Study of the possible link of 25-hydroxyvitamin D with Epstein-Barr virus and human herpesvirus 6 in patients with multiple sclerosis.

BACKGROUND AND PURPOSE: Although the causes of multiple sclerosis (MS) remain partially unknown, environmental and genetic factors are thought to play a role in its aetiopathogenesis. Hypovitaminosis D, Epstein-Barr virus (EBV) and human herpesvirus 6 (HHV-6) infections have been described as possible MS triggers. Our aim was to analyse the possible link between 25-hydroxyvitamin D [25(OH)D] and viruses in patients with MS. METHODS: We included 482 patients with MS in a 2-year study. Serum samples were collected to analyse 25(OH)D levels and, according to sample availability, antibody titres against EBV and HHV-6 by enzyme-linked immunosorbent assay. DNA was extracted from blood in order to analyse EBV and HHV-6 viral load by quantitative real-time polymerase chain reaction and to genotype MS-related single nucleotide polymorphisms (rs3135388, rs2248359 and rs12368653) when possible. RESULTS: The 25(OH)D levels were significantly higher in the first semester of the year than in the second. Carriers of the risk allele rs2248359-C showed lower 25(OH)D levels than non-carriers. For EBV, viral load was significantly higher when 25(OH)D levels were low, demonstrating an inverse correlation between 25(OH)D levels and EBV load. CONCLUSIONS: The 25(OH)D levels could be involved in the regulation of EBV replication/reactivation in patients with MS.

Disección carotídea secundaria a herida cervical por arma de fuego / Carotid dissection secondary to cervical wound by a firearm

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Estatus epiléptico no convulsivo revertido con levetiracetam endovenoso / Non-convulsive epileptic status reverted with intravenous levetiracetam

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[First tonic clonic generalized seizure: recurrence, and prognosis factors]. / Primera crisis tonicoclónica generalizada: implicaciones diagnósticas, pronósticas y terapéuticas.

OBJECTIVE: Previous epidemiologic studies have shown that around 5% of the population will suffer a tonic clonic seizure during their life. The aim of this study is to know how many and which of these people will suffer a second seizure and become epileptic. PATIENTS AND METHODS: 175 patients seen in the emergency department of the Vall d Hebron Hospital were included. They were divided in three groups according to the clinical suspicion of having had a seizure. Only the patients with low clinical suspicion and also normal EEG standard and EEG in sleep deprivation were excluded (16). The patients with previous episodes of lost of consciousness, previous episodes of possible mioclonias or absence were not excluded. RESULTS: After a first tonic clonic seizure the patients who did not receive treatment present a risk of relapse of 66% followed two years and the patients treated 46%. The difference between two groups was statistically significant. Dividing the patients according to the type of seizure: primary generalised, partial or nor localised we did not find differences in the risk of relapse. Dividing the patients according to their etiology we found that the group of patients with provoked seizures was different from the rest groups: symptomatic, genetic or cryptogenic and idiopathic, who had equal risk of recurrence. We found that the presence of previous episodes of lost of consciousness, the clinical suspicion and, probably (we obtained nearly statistical signification) de EEG and the presence of previous mioclonias or absences were risk factors. Other factor like age at the moment of the first episode, febrile seizures, familiar history, antecedents of stroke, encephalitis, neurosurgery and dementia were not related with the risk of relapse. CONCLUSIONS: With the exception of provoked seizures the rest of first tonic clonic seizures have a high risk of relapse (around 60 70%) and if they go with abnormal EEG, previous episodes of absences or mioclonias starting treatment must be considered.

Primera crisis tonicoclónica generalizada: implicaciones diagnósticas, pronósticas y terapéuticas / First tonic-clonic generalized seizure: recurrence, and prognosis factors

Introducción. Este estudio pretende determinar el riesgo de recidiva de pacientes con una primera crisis generalizada tonicoclónica (CGTC) y establecer en qué casos se indica iniciar tratamiento anticomicial en la primera crisis. Pacientes y métodos. 175 pacientes, no conocidos, epilépticos, que consultaron a los Servicios de Urgencias de los hospitales Vall d'Hebron. Se dividieron los pacientes en tres grupos, según el grado de sospecha clínica de haber sufrido una CGTC. Se excluyeron del estudio aquellos pacientes que presentaron episodio de baja sospecha clínica, con EEG y EEG en privación de sueño normal, y aquellos que presentaban otra causa de pérdida de conciencia (16). No se excluyeron los pacientes con episodios previos sugestivos de mioclonías, ausencias o pérdidas de conocimiento. Resultados. El porcentaje de recidiva tras un seguimiento de 2 años en los pacientes no tratados fue del 66 por ciento, y en los tratados, del 46 por ciento, y la diferencia fue estadísticamente significativa. Se dividió a los pacientes según el tipo de crisis sufrida: crisis parcial secundariamente generalizada, crisis primariamente generalizada o crisis no localizada; no obtuvimos diferencias respecto al riesgo de recidiva. Respecto a la etiología, las epilepsias provocadas presentan un riesgo de recidiva significativamente inferior al resto de etiologías (sintomáticas, idiopáticas o criptogénicas y genéticas).Son factores pronósticos: el grado de sospecha clínica, los episodios previos de pérdida de conciencia; con tendencia a la significación estadística: la presencia de foco irritativo en el EEG, actividad generalizada en el EEG en privación de sueño y las mioclonías o ausencias previas. No son factores pronósticos: la historia familiar, episodios previos de ictus, encefalitis, neurocirugía y demencia, ni la edad de presentación de la primera crisis. Conclusiones. A excepción de las primeras crisis de etiología provocada, el resto de primeras crisis tienen un alto riesgo de recidiva, que, si se acompaña de otros factores como EEG patológico o episodios previos de pérdida de conciencia, mioclonías o ausencias, puede que sea lícito iniciar tratamiento en la primera crisis (AU)