Contributions
Abstract: EP1507
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Background: Patients with multiple sclerosis (MS) frequently show difficulties in episodic memory, attention, information processing speed and executive functions. Some of them have selective deficits of a given cognitive domain, and different cognitive phenotypes involving memory or processing speed disturbances have been described.
Aim: To analyse the underlying patterns of damage in structural networks according to the cognitive phenotypes observed in a large sample of MS patients.
Methods: A cohort of 183 patients (age: 43.1±10 years; disease duration: 12.1±9.3 years; Expanded Disability Status Scale, EDSS: 2 (0-6.5)) was assessed by the Rao Battery. Whole brain structural connectivity was obtained from diffusion magnetic resonance imaging and mean fractional anisotropy (FA) in each connection was compared among patients' groups.
Results: Thirty-two patients (18%) showed memory impairment (z-score of Selective reminding test-delayed or Spatial recall tests-delayed below -1.5), 29 (16%) patients had attention deficits (below -1.5 z-score in Symbol Digit Modalities Test or Paced Auditory Serial Addition Task) and 21 (11%) had global impairment. The remaining 101 (55%) patients were cognitively preserved (CP). Patients with global impairment were older, more frequently secondary-progressive MS, and had higher EDSS score.
While connectivity was similar in patients with memory and attention phenotypes compared with CP patients (decreased FA in 6% of connections), those with global impairment displayed more widespread reduction in connectivity (decreased FA in 63% of connections). Patients with global impairment showed larger number of connections with reduced FA (adjusted p< 0.05) in frontal and parietal areas, and insula, compared with the other cognitive groups.
Conclusions: In contrast to patients with global impairment, those with predominant memory or attention deficits have similar brain connectivity to that seen in CP patients, suggesting that they are at an early stage of cognitive disability and do not have specific patterns of network modifications. Furthermore, the results reinforce the importance of the frontoparietal network damage in the development of cognitive deficits in MS.
Disclosure: ES received travel reimbursement from TEVA; EMH, ELS, CM, NB declare nothing to disclose; MS received speaker honoraria from Sanofi and Biogen, and funding from the Generalitat de Catalunya (SLT002/16/00354); NSV receives funding from the Spanish Government (Instituto de Salud Carlos III, Spain, and Fondo Europeo de Desarrollo Regional [FEDER, FI16/00251], and the Predoctoral Grant for Health Research) and received speaker honoraria from Genzyme, Merck-Serono, Biogen-idec, Bayer; EML received speaking honoraria from Biogen, Genzyme and Novartis, travel reimbursement from Roche, Sanofi-Genzyme and TEVA, and funding from the Spanish Government (Instituto de Salud Carlos III [CM13/00150; MV15/00012; JR16/00006]), Fundació Marató TV3 (20142030), GMSI (2016) and Fundació Cellex Barcelona; YB: received speaking honoraria from Biogen, Novartis and Genzyme; EHML has received honoraria from Biogen, Roche, Novartis and Sanofi for speaking, and a travel reimbursement from Roche, Biogen, Novartis and Sanofi; AS received compensation for consulting services and speaker honoraria from Bayer-Schering, Merck-Serono, Biogen-Idec, Sanofi-Aventis, TEVA and Novartis; SL received speaker honoraria from Biogen Idec, Novartis, Teva, Genzyme and Merck, and research support from the Spanish Government (PI15/00587).
Funding: This work was funded by a Proyecto de Investigacion en Salud (FIS 2015. PI15/00587, SL, AS) integrated in the Plan Estatal de Investigación Científica y Técnica de Innovación I+D+I and co-funded by the Instituto de Salud Carlos III-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER, "Otra manera de hacer Europa"); Red Española de Esclerosis Múltiple (REEM) (RD16/0015/0002, RD16/0015/0003, RD12/0032/0002, RD12/0060/01-02); TEVA SLU.
