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Join the ILAE at the 2019 International League Against Epilepsy (ILAE) British Branch Annual Scientific Meeting in Birmingham, UK, from the 2nd to the 4th October. The 3-day conference features a strong scientific programme with poster and oral presentations focusing on cutting edge basic and clinical research, innovative practice techniques and scientific topics including SUDEP, what is a seizure, advances in epilepsy surgery and the teenage brain. In addition, the programme includes a neurobiology of epilepsy session, co-hosted by Epilepsy Research UK, the Irish Branch session on FutureNeuro and the Neurosurgery Network meeting. The aim is to provide a high quality teaching experience, with the overall objective of improving epilepsy management in Britain.

Submission of abstracts for posters are invited, and submissions for two Gower Award categories. The meeting is a great opportunity in which to further your professional development by sharing your research ideas, networking with colleagues and building collaborative relationships.

14 CPD accreditation credits from the Royal College of Physicians have been applied for. Early bird rates available until the 5th August. ILAE British Branch members receive discounted registration. Bursaries are also available to attend the meeting.

Join the ILAE today, visit ww.ilaebritish.org.uk

To learn more and to register for the 2019 meeting, visit www.ilaebritishconference.org.uk

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Bial and Eisai have announced clinical practice data from the Euro-Esli study demonstrating clinical effectiveness of eslicarbazepine acetate, and that it is generally well tolerated as an adjunctive therapy in focal epilepsy patients with psychiatric comorbidities, including intellectual disability, compared with people with no psychiatric comorbidities.[1] The data, which add to the body of evidence on eslicarbazepine acetate as adjunctive therapy from Phase III studies,[2],[3],[4],[5] were published in Journal of the Neurological Sciences.[1]

Psychiatric comorbidities, including intellectual disability and depression, are common for adults who have epilepsy.[6],[7] Prevalence of psychiatric comorbidities may be twofold higher in adult patients with epilepsy compared to the general public, and up to a quarter of people diagnosed with epilepsy are estimated to have an intellectual disability.[6],[7] Psychiatric comorbidities can exacerbate the effects and increase the impact of epilepsy.[8] Furthermore, antiepileptic treatments can interfere with treatments for the psychiatric comorbidities, and thus adversely affect these psychiatric conditions. [9],[10] There are many considerations for treating this patient population, thereby complicating treatment choice.[10]

“The comorbidities of epilepsy represent a substantial burden for people with epilepsy. This data provides a significant insight into how eslicarbazepine acetate performs in a routine medical setting for these patients and the results are very encouraging, demonstrating eslicarbazepine acetate’s efficacy and tolerability as an adjunctive therapy in this sub-set of patients,”

Dr Colin Doherty, Consultant Neurologist, St James’s Hospital, Dublin, Ireland, and lead author of the Euro-Esli study.

This newly published data includes patient populations that are sometimes excluded from clinical trials, including those with psychiatric comorbidities, specific comorbidities of intellectual disability, or depression.[1],[11] Adverse events reported during this sub-cut of the Euro-Esli study are consistent with eslicarbazepine acetate’s safety profile established in Phase III studies.[1],[2],[3],[4],[5] Adverse events with eslicarbazepine acetate treatment were reported by 43.1% of people with psychiatric comorbidities (n=122/283) and 45.8% of people with intellectual disability (n=49/107). The most common adverse events were dizziness (11.4%; n=31/272), somnolence (8.8%; n=24/272) and fatigue (8.1%; n=22/272) for people with psychiatric comorbidities; and somnolence (10.1%; n=10/99), dizziness (7.1%; n=7/99) and fatigue (6.1%; n=6/99) for people with intellectual disability.[1]

