Abstract
psychosis following traumatic brain injury or allowed calculation of prevalence rates from data provided in the paper. We did computerassisted searches, scanned reference lists, searched journals and correspondedwith authorswherenecessary.We includedcase-control studies, cohort studies and family studies. Estimates of prevalence of psychosis from different studies were combined using fixed or random-effects meta-analysis, as appropropriate, with the data presented in forest plots. Heterogeneity among studies was estimated. Results: Our literature search and search of reference lists yielded 10015 references. The search was then limited to humans, which resulted in 9131 studies. Of these, 162 were considered to be potentially relevant. We excluded 154 studies, which did not meet inclusion criteria. We identified 8 studies which met our inclusion criteria, of which two were family studies, two were nested casecontrol studies and four were cohort studies. The overall pooled data revealed a significant association between TBI and subsequent psychosis (adjusted odds ratio=1.15, 1.04-1.26). However there was significant heterogeneity between the studies (Heterogeneity x=30.70 (d.f.=7) p=0.000; I=77.2%). Therefore,we decided to examine the family studies and case-control/cohort studies separately. Overall pooled data from the 6 population-based cohort and case-control studies showed an increased risk of development of schizophrenia or psychotic disorder in individuals who had been exposed to TBI (adjusted odds ratio=1.1, 1.005-1.231). However there was significant heterogeneity between the studies (Heterogeneity x=26.43 (d.f.=5); p<0.000; I=81.1%). Pooled data from the two family studies show an increased risk of schizophrenia after TBI in individuals who have a family history of schizophrenia (adjusted odds ratio=1.43, 1.14-1.8). There was no significant heterogeneity between the two studies. We were not able to examine the influence of location or age at onset of head injury. Discussion: We report an increased risk of psychosis following TBI. The increase among the general population is small about 10%but the risk ismore substantial among individualswhohave a family historyof schizophrenia or psychosis – about 43% increased risk. In particular, our findings point to the importance of gene-environment interaction in the etiology of psychosis following traumatic brain injury. Acknowledgements: Thisworkwas supportedbya Clinician Scientist Award to M. Cannon from the Health Research Board (Ireland).
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