We were unable to confirm improvement in survival using contem- porary supportive therapies and confirmed older age, male sex and bulbar onset as adverse prognostic factors. The increasing incidence is not explained by ageing of the population. doi:10.1016/j.jocn.2008.07.007 109. An Algorithm to Quantify UMN Involvement in ALS Jennica M. Winhammar a , Steve Vucic b , David Joffe a , Matthew Kiernan a , Dominic B. Rowe a a Royal North Shore Hospital b Prince of Wales Medical Research Institute Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegen- erative disease that produces weakness and ultimately death from respiratory failure. ALS results in the death of 500 Australians per year, with a median survival of only 2–3 years from diagnosis. Cur- rently there is no accurate objective measure of Upper Motor Neuron damage in ALS. Aim: The aim of this study was to use two methods, Transcranial Magnetic Stimulation (TMS) and Diffusion Tensor Imaging (DTI) to interrogate the UMN in ALS patients in comparison to control sub- jects. These tools were used to develop an algorithm to quantify UMN involvement in ALS. Method: TMS and DTI were performed in ten ALS patients and ten healthy control subjects. TMS is a method for neurophysiological assessment of UMN function and cortical abnormalities. DTI is a magnetic resonance method to investigate CST pathology. Results: TMS demonstrated an increase in excitability of corti- comotoneurons and a decrease in intracortical inhibition, contribut- ing to motor cortex excitability in ALS. The DTI studies identified considerable differences between ALS patients and controls in diffu- sivity along the CST between the internal capsule and midbrain in patients with ALS. Multiple correlations were demonstrated between the TMS and DTI parameters. An UMN algorithm was developed using TMS and DTI parameters that clearly distinguishes between ALS and control subjects. Conclusion: A SICI/DTI parameter algorithm is described that can be used to quantify UMN involvement in ALS. doi:10.1016/j.jocn.2008.07.008 110. CSF t-tau, p-tau and Amyloid Beta 1-42 in HIV Infection Bruce J. Brew a , Magnus Gisslen b , Louise Pemberton a , Paola Cinque c , Lars Hagberg b , Richard W. Price d , Kaj Blennow b , Serena Spudich d a St Vincent’s Hospital Sydney b Sahlgrenska Hospital, Sweden c San Raffaela Hospital, Italy d University of California San Francisco, United States Objective: Several studies have shown a link between HIV and Alzheimers dementias (HAD) (AD). There is increasing evidence that CSF levels of amyloid beta 1–42 (AB), t-tau, and p-tau can be used as ancillary tools for AD diagnosis and prediction. We sought to deter- mine whether these markers were abnormal in patients with and without ADC. Methods: CSF samples from cohorts of patients in Sydney, Gothe- borg, Milan and San Francisco were accessed. All patients had been neurologically evaluated and investigated as appropriate. HAD was diagnosed according to AAN criteria. CSF AB, t-tau and CSF p-tau levels were measured using an ELISA (Innogenetics). The lower limit of detections were: t-tau 75pg/ml, p-tau 16pg/ml and AB 20pg/ml. HIV negative out-of-hospital controls were used and a cohort of AD patients. Results: For the AB analyses there were 120 patients without HAD, 47 with stage 1 and 62 with stage 2; for p-tau there were 103, 20 and 40 patients while for t-tau there were 121, 45 and 49 patients. CSF AB levels were significantly reduced in HAD and t-tau levels increased compared to both the non demented group and HIV negative controls. The HAD group did not differ from the AD group. CSF p-tau concentrations however were not raised. Conclusions: That CSF AB and t-tau levels were abnormal in HAD and not different from AD points to similarities in basic pathogenetic mechanisms. However, the finding of normal CSF p-tau in HAD strongly suggests that it may be useful in differentiating the two conditions. doi:10.1016/j.jocn.2008.07.009 111. The ARCS: A One Minute 47 Second Cognitive Screen Peter W. Schofield a , Grant Lyall b , Stephen Lee b a University of Newcastle b Hunter New England Area Health Service Objective: To describe a novel cognitive screening instrument, the Audio Recorded Cognitive Screen (ARCS), and report on its per- formance in a mixed clinical sample. Method: Previously, we demonstrated that cognitive tests could be administered by a tape recorder to unsupervised subjects who write their responses in a booklet for later scoring (Schofield et al. JAGS 2003;3:415). The ARCS represents an extensive revision of the earlier instrument and is administered using a portable CD player. Testing lasts 34 minutes but the time-cost to the clinician is about 2 minutes (for scoring). Diagnoses (normal, mild cognitive impairment (MCI), demented) based on detailed neuropsychological and clinical evaluations were made on 92 outpatients, independent of ARCS and Mini Mental State Examination (MMSE) scores. Here, we compare discriminant validity of the ARCS with the MMSE in this clinical sample. Results: All 92 patients had been referred to the Neuropsychiatry Service for assessment. Thirty-five were judged to have no cognitive impairment, 34 MCI, and 23 dementia. In Analyses of Variance with bonferroni correction (F 2,89 = 38.9, p < .001), mean global score derived from the ARCS was significantly different for each of the 3 diagnostic groups. By contrast, group mean MMSE score (F 2,89 = 13.9, p < .001) differed between dementia and both normal and MCI groups, but not between normal and MCI groups. Mean scoring time for 10 randomly selected ARCS response booklets was 1 minute 47 seconds. Conclusion: The ARCS is highly efficient for the clinician and appears to have considerably better psychometric properties than the MMSE. doi:10.1016/j.jocn.2008.07.010 112. Discordance between valproate plasma levels and seizure suppression in a genetic rat model of absence epilepsy? Lenna Van Raay a , Terence J. O’Brien a , Margaret J. Morris b , Ronald C. Reed c , Robert E. Hogan d , Stefanie Dedeurwaerdere a 464 Abstracts / Journal of Clinical Neuroscience 16 (2009) 462–481