Self-administered cognitive behavior therapy (SCBT) has been shown to be an effective alternative to therapist-delivered treatment for panic disorder (PD). However, it is unknown whether combining SCBT and antidepressants can improve treatment. This trial evaluated the efficacy of SCBT and sertraline, alone or in combination, in PD.

Patients (n=251) were randomized to 12 weeks of either placebo drug, placebo drug plus SCBT, sertraline, or sertraline plus SCBT. Those who improved after 12 weeks of acute treatment received treatment for an additional 12 weeks. Outcome measures included core PD symptoms (panic attacks, anticipatory anxiety, agoraphobic avoidance), dysfunctional cognitions (fear of bodily sensations, agoraphobic cognitions), disability, and clinical global impression of severity and improvement. Efficacy data were analyzed using general and generalized linear mixed models.

Primary analyses of trends over time revealed that sertraline/SCBT produced a significantly greater rate of decline in fear of bodily sensations compared to sertraline, placebo/SCBT and placebo. Trends in other outcomes were not significantly different over time. Secondary analyses of mean scores at week 12 revealed that sertraline/SCBT fared better on several outcomes than placebo, with improvement being maintained at the end of continuation treatment. Outcome did not differ between placebo and either sertraline monotherapy or placebo/SCBT. Moreover, few differences emerged between the active interventions.

This trial suggests that sertraline combined with SCBT may be an effective treatment for PD. The study could not confirm the efficacy of sertraline monotherapy or SCBT without concomitant medication or therapist assistance in the treatment of PD.

We were interested in examining the relationship between socially relevant stimuli and decision processes in patients with schizophrenia.

We tested patients with schizophrenia and healthy controls on a stochastically rewarded associative learning task. Participants had to determine, through trial and error, which of two faces was associated with a higher chance of reward: one face was angry, the other happy.

Both patients and healthy controls were able to perform the task at above-chance accuracy, and there was no significant difference in overall accuracy between the groups. Both groups also reliably preferred the happy face, such that they selected it more often than the angry face on the basis of the same amount of positive versus negative feedback. However, patients were significantly more averse to the angry face, such that they chose it less often than control participants when the reward feedback strongly supported the angry face as the best choice.

Patients show an increased aversion to angry faces, in a task in which they must learn to associate rewards with expressions.

Elevated incidence of psychotic illness has been consistently shown among migrant populations. Ethnic density, the proportion of an ethnic group in a defined area, is cited as one factor with a reduced risk of psychosis where ethnicity is shared. However, UK studies have shown mixed results. We set out to re-examine the ethnic density effect at a greater level of geographic detail than previous studies.

Using a large sample of patient records from general practitioners in South East London, we were able to assess neighbourhood factors at the detailed lower super output area level. This comprises, on average, 1500 people compared with around 6000 per ward, the measure used in previous studies. We compared black (Afro-Caribbean) and white psychosis incidence by neighbourhood ethnic density over a 10-year period.

We found a clear negative association between ethnic density and psychosis incidence. In neighbourhoods where black people comprised more than 25% of the population, there was no longer a statistically significant ethnic difference in psychosis rates. However, where black people were less well represented, their relative risk increased nearly threefold [odds ratio (OR) 2.88, 95% confidence interval (CI) 1.89–4.39]. Furthermore, incidence rates for black people in the lowest density quintiles were over five times greater than in the most dense quintile (OR 5.24, 95% CI 1.95–14.07). However, at ward level this association was much weaker and no longer statistically significant.

Ethnic density is inversely related to psychosis incidence at a detailed local neighbourhood level.

Unlike civilian post-traumatic stress disorder (PTSD), the efficacy of sertraline for the treatment of combat-related PTSD has not yet been proven. The present study aimed to evaluate the clinical efficacy of sertraline against combat-related PTSD in a randomized, double-blind, placebo-controlled trial.

Seventy Iranian veterans of the Iran–Iraq war who met the DSM-IV criteria for diagnosis of PTSD were randomized to receive either flexibly dosed sertraline (50–200 mg/day) (n=35, completers=32) or placebo (n=35, completers=30) for 10 weeks. Efficacy was evaluated by the Impact of Event Scale – Revised (IES-R) and the Clinical Global Impression scale – Severity (CGI-S) and Improvement (CGI-I) ratings. Responder criteria were defined as a ⩾30% reduction in the IES-R total score plus a CGI-I rating of ‘much’ or ‘very much’ improved.

