Reduced negative symptoms may distinguish the clinical profile of patients with psychosis following traumatic brain injury from schizophrenia/schizoaffective disorder

Objective A comprehensive and standardized examination of the clinical presentation of psychosis following traumatic brain injury (PFTBI) has not been reported in the literature. This information is vital for the accurate diagnosis and efficacious treatment of these patients. Method Patients with PFTBI (n =10) and schizophrenia (n =23) participated in a comprehensive clinical assessment: the Structured Clinical Interview for DSM-IV-TR Axis I Disorders (SCID-I/P; First et al., 2002), the Positive and Negative Syndrome Scale (PANSS; Kay et al., 1987), the Scale for the Assessment of Positive Symptoms (SAPS; Andreasen, 1984), the Scale for the Assessment of Negative Symptoms (SANS; Andreasen, 1984), and the Thought Language and Communication Index (TLC; Andreasen, 1986). Scores from the patient groups were submitted to independent sample t-tests and independent samples Mann-Whitney U tests (normal and non-normal in distribution, respectively). Results PFTBI participants met the symptom and course criteria for schizophrenia (n = 6), schizoaffective disorder (n = 2), schizophreniform disorder (n = 1), and paranoid psychosis (n = 1). No significant differences between schizophrenia and PFTBI clinical profiles were found, with the exception of i) the PANSS negative total score, and ii) SAPS lifetime grandiose delusions. On both of these indices schizophrenia patients scored significantly higher than the PFTBI cohort. Conclusion The clinical profile of PFTBI appears to be comparable to schizophrenia/ schizoaffective disorder, perhaps with the exception of negative symptoms and lifetime (but not current) grandiose delusions. Reduced negative symptoms in PFTBI are a particularly critical finding given reports of the same in a small number of case studies (Batty et al., 2013). The thinning and hypoactivity of the cingulate cortex is believed to underlie negative symptoms in schizophrenia (Bersani et al., 2014), thus, the preservation of the cingulate cortex in PFTBI may neurologically explain these findings, and is an important next step in understanding clinical differences in PFTBI and schizophrenia