On the massive stellar population of the Super Star Cluster Westerlund 1

We present new spectroscopic and photometric observations of the young Galactic open cluster Westerlund 1 (Wd 1) that reveal a unique population of massive evolved stars. We identify ~200 cluster members and present spectroscopic classifications for ~25% of these. We find that all stars so classified are unambiguously post-Main Sequence objects, consistent with an apparent lack of an identifiable Main Sequence in our photometric data to V~20. We are able to identify rich populations of Wolf Rayet stars, OB supergiants and short lived transitional objects. Of these, the latter group consists of both hot (Luminous Blue Variable and extreme B supergiants) and cool (Yellow Hypergiant and Red Supergiant) objects - we find that half the known Galactic population of YHGs resides within Wd1. We obtain a mean V-M_V ~25 mag from the cluster Yellow Hypergiants, implying a Main Sequence turnoff at or below M_V =-5 (O7 V or later). Based solely on the masses inferred for the 53 spectroscopically classified stars, we determine an absolute minimum mass of \~1.5 x 10^3 Msun for Wd 1. However, considering the complete photometrically and spectroscopically selected cluster population and adopting a Kroupa IMF we infer a likely mass for Wd 1 of ~10^5 Msun, noting that inevitable source confusion and incompleteness are likely to render this an underestimate. As such, Wd 1 is the most massive compact young cluster yet identified in the Local Group, with a mass exceeding that of Galactic Centre clusters such as the Arches and Quintuplet. Indeed, the luminosity, inferred mass and compact nature of Wd 1 are comparable with those of Super Star Clusters - previously identified only in external galaxies - and is consistent with expectations for a Globular Cluster progenitor.Comment: A&A in press, 24 pages with 19 figures. For full resolution version see http://www.edpsciences.org/articles/aa/pdf/press-releases/PRAA200506.pdf (now correct url

The retention of lacosamide in patients with epilepsy and intellectual disability in three specialised institutions

Purpose: We describe the effectiveness of lacosamide as adjunctive therapy in patients with epilepsy and an intellectual disability. This information is relevant, as few data exist pertaining to this population with a high prevalence of (intractable) epilepsy. Methods: We performed a retrospective study in three specialised institutions. Inclusion criteria were (1) focal onset or symptomatic generalized (2) therapy-resistant epilepsy, (3) intellectual disability and (4) residence in a care-facility for people with intellectual disabilities (PWID). The primary outcome variables were the retention rates of lacosamide, estimated through Kaplan-Meier survival analysis. Secondary outcomes were reported seizure control, side effects and clinical factors influencing discontinuation. Results: One hundred and thirty-two patients were included. The median retention time of lacosamide in our cohort was four years. The estimated one-, two- and three-year retention rates of lacosamide were 64%, 57% and 56% respectively. Severity of intellectual disability and seizure type did not influence whether lacosamide was continued. In 48.5% of patients, a reduction of seizure activity was reported. Side effects were at least part of the reason for discontinuing treatment in 26.5% of all patients. Common side effects were tiredness/somnolence (in 30.3%), aggression/agitation (24.2%), and instable gait (15.2%). Five deaths during follow-up were considered unlikely to be related to the use of lacosamide. One patient died unexpectedly within two months of treatment onset, probably this was a case of SUDEP. Conclusion: These retention rates of lacosamide in PWID are similar to rates of previously registered anti epileptic drugs in PWID. Behavioural side effects were noted in a high proportion compared to the general literature on lacosamide. Other side effects were in line with this literature. Lacosamide seems effective and safe for PWID and refractory epilepsy. (C) 2017 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved

A new hyperekplexia family with a recessive frameshift mutation in the GLRA1 gene

Genetics of disease, diagnosis and treatmen

Chapter 14 entitled " Migraine and Epilepsy "

Migraine and epilepsy are both characterized by transient attacks of altered brain function with a clinical, pathophysiological and therapeutic overlap [1–9]. Furthermore, epilepsy and migraine may mimic each other. In particular, occipital lobe seizures may be easily misinterpreted as migraine with visual aura [10]. The frequency of epilepsy among people with migraine (range 1–17%) is higher than in the general population (0.5–1%), just as the prevalence of migraine among patients with epilepsy is also higher (range 8–15%) than that reported in healthy individuals [3, 11-16]. Especially in children this comorbidity is found often [17]. Some studies of the association between migraine and specific epilepsy syndromes, such as childhood epilepsy with occipital paroxysms and benign childhood epilepsy with centrotemporal spikes (CTS) were negative [6,18], but others were positive [3, 19-24]. An increase in (usually unspecific) electroencephalographic (EEG) abnormalities in patients suffering from migraine [9], has been considered as evidence of a relationship between migraine and epilepsy [10, 11]. The mechanism underlying the onset of a migraine attack is probably cortical spreading depression (CSD). Unlike epileptiform abnormalities in epilepsy attacks, CSD is not demonstrable in migraine patients which clearly hampers studies addressing the pathophysiological overlap between migraine and epilepsy attacks