On both intention-to-treat (ITT) and per protocol (completer) methods of analysis, the mean reductions in the IES-R total and subscale (re-experiencing/intrusion, avoidance/numbing and hyperarousal) scores (p<0.001) and also in the CGI-S score (p<0.01) were significantly greater in the sertraline group than in the placebo group. For the CGI-I, the mean endpoint score was significantly lower in the sertraline group than in the placebo group (p⩽0.001). The number of responders in the sertraline group was significantly higher than in the placebo group (44% v. 3%, p⩽0.001). Sertraline was well tolerated, with a 6% discontinuation rate as a result of adverse reactions.

The results of this study suggest that sertraline can be an effective, safe and tolerable treatment for combat-related PTSD in Iranian veterans.

Monoamine oxidase A (MAOA) is an important enzyme that metabolizes monoamines such as serotonin, norepinephrine and dopamine in the brain. In prefrontal cortex, low MAOA binding is associated with aggression and high binding is associated with major depressive disorder (MDD) and also risk for recurrence of depressive episodes. In rodent models, low MAOA levels are associated with increased aggression and fear conditioning, and decreased social and exploratory investigative behaviors. Our objective was to measure MAOA binding in prefrontal cortex and concurrently evaluate a broad range of validated personality traits. We hypothesized that prefrontal MAOA binding would correlate negatively with angry-hostility, a trait related to aggression/anger, and positively with traits intuitively related to adaptive investigative behavior.

Participants were aged 19–49 years, healthy and non-smoking. MAOA binding was measured with [11C]harmine positron emission tomography (PET) in prefrontal brain regions and personality traits were measured with the NEO Personality Inventory Revised (NEO PI-R).

Prefrontal MAOA binding correlated negatively with angry-hostility (r=−0.515, p=0.001) and positively with deliberation (r=0.514, p=0.001). In a two-factor regression model, these facets explained 38% of variance in prefrontal MAOA binding. A similar relationship was found in prefrontal cortex subregions.

We propose a new continuum describing the relationship between personality and MAOA: deliberate/thoughtful contrasting aggressive/impulsive. Additionally, the association between high MAOA binding and greater deliberation may explain why some people have moderately high levels of MAOA, although very high levels occur during MDD. In health, higher MAOA binding is associated with an adaptive personality facet.

Disturbances in social interaction are a defining feature of patients with borderline personality disorder (BPD). In this study, facial emotional expressions, which are crucial for adaptive interactions in social contexts, were assessed in patients with BPD in response to social exclusion.

We examined facial emotional reactions of 35 patients with BPD and 33 healthy controls when playing Cyberball, a virtual ball-tossing game that reliably induces social exclusion. Besides self-reported emotional responses, facial emotional expressions were analyzed by applying the Emotional Facial Action Coding System (EMFACS).

Patients with BPD showed a biased perception of participation. They more readily reported feeling excluded compared to controls even when they were included. In BPD, social exclusion led to an increase in self-reported other-focused negative emotions. Overall, EMFACS analyses revealed that BPD patients reacted with fewer positive expressions and with significantly more mixed emotional expressions (two emotional facial expressions at the same time) compared to the healthy control group when excluded.

Besides a negative bias for perceived social participation, ambiguous facial emotional expressions may play an important role in the disturbed relatedness in patients with BPD.

Catechol-O-methyltransferase (COMT) Val158Met has been associated with activity of the mesial temporal lobe during episodic memory and it may weakly increase risk for schizophrenia. However, how this variant affects parahippocampal and hippocampal physiology when dopamine transmission is perturbed is unclear. The aim of the present study was to compare the effects of the COMT Val158Met genotype on parahippocampal and hippocampal physiology during encoding of recognition memory in patients with schizophrenia and in healthy subjects.

Using blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI), we studied 28 patients with schizophrenia and 33 healthy subjects matched for a series of sociodemographic and genetic variables while they performed a recognition memory task.

We found that healthy subjects had greater parahippocampal and hippocampal activity during memory encoding compared to patients with schizophrenia. We also found different activity of the parahippocampal region between healthy subjects and patients with schizophrenia as a function of the COMT genotype, in that the predicted COMT Met allele dose effect had an opposite direction in controls and patients.

Our results demonstrate a COMT Val158Met genotype by diagnosis interaction in parahippocampal activity during memory encoding and may suggest that modulation of dopamine signaling interacts with other disease-related processes in determining the phenotype of parahippocampal physiology in schizophrenia.

