Abstracts / Journal of Clinical Neuroscience 15 (2008) 337–369 355

Results: Two of 35 (6%) patients had peri-operativestrokes. Sixteen of 32 (50%) with post-operative imaginghad new ischemic lesions including 5 of 6 with combinedcardiac valve and CABG surgery. There were a range of1–17 lesions, each <1 cm3 diameter except in 3 patientswith large confluent areas of ischemia. Twenty of 29(69%) patients with post-operative testing had significantcognitive declines in at least one domain (range 1–4),including all those with new ischemic lesions (p = 0.005).

Conclusion: Brain injury is common following cardiacvalve surgery: 6% have new neurological deficit and justover two thirds have measurable cognitive decline. Halfof the patients had new post-operative ischemic lesionson DWI and these appeared embolic in nature. To ourknowledge, this is the first study to link cognitive declineand cerebral ischemia. Cardiac surgery may be a usefulmodel of human stroke in late phase IIB trials of putativeneuroprotective therapies.

doi:10.1016/j.jocn.2007.07.049

439: Detection of large-scale deletions in mitochondrial DNA

using DNA extracted from salivary samples

Himesha Vandebona a, Con Yiannikas b, Carolyn M.

Sue a; a Department of Neurogenetics, Kolling Institute of

Medical Research, University of Sydney, Royal North Shore

Hospital, Australia; b Department of Neurology, Concord

Hospital, Australia

Background: Large deletions in mitochondrial DNA(mtDNA) are found in patients with chronic progressiveexternal ophthalmoplegia (CPEO). Southern blot analysisis the standard method to identify these mutations. Typi-cally, muscle tissue is used for this type of analysis becausedeletions are often not found in blood and other sources ofDNA do not provide adequate amounts of DNA for thetest.

Aim: To determine whether deletions in mtDNA can bedetected in the DNA extracted from salivary samples frompatients with CPEO.

Methods: We collected salivary samples from 3 patientswho were clinically diagnosed with CPEO. Samples werecollected into Oragene vials (Geneworks Pty. Ltd., SouthAustralia). DNA from saliva was extracted following themanufacturer’s instructions. DNA was also extracted fromblood samples obtained from patients. Five micrograms oftotal DNA from blood and saliva of each patient weredigested with BamH1 and SnaB1 restriction enzymes sep-arately and used for Southern blot analysis. The DNAwas hybridized with radio-labelled mitochondrial DNAprobes.

Results: We found large-scale deletions in the salivarysamples of two patients. In the third we detected multiplemtDNA deletions. No mtDNA deletion was identified inthe DNA extracted from the patients’ blood samples.

Conclusion: We conclude that Southern blot analysisusing salivary samples can successfully detect large-scalemtDNA deletions (>2 kb) in patients with CPEO. Salivarysamples are a convenient alternative source for screening ofmtDNA large-scale deletions and may avoid the need formuscle biopsy in patients requiring genetic analysis for thiscondition.

doi:10.1016/j.jocn.2007.07.050

440: Botulinum toxin (Dysport) in upper limb spasticity

following stroke – A placebo controlled study

Andrew Hughes a, Ian Baguley b, Stephen de Graaff c, LeoDavies d, Paul McCrory e, Joseph Sandanam b, Pesi

Katrak f; a Austin Hospital, Australia; b St. Joseph’s

Hospital, Sydney, Australia; c Caulfield General Medical

Centre, Melbourne, Australia; d Royal Prince Alfred

Hospital, Sydney, Australia; e Box Hill Hospital,

Australia; f Prince of Wales Hospital, Australia

Purpose: To assess the safety and efficacy of botulinumtoxin (Dysport) in the treatment of upper limb spasticityfollowing stroke.

Methods: A prospective, multicentre, placebo-con-trolled, double blind study was conducted using 2 treat-ments with botulinum toxin or placebo at 12 weekintervals in 102 patients with post-stroke upper limb spas-ticity. Adverse events were recorded to assess safety. Scalesof quality of life (primary end point), spasticity, functionalstatus, goal attainment, depression, pain, patient disability,carer burden and global benefit were used to assessefficacy.

Results: Six patients withdrew before randomisationleaving 96 patients available for intention to treat analy-sis. Mean age was 59.5 years (SD 13.2 years) and patientswere enrolled a mean of 5.9 years (SD 10.5 years) follow-ing their stroke. Adverse events occurred equally in thosetreated with botulinum toxin or placebo. Eighteen seriousadverse events were reported in 11 patients resulting in 2patients being withdrawn from the study. However, noserious adverse events were classified as possibly or prob-ably related to treatment. Botulinum toxin lead to a sig-nificant reduction in spasticity compared to placeboacross all three joints studied (fingers, wrist and elbow)at all time points after the first injection. Significantimprovement compared to placebo was also seen in thepatient rated functional outcome measure, the goal attain-ment scale, global benefit and pain (only after the initialinjection). However no significant improvement was seenin depression, patient disability, carer burden or qualityof life.