Psychiatric comorbidities

  • Treatment with eslicarbazepine acetate in people with psychiatric comorbidities showed a responder rate of 83.1% (n=128/154) (defined by ≥50% seizure frequency reduction from baseline) at 12 months, compared with 82.5% (n=326/395) of people without psychiatric comorbidities (p=0.871). Seizure freedom was achieved by 51.3% of people with psychiatric comorbidities (n=79/154) (defined as no seizures since at least the prior visit) at 12 months with eslicarbazepine acetate treatment, compared with 51.4% (n=203/395) of people in the no psychiatric comorbidities group (p=0.984).[1]
  • Adverse events were reported by 43.1% of people with psychiatric comorbidities (n=122/283) compared to 30.5% of people without psychiatric comorbidities (n=261/855; p<0.001). Psychiatric adverse events were reported by 3.7% of people with psychiatric comorbidities (n=10/272) compared to 1.8% of people without psychiatric comorbidities (n=15/822; p=0.076). Discontinuation of treatment with eslicarbazepine acetate due to adverse events occurred in 17.2% of people with psychiatric comorbidities (n=45/262) compared with 11.6% of people without psychiatric comorbidities (n=94/811; p=0.019).[1]

Intellectual disability

  • Treatment with eslicarbazepine acetate in people with intellectual disability showed a responder rate of 60.3% (n=35/58) at 12 months, compared with 76.6% (n=222/290) of people without intellectual disability (p=0.010). Seizure freedom was achieved by 22.4% of people with intellectual disability (n=13/58) at 12 months with eslicarbazepine acetate treatment, compared with 43.1% (n=125/290) of people without intellectual disability (p=0.003).[1]
  • Adverse events were reported by 45.8% of people with intellectual disability (n=49/107) compared to 32.6% of people without intellectual disability (n=275/844; p=0.007). Cognitive adverse events were reported by 4.0% of people with intellectual disability (n=4/99) compared to 3.8% of people without intellectual disability (n=31/809; p=0.919). Discontinuation of treatment with eslicarbazepine acetate due to adverse events occurred in 22.4% of people with intellectual disability (n=22/98) compared with 14.8% of people without intellectual disability (n=117/789; p=0.050).[1]

Depression

  • Treatment with eslicarbazepine acetate in people with depression showed a responder rate of 81.0% (n=51/63) at 12 months, compared with 82.9% (n=402/485) of people without depression (p=0.703). Seizure freedom was achieved by 46.0% (n=29/63) of people with depression at 12 months with eslicarbazepine acetate treatment, compared with 52.0% (n=252/485) of people without depression (p=0.376).[1],[12]
  • Adverse events were reported by 42.6% of people with depression (n=60/141) compared to 32.4% of people without depression (n=322/993; p=0.017). Psychiatric adverse events were reported by 4.4% of people with depression (n=6/136) compared to 2.0% of people without depression (n=19/955; p=0.074). Discontinuation of treatment with eslicarbazepine acetate due to adverse events occurred in 18.5% of people with depression (n=24/130) compared with 12.1% of people without depression (n=114/939; p=0.044).[1]

The Euro-Esli study presents a clinical practice data set of eslicarbazepine acetate with 2,058 patients included.[13] The Euro-Esli study has a broad set of inclusion/exclusion criteria, allowing for the representation of people with conditions sometimes excluded from clinical trials.[13],[14] The Euro-Esli study includes a diverse patient population with challenging comorbidities, and provides robust evidence to support clinical practice and treatment decisions.[13],[14]

Eslicarbazepine acetate is approved in the European Union (EU) as adjunctive therapy in adults, adolescents and children aged above 6 years, with partial-onset seizures with or without secondary generalisation.[15] Eslicarbazepine acetate has also been approved in the EU as monotherapy in the treatment of partial-onset seizures, with or without secondary generalisation, in adults with newly diagnosed epilepsy in 2017.[15]

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Rajith de Silva
Emaildesilva63@aol.com

Conflict of interest statement: None declared.

Date first submitted: 22/02/19

Acceptance date: 25/02/19

Published online first: 3/6/19

The year was 1994, and I had just completed my stint in research in Creutzfeldt-Jakob disease (CJD) with Bob Will, at the National Surveillance Unit in Edinburgh, UK.  Some of the work I had done with the team had been accepted for presentation at a joint ABN/ANA conference in San Francisco.  I set off proudly, clutching two posters, accompanied by one of the Neuropathologists from the unit – James Ironside.  San Francisco was of course the base of Stanley Prusiner, who had proposed the “prion” hypothesis, as the explanation for some of the unique aspects of the spongiform encephalopathies.  At the time the theory was still under scrutiny and the subject of much debate (although a few years later Prusiner was partially vindicated by the award of the Nobel prize in Medicine; the same mechanism is now thought to underlie many more (possibly all?) degenerative disorders affecting the brain associated with abnormal proteins, including (perhaps) Parkinson’s disease).  It seemed appropriate that James and I should visit Prusiner in his laboratory, during our visit.  It smacked a little of paying homage, but we were excited by the prospect of meeting this controversial character, and it was simply too good an opportunity to miss.

