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.
"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). "
"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. "
[Show abstract][Hide abstract] ABSTRACT: There is a large literature showing that unemployment has a negative effect on mental health, but little evidence exists on how mental illness affects the unemployeds’ chances of re-employment or the risk of labour market exit. We study how purchase of pharmaceutical products for severe mental illnesses during unemployment affects re- employment and labour market exit probabilities. Within the framework of a multivariate duration model we apply the ‘timing-of-events’ method, which explicitly makes use of the information that pharmaceutical treatment can begin at different points of time during an unemployment spell. In the absence of instrumental variables this method allows for causal inference in presence of unobserved heterogeneity, but at the cost of strong assumptions. The basis for our analysis is state-of-the-art register-based data, which gives insight on the timing, type, and volume of drug purchase as well as labour market histories for a random sample of the Danish population. We find a significant and strong negative effect of periods with drug treatment on the employment chances. During the treatment with drugs, the job-finding rate is reduced substantially relative to what it would have been in absence of a drug treated mental illness. Importantly, our results not only show that drug treated mental illness prolongs the unemployment duration, but it also increases the labour market exit rate.
"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. "
[Show abstract][Hide abstract] ABSTRACT: Schizophrenia is a devastating disease that affects approximately 1% of the population across cultures. Its neurobiological underpinnings are still unknown. Accordingly, animal models of schizophrenia often lack construct validity. As concordance rate in monozygotic twins amounts to only 50%, environmental risk factors (e.g. neurotrauma, drug abuse, psychotrauma) likely act as necessary 'second hit' to trigger/drive the disease process in a genetically predisposed individual. Valid animal models would have to consider this genetic-environmental interaction. Based on this concept, we designed an experimental approach for modeling a schizophrenia-like phenotype in mice. As dysfunction in synaptic transmission plays a key role in schizophrenia, and complexin2 (CPLX2) gene expression is reduced in hippocampus of schizophrenic patients, we developed a mouse model with Cplx2 null mutation as genetic risk factor and a mild parietal neurotrauma, applied during puberty, as environmental 'second hit'. Several months after lesion, Cplx2 null mutants showed reduced pre-pulse inhibition, deficit of spatial learning and loss of inhibition after MK-801 challenge. These abnormalities were largely absent in lesioned wild-type mice and non-lesioned Cplx2 null mutants. Forced alternation in T-maze, object recognition, social interaction and elevated plus maze tests were unaltered in all groups. The previously reported mild motor phenotype of Cplx2 null mutants was accentuated upon lesion. MRI volumetrical analysis showed a decrease of hippocampal volume exclusively in lesioned Cplx2 null mutants. These findings provide suggestive evidence for the 'second hit' hypothesis of schizophrenia and may offer new tools for the development of advanced treatment strategies.
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