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Case Report: A woman, treated with immunomodulatory and immunosuppressive drugs for multiple sclerosis, developed macular oedema 4 months after oral fingolimod administration. The patient was previously seen by an ophthalmologist, with a normal anterior segment and funduscopic examination. Four months after the treatment she referred to decreased visual acuity in both eyes. The funduscopic and OCT examination now revealed cystoid macular oedema (CME)., Discussion: Attention to visual changes and periodic funduscopic examinations are an important part of monitoring while using fingolimod. In our patient early recognition and discontinuation of fingolimod did not result in resolution of the CME., (Copyright © 2011 Sociedad Española de Oftalmología. Published by Elsevier Espana. All rights reserved.)

Introduction: This study outlines the design of an electronic register of patients with multiple sclerosis who began treatment with fingolimod in Spain. The system is intended to serve as a tool to monitor its utilisation in daily clinical practice and thus allow optimisation of the way it is used., Aims: To establish the profile of patients with multiple sclerosis undergoing treatment with fingolimod and to determine the effectiveness and safety of this treatment in daily clinical practice., Development: An observation-based, retrospective and prospective, multi-centre registry is set up, which will be active for five years. Forty neurologists working in Spain will participate in the project. Patients treated with fingolimod who fulfil the selection criteria will be included in the study. The effectiveness variables that will be evaluated are: disability measured by means of the Expanded Disability Status Scale, the rate of attacks, T1 gadolinium-enhancing lesions and new lesions in T2, and the percentage of patients who were free of activity and those who require concomitant treatments. The tolerability variables that will be evaluated are: the rate of patients who present events and adverse reactions, respectively, with a separate analysis of those presenting after the first dose or that are related to the fingolimod risk management plan and the treatment dropout rate., Conclusions: New pharmaceuticals that have only recently been commercialised require more information about their effectiveness and safety, beyond the controlled environment of a clinical trial. Initiatives involving electronic registries such as the Gilenya register are a solution that can respond to such needs by providing information in the shortest possible time about the most suitable management in order to be able to make the best and most efficient use of it.

Introduction: Fingolimod is the first approved drug with oral availability for the treatment of relapsing multiple sclerosis., Aims: To review the mechanism of action of fingolimod and its relationship with the development of infections. To propose preventive measures for those patients who are receiving the drug or will initiate a new treatment. In addition, the role of fingolimod in the development of progressive multifocal leukoencephalopathy on the basis of recent knowledge of its pathophysiology will be discussed., Development: The mechanism of action of fingolimod is based on an antagonic effect on the sphingosine 1-phospate receptors that will generate an inhibition of the egress of naive and central memory lymphocytes into the bloodstream, allowing the free recirculation of memory effectors T lymphocytes. This effect will produce lymphopenia. Fingolimod-associated lymphopenia is a consequence of lymphocyte redistribution, and it is selective and reversible. There is no evidence of higher number of opportunistic and non-opportunistic infections in comparison to placebo or interferon beta-1a in patients receiving fingolimod. However, two patients developed severe herpetic infections under fingolimod., Conclusions: Fingolimod induce a selective and reversible lymphopenia that, taking into account the most recent available data, does not seem to be associated with higher risk of opportunistic infections due to a preservation of immuno-surveillance. The risk of herpesvirus infection should be taken into consideration and more studies are warranted to confirm if an association of these infections with the use of fingolimod exists.

The present work is a review of the new anti-epileptic drug felbamate. Felbamate is a dicarbonate with antiepileptic effects in partial attacks and in Lennox-Gastaut syndrome. This new drug is especially interesting since its pharmacological action on test animals would indicate a wider anti-epileptic spectrum of activity than most other such drugs. We review the clinical pharmacology of felbamate, its development as a new antiepileptic and the new clinical control type trials carried out into epilepsy. We also give a summary of clinical trial experiments performed using felbamate in the treatment of partial refractory attack and of Lennox-Gastaut syndrome. Felbamate has turned out to be the first anti-epileptic with specific efficacy in Lennox-Gastaut syndrome. Felbamate was approved as an anti-epileptic by the United States Food And Drug Administration in July 1993 for clinical use with children suffering from Lennox-Gastaut syndrome and with adults having partial epileptic attacks. 1994 saw some cases of aplastic anaemia and liver failure associated with treatment using felbamate which called for a reevaluation of the benefit-risk factors of the drug. Its use in the European Union was restricted to Lennox-Gastaut syndrome, and rigorous liver function and haematological controls were set up in patients so treated. In the United States the FDA also allows treatment using felbamate of partial attacks not responding to any type of medicine.