The conference passed without event, and my posters were accorded the appropriate lack of interest they deserved.  Undeterred, James and I set off for Parnassus Heights one October morning, to the UCSF campus there.  Prusiner breezed in, a few minutes late, but was polite, genial and duly condescending.  We had gone armed with more data from the unit.  Variant CJD had not yet appeared, but James, Bob and others were already engaged in an intensive (and ultimately rewarding) surveillance exercise.  We showed Prusiner the data we had been collecting, and he listened patiently to us, rather like a kind Montessori teacher.  His time was clearly precious, and after half an hour, he indicated that our time was up by looking at his watch very deliberately.

We hastily concluded our chat, and got ready to leave.  Prusiner, perhaps feeling a little sorry for us by then, started asking what we planned to do the rest of the day.  The conference organisers had arranged various excursions after the meeting, one of which was a walking tour of San Francisco’s fabled Chinatown.   Our meeting with this famous scientist took a surreal turn at this point, when I explained that I was hoping to join this tour that afternoon.  Prusiner reposted by asking what time I needed to be at the airport.  I looked at him curiously, but also with some bewilderment.  Did he not know that there was a Chinatown in his own City, and that you didn’t need to fly to get there?  Was he really the great man…and, crucially, should he be a Nobel prize contender?  It dawned on me that he had not understood my British-Sri Lankan accent, and thought that I was going to visit China!  More explanations followed, and we departed, flushing.

Prusiner did receive the Nobel prize in 1997, and many more accolades followed.  Our meeting with him took place at a heady time: the world was fascinated by these disorders and the potential impact of Bovine Spongiform Encephalopathy on humans.  Neuroscientists too were intrigued by “prion” biology, and the extent to which Prusiner’s theory accounted for our clinical and laboratory observations.  It was a privilege meeting him, seemingly at the height of his career, that day, although from his perspective it was a considerably more pedestrian encounter, I suspect.  However puerile, what made the memory of that meeting indelible for me was a rather embarrassing misunderstanding – one which did make me query, however briefly, his brilliance!

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Biogen and the Douglas Grant Rehabilitation Centre, NHS Ayrshire & Arran, Scotland have announced the launch of multiple sclerosis awareness campaign, 1MSg (One Message), on World MS Day, encouraging ‘lost’ MS patients to re-engage with the support available to them.

Research conducted by the MS Trust found that one in 10 people living with MS had seen neither an MS-specialist nurse nor a neurologist in the past year1, and so will not have received the comprehensive annual review recommended by the National Institute for Health and Care Excellence (NICE)2. In addition to this, there are a number of people with MS not currently known to  MS-specialists at all – those ‘lost to follow-up’. A report published by the MS Society demonstrates that there is now consensus amongst MS experts to indicate that early treatment is key in improving long-term health outcomes, slowing down irreversible damage, and reducing relapses3.

The 1MSg campaign encourages people with MS to ‘take control and know their choices’, and the Douglas Grant Rehabilitation Centre calls on patients to come back and find out what options may be available to them. Dr Jenny Preston, Consultant Occupational Therapist, Clinical Lead Neurological Rehabilitation Douglas Grant Rehabilitation Centre, NHS Ayrshire & Arran, said:

This campaign underlines the importance for people living with multiple sclerosis to get in touch with us if they haven’t had a review appointment for more than year. It is vital that we keep in touch with our patients so we are aware of how they are managing their health. We can also keep them up-to-date with new medications and treatments that could really benefit them.

