Existing Methodological Limitations and Future Recommendations

As discussed throughout this chapter, substantial methodological weaknesses are a frequent theme in the PFTBI literature. Data pooling, despite discordant information,

represents one of the more flawed practices. Chart review-based studies, which constitute the majority of available research, tend to draw conclusions about symptom trends even where substantial amounts of data are missing on measures of interest (Burg et al., 1996; Fujii & Ahmed, 2002). Similarly, critical literature reviews have typically pooled data from studies with incompatible methodologies and attempted to draw meaningful conclusions about PFTBI cohorts as a whole (e.g., Davison & Bagley, 1969).

Recruitment is often confined to hospital inpatients or chart information taken from inpatient wards, and in one circumstance potential cases were sought from a list of TBI patients referred for further neuropsychological testing (Fujii & Ahmed, 2001). These are the worst cases and miss mild to moderate brain injured patients who may be experiencing mild psychotic symptoms (Burg et al., 1996; Fujii & Ahmed, 2001; Malaspina et al., 2001), or experiencing other psychiatric symptoms that are inadvertently concealing their symptoms of

0 10 20 30 40 50 60 70 80 90

Frontal Temporal (Left) Temporal (Right) Parietal (Left) Parietal (Right) Basal 50% 87.5% 75% 12.5% 25% 12.5% M ean P er ce n tage (% ) ( N =8) Lesion Location

Table 2.4

PFTBI Localisation to Date

Author Year N (nΨ) Diagnosis (%)*

Localisation method Hemisphere Lobe Notes Achte et al. 1969 3552 (317) SCZ (24%) pSCZ (22%) Case record descriptions Bilateral Frontal (23.8%) Temporal (20.4%) Parietal (15.3%) Basal (14.3%)

Basal lesions most frequently psychotic

Bamrah & Johnson 1991 1 SCZf CT Generalised

atrophy

Frontal Buckley et al. 1993 5 SLP (60%)

SaLP (40%)

MRI Left Temporal Left temporal lesions in SLP

cleanly differentiated groups Fujii & Ahmed 1996 15 PFTBI EEG/SPECT/CT/MRI Bilateral Temporal/Frontal Right temporal lesions most

common

Fujii & Ahmed 2002 69 PFTBI EEG/CT/MRI Fontal (33.3%)

Temporal (21.7%) Ventricles (15.9%)

Hillbom 1960 3552

(498)

TBI & Ψ† Case record descriptions

Bilateral Temporal Left (and bilateral) temporal lesions most frequently psychotic

Sachdev et al. 2001 90 (45) SLP CT Bilateral Temporal/Parietal

Wilcox & Nasrallah 1987 659 (200)

PFTBI (11%) Case record descriptions

Bilateral Temporal * The percentage value is provided in the ‘Diagnosis’ column where this number differs from (nΨ).

psychosis (i.e., symptoms of depression co-occurring with affective flattening, Fleminger, 2008; Koponen et al., 2002; Mainio et al., 2007). There are a number of indications in the literature that mild injury can precede the development of psychosis. For example, higher rates of psychosis have been shown in patients who have suffered a mild injury when compared with those who have suffered a severe injury on two occasions; Achte et al. (1969) and Fujii et al. (2004). Further, Fujii and Ahmed (2002) reported that PFTBI patients with milder injury tended to have shorter onset latency (i.e., the period between injury and the development of psychotic symptoms).

Related to a bias in recruitment, a number of studies, particularly in the earlier research, have reported on servicemen/war veterans with penetrating skull injuries (Achte et al., 1969; Corcoran & Malaspina, 2007; David & Prince, 2005; Davison & Bagley, 1969). While these data are valuable because of their robust sample sizes, there are obvious limitations to their

generalisability to later PFTBI populations, both because of the inflated rates of skull penetrating injuries, and the introduction of additional confounding psychopathology that may be specific to war injuries, for example, post-traumatic stress disorder.

