ity, many weeks before the development of axonal loss. The role ofaxonal ion channel dysfunction is being increasingly recognised inneurological disease, with a consequent shift to translational studiesconcerning early diagnosis and better treatment for these disorders.

doi:10.1016/j.jocn.2010.07.046

46. Limiting and repairing the damage in multiple sclerosisAlastair Compston

University of Cambridge, UK

When the 1st edition of what subsequently became McAlpine’sMultiple Sclerosis appeared in 1955, the authors could say nothingof substance relating to the aetiology, pathogenesis or treatment ofthe disease. Within a few years Ian McDonald changed the studyof multiple sclerosis from a system based on exploratory but dis-jointed approaches into a highly productive discipline grounded infirst class clinical science. In the 1960s, he characterised the physiol-ogy and morphology of demyelination and remyelination in the cen-tral nervous system; in the 1970s, with the late Martin Halliday, hepioneered laboratory methods for supplementing the clinical diag-nosis of multiple sclerosis; in the 1980s, he realised that magneticresonance imaging could be used to illuminate the nature of inflam-matory brain disease; and his work provided laboratory measuresfor charting the efficacy of the first wave of disease modifying treat-ments when these were introduced in the mid-1990s. Those treat-ments raised expectations amongst affected individuals and weresafe but of limited efficacy. Meanwhile contemporary neurobiology,neuropathology, molecular genetics and immunology was providingthe framework for a modern synthesis of the aetiology and patho-genesis of multiple sclerosis, and developing strategies for limitingand repairing the damage. In turn, these ideas raised new questionsrelating to the interplay of inflammation and neurodegeneration andchallenged the assumption that multiple sclerosis is a single disease.

The 2010 McDonald Lecture will draw on this history and tell thestory of how the use of alemtuzumab has explored the relative con-tribution of inflammatory and neurodegenerative events underlyingthe natural history of multiple sclerosis as this evolves from therelapsing-remitting to progressive phase of the disease; identifiednovel mechanisms of symptom production reflecting altered axonalstructure and function; provided a ‘human’ model of lymphocytereconstitution that explains general principles of human autoimmu-nity; demonstrated the importance of timing in order to achieve highefficacy for immunological treatments in multiple sclerosis; andshown that lymphocyte depletion early in the course of relapsing-remitting multiple sclerosis not only stabilises the natural historyof the disease but may also enable recovery of existing disabilities.

doi:10.1016/j.jocn.2010.07.047

47. On the shoulders of giants: The brain foundation 1970–2010G. Michael Halmagyi

Royal Prince Alfred Hospital, NSW

The Australian Neurological Foundation (later to become theBrain foundation) was the brainchild of a previous generation ofneurologists and neurosurgeons. Its inaugural meeting was held3 pm on Saturday 16th May 1970 at the Canberra Hotel, Common-wealth Avenue, Canberra under the patronage of former Governor-General The Rt Hon Lord Casey of Berwick KG, GCMG, CH, DSO,

MC, KStJ, PC. Directors who were members of the Australian Associ-ation of Neurologists (later to become the Australia and New ZealandAssociation of Neurologists) were Professor Keith Bradley, Dr. JohnGame, Dr. Byron Kakulas, Prof James Lance, Dr. Barrie Morley, Dr.E. Graeme Robertson, Dr. George Selby and Prof. Sir SydneySunderland.

The basic reason for the creation of the Foundation was in factthat there were in-sufficient para-clinical scientists and scientificfacilities directly available to those neurologists and neurosurgeonswho are at present treating the patients, and endeavouring at thesame time to conduct research into their diseases in the teachinghospitals. The greatest and most immediate need was to fill thatgap. State surveys revealed deficiencies in almost all aspects of theexisting facilities available for the application of modern scientificknowledge and techniques to the treatment of patients and researchinto the causes of their diseases, in terms of personnel, equipmentand facilities. The degree of deficiency in the various fields variedin the different States, as may have been expected. A commondenominator was found to be, as expected, the lack of ancillary sci-entific services required by the clinicians to give their patients thefull advantage of available modern scientific knowledge and tech-niques in their diagnosis and treatment. The most basic of thesewas the lack of neuropathological services. In some States, therewas a disconcerting lack of even more basic clinical facilities suchas beds and basic resident medical staff.

