or a defect of a pathway which normally degrades mis- folded proteins. doi:10.1016/j.jocn.2007.07.065 456: Utilisation of intravenous immunoglobulin in New Zealand: A clinical audit David O. Hutchinson a , Richard Charlewood b , Peter Flanagan b , Terry Mitchell a ; a Auckland City Hospital, New Zealand; b NZ Blood Service, New Zealand Purpose: To explore the utilisation patterns of IVIG across different regions of New Zealand (NZ), and to audit the appropriateness of its use in a subset of patients. Methods: We accessed NZ Blood Service and other data to determine the quantities of IVIG issued by each District Health Board (DHB) during 2004, and the indications. In a later prospective audit performed over 6 months we col- lected data on all utilisation in eight DHB. The indications for IVIG were checked for compliance with the Australian Health Minister’s Advisory Council (AHMAC) and Auck- land District Health Board (ADHB) guidelines. Results: Retrospective audit: The rates at which IVIG was pre- scribed varied 11-fold across the different DHB, from 100.5g/1000 population in Capital & Coast DHB to 8.8g/ 1000 in Nelson-Marlborough DHB. The Auckland DHB (and to a lesser extent some other DHB) provided substan- tial amounts of IVIG to treat patients resident in other DHB. Eccentric patterns of utilisation (e.g. obstetric) were found in some regions. Prospective audit: We captured 466 treatment episodes. Primary antibody deficiency was by far the most frequent diagnosis. Five diagnoses accounted for 69% of the total IVIG utilisation. 80.6% of the diagnoses were in AHMAC category 1 (convincing evidence of benefit) and 71.5% were approved diagnoses in the ADHB guidelines. Compliance with the two sets of guidelines varied significantly across the different DHB. Conclusion: A limited set of disorders accounts for most of the IVIG prescribed in NZ. The wide variation in the pat- terns of utilisation in different regions is probably due to a range of factors and could usefully be studied further. There is almost certainly under- and overutilisation in some regions for certain diagnostic categories. Up-todate, evi- dence-based guidelines and a rigorous authorisation process have the potential to promote appropriate utilisation. doi:10.1016/j.jocn.2007.07.066 457: Sensory nerve excitability in cancer patients treated with oxaliplatin Cindy Shin-Yi Lin a , Arun Krishnan a , David Goldstein b , Michael Friedlander b , Matthew Kiernan a ; a Prince of Wales Medical Research Institute, Prince of Wales Hospital, Australia; b Prince of Wales Hospital, Australia Purpose: Nerve dysfunction is a common side effect of oxaliplatin chemotherapy, typically occurring in a dose- dependent manner, so that the higher the dose and the longer exposure time, the more likely neuropathy is to occur. Immediately after administration of oxaliplatin, patients report sensory symptoms, such as paraesthesia in the hands triggered or aggravated by cold exposure. Methods: To investigate the pathophysiology of oxalipl- atin-induced neurotoxicity, nerve excitability studies were undertaken on sensory axons before and after individual paired treatment cycles. Stimulus responses, strength-dura- tion time constant (SDTC), threshold electrotonus (TE), recovery cycles and current-threshold relations were recorded from a total of 198 cycles of therapy (cycle range: 1-12) in 42 patients. Results: From the 77 paired cycles, using pre-infusion data from each cycle as the controls, refractoriness decreased significantly by 6.9 ± 2.7% (p < 0.01), relative refractory period (RRP) was shortened by 1.13 ± 1.0 ms (p < 0.01), superexcitability decreased by 1.4 ± 0.5% (p < 0.01) and TE hyperpolarizing (90–100 ms) increased by 4.9 ± 2.5% (p < 0.05) (mean difference ± SE, paired t- test). Further analysis after categorising 77 paired cycles into early (cycles 1–4) and late (cycles 5–12) groups estab- lished that the early cycles of treatment had greater effects on excitability parameters. Later cycles correlated with prolongation in latency (p < 0.001), perhaps reflecting the development of neuropathy. Conclusions: In total, these studies demonstrate that the neurotoxic effects of oxaliplatin may relate to altered axo- nal Na+ channel function similar to previously docu- mented effects of tetrodotoxin-induced neurotoxicity. The correlation between cycle number and changes in excitabil- ity parameters further confirms the cumulative-dose effect of oxaliplatin and suggests a clinical use for nerve excitabil- ity testing in predicting neurotoxicity. doi:10.1016/j.jocn.2007.07.067 458: Vestibular, saccadic and fixation abnormalities in genetically confirmed Friedreich Ataxia Michael C. Fahey a , Owen White b , Phillip D. Cremer c , Lynette Millist b , Swee Aw d , Louise A. Corben a , Andrew Churchyard e , Martin B. Delatycki a ; a Murdoch Childrens Research Institute, Australia; b Royal Melbourne Hospital, Australia; c Royal North Shore Hospital, Australia; d Royal Prince Alfred Hospital, Australia; e Southern Health, Australia Aim: To assess eye movement abnormalities in Friedr- eich ataxia (FRDA) and compare these results to clinical measures 362 Abstracts / Journal of Clinical Neuroscience 15 (2008) 337–369