Find out more at www.1msg.co.uk/

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JMS Pearce MD, FRCP Emeritus Consultant Neurologist, Department of Neurology, Hull Royal Infirmary, UK.
Correspondence to: J.M.S. Pearce, 304 Beverley Road Anlaby, East Yorks, HU10 7BG, UK.
Emailjms.pearce@me.com

Conflict of interest statement: None declared.

Date first submitted: 20/10/18

Acceptance date: 25/10/18

Published online first: 29/5/19

Featured image: WJ Adie
From: Alastair Compston; Idiopathic narcolepsy: a disease sui generis; with remarks on the mechanisms of sleep. By WJ Adie. Brain, 2008;131:2532–2535, https://academic.oup.com/brain/article/131/10/2532/1746741

The harmless condition of a dilated pupil which reacts abnormally slowly (myotonic) to light and convergence was fully described in 1931 by William John Adie (1886 – 1935),1 of the National Hospital, Queen Square.

I wish to draw attention to a benign symptomless disorder characterized by pupils which react on accommodation but not to light, and by absent tendon reflexes. Five of the six cases I am about to describe came under my notice in the course of a few weeks;… Though harmless in itself it merits recognition because it is often mistaken for a manifestation of syphilis of the nervous system, with unfortunate consequences… Mr. Foster Moore has described seven cases under the title ‘Non-luetic Argyll Robertson pupil.2

Usually seen in females, in 80% cases it is unilateral. Adie was not the first to observe this uncommon curiosity and its variant manifestations. In 1818 the London ophthalmologist, James Ware (1756–1815), described a patient who may have had a myotonic pupil.3 His patient, whose pupillary abnormality had been known for twenty years, was:

A lady between thirty and forty years of age, the pupil of whose right eye, when she is not engaged in reading, or in working with her needle, is always dilated very nearly to the rim of the cornea; but whenever she looks at a small object, nine inches from the eye, it contracts, within less than a minute, to a size nearly as small as the head of a pin. Her left pupil is not affected like the right; but in every degree of light and distance, it is contracted rather more than is usual in other persons.… Several instances have come under my notice, in which the pupil of one eye has become dilated to a great degree, and has been incapable of contracting on an increase of light,

Adie stated: ‘The tonic or myotonic pupillary reaction was first described in 1902 by Saenger in the left pupil of a 34 year old woman)4 and by Strasburger in a 17 year old man5 independently.6  Later in the same year both Saenger and Nonne reported further cases for which Saenger proposed the name ‘myotonic pupillary movement’ to distinguish it from other forms of mydriasis or abnormal pupillary reflexes. Later, Adie related ‘atypical ‘forms, less clearly defined, but he included some forms of ‘internal ophthalmoplegia and complete light rigidity with atonic convergence reaction.’

Before Adie, Hughlings Jackson in 1881 had also clearly described the same disorder:7

A woman aged 26 was sent to see me simply because the right pupil was much larger than the left. It had been so three years…the right pupil was dilated and absolutely motionless to light, and also during accommodation, yet the accommodation itself on this side was perfect; this was severely tested by Mr Couper…this case at first puzzled me…It occurred to me to test the knees. Neither I nor Mr Couper found the smallest trace of the knee phenomenon [knee jerk]. Several times did I pertinaciously inquire for other symptoms of tabes; there were no other symptoms of any kind.…Dr Buzzard …confirmed the above observations.8

In 1906 Markus had described an isolated case of partial iridoplegia,9 and Weill and Reys10 also described a tonic pupil reactions to convergence and accommodation with areflexia. Some reports bear their names as eponyms.

Adie’s more detailed, classic paper in 1932,11 described 22 patients, with absent tendon reflexes, and noted 44 reported cases of tonic pupil in nine of which there were absent tendon reflexes. In this account he outlined four incomplete forms (the last would not now be accepted)

1. The complete form—typical tonic pupil and absence of reflexes.

2. Incomplete forms : a) tonic pupil alone; b) atypical phase of the tonic pupil alone (iridoplegia; internal opthalmoplegia); c) atypical phases of the tonic pupil with absent reflexes; d) absent reflexes alone.

