Contributions
Abstract: 225
Type: Oral
Abstract Category: Pathology and pathogenesis of MS - Imaging
Background: Previous studies have identified strong effects of grey matter (GM) atrophy and white matter (WM) tissue integrity loss on cognition in multiple sclerosis (MS). Currently, however, it is difficult to study compartment-specific effects, as GM atrophy and WM damage frequently overlap in time.
Objective: To investigate the relationship between cognitive dysfunction and WM integrity loss, in patients with and without GM atrophy.
Methods: A total of 330 MS patients (disease duration 14.6 ± 8.4 years) and 96 matched healthy controls underwent volumetric and diffusion-tensor MR-imaging as well as extensive neuropsychological testing. Cortical and deep GM volumes, as well as extent and severity scores of FA-derived WM damage were calculated using FSL. Cognitive and volumetric Z‑scores were corrected for normal effects of age, sex and education, as present in healthy controls. Cognitive impairment was defined as Z< -1.5 below controls on at least two tests, and atrophy as Z< -1.5 for both cortical and deep GM volumes. In patients with and without atrophy, cognitive groups (i.e., impaired and preserved) were compared for extent and severity of damage, as well as descriptive variables.
Results: Combined deep and cortical GM atrophy was seen in 67 patients, while 133 patients showed no GM atrophy. Of these two patient groups, 75% and 32% showed cognitive impairment, respectively. Isolated deep GM atrophy was seen in 126 patients (46% cognitive impairment), while isolated cortical atrophy was much rarer (six patients, of whom two showed cognitive impairment). In patients without deep nor cortical GM atrophy, cognitive impairment was associated with a lower level of education (p< 0.001), with no difference in WM integrity. In the combined atrophy group, cognitive impairment was only related to a worse WM damage extent and severity (p< 0.001 for both). Effects of gender, age, disease duration and MS phenotype did not survive Bonferroni correction.
Conclusion: Cognitive impairment is more common in, but not unique to, patients with deep or cortical GM atrophy. In patients without deep nor cortical GM atrophy, cognitive impairment is explained by a lower level of education but not by the extent and severity of WM integrity loss. A higher extent and severity of WM damage was only related to cognitive impairment in patients with concomitant GM atrophy. Future longitudinal studies are needed to elucidate the order of WM and GM damage.
Disclosure: A.J.C. Eijlers: nothing to disclose and receives research support from the Dutch MS Research Foundation, grant 14-358e
K.A. Meijer: nothing to disclose and receives funding from a Biogen research grant
Q. van Geest: nothing to disclose and receives funding from a Novartis research grant
J.J.G. Geurts: nothing to disclose
M.M. Schoonheim: nothing to disclose and receives research support from the Dutch MS Research Foundation, grant 13-820
Abstract: 225
Type: Oral
Abstract Category: Pathology and pathogenesis of MS - Imaging
Background: Previous studies have identified strong effects of grey matter (GM) atrophy and white matter (WM) tissue integrity loss on cognition in multiple sclerosis (MS). Currently, however, it is difficult to study compartment-specific effects, as GM atrophy and WM damage frequently overlap in time.
Objective: To investigate the relationship between cognitive dysfunction and WM integrity loss, in patients with and without GM atrophy.
Methods: A total of 330 MS patients (disease duration 14.6 ± 8.4 years) and 96 matched healthy controls underwent volumetric and diffusion-tensor MR-imaging as well as extensive neuropsychological testing. Cortical and deep GM volumes, as well as extent and severity scores of FA-derived WM damage were calculated using FSL. Cognitive and volumetric Z‑scores were corrected for normal effects of age, sex and education, as present in healthy controls. Cognitive impairment was defined as Z< -1.5 below controls on at least two tests, and atrophy as Z< -1.5 for both cortical and deep GM volumes. In patients with and without atrophy, cognitive groups (i.e., impaired and preserved) were compared for extent and severity of damage, as well as descriptive variables.
Results: Combined deep and cortical GM atrophy was seen in 67 patients, while 133 patients showed no GM atrophy. Of these two patient groups, 75% and 32% showed cognitive impairment, respectively. Isolated deep GM atrophy was seen in 126 patients (46% cognitive impairment), while isolated cortical atrophy was much rarer (six patients, of whom two showed cognitive impairment). In patients without deep nor cortical GM atrophy, cognitive impairment was associated with a lower level of education (p< 0.001), with no difference in WM integrity. In the combined atrophy group, cognitive impairment was only related to a worse WM damage extent and severity (p< 0.001 for both). Effects of gender, age, disease duration and MS phenotype did not survive Bonferroni correction.
Conclusion: Cognitive impairment is more common in, but not unique to, patients with deep or cortical GM atrophy. In patients without deep nor cortical GM atrophy, cognitive impairment is explained by a lower level of education but not by the extent and severity of WM integrity loss. A higher extent and severity of WM damage was only related to cognitive impairment in patients with concomitant GM atrophy. Future longitudinal studies are needed to elucidate the order of WM and GM damage.
Disclosure: A.J.C. Eijlers: nothing to disclose and receives research support from the Dutch MS Research Foundation, grant 14-358e
K.A. Meijer: nothing to disclose and receives funding from a Biogen research grant
Q. van Geest: nothing to disclose and receives funding from a Novartis research grant
J.J.G. Geurts: nothing to disclose
M.M. Schoonheim: nothing to disclose and receives research support from the Dutch MS Research Foundation, grant 13-820