Entrevista exclusiva con el dr. Eugen Trinka sobre epilepsia

La epilepsia afecta a 50 millones de personas en todo el mundo, de los cuales alrededor de 6 millones son europeos. Los últimos avances médicos sobre esta enfermedad fueron abordados en Berlín durante el Congreso de la Academia Europea de Neurología( EAN2015). Noticias de Salud estuvo presente en el evento. Exactamente en el Seminario organizador por EISAI sobre los nuevos avances del medicamento Fycompa( Peramparel).
En exclusiva hablamos con uno de los más importantes expertos a nivel mundial en esta enfermedad, el dr Eugen Trinka( de Salzburgo, Austria). En la charla nos habla de la epilepsia, su tratamiento médico, el estigma social que todavía representa esta enfermedad y cómo afecta a edades más jóvenes en los últimos tiempos.

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El fármaco innovador Fycompa® (perampanel) demuestra mejor control de las crisis en la epilepsia generalizada idiopática en dos nuevos estudios

Hoy, en el primer Congreso de la Academia Europea de Neurología (EAN, European Academy of Neurology), celebrado en Berlín, Alemania, se han presentado nuevos datos importantes sobre el tratamiento con Fycompa® (perampanel) administrado una vez al día. En un análisis de subgrupos se evaluaron los efectos de perampanel adyuvante en las crisis de ausencia y mioclónicas en pacientes con epilepsia generalizada idiopática. Un segundo análisis comunicó que la reducción de las crisis tónico-clónicas generalizadas primarias (PGTC) observada en el estudio en fase III era independiente de la edad, el sexo o la raza.

Perampanel, un tratamiento oral con ajuste sencillo de la dosis, está indicado actualmente para el tratamiento adyuvante de las crisis de inicio parcial, con o sin generalización secundaria, en pacientes con epilepsia de 12 años y mayores. El 27 de mayo de 2015, perampanel recibió un dictamen favorable del CHMP para la indicación para las crisis PGTC, y es el único fármaco antiepiléptico (FAE) que actúa selectivamente en los receptores AMPA, una proteína del cerebro que desempeña una función clave en la propagación de las crisis. Este mecanismo de acción es diferente al de los demás FAE actualmente disponibles.

"Para los pacientes con crisis PGTC no controladas, las opciones de tratamiento son limitadas, y perampanel es un tratamiento innovador con un modo de acción único y buena tolerabilidad", comenta Bernard Steinhoff, Director Médico y Consejero Delegado, Centro Kork de la Epilepsia, Alemania.

Las crisis tónico-clónicas generalizadas pueden ser un tipo de epilepsia peligroso. Las crisis comienzan con una pérdida de conciencia y la contracción repentina de los músculos, lo que puede provocar la caída de la persona que las sufre (fase tónica). A continuación aparecen convulsiones violentas (fase clónica) hasta que los músculos finalmente se relajan. Entre el 20% y el 40% de las personas con epilepsia de diagnóstico reciente son o se volverán refractarias al tratamiento, con el posible empeoramiento de su calidad de vida.

Los subanálisis forman parte del primer ensayo en fase III, aleatorizado, doble ciego y controlado con placebo para evaluar la eficacia y seguridad de perampanel adyuvante en el tratamiento de las crisis PGTC, en pacientes de 12 años o mayores con epilepsia generalizada idiopática. En este estudio se aleatorizó a 164 pacientes, de los cuales 81 recibieron el tratamiento con perampanel y 81 placebo. Los resultados del estudio 332 muestran una mayor reducción en la frecuencia de las crisis PGTC en pacientes tratados con perampanel, en comparación con aquellos que recibieron placebo (un 76,5% frente a un 38,4%, respectivamente; P<0 39="" 50="" 64="" a="" ambi="" con="" crisis="" de="" del="" en="" frente="" fue="" i="" la="" mayor="" n="" nbsp="" pacientes="" perampanel="" pgtc="" placebo="" que="" respectivamente="" respuesta="" style="box-sizing: border-box; line-height: 1.4; margin: 0px;" tasa="" un="">P

=0,0019). Estos dos aspectos son los criterios de valoración principales. Asimismo, el 31% de los pacientes no sufrió ninguna crisis durante el período de mantenimiento de 13 semanas, cuando se les trató con perampanel como tratamiento adyuvante, en comparación con el 12% del grupo con placebo. Los pacientes tratados con perampanel también presentaron mejor calidad de vida en todos los ámbitos valorados, incluidas actividades cotidianas, cognición y ansiedad. El perfil de acontecimientos adversos de este estudio resultó similar al observado en otros estudios de perampanel. La mayor parte de los acontecimientos adversos de ambos grupos de tratamiento se consideraron de naturaleza leve a moderada, siendo los más frecuentes mareos, fatiga, cefalea, somnolencia e irritabilidad.

