Traumatic brain injury in individuals at clinical high risk for psychosis
Introduction
A traumatic brain injury (TBI) is characterized as an alteration in brain functions caused by an external force (Reis et al., 2015). A TBI is known to lead to a variety of psychiatric problems in as high as one third of those who suffer a TBI, such as mood and anxiety disorders, personality changes, as well as impairments in Intelligence Quotient (IQ) and neurocognition (Deb et al., 1999, Kim et al., 2007, Konigs et al., 2015, Masel and DeWitt, 2010, Nicholl and LaFrance, 2009). More recent work suggests that a TBI may also be a risk factor for psychosis. In particular, a recent meta-analysis reported that a TBI significantly increased the risk of later development of schizophrenia by approximately 60% (Molloy et al., 2011). However, estimates of increased risk vary widely according to sample selection, with risk estimates typically elevated and more likely to be inaccurate in psychotic samples where TBI history is taken retrospectively, relative to estimates drawn from patients with a TBI who later develop psychosis (Batty et al., 2013). Moreover, it is difficult to determine whether a TBI leads to psychosis or whether an individual was already on a course towards psychosis prior to the injury (David and Prince, 2005). Interpretation is further complicated by the retrospective manner in which data on TBI were collected in schizophrenia samples (Molloy et al., 2011).
The risk of psychosis following a TBI is highest in individuals with a family history of the disorder (Kim, 2008) suggesting that the relationship of TBI to schizophrenia may involve a combination of a genetic predisposition to psychosis and environmental insult to the brain (AbdelMalik et al., 2003). Even in those at risk for psychosis, those with a family history reportedly experienced a greater number of lifetime head injuries compared to a healthy control group as evaluated with the Traumatic Brain Injury Interview, a 24 question clinician-rated scale (Stowkowy and Addington, 2013). Moreover, people at CHR of psychosis reported higher rates of trauma and bullying compared to healthy controls (Addington et al., 2013, Bechdolf et al., 2010) and it has been found that adolescents with a history of TBI are vulnerable to psychological and behavioral harms that co-occur with their history of TBI (Ilie et al., 2014).
However, it is unknown whether CHR individuals who had experienced a mild TBI also report significantly greater rates of trauma and bullying. This is an important consideration, as approximately 35% of people at CHR of psychosis will go on to develop a full blown psychotic disorder (Fusar-Poli et al., 2012). Thus this population offers a window of opportunity to evaluate the presence of TBI in people who have a greater risk of developing psychosis compared to the general population. These individuals present with attenuated psychotic symptoms, brief intermittent psychotic symptoms, or have a genetic risk for the disorder and a recent decline in functioning (McGlashan et al., 2010). The CHR cohort offers a unique opportunity to examine the prevalence of TBI and its impact on IQ prior to the onset of psychosis in people with a greater probability of developing a psychotic disorder relative to the general population, but who do not have a full blown psychotic disorder as in the retrospective research described above. However, TBI is typically an exclusion criteria in studies of clinical high risk. In the North American Prodromal Longitudinal Study (NAPLS 2) there were clear exclusion criteria with respect to moderate and severe TBI, typical of other studies (Brewer et al., 2005). The aims of the current study were to evaluate, in a large sample of youth at CHR of psychosis the prevalence of mild TBI, whether it was related to positive symptoms, differences in IQ, past experiences of trauma and bullying, and the relationship of mild TBI to later transition to psychosis.
Section snippets
Participants
All participants were recruited as part of the eight-site NAPLS 2 study (Addington et al., 2012), which was established to investigate predictors and mechanisms of transition to psychosis. As described in Addington et al. (2012) all participants are help-seekers and were responding to similar recruitment strategies across sites. All participants were screened for TBI at the initial screening visit. This paper reports on the 747 CHR participants that completed the Traumatic Brain Injury
Results
The sample consisted of 278 HC participants (140 males, 138 females) and 747 CHR participants (428 males, 319 females). Groups did not significantly differ on sex. HC's were significantly older (M = 19.8, SD = 4.7 vs M = 18.5, SD = 4.2, t = 4.16, p < 0.01) and had more years of education (M = 12.7, SD = 3.6 vs. M = 11.3, SD = 2.8, t = 6.71, p < 0.001) than CHR participants. Groups did not significantly differ on race and the majority of each group, approximately 60%, were White, Middle Eastern or Latin American.
As
Discussion
The purpose of this study was to investigate, in a large sample of individuals at CHR of psychosis, the prevalence of mild TBI, whether it was related to past trauma and other relevant correlates and the relationship of mild TBI to later transition to psychosis.
The finding that a greater proportion of CHR participants reported experiencing a mild TBI than HCs is consistent with the literature in people with schizophrenia, who are more likely to have a history of TBI in comparison to their
Conflict of interest
The authors report no conflict of interest.
Authors' contributions
SD and LB were responsible for performing analyses and writing the manuscript. JA, TDC, KSC, BAC, DOP, LJS, THM, MTT, EFW, SWW, were responsible for all aspects of the NAPLS-2 study including study design, obtaining funding, data collection, and all contributed to the writing of the final version of the manuscript. TDC was responsible for the neuroimaging analysis and AA performed the functional connectivity analysis. DHM assisted in the conceptualization of the analysis for this study and
Role of funding source
This study was supported by the National Institute of Mental Health (grant U01MH081984 to Dr Addington; grants U01 MH081928; P50 MH080272; Commonwealth of MassachusettsSCDMH82101008006 to Dr Seidman; grants R01 MH60720, U01 MH082022 and K24 MH76191 to Dr Cadenhead; grant U01MH081902 to Dr Cannon; P50 MH066286 (Prodromal Core) to Dr Bearden; grant U01MH082004 to Dr Perkins; grant U01MH081988 to Dr Walker; grant U01MH082022 to Dr Woods; and UO1 MH081857-05 grant to Dr Cornblatt. The NIMH had no
Acknowledgements
J Stowkowy, T Raedler, L McGregor, D Marulanda, L Legere, L Liu, C Marshall, E Falukozi, E Fitton, L McAusland, K Smith (University of Calgary). T Alderman, K Shafer, I Domingues, A Hurria, H Mirzakhanian (UCSD). B Walsh, J Saksa, N Santamauro, A Carlson, J Kenney, B Roman (Yale University). K Woodberry, AJ Giuliano, W Stone, JM Rodenhiser, L Tucker, R Serur, G Min, R Szent-Imrey (Beth Israel Deaconess Medical Center/Harvard). C Bearden, P Bachman, J Zinberg, S DeSilva, A Andaya, S Uguryan
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