At about the same time, Gordon Holmes found 19 patients with the myotonic pupils, characterised in his Introduction to Clinical Neurology:

By very slow contraction on convergence, and even slower relaxation. The reflex to light is often lost too. One or both eyes may be affected.

His 1931 paper described it and its association with symptoms of other diseases of the nervous system:

Frequently no change in the size of the pupil was visible immediately on convergence, but when this was maintained for a few seconds the pupil slowly and gradually grew smaller, till its diameter equalled or was even narrower than that of the normal eye. The rate of contraction varied very much…When contracted the pupil remains constant and when convergence is relaxed it dilates slowly… In the present state of our knowledge a separation of those cases in which the tendon jerks are absent from those in which they persist is unjustifiable . . . the similarity of the symptoms in all these cases naturally suggests a common aetiology.12

Edwin Bramwell linked Holmes’s name with Adie’s in 1936.13 The brilliant George Bruyn mischievously pointed to the ‘peculiarity’ that Morgan, Symonds, Holmes and Adie all published at about the same time, in different journals without referring to each other, yet they knew each other well at Queen Square.1 However Adie’s second paper (1932) did mention Holmes’s work .11

The credit must be Adie’s for stressing its harmless nature and crucially by distinguishing it from neurosyphilis. Adie did not claim originality, recognizing several earlier accounts. He acknowledged that Morgan and Symonds had recorded:

IN Guy’s Hospital Reports for 1927 Dr. Symonds and I drew attention to a small group of cases in which certain abnormalities of the pupil, including inequality and defective reaction to light and convergence, and also some affection of accommodation, were associated with a pathological absence or diminution of the tendon- jerks.14

It was previously confused with the Argyll Robertson pupil associated with luetic tabes dorsalis or General Paralysis of the Insane, characterised by: a loss of both direct and consensual light reflexes; pupillary inequality; irregularity and iris atrophy without reaction to light. Adie clearly distinguished this from his myotonic (Pseudo-Argyll Robertson) pupil.

Since Adie’s descriptions,2,6,11 this conception of an atypical tonic pupil has been widened,15 which unnecessarily complicates a diagnosis which is secure if clinical observations are precisely observed.

Pathogenesis

Stanley Graveson (1915-1976) studied 15 patients, three men, 12 women, aged 12 to 55.16 He set out to illuminate: (1) the site of the anatomical lesion and (2) the nature and specificity, or otherwise, of the underlying pathological process. Two types of tonic pupil were distinguished, (a) the fixed type, and (b) the ordinary type of tonic pupil. The only common features of this latter variety are (1) their regularity of shape or position of the pupil and (2) the slowness of pupillary dilatation after convergence. Graveson pointed out that the lesion had to be on the efferent limb of the light reflex arc, to account for the absence of a light response in a unilateral tonic pupil with a simultaneous brisk consensual response in the normal pupil. The prompt reaction of the pupil to pilocarpine meant that the muscle of the iris could not be at fault.

The pathogenesis remained uncertain. Adie had reported: ‘all we can say is that the ocular and reflex signs we have considered seem to be the expression of a kind of perversion of nervous activity of which, at present, we can form no conception.’ Harriman and Garland however, clarified matters in a minutely examined autopsy case in 1968 that showed the causal neuronal degeneration in the ciliary ganglion, denervation of ciliary body, partial atrophy of pupilloconstrictor muscle—all on the right, affected side. The site of the lesion responsible for areflexia was less conclusive, but they noted a selective degeneration of neurones in dorsal root ganglia, possibly those supplying muscle spindles. This was consistent with a neurophysiological reduction in size of the H waves, evidence of depression of the monosynaptic spinal reflex arc, previously observed.17 It confirmed the similar complete loss of ciliary ganglion cells in the only other autopsied case at the time,18 and fits with the known denervation cholinergic hypersensitivity of the pupil to methacholine and pilocarpine.