El desarrollo de perampanel demuestra el compromiso de Eisai con el área terapéutica de la epilepsia, y supone un ejemplo más de la contribución de la compañía para abordar las diversas necesidades y aportar cada vez mayores beneficios a los pacientes y sus familias, como lo muestra su misión human health care (hhc).

Birth season affects your mood in later life

New research shows that the season you are born has a significant impact on your risk of developing mood disorders. People born at certain times of year may have a greater chance of developing certain types of affective temperaments, which in turn can lead to mood disorders (affective disorders). This work is being presented at the European College of CNP Congress in Berlin.

Seasons of birth have traditionally been associated with certain personality traits, such as novelty seeking, and various folklore justifications, such as astrology, have sought to explain these associations. Now a group of researchers from Budapest, Hungary, are presenting a study which links birth season with temperament.

According to lead researcher, Assistant Professor Xenia Gonda

“Biochemical studies have shown that the season in which you are born has an influence on certain monoamine neurotransmitters, such as dopamine and serotonin, which is detectable even in adult life. This led us to believe that birth season may have a longer-lasting effect. Our work looked at over 400 subjects and matched their birth season to personality types in later life. Basically, it seems that when you are born may increase or decrease your chance of developing certain mood disorders”.

“We can’t yet say anything about the mechanisms involved. What we are now looking at is to see if there are genetic markers which are related to season of birth and mood disorder”.

The group found the following statistically significant trends:

·         cyclothymic temperament (characterized by rapid, frequent swings between sad and cheerful moods), is significantly higher in those born in the summer, in comparison with those born in the winter.

·         Hyperthymic temperament – a tendency to be excessively positive -  were significantly higher in those born in spring and summer

·         Those born in the winter were significantly less prone to irritable temperament than those born at other times of the year.

·         Those born in autumn show a significantly lower tendency to depressive temperament than those born in winter.

Commenting for the European College of Neuropsychopharmacology, Professor Eduard Vieta (Barcelona) XY said:

"Seasons affect our mood and behavior. Even the season at our birth may influence our subsequent risk for developing certain medical conditions, including some mental disorders. What's new from this group of researchers is the influence of season at birth and temperament. Temperaments are not disorders but biologically-driven behavioral and emotional trends. Although both genetic and environmental factors are involved in one's temperament, now we know that the season at birth plays a role too. And the finding of "high mood" tendency (hyperthymic temperament) for those born in summer is quite intriguing."

Researchers find why depression and ageing linked to increased disease risk

 Psychological stress and stress-related psychiatric disorders are associated with increased risk for aging-related diseases, but the molecular mechanisms underlying this relation are unknown. Understanding these mechanisms may contribute to the development of targeted preventive strategies and new or improved treatments for these devastating diseases. This work is presented at the European College of Neuropsychopharmacology congress in Berlin.

Now an international group of researchers from Germany and the US has found that both ageing and depression are associated with changes in the FKBP5 gene. Genes can be regulated by the addition or removal of methyl (CH3) groups to an area of the gene.  The researchers found that ageing can decrease this methylation process, causing the FKBP5 gene to be overexpressed. They also found that when someone is depressed, this demethylation process is accelerated even further.

In a second finding they found that this increased FKBP5 expression is associated with increases in biochemical markers of inflammation and cardiovascular risk.

According to lead researcher, Dr Anthony Zannas (Max Planck Institute of Psychiatry, Munich):

“We found that both aging and depression seem to lead to changes in how DNA is processed, and that this can control the expression of genes that regulate how we respond to stress. These changes are associated with increased inflammation, and we believe that this may lead to the increased risk for several aging-related diseases, such as cardiovascular diseases and neuropsychiatric disorders, that has been observed in chronically stressed and depressed individuals.

Our work shows that risk for aging-related diseases could be conferred by epigenetic changes of stress-related genes and resultant increases in the expression of inflammation markers. It’s too early to say that we are seeing a cause and effect, so we need to confirm the findings by using larger samples and uncover the mechanisms using animal models. If we can do that, we may have the opportunity to develop tests for age-related diseases and new ways to prevent the harmful effects of stress”.

