Cortico-juxtacortical involvement increases risk of epileptic seizures in multiple sclerosis.

OBJECTIVES: Previous studies have reported an increased risk for epileptic seizures in multiple sclerosis (MS) patients. However, data on the pathogenesis of seizures remain inconclusive. The aim of our study is to evaluate prevalence, clinical and paraclinical features of epileptic attacks in our MS cohort and to search MS-specific risk factors for epileptic seizures. MATERIALS AND METHODS: In this cohort of 428 MS patients, 13 patients were identified with epileptic seizures occurring at any point during the course of MS including at MS onset. As a control group, we selected 26 MS patients without seizures and matched for gender, age and date of MS onset. We compared demographic features and clinic-radiological findings between the both groups. RESULTS: Thirteen patients (3%) were identified as having epileptic attacks. Ten patients (77%) experienced focal seizures, half of whom had confirmed secondary generalization. We did not find an association between seizures and disease course. Most patients had a single or few (2-5) seizures. MS patients with seizures had a significantly higher number of cortical and juxtacortical lesions on T2-weighted/fluid attenuation inversion recovery magnetic resonance imaging than control group [OR = 2.6 CI95% (1.0-6.5); P = 0.047]. CONCLUSIONS: Our findings support a credible role of cortical and juxtacortical involvement in the development of epileptic seizures in MS.

[Fingolimod: effectiveness and safety in routine clinical practice. An observational, retrospective, multi-centre study in Navarra, Gipuzkoa and La Rioja]. / Fingolimod: efectividad y seguridad en la practica clinica habitual. Estudio observacional, retrospectivo y multicentrico en Navarra, Gipuzkoa y La Rioja.

AIM: To evaluate the effectiveness and safety of fingolimod in clinical practice in Navarra, Gipuzkoa and La Rioja regions. PATIENTS AND METHODS: We conducted a retrospective multi-centre study with recurrent multiple sclerosis patients treated with fingolimod, following the product data sheet. The following data were evaluated: annualised relapse rate (ARR), percentage of patients free from relapses, disability using the Expanded Disability Status Scale (EDSS) and the percentage of patients without gadolinium-enhancing lesions. RESULTS: A total of 113 patients were treated with fingolimod: 6% were naive, and 58% and 35% were patients previously treated with an immunomodulator and natalizumab, respectively. Fingolimod lowered the ARR after the first (67%; 1 to 0.3; p < 0.0001) and second (89%; 1 to 0.1; p < 0.0001) years of treatment, and thus the number of patients free from relapses during the treatment increased. The baseline EDSS was 3 and after treatment with fingolimod was 2.5 in both years. The percentage of patients without gadolinium-enhancing lesions after the first year of treatment was 77%. Similar results were observed in naive patients and in those previously treated with an immunomodulator. In patients previously treated with natalizumab no changes were observed following the treatment. CONCLUSIONS: The use of fingolimod in clinical practice showed an effectiveness similar to that observed in clinical trials. There were no changes in the ARR after changing from natalizumab, and only one patient presented a 'relapse' after withdrawal of natalizumab. Fingolimod acts like a safe drug, with scarce side effects and a low percentage of drop-outs.

TITLE: Fingolimod: efectividad y seguridad en la practica clinica habitual. Estudio observacional, retrospectivo y multicentrico en Navarra, Gipuzkoa y La Rioja.Objetivo. Evaluar la efectividad y seguridad del fingolimod en la practica clinica en las regiones de Navarra, Gipuzkoa y La Rioja. Pacientes y metodos. Estudio retrospectivo y multicentrico de pacientes con esclerosis multiple recurrente tratados con fingolimod, siguiendo la ficha tecnica. Se evaluo la tasa anualizada de brotes (TAB), el porcentaje de pacientes libres de brotes, la discapacidad usando la escala expandida del estado de discapacidad (EDSS) y el porcentaje de pacientes sin lesiones captantes de gadolinio. Resultados. Un total de 113 pacientes fueron tratados con fingolimod: el 6%, naive, y el 58% y 35%, pacientes tratados previamente con inmunomodulador y natalizumab, respectivamente. El fingolimod disminuyo la TAB tras el primer (67%; 1 a 0,3; p < 0,0001) y segundo (89%; 1 a 0,1; p < 0,0001) año de tratamiento, y aumento asi el porcentaje de pacientes libres de brotes durante el tratamiento. La EDSS basal fue 3 y despues del tratamiento con fingolimod fue 2,5 en ambos años. El porcentaje de pacientes sin lesiones captantes de gadolinio tras el primer año de tratamiento fue del 77%. Resultados similares se observaron en los pacientes naive y en los tratados previamente con inmunomodulador. En los pacientes tratados previamente con natalizumab no se observaron cambios tras el tratamiento. Conclusiones. El uso del fingolimod en la practica clinica mostro una efectividad similar a la eficacia observada en ensayos clinicos. No hubo cambios en la TAB al cambiar desde natalizumab, y solo un paciente tras suspender el natalizumab presento 'rebrote'. El fingolimod se comporta como un farmaco seguro, con escasos efectos adversos y con un bajo porcentaje de abandonos.

[Cognitive deterioration in multiple sclerosis]. / Deterioro cognitivo en la esclerosis múltiple.

Amongst the varied symptomology of multiple sclerosis is to be found the alteration of higher functions (cognitive deficit), which has considerable repercussions on the quality of life of patients. The old descriptions of the disease rarely differentiate cognitive affectation from the more general category of "mental symptoms", which also includes a broad range of affective disorders. Towards 1960 neuropsychological tests began to be employed, and it was from the 1970s onwards that a clear distinction was drawn between deterioration of the higher functions and psycho-affective aspects in the disease. The pattern of cognitive deterioration in patients with multiple sclerosis is not uniform. During the initial phases of the disease it is, in general, light and it has an insidious start, although inter-individual variability is wide, depending on the predominant pathological alterations in the lesions and on their number and localisation. In more severe cases, it is possible to include within the debatable term of subcortical dementia, intellectual slowness, problems of attention, alterations in abstract reasoning, shortcomings in the resolution of problems and memory dysfunction. It is an almost invariable complication of the advanced stages of the disease, since the lesions characterised by axonal loss affect broad areas of white matter, which determines the deafferentation of several areas of cortical association. There does not appear to be any correlation between cognitive deterioration and the variables of the disease considered in an independent way, such as demographic data, clinical course, alterations of mood, consumption of medicines or fatigue. Although, evidently, the disease's progressive secondary forms of greater duration and the accumulation of lesions are what present the greatest deterioration. With present-day techniques of neuroimaging it has been possible to show a correlation between cognitive deterioration and the existence of an increase in ventricular size, periventricular lesions and atrophy of the callous body.

[Supranuclear gaze palsy following extracorporeal surgery with induced hypothermia. Report of two cases]. / Parálisis supranuclear de la mirada tras cirugía extracorpórea con hipotermia inducida. A propósito de dos casos.

Although up to 5-20% of the patients who underwent surgery with hypothermia and cardiac arrest may present neurological complications, just a few cases of ocularmotor disorders have been described. Acquired supranuclear ocular motor paresis (ASOMP) is a rare disorder characterized by impairment in volitional and reflex saccades and smooth pursuit in one or more directions of gaze with intact extraocular movements in response to vestibular estimulation. We present two cases of acquired supranuclear ocular motor paresis associated with a peculiar gait disorder. Although a partial improvement was observed, both patients continue with ocular motor paresis in vertical direction after one year of evolution. A selective vulnerability of certain brainstem neuronal groups would explain the pathophysiology of these symptoms.