Our founders should be pleased with us. In our 40th year we areweathering the global financial crisis; our corpus is around$7,000,000 – it was just over $1,500,000 in 2004. In 2009 it was pos-sible to give over $450,000 in competitive grants (with an additional$300,00 from the Australian Competitive Grants Register awardedthrough the Department of Industry, Innovation Science andResearch) at the last round in 2009, with 8 of the 14 successful appli-cants being members of ANZAN. The scientific advisory committeeheaded by Matthew Kiernan ranked 173 applications in order ofmerit. We will maintain the same level of funding in 2010 as 2009and encourage young clinician scientists to apply. Applications close30th of June at www.brainaustralia.org.au. The website has over6,000,000 hits a year and needs constant attention to content.

Current ANZAN member directors under the patronage of Emer-itus Professor James W. Lance AO, CBE, MD, FRCP, FRACP are: JohnCorbett, Geoff Donnan, Matthew Kiernan (vice-president, medical),Michael Halmagyi (president), Pam McCombe and Dominic Rowe.

doi:10.1016/j.jocn.2010.07.048

48. Controversies in the management of acute strokeAlan Barber

University of Auckland and Centre for Brain Research, New Zealand

It is now 15 years since the NINDS trial results were publishedshowing that thrombolytic therapy with intravenous recombinanttissue plasminogen activator (tPA) reduces death and disability inischemic stroke patients treated within three hours. More recently,the ECASS III study showed that the benefit of tPA is still seen inpatients treated out 4.5 hours. The results of the European SITS-MOST observational study has shown that concerns about the appli-cability of the results from randomised controlled trials, to day today clinical practice, are unfounded. Why is it then that in 2009the National Stroke Foundation audit of almost all Australian andNew Zealand hospitals found that fewer than 1 in 25 ischemic strokepatients are actually treated with thrombolytic therapy? Other ther-apies aimed at restoring cerebral blood flow such as intra-arterialthrombolysis and clot retrieval devices, are increasingly being used

1624 Abstracts / Journal of Clinical Neuroscience 17 (2010) 1610–1638

in North American and some Australasian centres. Is the use of thesetherapies justified on the basis of the current evidence? Does theimprovement in mortality seen in patients with malignant middlecerebral artery territory infarction undergoing decompressive crani-ectomy come at the cost of increased numbers of patients living withsevere disability? Or is hemicraniectomy a useful therapeutic addi-tion? Other therapies such as transcranial sonolysis or near infraredlaser therapy have also been shown to be of promise in strokepatients. Is the rationale behind these therapies sound and are thepositive study results simply a statistical aberration? These andother controversial new stroke therapies will be presented.

doi:10.1016/j.jocn.2010.07.049

49. Idiopathic intracranial hypertensionJohn King

University of Melbourne and Royal Melbourne Hospital, VIC

Idiopathic Intracranial Hypertension (IIH) presents neurologistswith important diagnostic and therapeutic challenges. There is apotential for misdiagnosis unless thorough clinical assessment, lum-bar puncture and MRI/MRV are carried out.

The aim of treatment is relief of symptoms and preservation ofvision. Most patients can be managed by medical treatment to lowerintracranial pressure, weight reduction and regular follow-up untilthe patient is in remission.