The FKBP5 gene is found on chromosome 6 in humans. It codes the FK506 binding protein 5, also known as FKBP5. This protein is known to play a role in stress responses, immune regulation and basic cellular processes involving protein folding.

Commenting on the work for the ECNP, Professor Bill Deakin (Manchester) said:

“There is a growing realisation that depression is one expression of a set of vulnerabilities for a range of disorders associated with age including obesity, diabetes, cerebro-vascular disease and dementia. Zannas and colleagues are now beginning to unpick some of the first molecular mechanisms of the shared risk. The focus is on FKBP5 a protein transcription factor that regulates several genes relevant to depression (via stress hormones) and to disorders such as Alzheimer’s disease.

Experiencing trauma in childhood and ageing have long-term influences on activity of the gene for FKBP5. This epigenetic regulation is abnormal in people with depression. It is early days and these findings need to be confirmed in definitively large populations. Nevertheless, the results point the way to finding molecular subtypes of depression with specific treatments targeted on transcription factors and epigenetic mechanisms”.

Pathological gambling is associated with altered opioid system in the brain, and a reduced feeling of euphoria when compared to healthy volunteers.

All humans have a natural opioid system in the brain. Now new research, presented at the ECNP Congress in Berlin, has found that the opioid system of pathological gamblers responds differently to those of normal healthy volunteers. The work was carried out by a group of UK researchers from London and Cambridge, and was funded by the Medical Research Council. This work is being presented at the European College of Neuropsychopharmacology congress in Berlin.

Gambling is a widespread behaviour with about 70% of the British population gambling occasionally. However In some individuals, gambling spirals out of control and takes on the features of an addiction − pathological gambling, also known as problem gambling. The 2007 British Gambling Prevalence Survey estimated that 0.6% of UK adults have a problem with gambling, equivalent to approximately 300,000 people, which is around the total population of a town like Swansea. This condition has an estimated prevalence of 0.5−3% in Europe.

The researchers took 14 pathological gamblers and 15 healthy volunteers, and used PET scans (Positron Emission Tomography scans) to measure opioid receptor levels in the brains of the two groups. These receptors allow cell to cell communication – they are like a lock with the neurotransmitter or chemical, such as endogenous opioids called endorphins, acting like a key. The researchers found that there were no differences between the receptor levels in pathological gamblers and non-gamblers. This is different to addiction to alcohol, heroin or cocaine where increases are seen in opioid receptor levels.

All subjects were then given an amphetamine tablet which releases endorphins, which are natural opiates, in the brain and repeated the PET scan. Such a release – called an ‘endorphin rush’- is also thought to happen with alcohol or with exercise.  The PET scan showed that the pathological gamblers released less endorphins than non-gambling volunteers and also that this was associated with the amphetamine inducing less euphoria as reported by the volunteers (using a self-rating questionnaire called the ‘Simplified version of the amphetamine interview rating scale’, or SAIRS).

As lead researcher Dr Inge Mick said:

““From our work, we can say two things. Firstly, the brains of pathological gamblers respond differently to this stimulation than the brains of healthy volunteers. And secondly, it seems that pathological gamblers just don’t get the same feeling of euphoria as do healthy volunteers. This may go some way to explaining why the gambling becomes an addiction”.

“This is the first PET imaging study to look at the involvement of the opioid system in pathological gambling, which is a behavioural addiction. Looking at previous work on other addictions, such as alcoholism, we anticipated that pathological gamblers would have increased opiate receptors which we did not find, but we did find the expected blunted change in endogenous opioids from an amphetamine challenge. These findings suggest the involvement of the opioid system in pathological gambling and that it may differ from addiction to substances such as alcohol. We hope that in the long run this can help us to develop new approaches to treat pathological gambling”

Speaking on behalf of the ECNP, Professor Wim van den Brink (Amsterdam), Chair of the Scientific Committee for the Berlin Congress, said:

“At the moment, we find that treatment with opioid antagonists such as naltrexone and nalmefene seem to have a positive effect in the treatment of pathological gambling, and that the best results of these medications are obtained in those problem gamblers with a family history of alcohol dependence. But this report from Dr Mick and colleagues is interesting work, and if confirmed it could open doors to new treatment methods for pathological gamblers”.