Abstract: EP1507
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Background: Patients with multiple sclerosis (MS) frequently show difficulties in episodic memory, attention, information processing speed and executive functions. Some of them have selective deficits of a given cognitive domain, and different cognitive phenotypes involving memory or processing speed disturbances have been described.
Aim: To analyse the underlying patterns of damage in structural networks according to the cognitive phenotypes observed in a large sample of MS patients.
Methods: A cohort of 183 patients (age: 43.1±10 years; disease duration: 12.1±9.3 years; Expanded Disability Status Scale, EDSS: 2 (0-6.5)) was assessed by the Rao Battery. Whole brain structural connectivity was obtained from diffusion magnetic resonance imaging and mean fractional anisotropy (FA) in each connection was compared among patients' groups.
Results: Thirty-two patients (18%) showed memory impairment (z-score of Selective reminding test-delayed or Spatial recall tests-delayed below -1.5), 29 (16%) patients had attention deficits (below -1.5 z-score in Symbol Digit Modalities Test or Paced Auditory Serial Addition Task) and 21 (11%) had global impairment. The remaining 101 (55%) patients were cognitively preserved (CP). Patients with global impairment were older, more frequently secondary-progressive MS, and had higher EDSS score.
While connectivity was similar in patients with memory and attention phenotypes compared with CP patients (decreased FA in 6% of connections), those with global impairment displayed more widespread reduction in connectivity (decreased FA in 63% of connections). Patients with global impairment showed larger number of connections with reduced FA (adjusted p< 0.05) in frontal and parietal areas, and insula, compared with the other cognitive groups.
Conclusions: In contrast to patients with global impairment, those with predominant memory or attention deficits have similar brain connectivity to that seen in CP patients, suggesting that they are at an early stage of cognitive disability and do not have specific patterns of network modifications. Furthermore, the results reinforce the importance of the frontoparietal network damage in the development of cognitive deficits in MS.
Disclosure: ES received travel reimbursement from TEVA; EMH, ELS, CM, NB declare nothing to disclose; MS received speaker honoraria from Sanofi and Biogen, and funding from the Generalitat de Catalunya (SLT002/16/00354); NSV receives funding from the Spanish Government (Instituto de Salud Carlos III, Spain, and Fondo Europeo de Desarrollo Regional [FEDER, FI16/00251], and the Predoctoral Grant for Health Research) and received speaker honoraria from Genzyme, Merck-Serono, Biogen-idec, Bayer; EML received speaking honoraria from Biogen, Genzyme and Novartis, travel reimbursement from Roche, Sanofi-Genzyme and TEVA, and funding from the Spanish Government (Instituto de Salud Carlos III [CM13/00150; MV15/00012; JR16/00006]), Fundació Marató TV3 (20142030), GMSI (2016) and Fundació Cellex Barcelona; YB: received speaking honoraria from Biogen, Novartis and Genzyme; EHML has received honoraria from Biogen, Roche, Novartis and Sanofi for speaking, and a travel reimbursement from Roche, Biogen, Novartis and Sanofi; AS received compensation for consulting services and speaker honoraria from Bayer-Schering, Merck-Serono, Biogen-Idec, Sanofi-Aventis, TEVA and Novartis; SL received speaker honoraria from Biogen Idec, Novartis, Teva, Genzyme and Merck, and research support from the Spanish Government (PI15/00587).
Funding: This work was funded by a Proyecto de Investigacion en Salud (FIS 2015. PI15/00587, SL, AS) integrated in the Plan Estatal de Investigación Científica y Técnica de Innovación I+D+I and co-funded by the Instituto de Salud Carlos III-Subdirección General de Evaluación and the Fondo Europeo de Desarrollo Regional (FEDER, "Otra manera de hacer Europa"); Red Española de Esclerosis Múltiple (REEM) (RD16/0015/0002, RD16/0015/0003, RD12/0032/0002, RD12/0060/01-02); TEVA SLU.