Where medical treatment fails and there is loss of visual acuityand/or field, surgical options should not be delayed. There are no evi-dence-based guidelines to assist the clinician but lumbo-peritonealor ventriculo-peritoneal shunting, optic nerve sheath fenestrationand dural venous sinus stenting have all been reported to be effec-tive. All the procedures have their advantages and disadvantagesand all may fail no matter what procedure is used. Once again regu-lar review by the neurologist is necessary to avoid permanent visualloss.

doi:10.1016/j.jocn.2010.07.050

50. Does the principle of minimum work apply at the carotidbifurcation?G. Das, R. Beare, M. Ren, W. Chong, V. Srikanth, T.G. Phan

Stroke and Ageing Research Group, Monash Medical Centre, VIC

Background: There is recent interest in the role of carotid bifurca-tion anatomy, geometry and hemodynamic factors in the pathogen-esis of carotid artery atherosclerosis. Investigators have drawnparallel between certain anatomical and geometric configuration atthe carotid bifurcation and its exposure to disturbed flow. Anintriguing idea is that the vascular dimensions of the intracranialcarotid artery may be optimally designed such that there is mini-mum work to maintain blood and pump it through a vascular sys-tem. It has been proposed that this occurs when the exponentpower relationship between the radii of the parent artery and thedaughter arteries is 3. In this study, we evaluate if the dimensionsof bifurcation of the extracranial carotid artery follows this principleof minimum work.

Methods: This study involved subjects who had CT angiographyat Monash Medical Centre between 2006–2007. Subjects with lumi-nal stenosis >30% were excluded. Following segmentation of the car-otid artery, the radii and areas of the common carotid/parent artery

and the two daughter arteries (internal and external carotid arteries)were determined. A non-linear equation solver was used to deter-mine the optimum value of power n.

Results: When the equation was solved for radius, the value of nranged from 1.4 to 1.8.

Conclusion: Our findings indicate that the principle of minimumwork (as defined by power n of 3) may not apply at the carotid bifur-cation and may suggest that additional factors play a role in the rela-tionship between the parent and daughter vessels radii.

doi:10.1016/j.jocn.2010.07.051

51. Bilateral frontal periventricular locations of cerebral whitematter lesions show greatest covariance with poorer gaitVelandai Srikanth a, Thanh G. Phan a, Jian Chen a, Richard Beare a,Jenny Stappleton a, David C. Reutens b

a Stroke and Ageing Research Group, Monash Medical Centre, VICb Queensland Brain Institute, University of Queensland, QLD

Background: Ageing is associated with a slowing and hesitancy ofgait, and in some, this may take the form of a more serious gaitapraxia. Greater volume of cerebral white matter lesions (WML) isassociated with poorer gait. One possible causal mechanism for thisis that WML disconnect neural networks specifically involved in gait.We hypothesised that WML associated with gait impairment arepreferentially distributed in regions related to the control of gait.

Methods: High-resolution brain MRI and computerised gait anal-ysis were performed on 385 participants in the population-basedTasmanian Study of Cognition and Gait (TASCOG). A composite gaitfactor was derived using factor analysis. Semiautomated segmenta-tion was used to identify lesion-affected voxels. The multivariatevoxel-based method of partial least squares regression was used todetermine which systems of WML voxels showed greatest covari-ance with gait independent of other WML voxels.

Results: Systems of WML affected voxels in bilateral frontal andperiventricular regions demonstrated greatest covariance withpoorer gait. The location of these voxels corresponded mainly tomajor anterior projection fibres (anterior and superior thalamic radi-ations, corticopontine and corticospinal tracts), adjacent parts ofanterior association fibres (corpus callosum, superior longitudinalfasciculus, short association fibres).

Conclusion: WML may contribute to age-related gait decline bydisrupting frontally located afferent and efferent projection andassociation tracts known to be involved in the execution of plannedmovement.

doi:10.1016/j.jocn.2010.07.052

52. The role of ABCD2 in predicting stroke recurrence in theAustralian settingLauren Sanders a, Velandai Srikanth a, Helen Pshigohios b, KittyWong a, Dave Ramsay b

a Stroke and Ageing Research Group, Monash Medical Centre, VICb Monash Medical Centre,VIC

Background: To determine the accuracy of the ABCD2 tool in pre-dicting stroke outcome in an Australian cohort of patients.

Method: This is a retrospective cohort study. The setting is anurban tertiary referral hospital in Melbourne, Australia. All adultspresenting with suspected Transient Ischaemic Attack (TIA) who

Abstracts / Journal of Clinical Neuroscience 17 (2010) 1610–1638 1625