References

  1. Bruyn GW, Gooddy W. Adie’s syndrome. In: Neurological Eponyms. edited Peter J. Koehler PJ, Bruyn GW, Pearce JMS. Oxford, OUP 2000;181-185.
  2. Adie W. J. Pseudo-Argyll Robertson pupils with absent tendon reflexes. Br Med J 1931;1:1091.
  3. Ware J. Observations relative to the near and distant sight of different persons. Phil Tr Roy Soc London 1813;103:36-38.
  4. Saenger A. Myotonic Pupil Movement .Neurol Centralbl 1902;21:837 and 1137.
  5. StrasburgerJ. Sluggishness of the Pupil to Accommodation and Convergence. Neurol.ZbI 1902;21,738 and 1052.
  6. Adie WJ. Tonic Pupils and absent tendon reflexes: A benign disorder sui generis; its complete and incomplete forms. Brain. 1932;55,98-113.
  7. Pearce JMS. Hughlings Jackson and the Holmes-Adie tonic pupil. J Neurol Neurosurg Psychiatry 1995; 58 (1): 87
  8. Jackson JH. Paralytic affections. 1. On eye symptoms in locomotor ataxy. Tr ophthal Soc. UK. 1881; 1 :139-54.
  9. Markus Ch. Notes on a peculiar pupil-phenomenon in cases of partial iridoplegia. Trans Ophthal Soc UK. 1906;26:50-58.
  10. Weill G, Reys L. Rev de l’accomodation avec areflexie a la lumiere chez un sujet de crises tetanoides et d’areflexie. Revue d’Oto-Neuro-Ophtalmologie. 1926;4: 433–441.
  11. Adie WJ. Complete and incomplete forms of the benign disorder characterised by tonic pupils and absent tendon reflexes. Br J Ophthalmol. 1932;449-60.
  12. Holmes G. Partial iridoplegia associated with symptoms of other diseases of the nervous system. Trans ophthal Soc. UK. 1931; 51 : 209-28.
  13. Bramwell E. The Holmes-Adie Syndrome. A Benign Clinical Entity which Simulates Syphilis of the Nervous System. Edinburgh Med. Jour., New Series. 43:1936;83-91
  14. Morgan, OG. and Symonds, CP. Internal Ophthalmoplegia with Absent Tendon-jerks. Proceedings of the Royal Society of Medicine 1931; pp.41-43.
  15. Lowenstein, O., and Friedman, E. D. (1942). Arch. Ophthal., Chicago, 28, 1042.
  16. Graveson G. S. The Tonic Pupil. J. Neurology Neurosurgery & Psychiatry. 1949;12:219-30.
  17. Harriman DGF, Garland H. The pathology of Adie’s syndrome. Brain 1968; 91 ;401-18.
  18. Ruttner, F. Die tonische Pupillenreaktion. Mschr Psychiat Neurol. 1947;114:265–286.
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The charity, Young Epilepsy, has launched a new online resource for education professionals, which provides access to information and practical tools enabling them to better support the children with epilepsy who are under their care.

A survey of 600 adults working in the education sector – including teachers, administrators, and catering assistants- was commissioned by the charity, and found that four in 10 education professionals would not be able to help a student having an epileptic seizure1.

On average epilepsy affects 112,000 children and young people across the UK2, but two-thirds of those polled have had no training about how to support the children with epilepsy in their care, including what to do in the event of a seizure1.

Other results confirmed that only 29 per cent knew that they should time the length of seizure and a third confirmed they wouldn’t know when to call for an ambulance in the event of a seizure1.  Experts recommend you ring 999 if you know it’s their first seizure or if the seizure lasts for more than five minutes as prolonged seizures can result in status epilepticus, a potentially fatal condition.

The Online Guide for Schools contains essential information for anyone working with young people who have epilepsy and is available to access completely free of charge at www.youngepilepsy.org.uk/guideforschools.

Sharon White, Chief Executive of the School and Public Health Nurses Association (SAPHNA) said: “We welcome this resource which provides much needed updated guidance and, in doing so, further raises awareness of epilepsy in young people.”

Many of those polled were not aware of the different types of seizure a young person can experience. Three quarters were unaware falling to the ground and getting straight back up again could indicate that a young person is having a seizure, or experiencing strange tastes and smells (55 per cent), or staring blankly as if daydreaming (29 per cent)1.

A further survey of 356 young people with epilepsy and their parents undertaken by Young Epilepsy, found 37 per cent of young people do not have an Individual Health Care Plan at school – these plans set out key information to ensure young people are safe and included in all aspects of school life.