Diagnostic criteria, concerning both the identification of a traumatic brain injury and the presence of psychosis, are often not standardised (e.g., Achte et al., 1969). A significant traumatic brain injury is commonly identified in research by self-report, and the relevant details are obtained from a patient’s recall of the prior injury. As noted earlier, in some instances this is drawn from a simple yes/no response to one question (Fann et al., 2004; Silver et al., 2001). Elsewhere however, there are strict criteria applied to determine the existence and severity of a traumatic brain injury (Deb, Lyons, Koutzoukis, Ali, & McCarthy, 1999; Max et al., 1997). Similarly, a number of different methods have been used to define TBI severity; Glasgow Coma Scale (GCS; Teasdale & Jennett [1974], e.g., Max et al., 1997), duration of loss of consciousness (Buckley et al., 1993; Hoofien et al., 2001), length of coma, duration of post-traumatic amnesia (PTA; Koponen et al., 2006), and ICD-10 codes (Fujii & Ahmed, 2002; Harrison et al., 2006). These are not necessarily compatible and thus make the task of determining a relationship between injury severity and psychotic outcome difficult.

Psychotic patients are also more likely to want to attribute their psychiatric disturbances to a physical cause, and thus, more likely to report a TBI. In some cases, diagnoses of psychosis have been made from available chart notes alone (Corcoran & Malaspina, 2007; Kim, 2008). As

discussed in Section 2.2, disparity is also shown in the concepualisation of the subsequent psychotic symptoms; some research has focused on elucidating the potential for organic schizophrenia

(AbdelMalik et al., 2003; Corcoran & Malaspina, 2007; Kim, 2008; Malaspina et al., 2001; Nielsen et al., 2002), whereas others have conceptualised the link to psychotic symptoms along a continuum

(Buckley et al., 1993; David & Prince, 2005; McAllister & Ferrell, 2002; Wilcox & Nasrallah, 1986).

Retrospective recall bias is a further considerable issue in PFTBI investigations. Much of the work has relied on recall for a number of criteria, especially when collecting data relating to

personal and family history (e.g., Burg et al., 1996). This is shown most in large community-based prevalence investigations where questionnaires are widely distributed (Fann et al., 2004; Silver et al., 2001). Generally, relying on recall is subject to potential inaccuracies, and this risk is

exacerbated within brain injured and potentially psychotic populations who are known to carry cognitive and neuropsychological deficiencies, particularly in memory (Malaspina et al., 2001; Silver et al., 2001).

Further inconsistencies arise in the recording and assessment of personal and family history of psychosis. Research has both; (i) failed to assess personal history of psychosis in those

presenting with PFTBI (Burg et al., 1996; Fujii & Ahmed, 2002), and (ii) collapsed groups with and without psychoses prior to a TBI in their investigations (Fann et al., 2004). It is essential that these are reliably recorded and separated in analyses to work toward understanding the nature and/or direction of the relationship between psychoses and traumatic brain injury. Because genetic liability in schizophrenia is well established (Kim, 2008; Kumar et al., 2010), family history should also be reliably ascertained to move toward assessing potential aetiological (i.e., genetic) similarities between PFTBI and schizophrenia.

Many of the limitations discussed here are at least partially a consequence of the inherent difficulties in the recruitment and assessment of a PFTBI cohort. If the existing prevalence estimates are accurate then prevalence appears to be between 0.7% and 9.2% of patients who sustain a TBI (Davison & Bagley,1969; Fujii et al., 2004). This would explain the prominence of case study and retrospective chart or database reviews in the literature. Nonetheless, theorised conceptual models of the relationship between traumatic brain injury and psychosis are premature until substantial investigations, that are comprehensive and standardised, and that address the methodological confounds discussed in this review, are undertaken. This is required across all domains reviewed here. Only then can we begin to obtain a true picture of the PFTBI phenomenon.

Chapter 3: Cognitive Neuropsychological Deficits in Psychosis