Contributions
Abstract: EP1539
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Neuropsychology
Background: Cognitive dysfunction of patients with multiple sclerosis (PwMS) has been correlated with brain atrophy and neurodegeneration. We hypothesized that potentially treatable inflammatory mechanisms are also important for the pathogenesis of cognitive dysfunction of PwMS. If so, cognitive dysfunction may predict therapeutic response to potent, anti-inflammatory disease modifying drugs.
Aim: To explore whether the therapeutic response to natalizumab is modified by baseline cognitive function or level of disability (EDSS).
Methods: 76 relapsing-remitting PwMS completed a standardized validated computerized cognitive assessment battery (NeuroTrax) with analysis of age-and education-adjusted individual cognitive domain scores and a global cognitive (average) summary score (GCS). Cognitive scores and EDSS were evaluated twice: at baseline and after a time interval of 9-27 months of treatment with natalizumab. Repeated measures ANOVA was used to estimate the effects of baseline EDSS and GCS on the changes in EDSS and GCS after treatment, while controlling for the inter-evaluation time.
Results: 76 PwMS were evaluated [female: 54 (71%); EDSS 3.5±2; education: 14.8±2.7 years; time between evaluations:16.8±4.6 months]. A significant interaction was found between baseline global cognitive score and change in EDSS after natalizumab infusions [F(1,71)=4.6, P=0.035]. EDSS and GCS changes after natalizumab were not significantly modified by baseline EDSS. In line with our hypothesis, patients with low baseline cognitive scores (GCS of at least 1SD below age- and education-adjusted average) showed greater improvement in EDSS after treatment compared with patients with better cognitive function at baseline. GCS scores were also improved after natalizumab [F(1,71)=6.3, P=0.02]. An improvement of at least 0.5SD in GCS was noted in 17% of the patients.
Conclusion: Cognitive impairment predicts therapeutic response to natalizumab and may improve after treatment with natalizumab. Cognitive dysfunction in PwMS may not necessarily imply irreversible brain damage, but may be also due to ongoing inflammation that is amenable to treatment.
Disclosure: All authors have nothing to disclose
Abstract: EP1539
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Neuropsychology
Background: Cognitive dysfunction of patients with multiple sclerosis (PwMS) has been correlated with brain atrophy and neurodegeneration. We hypothesized that potentially treatable inflammatory mechanisms are also important for the pathogenesis of cognitive dysfunction of PwMS. If so, cognitive dysfunction may predict therapeutic response to potent, anti-inflammatory disease modifying drugs.
Aim: To explore whether the therapeutic response to natalizumab is modified by baseline cognitive function or level of disability (EDSS).
Methods: 76 relapsing-remitting PwMS completed a standardized validated computerized cognitive assessment battery (NeuroTrax) with analysis of age-and education-adjusted individual cognitive domain scores and a global cognitive (average) summary score (GCS). Cognitive scores and EDSS were evaluated twice: at baseline and after a time interval of 9-27 months of treatment with natalizumab. Repeated measures ANOVA was used to estimate the effects of baseline EDSS and GCS on the changes in EDSS and GCS after treatment, while controlling for the inter-evaluation time.
Results: 76 PwMS were evaluated [female: 54 (71%); EDSS 3.5±2; education: 14.8±2.7 years; time between evaluations:16.8±4.6 months]. A significant interaction was found between baseline global cognitive score and change in EDSS after natalizumab infusions [F(1,71)=4.6, P=0.035]. EDSS and GCS changes after natalizumab were not significantly modified by baseline EDSS. In line with our hypothesis, patients with low baseline cognitive scores (GCS of at least 1SD below age- and education-adjusted average) showed greater improvement in EDSS after treatment compared with patients with better cognitive function at baseline. GCS scores were also improved after natalizumab [F(1,71)=6.3, P=0.02]. An improvement of at least 0.5SD in GCS was noted in 17% of the patients.
Conclusion: Cognitive impairment predicts therapeutic response to natalizumab and may improve after treatment with natalizumab. Cognitive dysfunction in PwMS may not necessarily imply irreversible brain damage, but may be also due to ongoing inflammation that is amenable to treatment.
Disclosure: All authors have nothing to disclose