A number of the young people have been unnecessarily excluded from activities or opportunities at school, purely due to their condition3.

Young Epilepsy’s research also shows that many young people with epilepsy have a significant difficulty in some area of cognition or behaviour; a consequence of epilepsy that’s rarely addressed when discussing the condition, but can have a profound effect on educational development, without the right support and guidance3.

Mark Devlin, Chief Executive of Young Epilepsy said: “We know that our colleagues working in any education setting are facing many challenges every day, and most are doing a fantastic job in ensuring that every child in their care is being fully supported.

“But these latest figures show that children with epilepsy are struggling to have their conditions fully understood by the people who are playing an essential role in their educational and emotional development.

“It is our hope that this fantastic new online resource gives teachers the opportunity to learn more about epilepsy and allow the young people in their care to be fully supported to learn and be included in school life to the full.”

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Elekta has announced that Elekta Unity, a transformative magnetic resonance radiation therapy (MR/RT) system that enables personalised precision radiation medicine, is in clinical use at The Christie NHS Foundation Trust. Elekta Unity combines two technologies: a state-of-the-art 1.5T MRI scanner and a best-in-class 7 MV linear accelerator, driven by breakthrough real-time adaptive radiotherapy software. It provides the ability to reshape the dose based on daily changes in shape, size and position of the tumour and surrounding healthy anatomy, as visualised with MRI, and then enables accurate dose delivery with real-time visualisation of the tumour.

“Tumours are mobile, and they can change in size, shape and location within the body as a result of treatment, disease progression or regression, and normal physiologic activity such as breathing and digestion,” said Professor Ananya Choudhury, Chair and Honorary Consultant in Clinical Oncology at the Christie NHS Trust Foundation. “Prior to Unity, we did not have the technology to assess these changes on a daily basis. Unity provides an exciting new capability to provide patients with the best and precise cancer care possible. As the most advanced approach to radiation therapy, Unity gives us the ability to adapt treatment in real time to optimise radiation delivery to the tumour while sparing nearby healthy tissue.”

“The Christie NHS Foundation Trust was a founding member of the global consortium that helped develop Unity. We are very enthusiastic about this new technology due to the ability to see what we treat in real time and the potential to improve our radiotherapy treatments,” said Professor Corinne Faivre-Finn, Honorary Consultant Clinical Oncologist and Professor of Thoracic Radiation Oncology at the Christie NHS Trust Foundation. “Not only will Unity allow more precise delivery of radiation in cancers typically treated with this important form of therapy, it will also open the door to using radiation therapy in hard-to-treat cancers. We are gratified to see our vision of next-generation radiation therapy realised and available now to the patients we serve.”

To learn more, visit elekta.com/Unity.

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The Neurokinex Charitable Trust is now able to offer bursaries to children living with paralysis at its Neurokinex Kids centre in Gatwick thanks to receiving £20,000 in funding from The Peter Harrison Foundation Community Fund. The ‘small grants fund’ organisation supports local community and voluntary groups and this award is part of its ‘Special Needs and Care for Children and Young People’ programme.

The Neurokinex Kids Centre Sponsorship Fund will allow access to cutting-edge neurological rehabilitation for eligible children living with all forms of paralysis, including spinal cord injury, stroke, transverse myelitis and cerebral palsy.

Neurokinex is a leading, not-for-profit provider of activity-based rehabilitation. Established in 2013, it is the first and only International affiliate of the Christopher & Dana Reeve Foundation’s NeuroRecovery Network®. Neurokinex sets out to ‘redefine possibilities’ for people with paralysis: its programmes stimulate and load the entire nervous and musculoskeletal systems through carefully crafted, task-specific exercises with the assistance of skilled therapists.

The Neurokinex Kids centre for paediatric neurorecovery opened its doors in April 2018 at the Neurokinex Gatwick site.  Neurokinex paediatric beneficiaries take part in activities such as active standing, cycling, swinging, climbing and walking, tailored to their neurological impairment. This offers children a multitude of benefits including improvements in neurological function, muscle bulk and quality, cardiovascular health, strength and stamina, balance and trunk control, skin and bone health, range of motion and psychological wellbeing.

