A brief neurocognitive assessment of patients with psychosis following traumatic brain injury (PFTBI): Use of the Repeatable battery for the Assessment of Neuropsychological Status (RBANS)

Highlights

• The PFTBI cognitive neuropsychological profile is significantly and substantially impaired.

• PFTBI deficits exceed those demonstrated in TBI and schizophrenia alone.

• The RBANS is an effective method of neuropsychological assessment in PFTBI.

• This is the first standardised neuropsychological assessment of a cohort of PFTBI patients.

Abstract

Patients who develop psychosis following a traumatic brain injury (PFTBI) show impaired neurocognition; however, the degree of impairment has not been empirically investigated using a standardised battery. We administered the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) to patients with PFTBI (n=10), and to three groups of controls: traumatic brain injury (TBI) (n=10), schizophrenia (n=23), and nonclinical controls (n=23). The results confirmed that the cognitive neuropsychological profile of dually-diagnosed patients with PFTBI is significantly and substantially impaired. Seventy per cent of patients with PFTBI received a neuropsychological classification between the “extremely low” and “low average” ranges. Group-wise analyses on the RBANS indices indicated that patients with PFTBI had the lowest (Immediate Memory, Attention, Delayed Memory, Total Score), or equal lowest (visuospatial, equivalent with schizophrenia patients) scores, with the exception of the Language Index where no group differences were shown (however, the mean PFTBI score on the Language Index was two standard deviations below the RBANS normative score). These findings provide novel evidence of impaired cognitive neuropsychological processing in patients with PFTBI using a standardised and replicable battery.

Introduction

Psychosis following a traumatic brain injury (PFTBI) is estimated to occur in up to 10% of patients who sustain a traumatic brain injury (TBI) (Davison and Bagley, 1969; Fujii et al., 2004). Aetiological theories primarily highlight the role of the TBI in activating a premorbid psychosis proneness and/or initiating structural and functional neurological changes that underpin the development of new psychotic symptoms (see Batty et al. (2013) for review). However, the substantial morbidity of PFTBI patients has meant that empirical evidence is lacking.

The extent of neurocognitive deficits in PFTBI has rarely been empirically investigated, with the majority of existing data having been drawn from case studies and retrospective chart reviews. This is problematic given that the pooled analysis of single case studies compromises the comparability of assessment protocols, and small group case studies compromise statistical power, making it difficult to draw definitive conclusions with confidence. The standardised measurement of neurocognitive deficits in patients with PFTBI is critical to aspects of their diagnosis and long-term care. To date, deficits in language, verbal learning and verbal memory appear consistently in the existing literature (see Batty et al. (2013) for a comprehensive review) (Bamrah and Johnson, 1991, Sachdev et al., 2001, Fujii and Ahmed, 2002, Fujii et al., 2004). However, other aspects of neurocognition have been reported as intact in some cases. For instance, a retrospective chart review reported cognitive neuropsychological data for 17 patients with PFTBI, demonstrating memory impairment in 59%, executive dysfunction and visuospatial impairment in 41%, and language and attention deficits in only 12% (Fujii and Ahmed, 2002).

Large bodies of empirical work in patients with either schizophrenia or traumatic brain injury (TBI) have established much broader and encompassing neurocognitive deficits in these patient cohorts. Both schizophrenia and TBI are associated with extensive deficits in visual-perceptual processing (e.g., Brosseau-Lachaine et al., 2008; Ponsford et al., 2011; Landgraf et al., 2011), language and communication (e.g., DeLisi, 2001; Covington et al., 2005; LeBlanc et al., 2006), memory (e.g., Lezak, 1979; Vakil, 2005; Gur and Gur, 2013; Lett et al., 2014), and executive function (e.g., Ponsford and Kinsella, 1992; Rios et al., 2004; Eisenberg and Berman, 2010; Breton et al., 2011), with fatigue and loss of concentration/attention exacerbating these deficits further. Established impairments in schizophrenia and TBI suggest that further research into the cognitive neuropsychological profile in PFTBI is needed to address apparent discrepancies in the existing literature.

The Repeatable Battery for the Assessment of Neuropsychological Status (RBANS; Randolph, 1998) has potential as an appropriate test of neurocognition in PFTBI¹. The RBANS assesses attention, language, visuospatial/constructional ability, and immediate and delayed memory, in a relatively brief, and yet comprehensive, one-on-one administration (Randolph, 1998). The clinical validity of the RBANS has been established by various studies that have illustrated sensitivity in the detection of neurocognitive impairments in both schizophrenia (Wilk et al., 2004, Gogos et al., 2010) and TBI (Randolph, 1998, Carone et al., 2004, McKay et al., 2007). Furthermore, the RBANS has demonstrated comparable sensitivity to more extensive alternative measures in both patient groups: Wechsler, 1997a, Wechsler, 1997b assessments in schizophrenia (i.e. Wechsler Adult Intelligence Scale, 3rd Edition [WAIS-III] and Wechsler Memory Scale, 3rd Edition; Gold et al., 1999), and the WAIS-III (Wechsler, 1997a) and California Verbal Learning Test, 2nd Edition (Delis et al., 2000) in TBI (McKay et al., 2007).

The purpose of the current study was to determine the neuropsychological profile of a sample of patients with PFTBI using the RBANS (Randolph, 1998). To our knowledge, this is the first systematic and standardised neuropsychological assessment of PFTBI. RBANS scores from patients with PFTBI were compared with TBI, schizophrenia, and nonclinical control groups. Given their dual diagnosis, we expected that patients with PFTBI would show significant impairment on each domain of the RBANS relative to all three control cohorts. To date, this is only partially demonstrated in the literature.