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Background and purpose: Oral or intravenous methylprednisolone (≥500 mg/day for 5 days) is recommended for multiple sclerosis (MS) relapses. Nonetheless, the optimal dose remains uncertain. We compared clinical and radiological effectiveness, safety and quality of life (QoL) of oral methylprednisolone [1250 mg/day (standard high dose)] versus 625 mg/day (lesser high dose), both for 3 days] in MS relapses. Methods: A total of 49 patients with moderate to severe MS relapse within the previous 15 days were randomized in a pilot, double‐blind, multicentre, non‐inferiority trial (ClinicalTrial.gov, NCT01986998). The primary endpoint was non‐inferiority of the lesser high dose by Expanded Disability Status Scale (EDSS) score improvement on day 30 (non‐inferiority margin, 1 point). The secondary endpoints were EDSS score change on days 7 and 90, changes in T1 gadolinium‐enhanced and new/enlarged T2 lesions on days 7 and 30, and safety and QoL results. Results: The primary outcome was achieved [mean (95% confidence interval) EDSS score difference, −0.26 (−0.7 to 0.18) at 30 days (P = 0.246)]. The standard high dose yielded a superior EDSS score improvement on day 7 (P = 0.028). No differences were observed in EDSS score on day 90 (P = 0.352) or in the number of T1 gadolinium‐enhanced or new/enlarged T2 lesions on day 7 (P = 0.401, 0.347) or day 30 (P = 0.349, 0.529). Safety and QoL were good at both doses. Conclusions: A lesser high‐dose oral methylprednisolone regimen may not be inferior to the standard high dose in terms of clinical and radiological response. [ABSTRACT FROM AUTHOR]

Carmona O, Masuet C, Santiago O, Alía P, Moral E, Alonso-Magdalena L, Casado V, Arbizu T. Multiple sclerosis and cognitive decline: is ApoE-4 a surrogate marker? Acta Neurol Scand: 2011: 124: 258-263. © 2011 John Wiley & Sons A/S. Background - The role of the apolipoprotein E (ApoE) polymorphism has been well demonstrated in neurodegenerative disorders such as Alzheimer. However, its role in multiple sclerosis (MS) remains unclear. Aims - The aims of our study were as follows: (i) to assess whether ApoE-4 might be a surrogate marker of cognitive decline in MS; (ii) to confirm the presence of cognitive impairment in mildly disabled patients treated with interferon-beta; and (iii) to analyse the correlation between cognitive disturbances and clinical variables. Material and methods - Fifty relapsing-remitting MS patients underwent a battery of neuropsychological tests and were genotyped for ApoE. Their scores were compared with those of 35 controls. Results - No association was found between ApoE-4 and cognitive impairment. Significant differences in most domains were observed between MS and the control group. Cognitive decline was not related to disability progression. Conclusion - No association between cognitive impairment and ApoE-4 or clinical markers was detected in our MS patients. [ABSTRACT FROM AUTHOR]

Objective A post-hoc analysis of the data from a randomised clinical trial involving prescription of antipsychotic treatment to never treated first-onset psychotic patients was used to compare the weight change after 6-week olanzapine treatment (standard tablets vs. orally disintegrating formulation). Method In the subgroup of 38 patients randomised to olanzapine, standard olanzapine tablets were non-randomly and consecutively prescribed to the first 19 patients, with the orally disintegrating formulation being prescribed to the following 19 patients. Results After 6-week treatment with olanzapine, a significant higher increase in weight was noted in those patients on standard tablets (mean weight increase 6.3 ± 1.9 Kg) as compared to those on orally disintegrating olanzapine (mean weight increase 3.3 ± 3.2 Kg) (F = 7.7; p = 0.009). BMI increase was also significantly higher in the olanzapine tablet group (mean increase of 2.1 Kg/m2 as compared with 1.1 Kg/m2 in the orally disintegrating group) (F = 4.7; p = 0.036). Substantial weight gain (SWG) (≥7% increase from baseline weight) was noted in 84.2% (n = 16) of the olanzapine tablet patients and in 31.6% (n = 6) of the orally disintegrating olanzapine patients, with the olanzapine tablet group showing a significant increase in the mean percentage of weight gain (F = 4.0; p = 0.014). Conclusions Partial sublingual absorption occurring with orally disintegrating olanzapine may bypass gastrointestinal metabolisation and hence lead to differences in metabolite versus parent compound ratios. However, the need arises to replicate the present study with a longer follow-up. Copyright © 2007 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Alonso-Magdalena L, Romero-Pinel L, Moral E, Carmona O, Gubieras L, Ramón JM, Martínez-Yélamos S, Arbizu T. Anticipation of age at onset in multiple sclerosis: methodologic pitfalls. Acta Neurol Scand: 2010: 121: 426–428. © 2010 John Wiley & Sons A/S. Background/aim – There are several reports that claim anticipation in complex or polygenic diseases such as multiple sclerosis (MS), Crohn disease or schizophrenia. The aim of the present study was to assess age at onset of MS during the last 60 years in the region of Costa de Ponent (Barcelona, Spain) showing how apparent changes in age at onset between generations can be an artefact of analysis based on cohorts that have not been followed enough time. Methods – The study comprised 1100 patients diagnosed of MS. The method used to correct for follow-up time bias involves constructing comparison cohorts that had been observed for the same amount of time. To ensure equal follow-up times, we restricted our analysis to patients whose onset was by 37 years of age (percentile 75) and were at least 37 years old. We analysed differences in age at onset using log-rank test to compare survival curves estimated by Kaplan–Meier method. Results – Age at onset decreases progressively from older to younger generations. However, when adjustment to equal follow-up time was done, anticipation in age at onset was not found. Conclusion – Anticipation of age at onset is undetectable when adjusted for follow-up time. [ABSTRACT FROM AUTHOR]