“Securing this funding from The Peter Harrison Foundation will be life-changing for some of our young beneficiaries,” Kate Thornton-Jones, Fundraising Director for Neurokinex. “A spinal cord injury at any age is devastating, but it’s particularly serious in the very young.  That said, children’s bodies are highly adaptable and if injured youngsters are able to access quality rehabilitation, we can work together to maximise their rehabilitation. We are very grateful to The Peter Harrison Foundation whose generosity in funding these bursaries will support more families and ensure their children can access our support.”

Please contact trustees@neurokinex.orgtrustees@neurokinex.org for information on how to apply.

www.neurokinex.org

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Eisai and the UK Dementia Research Institute (UK DRI) have announced the launch of a joint collaboration to support the advancement in dementia research. This first-of-its-kind industry collaboration for the UK DRI aims to deliver innovative research that translates into improvements in diagnosis, treatment and prevention of all types of dementia.

There are approximately 850,000 people with dementia in the UK, with numbers set to rise to over one million by 2025.1 As the ageing of the global population gathers pace, the number of dementia patients worldwide is expected to follow this trend, with the total number of people with dementia projected to reach 82 million in 2030 and 152 million in 2050.2

To combat this global issue, the UK DRI draws together world-leading expertise into a single national institute that conducts research into all aspects of dementia including Alzheimer’s disease, Parkinson’s disease, frontotemporal dementia, vascular dementia, and Huntington’s disease.

Eisai is delighted to initiate this joint programme with the UK Dementia Research Institute, bringing new ideas and cutting-edge science to the significant challenge of dementia. As the UK Dementia Research Institute’s first joint collaboration with industry, this programme will provide an environment in which post-doctoral researchers at the forefront of dementia research in the UK can demonstrate the potential of their research to develop treatments for dementia patients.”

Dr Andy Takle, Executive Director and Head, Eisai Hatfield Research Laboratories.

Researchers will benefit from both the UK DRI’s state-of-the-art research facilities and Eisai’s drug discovery and translational expertise, and will support the work of the UK DRI in striving to elucidate novel drug discovery targets and mechanisms, develop new dementia models, and accelerate the linkage of these research results to diagnostics, treatment and care.

This collaboration is a wonderful example of the UK DRI’s desire to work with industry for the greater good of dementia science and patient outcomes. We are grateful for the investment and partnership of Eisai, and indeed for the work of all the dedicated researchers trying to move to new frontiers in addressing dementia. We look forward to seeing more fresh thinking on dementia, and to welcoming our colleagues at Eisai to the UK DRI community of ideas and energy.

Dr Adrian Ivinson, UK DRI Director and COO

Eisai has been conducting research on neurodegenerative diseases in the UK since 1990. In 2012 the company began a research collaboration with University College London (UCL) which will run until 2023, and was established as part of the company’s ‘Open Innovation’ strategy to collaborate with leading researchers and translate new research findings into innovative treatments for patients with neurodegenerative diseases.

References:

  1. The Alzheimer’s Society. Facts for the media. https://www.alzheimers.org.uk/about-us/news-and-media/facts-media. Last accessed May 2019.
  2. Alzheimer’s Disease International. World Alzheimer Report 2018.  https://www.alz.co.uk/research/WorldAlzheimerReport2018.pdf. Last accessed May 2019.
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Neurology Formative Test Questions In Collaboration with The Association of British Neurologists

Now in its third year, the 2019 Neurology Formative Test Questions are brought to you by the Neurology team in South Wales.

The questions will close at midnight on 26 May 2019. They are free to everybody with an ebrain account or access can be purchased for 10 euros (see http://www.ebrain.net/neurology-formative-test/). Before you can start, you will be asked to submit one question that can be used in subsequent years – further guidance is available on the questions page. On completion, you will be able to produce a certificate of participation and claim 2 CPD points.

You can do some of the test questions then come back later, there is no time limit, and retakes are allowed. The 2017 and 2018 questions are still available on ebrain for practice, and these have been popular before and during the test period so far.

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