=.10, controlled for age, sex, body size) predicted UE z-score with all MRI predictors.
Results: The total model accounted for 38.0% of the variance in the UES (F[7,97]=8.48, p< .001), with poorer performance independently predicted by higher cervical lesion count (rp=-.294, p=.003) and lower normalized thalamic (rp=.326, p=.001), cerebellar (rp=.289, p=.004), and putaminal (rp=.216, p=.032) volumes. A second round of analysis was done controlling for cerebellar and pyramidal functional system scores (FSS), but the results remained unchanged.
Conclusion: In our population of early MS/CIS patients, the UES was independently predicted by cervical cord lesion count and thalamic, cerebellar, and putaminal volumes. Furthermore, the relationship between the UES and these predictors remained independent of cerebellar and pyramidal FSS, demonstrating that our composite metric identified disease burden that cannot be captured with routine clinical evaluation.
Disclosure:
Asaff Harel has received consulting fees from Teva pharmaceuticals.
Stephen Krieger has received compensation for consulting and advisory board work with Acorda Therapeutics Inc.; Bayer; Biogen; EMD Serono (Merck & Co., Inc.); Genentech; Genzyme; Mallinckrodt; Novartis; and Teva Pharmaceutical Industries Ltd. and has given non-promotional lectures with Biogen.
Oluwasheyi Ayeni has no relevant disclosures.
Rachel Brandstadter has no relevant disclosures.
Christina Lewis has no relevant disclosures.
Aaron Miller has received research support from BiogenIdec, Genzyme/sanofi, Mallinckrodt (Questcor), Novartis, Roche /Genentech, MedDay; consulting fees from Accordant Health Services (Caremark), Acorda, Adamas, Alkermes, Biogen Idec, Celgene, EMD Serono ( Merck Serono), Genzyme/Sanofi, Mallinckrodt (Questcor), Mapi-Pharma, Novartis, Roche/Genentech; and speaking fees from Biogen Idec (unbranded disease awareness programs only) and Genentech/Roche (unbranded programs only).
Gabrielle Pelle has no relevant disclosures.
Fred Lublin has received research support from Biogen Idec; Novartis Pharmaceuticals Corp; Teva Neuroscience, Inc.; Genzyme; Sanofi; Celgene; Transparency Life Sciences; NIH; NMSS, consulting fees from Bayer HealthCare Pharmaceuticals; Biogen Idec; EMD Serono, Inc.; Novartis; Teva Neuroscience; Actelion; Sanofi/Genzyme; Acorda; Questcor/Malinckrodt; Roche/Genentech; MedImmune; Osmotica; Xenoport, Receptos/Celgene; Forward Pharma; Akros; TG Therapeutics; Abbvie; Toyama; Amgen; Medday; Atara Biotherapeutics; Polypharma, speaking fees from Genentech (non-promotional); Genzyme (non-promotional), and has been co-chief editor of Multiple Sclerosis and Related Disorders.
James Sumowski has no relevant disclosures.