Schizophrenia-like psychosis following traumatic brain injury: A chart-based descriptive and case-control study

School of Psychiatry, University of New South Wales and Neuropsychiatric Institute, Prince of Wales Hospital, Randwick, Australia.
Psychological Medicine (Impact Factor: 5.94). 03/2001; 31(2):231-9. DOI: 10.1017/S0033291701003336
Source: PubMed


Head injury has been reported to increase the likelihood of the development of schizophrenia-like psychosis (SLP), but its features and risk factors have been insufficiently investigated.
Between 1987 and 1997, we examined 45 referred patients with SLP following brain trauma. These subjects were matched with 45 head-injured subjects without SLP on age (current and at injury) and gender, and their case records reviewed systematically. The groups were compared and logistic regression analyses performed.
The psychoses had a mean age of onset of 26.3 years, a mean latency of 54.7 months after head injury, usually a gradual onset and a subacute or chronic course. Prodromal symptoms were common and depression often present at onset. Paranoid delusions and auditory hallucinations were the predominant features, with formal thought disorder, catatonic features and negative symptoms being uncommon. The SLP group had more widespread brain damage on neuroimaging, especially in the left temporal and right parietal regions, and were more impaired cognitively. Fewer (non-significantly) SLP subjects had epilepsy which was more likely to be well-controlled in this group. On regression analysis, a positive family history of psychosis and duration of loss of consciousness were the best predictors of SLP.
Head injury-related psychosis is usually paranoid-hallucinatory and subacute or chronic in its presentation. A genetic predisposition to schizophrenia and severity of injury with significant brain damage and cognitive impairment may be vulnerability factors.

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    • "Psychosis following traumatic brain injury (PFTBI) is a complex dual diagnosis with the potential for neurocognitive deficits identified both post traumatic brain injury (TBI) and in schizophrenia. Although the PFTBI literature is limited (see Batty et al., 2013 for review), language deficits in this cohort have been reported with respect to impaired verbal learning (Bamrah and Johnson, 1991), language (n = 2; Fujii and Ahmed, 2002), WAIS vocabulary (Fujii et al., 2004), and verbal memory (Sachdev et al., 2001; Fujii et al., 2004). In TBI, language and communication impairments are well documented, including, but not limited to, lexical comprehension and production, semantics, discourse processes, and reading/listening skills (Hinchliffe et al., 1998; Ewing-Cobbs and Barnes, 2002; Moran and Gillon, 2004; LeBlanc et al., 2006). "
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    • "The presence of a psychotic disorder has been related to brain tumors (Lisanby et al., 1998), drug abuse (Hambrecht and Hafner, 1996), and head injury (Sachdev et al., 2001). Which, again, underlines the importance of controlling for the presence of somatic illnesses. "
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    • "In Cplx2 −/− mice, a mild behavioral phenotype consists of slight motor deficit and, inconsistently, impaired learning in Morris water maze (Glynn et al. 2003, 2007; Yamauchi et al. 2005). Neurotrauma is one potential risk factor for schizophrenia (Malaspina et al. 2001; McAllister 1998), and particularly lesions affecting the right parietal lobe have been associated with schizophrenia-like psychosis (Sachdev et al. 2001; Zhang & Sachdev 2003). As in a pivotal longitudinal study on patients with childhood onset schizophrenia, again the parietal cortex evolved as starting point of cortical gray matter loss (Thompson et al. 2001), we developed a mouse model, where a small standardized lesion is set during puberty onto the right parietal cortex. "
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