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RAatE 2011Monday 28th NovemberUniversity of Warwick Conference Centre, CoventryDelegate RegistrationRAatE 2011 is the only UK conference focused on the latest innovations anddevelopments in Assistive Technology. This conference will be of interest toeveryone who uses, works with, develops or conducts research on AssistiveTechnologies (AT).This year's event is run in association with the Health Design & TechnologyInstitute at Coventry University. The HDTI seeks to develop new products andnew systems of care provision for the assisted living sector.The conference program has, over the past years, regularly included newtechnological developments, service innovations, results of formal researchprojects, service based research and development and a wide range of otherstimulating topics.Known as a friendly and productive conference, RAatE offers you a chance tomeet and share knowledge and experience with other people working in AT.RAatE 2011 is delighted to announce this year's keynote speaker as Dr. RogerSmith, Fellow of RESNA and Professor of Occupational Science and Technologyat the College of Health Sciences and the University of Wisconsin, Milwaukee.Dr Smith has published and presented in the area of disability access, assistivetechnology and functional performance measurement and has also secured over$8m of funding for research and projects relating to disability and rehabilitation.Paper presentations at RAatE 2011 will include:• Case studies of innovative AT in practice• Developments & challenges in wheelchair services• Emerging technologies & recent advances in AT• New service demands: Commissioning of re-ablement & AT services• Services – Aspects of service deliveryTo book your place at RAatE 2011 register online at www.raate.org.uk.Cost is £150.Neurology and PsychiatrySpRs Teaching Weekend9 to 11 December 2011, St Anne’s College – OxfordTopics to include: Neurological and psychiatric history takingand examination • Investigations (MRI, EEG)• Psychological presentations of neurological disorder• ‘neurological’ presentations of psychological disorders and thebiological basis of psychiatric symptoms.Course Fee: £250 (Includes two nights’ bed & breakfast, lunches,morning and afternoon coffee/tea and Friday night dinner).BNPA 25thAnnual General Meeting9/10 February 2012Venue: The Institute of Child Health, Guilford St, LondonTopics to include: Huntington’s Disease • Tropical Neuropsychiatry• Conversion Disorder in the developing world • NeuropsychiatryResearch Update • Networks and Rhythms in Health and Disease• What the eye does not see – psychology of magicFor outline programme and registration form visit:www.bnpa.org.ukFor details of exhibition/sponsorship opportunities,contact: Jackie Ashmenall onPhone/Fax: 020 8878 0573/Phone: 0560 1141307Email: admin@bnpa.org.uk or jashmenall@yahoo.comEUROPEAN CHARCOTFOUNDATIONUNIVERSITY CLASSES VIIIEUROPEAN CHARCOTFOUNDATIONSYMPOSIUMFocused on Symptomatic TreatmentsAn Educational Programme onMultiple SclerosisNovember 30, 2011, Marbella, SpainFaculty:M.P. Amato, G. Comi, G. Edan, O. Fernandez, C. Fowler, J. Haas,R. Hupperts, L. Kappos, J. Palace, K. Selmaj, P. Soelberg Soerensen.Call for European Charcot Foundation young investigatorstravel grantsThe European Charcot Foundation is pleased to announce thatthey will provide an unrestricted educational grant to sponsor alimited number of young investigators with a travel grant of€1500,- to attend the University Classes in Multiple Sclerosis VIII.Young investigators are invited to apply before October 15, 2011.Conditions for applications are available on our website.Towards Personalized Treatment inMultiple SclerosisDecember 1, 2 and 3, 2011, Marbella, Spain17th European CharcotFoundation LectureProf. X. Montalban‘Towards Treatment of Persons with Multiple Sclerosis:on detour and access’Sessions on:• Rationale for personalized treatment in face of diseasecomplexity• Tools for prognosis• Treatment heterogeneity, targets and risks• Treatment in practice• Partnership• Personalized treatment, partnership and disease complexityFor detailed information and registration visit our website www.charcot-ms.eu32 > <strong>ACNR</strong> > VOLUME 11 NUMBER 4 > SEPTEMBER/OCTOBER 2011
CONFERENCE REPORTSBasal Ganglia at the Base of the CN TowerConference details: 5-9 June 2011; Movement Disorders Conference, Toronto, Canada. Reviewed by: Dr Tom Foltynie, Consultant Neurologist, Queen Square, London.So what’s new in Movement Disorders? Ofcourse there’s a growing trend to keepnew unpublished data to yourself thesedays, lest your rivals and competitors getwind of your latest breakthrough, but despitethis, MDS 15 in Toronto had plenty of novelty.PD Mechanisms and PathogenesisYou come all the way to Canada and yet itturns out that one of the star talks of theweek hails from Sheffield, UK. I’d not heardPeter Redgrave speak before, but he gave adelightful talk as part of an Obeso/ Brown/Redgrave basal ganglia trio. He explained theevolutionary existence of the basal gangliawell ahead of the development of the cortexand the fact that it has a clear role in actionselection in response to diverse environmentalstimuli. He elaborated that we shouldthink of our behaviour as either “goaldirected “ or “habitual”, with distinct