O:33 Is the risk of intellectual disability, rare syndromes or epilepsy elevated in the children of women with a psychotic illness? Results from a Western Australian population-based cohort study
V.A. Morgan∗, S. Zubrick, C. Bower, A.V. Jablensky
Neuropsychiatric Epidemiology Research Unit, UWA School of Psychiatry & Clinical Neurosciences, Perth, Australia
Aims The risk of schizophrenia is elevated among persons with an intellectual disability (∼3% compared to a general population figure of ∼1%). We used a record linkage study design to examine whether the risk of intellectual disability and rare syndromes was increased among a population-based cohort of children of mothers with a psychotic illness.
Methods We linked 79,599 women on the Western Australian psychiatric case register and 308,022 births on the midwives database, identifying mothers with schizophrenia (382 mothers, 618 children), bipolar disorder (763 mothers, 1301 children) and unipolar depression (686 mothers, 1255 children) who gave birth 1980–1992. Comparison mothers (1831 mothers, 3129 children) were randomly selected from mothers on the midwives database with no recorded history of psychiatric illness. Additional offspring data came from the intellectual disability, birth defects and hospital morbidity registers.
Results We found a significantly increased risk of intellectual disability for all three groups of case children: the odds ratio was highest for children of mothers with schizophrenia. The increased risk was not related to the presence of obstetric complications or the timing of illness onset. There was a significantly elevated risk of epilepsy in the bipolar group only. Case children had unusually high rates of rare syndromes; the syndromes identified varied by maternal diagnostic status.
Conclusions The risk of intellectual disability was elevated for children of mothers with psychosis. Some rare syndromes were identified but their distribution was specific to maternal diagnostic status. Our data point to underlying genetic risk factors of varying diagnostic specificity.
O:34 Lifetime prevalence of psychosis by age 21 in an Australian birth cohort
J. Welham∗, G. Williams, J. Najman, W. Bor, M. O'Callaghan, S. Saha, J. McGrath
∗Queensland Centre for Mental Health (QCMHR), The Park Centre for Mental Health, Wacol, QLD 4076, Australia
O:35 Cognition and Brain in Children with 22q11.2 Deletion Syndrome
L.E. Campbell∗, A.F. Stevens, R. Azuma, R.G. Morris, D.G.M. Murphy, K.C. Murphy
King's College London, Institute of Psychiatry, UK. Centre for Mental Health, University of Newcastle, Australia
Background Velo-cardio-facial syndrome or 22q11.2 deletion syndrome (22qDS) is the most common known microdeletion syndrome characterised by a high frequency of congenital heart disease, characteristic dysmorphology, structural brain anomalies, learning disabilities and psychiatric disorder in particular schizophrenia.
Method In this study, our aim was twofold: 1) to characterise memory, executive function and attentional abilities of children with 22qDS (N = 47) compared with age, gender and parental socioeconomic status matched sibling controls (N = 26); and to 2) relate cognitive function to structural brain anatomy. We used standardised neuropsychological batteries, the Children's Memory Scale (CMS), the Cambridge Automated Neuropsychological test battery (CANTAB) and the Maudsley attention and response suppression task battery (MARS). In addition, topographically unrestricted voxel-based morphometry as well as regions of interest (ROI) analysis was utilised to investigate structural neural correlates of cognitive impairments.
Results Overall, the 22qDS group had reduced memory scores, with specific deficits in visual memory and in particular facial recognition memory, and executive dysfunctions in areas such as planning, working memory, and motor organisation. These cognitive deficits were associated with structural brain anomalies, primarily in the medial frontal, temporal and cerebellar grey matter.
Conclusions This complex cognitive phenotype is probably the effect of differential genetically determined brain structural development.
O:36 Brain and Behaviour in Children with 22q11.2 Deletion Syndrome: A Volumetric and Voxel-Based Morphometry MRI Study
L.E. Campbell∗, E.M. Daly, F. Toal, A.F. Stevens, R. Azuma, M. Catani, V. Ng, T. Van Amelsvoort, X. Chitnis, W. Cutter, D.G.M. Murphy, K.C. Murphy
King's College London, Institute of Psychiatry, UK. Centre for Mental Health, University of Newcastle, Australia
Background 22qDS is a genetic disorder characterised by learning disability and a high prevalence of psychosis, and associated with variably sized deletions of 22q11.2. However, there have been few large quantitative studies of the effects of the deletion on brain anatomy and the relationship between brain and behaviour.
Method We studied the neuroanatomy of 39 children (6–16 years) with 22qDS and 26 siblings using automated voxel-based morphometry and manually traced region-of interest analyses. Also, we investigated whether those brain regions which differed significantly between groups were related to behavioural differences within children with 22qDS.
Results Using VBM analysis we found, after correction for IQ, that individuals with 22qDS compared to controls had a significant reduction in cerebellar grey matter, and white matter reductions in the frontal lobe, cerebellum and internal capsule. Using ROI analyses we found that people with 22qDS reduced bulk volume bilaterally in the occip-ital-parietal lobes, but a larger right caudate nucleus and lateral ventricles. Within people with 22qDS there was a significant positive correlation between grey matter volume and severity of; 1) schizotypy in the temporo-occipital regions and the corpus striatum, 2) emotional problems and social behavioural difficulties in the fronto-striatal regions.
Conclusions Subjects with 22qDS have widespread changes in brain anatomy, particularly affecting white matter, basal ganglia and cerebellum. Also within 22qDS regionally specific differences in brain development may partially underpin behavioural differences. We suggest that there is preliminary evidence for specific vulnerability of the fronto-striatal and cerebellar-cortical networks in 22qDS.
