Results: There was significant positive correlation between DCI and left inferior frontal (Brodmann Area [BA]-47), right superior frontal [BA-10], right medial frontal [BA-6], bilateral middle temporal [BA-21], left cingulate [BA-31] & right post-central [BA-3] gyri and significant negative correlation between DCI and left parahippocampal [BA-19], right supramarginal [BA-39], right fusiform [BA-37], left pre-central [BA-6], left middle temporal [BA-39] gyri and right cerebellum (uncorrected- p ≤0.001; SVC-p < 0.05). In males, there was a trend towards significant positive correlation between DCI and AAO, after controlling for the potential age effects (correlation co-efficient= 0.6; p = 0.079). Discussion: To the best of our knowledge, this is the first time VBM study to examine GM volume correlates of DCI in antipsychotic-naïve schizophrenia patients. Lesser DCI was associated predominantly with decreased frontal & temporal GM volumes. The findings offer support to the neurodevelopmental pathogenesis in schizophrenia. On the contrary, increased parahippocampal and inferior parietal lobule GM volumes (regions implicated in the genesis of first rank symptoms) were associated with lesser DCI which might offer partial explanation to first rank symptoms being less common in younger AAO patients. This possibility is further strengthened by the trend-level relationship suggesting younger AAO male patients having lesser DCI. Together, these findings support a possible clinical role for DCI in early identification of neurodevelopmentally more-impaired patients with poorer outcome. Moreover, the contrasting GM volume correlations need further research to elucidate the probable differential impact of neurodevelopmental insult on brain morphology in schizophrenia. doi:10.1016/j.schres.2010.02.805 Poster 45 CORTISOL RESPONSIVITY AND PRODROMAL SYMPTOMS AMONG INDIVIDUALS AT CLINICAL HIGH RISK FOR PSYCHOSIS Gisela Sugranyes 1 , Judy Thompson 2 , Renee Saenger 2 , Scott Schobel 2 , Anjuli Singh 2 , Lauren Bodkin 2 , Cheryl M. Corcoran 2 1 Programa Esquizofrenia Clinic, Hospital Clinic Barcelona, Barcelona, Spain; 2 Columbia University, Department of Psychiatry New York, NY, USA Background: The stress-vulnerability model has been widely accepted as contributing to the onset and progression of psychotic disorders. Specifically, the Hypothalamic Pituitary Adrenal Axis (HPAA) is thought to act as a mediator between the experience of psychosocial stress and psychotic symptoms. Studies to date assessing the HPAA in subjects defined as being at clinical high risk of psychosis have yielded inconsistent results. The purpose of the present study was to examine the relationship between cortisol responsivity to a neuropsychological stressor and psychotic-like symptoms, among a sample of patients identified as prodromal for psychosis. Methods: Twenty five patients defined as prodromal for psychosis according to the Structured Interview for Prodromal Syndromes were evaluated cross-sectionally. Salivary cortisol levels were measured at baseline (11.30am) (c1) and repeated one hour later (c2), after neuropsychological testing (Wechsler Memory Scale-Revised). Corti- sol responsivity was defined as the difference between "stress reactive" cortisol (cortisol secretion in response to the neuropsycho- logical stressor) and baseline cortisol (c2-c1). Depressive and anxiety symptoms were assessed using standardized measures (Hamilton Rating Scales), as was history of childhood trauma experiences (Early Trauma Inventory). Data distributions of the primary variables of interest were examined, and extreme outliers were removed. Spear- man correlational analyses were used to address the primary hypotheses of the study. Results: The 23 high risk participants included in the final analysis ranged from 13 to 24 years old (mean(M)=18.2 years; standard deviation(SD) = 3.1 years). 21(91.3%) were male, 13 (56.5%) Caucasian, 6(26.1%) Hispanic, 2(8%) Afro-American, and 2(8.7%) multi-racial. 9 (39.1%) were taking antidepressant medication, of which 5 were also receiving antipsychotics. Base- line cortisol (c1) ranged from 1.0 to 4.6 (M=2.0, SD=.87), and "stress reactive" cortisol (c2), from 0.7 to 4.3 (M =1.97;SD= .91). No significant correlation was found between either baseline (c1) or cortisol responsivity (c2-c1) and total positive (baseline r s = -.15;p=.49 ; responsivity r s = .23;p = .28), anxiety (baseline r s = -.26;p = .23 ; responsivity r s = .23;p = .28) or depressive (baseline r s = -.042;p = .85 ; responsivity r s = -.01;p = .97) symp- toms. In exploratory analysis of individual items of the Scale of Prodromal Symptoms, D3 ("Motor disturbances") was found to be positively associated with cortisol responsivity (r s = .42;p = .04). Visual inspection through scatterplots suggested that this asso- ciation was not being driven by medication status. Univariate analysis of history of early trauma, medication status and socio- demographic factors revealed no significant associations with the primary variables. Discussion: Contrary to our hypothesis, no significant correla- tions were found between cortisol responsivity, a correlate for impaired stress tolerance, and positive or affective symptoms. This is in line with the mixed results in the current literature, though the small sample size and the lack of formal control for confounders make it necessary to interpret this negative finding with caution. The significant association found between cortisol responsivity and motor disturbances in our exploratory analysis has been reported by other authors, and we provide further evidence for the association between these two putative biorisk markers for psychosis. Further, larger studies are warranted in order to help understand the role of the HPAA in the expression of psychosis. doi:10.1016/j.schres.2010.02.806 Poster 46 THE EFFECT OF EXTREME PREMATURITY AND VERY LOW BIRTH WEIGHT IN EARLY DEVELOPMENTAL MARKERS: A DERMATOGLYPHIC STUDY Nadia Vilahur 1,3 , Matthew P.G. Allen 2 , Muriel Walshe 2 , Chiara Nosarti 2 , Larry Rifkin 2 , Robin Murray 2 , Araceli Rosa 1,3 1 Unitat d'Antropologia, Departament de Biologia Animal, Facultat de Biologia, Universitat de Barcelona Barcelona Spain; 2 King's College London, Institute of Psychiatry London United Kingdom; 3 CIBER de Salud Mental (CIBERSAM), Instituto de Salud Carlos III Madrid Spain Background: Individuals who are born very preterm (VPT; before 33 weeks'gestation) are prey to adverse environmental insults, which may act in the prenatal and neonatal periods. In the neonatal periods, these insults are well-recognised, and include hypoxia, ischaemia, sepsis and under nutrition (Hoon et al. 1995). Prenatally, VPT birth may also be the outcome of pregnancies which are already showing signs of growth restriction of the fetus. The survivors of very preterm birth show an excess of neurological and cognitive impairment (Allin M et al. 2006, Bhutta et al. 2002), as well as a variety of structural brain abnormalities in later life (Stewart et al. 1999). However, it is unclear whether these abnormalities reflect neurodevelopmental events that take place in utero, processes taking place post-natally or a combination of both. Dermatoglyphics and the central nervous system share a Abstracts 436