anatomicalcircuits from cortex to basal ganglia. Heproposed that Parkinson’s disease (PD)patients are trapped in the goal directedbehaviour circuit, and have lost the habitualpathways responsible for automatic walking,postural reflexes and sequential motorprogrammes. There must also be distortion atthe point of convergence between thesecircuits, explaining why even voluntarymovements become slower and moreeffortful.We have long known about interrelatedpathways of proteasomal dysfunction andmitochondrial dysfunction in the neurodegenerativeprocess. It seems that mitochondrialdysfunction and removal (mitophagy)and ongoing replenishment through biogenesisis repeatedly being identified as criticalin PD pathogenesis. Serge Przedborksi gave auseful review of the last 20 years progresssince MPTP toxicity was first identified, allthe way to the recent identification of PGC1αand PARIS (parkin interacting substrate) allwith respect to the mitochondrial pathways.To add further detail, David Park reviewed hiswork on Calpain, cdk-5 and prx-2 that relateoxidative stress mediated by mitochondrialdysfunction with subsequent cell death,while Valina Dawson reviewed some of herunpublished cell biology that has beenrecently discovered, relating oxidative stressas a cause for mitochondrial dysfunctionand subsequent nuclear DNA damage. A keypart of this pathway is PARP-1, and PARP-1inhibitors that cross the blood brain barrierhave been identified and shown to beprotective in vitro and in animal models ofPD. The field has also been greatly advancedby the work of Heidi Macbride who showedreal time fission/fusion and budding of mitochondria,and their dynamic movementthrough the cytosol and into and out of theCN Tower, Toronto, Cananda.Tom Foltynie.nucleus. A novel PD gene VPS35 appears toplay a role in the process of mitochondrialbudding.... watch out for this.The take home message seems to be thatPD pathogenesis undoubtedly involvesproteotoxicity, mitochondrial dysfunctionand neuroinflammation, all interacting withmultiple points for potential therapeuticintervention.TherapeuticsCarl Clarke presented the evidenceregarding treatments for advanced PD.Despite its widespread use, we have littleactual “Evidence” to justify the use ofApomorphine, evidence from only smallnumbers of patients for Duodopa but datafrom trials involving large numbers ofpatients undergoing Deep Brain Stimulation(DBS). While experienced clinicians haveplenty of their own anecdotal experience tounderwrite the use of all three of theseagents in appropriate patients, will thisevidential thin-ice jeopardise our ability tooffer these treatments in these harsheconomic times? Dr Clarke predicted thatcost effectiveness data that is soon to emergefrom the PD surg trial may further jeopardisethe availability of these treatments foradvanced PD patients – I for one, really dohope not.Dr Clarke also discussed the plausibility ofa randomised trial comparing the efficacy ofthese three expensive treatments, andpointed out that this is highly unlikely giventhe need for companies to protect theircommercial interests, and the impossibilityof effective treatment blinding. Even iffinanced, such a trial would prove difficultgiven that different patients and cliniciansalready have well established prejudices/preferences regarding these disparate treatments.In my own opinion, I have no doubtthat one size does not fit all in advanced PDand an attempt to define choice one, twoand three that suits all comers is far toosimplistic. Long term improvements in functionand quality of life can be highly variablein response to these treatments dependingon patient phenotype such as age / severityof motor symptoms / motor phenotype /extent of cognitive impairment / other nonmotor symptoms.To complicate the PD therapeutic horizonfurther, there is no shortage of new andevolving treatments for PD. Olivier Rascolgave a whirlwind tour through these, bothdopamine and non-dopaminergic, oral andinhaled (Apomorphine) as well as thesurgical (particularly the gene therapyapproaches). There is growing interest in theuse of the cholinesterase inhibitors ormethylphenidate as treatments for doparefractory falls in PD, and preliminary dataneeds to be confirmed or refuted in futuretrials.I was keen to hear whether there havebeen further developments in DBS andindeed there were a whole bunch of postersdemonstrating the long term benefits of Sub-Thalamic nucleus (STN) DBS in PD, and highlightingits use in Chorea-acanthocytosis,Tourette syndrome and many forms ofdystonia. Jerry Vitek reminded us of thepossible under-investigated merits of GlobusPallidus externa (GPe) DBS, and Paul Krackreviewed the non-motor issues surroundingthe use of DBS. The most innovative talkcame from Peter Tass who described a novelway of applying different frequency DBS toadjacent populations of cells to de-synchronisetheir activity and lead to prolongednormalisation of firing patterns, thus makinga huge saving on electrical energy required<strong>ACNR</strong> > VOLUME 11 NUMBER 4 > SEPTEMBER/OCTOBER 2011 > 33
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Page 8 and 9: C O N T E N T SCONTENTSSEPTEMBER/OC
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Page 26 and 27: REHABILITATION ARTICLEEffectiveness
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