Conclusions: Botulinum toxin is a safe treatment forpost-stroke upper limb spasticity. Despite significantimprovements in spasticity and patient rated functionaloutcome and goal attainment scales there was no reduction

356 Abstracts / Journal of Clinical Neuroscience 15 (2008) 337–369

in patient disability, carer burden, or improvement in qual-ity of life. This apparent incongruity will be discussed.

doi:10.1016/j.jocn.2007.07.051

441: Cardiovascular autonomic function tests: Normative

data

Jeyaraj D. Pandian a, Kaye Dalton a, Justin R. Scott b,

John D. O’Sullivan a, Stephen J. Read a, Robert D.

Henderson a; a Department of Neurology, Royal Brisbane

and Women’s Hospital, Australia; b Queensland Institute of

Medical Research, Australia

Little information is available from Australasia regard-ing normative data for cardiovascular autonomic functiontests (AFTs), especially beyond age 60 years.

Purpose: To derive normative data for heart rate (HR)and blood pressure (BP) responses to deep breathing(DB), Valsalva manoeuvre (VM) and tilt-up.

Methods: We performed cardiovascular AFTs in 48healthy subjects. The average HR differences to DB(HRDB), Valsalva ratio (VR), magnitude of differentphases of Valsalva, BP recovery time (PRT 100 and PRT50), HR and BP changes on tilting were calculated usingstandard methods. Pearson’s correlation coefficient andmultivariate analysis were used.

Results: The mean age was 58 ± 14.5 years (range 20–82years), 29 (60%) were men. The HRDB declined with age(p < 0.0001) and was greater in females (p = 0.005). Age-gender interaction was seen among females for HRDB(�0.27, p < 0.01). VR showed a decline with age(p = 0.0009) without gender interaction. The systolic BP’searly phase II, late phase II and phase 3 amplitude inVM showed an inverse relationship with age. The systolicBP recovery time was not affected by age, gender, bodymass index (BMI), height and weight, whereas other auto-nomic parameters showed an inverse relationship withheight and BMI. The HR increments during tilt decreasedwith age whereas systolic BP reduction at 3 min and 5 minincreased with age.

Conclusions: Age has a significant effect on most of theAFT variables. The systolic BP recovery time did not showany age and gender effect which might be of importance inthe evaluation of adrenergic failure.

doi:10.1016/j.jocn.2007.07.052

442: Arterial stiffness is associated with left ventricular

hypertrophy among ischemic stroke patients

Deidre A. De Silva a, Fung Peng Woon b, Christopher

P.L.H. Chen c, Hui Meng Chang a, Tian Hai Koh b, James

Cameron d, Bronwyn Kingwell e, Meng Cheong Wong a;a National Neuroscience Institute, Singapore General

Hospital campus, Singapore; b National Heart Centre,

Singapore; c National Medical Research Council,

Singapore; d Monash University, Australia; e Baker

Medical Research Institute, Australia

Purpose: Arterial stiffness is a recognized risk factor foratherosclerosis. Left ventricular hypertrophy (LVH) is amarker of cardiac damage, most commonly due to hyper-tension. Both are known to be associated with higher car-diovascular mortality. Our research group previouslydemonstrated that hypertension is independently associ-ated with arterial stiffness among ischemic stroke patients.We aimed to study the association of LVH with arterialstiffness among ischemic stroke patients.

Methods: We studied 331 ethnic Chinese and SouthAsian patients admitted to the Singapore General Hospitalwith acute ischemic stroke. Arterial stiffness was measuredby central pulse wave velocity (cPWV) determined byapplanation tonometry. LVH was defined as R waves > 25mm in V5/V6 or (R wave in V5/V6 + S wave in V1/V2) > 35 mm.

Results: The patients’ characteristics were median age 62years, 68% male, 76% Chinese, 24% South Asian, 79% hyper-tensive, 51% diabetic, 22% with known ischemic heartdisease (IHD) and 31% with LVH. Median cPWV was11.4m/s (range 4.7–19.7). As expected we found that cPWVwas higher among hypertensives (12.4m/s) than non-hyper-tensives (10.3m/s) (p < 0.001), diabetics (12.6m/s) than non-diabetics (11.3m/s) (p < 0.001) and patients with LVH(12.8m/s) than those without (11.6m/s) (p = 0.001). Therewas a significant correlation between increased cPWV andolder age (p < 0.001). cPWV was not associated with ethnic-ity (p = 0.105), gender (p = 0.272) and IHD (p = 0.248). Inmultivariate regression analysis, older age (p < 0.001), hyper-tension (p < 0.001), diabetes (p = 0.001) or presence of LVH(p = 0.028) were independently associated with cPWV.

Conclusions: We describe a novel association betweenLVH and arterial stiffness among ischemic stroke patients.Further research is required to uncover the reasons for thisassociation. One possible reason is LVH reflects poor bloodpressure control which is involved in the pathogenesis ofarterial stiffening. The other possibility is stiff large arterieslead to LVH due to increased cardiac output resistance.

doi:10.1016/j.jocn.2007.07.053

443: Central nervous system demyelination complicating

tumour necrosis factor-a inhibitor therapy

Kaitlyn L. Sharp a, Armin Mohamed a, Michael Barnett b,

Judith M. Spies a; a Department of Neurology, Royal Prince

Alfred Hospital, Australia; b Department of Neurology, St.

George Hospital, Australia

Introduction: CNS demyelination is a rare but seriousand debilitating complication of tumour necrosis factor