While anxiety has been associated with exaggerated emotional reactivity, depression has been associated with blunted, or context insensitive, emotional responding. Although anxiety and depressive disorders are frequently co-morbid, surprisingly little is known about emotional reactivity when the two disorders co-occur.

We utilized the emotion-modulated startle (EMS) paradigm to examine the effects of a concurrent depressive episode on emotional reactivity in young adults with anxiety disorders. Using an archival dataset from a multi-disciplinary project on risk factors in childhood-onset depression, we examined eye-blink startle reactions to late-onset auditory startle probes while participants viewed pictures with affectively pleasant, unpleasant and neutral content. EMS response patterns were analyzed in 33 individuals with a current anxiety (but no depressive) disorder, 24 individuals with a current anxiety disorder and co-morbid depressive episode and 96 healthy controls.

Control participants and those with a current anxiety disorder (but no depression) displayed normative linearity in startle responses, including potentiation by unpleasant pictures. By contrast, individuals with concurrent anxiety and depression displayed blunted EMS.

An anxiety disorder concurrent with a depressive episode is associated with reactivity that more closely resembles the pattern of emotional responding that is typical of depression (i.e. context insensitive) rather than the pattern that is typical for anxiety (i.e. exaggerated).

Direct comparisons of brain function between obsessive compulsive disorder (OCD) and other anxiety or OCD spectrum disorders are rare. This study aimed to investigate the specificity of altered frontal-striatal and limbic activations during planning in OCD, a prototypical anxiety disorder (panic disorder) and a putative OCD spectrum disorder (hypochondriasis).

The Tower of London task, a ‘frontal-striatal’ task, was used during functional magnetic resonance imaging measurements in 50 unmedicated patients, diagnosed with OCD (n=22), panic disorder (n=14) or hypochondriasis (n=14), and in 22 healthy subjects. Blood oxygen level-dependent (BOLD) signal changes were calculated for contrasts of interest (planning versus baseline and task load effects). Moreover, correlations between BOLD responses and both task performance and state anxiety were analysed.

Overall, patients showed a decreased recruitment of the precuneus, caudate nucleus, globus pallidus and thalamus, compared with healthy controls. There were no statistically significant differences in brain activation between the three patient groups. State anxiety was negatively correlated with dorsal frontal-striatal activation. Task performance was positively correlated with dorsal frontal-striatal recruitment and negatively correlated with limbic and ventral frontal-striatal recruitment. Multiple regression models showed that adequate task performance was best explained by independent contributions from dorsolateral prefrontal cortex (positive correlation) and amygdala (negative correlation), even after controlling for state anxiety.

Patients with OCD, panic disorder and hypochondriasis share similar alterations in frontal-striatal brain regions during a planning task, presumably partly related to increased limbic activation.

The aim of this study was to investigate three main aspects of executive functions (EFs), i.e. shifting, updating and inhibition, in adolescents engaging in non-suicidal self-injury (NSSI) as compared with healthy controls.

EFs were assessed using the Intra/Extradimensional Set Shift, the Spatial Working Memory (SWM) Test and the Stop Signal Test (SST) from the Cambridge Neuropsychological Test Automated Battery (CANTAB), in a high-severity NSSI group (n=33), a low-severity NSSI group (n=29) and a healthy control group (n=35). Diagnostic characteristics were examined using the Kiddie-Sads-Present and Lifetime Version.

There were group differences on the SWM Test. A trend towards an interaction effect of sex revealed that males in the high-severity NSSI group made significantly more errors than males and females in the control group. Both males and females in the high-severity NSSI group made poor use of an efficient strategy in completing the test. The low-severity NSSI group performed poorly on the SST, making more errors than the control group and showing an impaired ability to inhibit initiated responses, as compared with the high-severity NSSI group. There were group differences in frequencies of current and previous major depressive disorder. However, no effects of these diagnoses were found on any of the EF tests.

This study demonstrates that NSSI subgroups have distinct deficits in EFs. The high-severity NSSI group has working memory deficits, while the low-severity NSSI group has impaired inhibitory control. This supports the emotion regulation hypothesis.

Current rodent models emphasize the joint action of the stress mediators noradrenaline (NE) and cortisol (CORT) in conferring a memory advantage of emotional over neutral stimuli.

Using a pharmacological strategy of tackling this stress-related mechanism to enhance human episodic (autobiographical) memory, we measured amygdala-hippocampal responses during encoding of emotional and neutral stimuli with functional magnetic resonance imaging in 51 healthy subjects under four pharmacological conditions in a double-blind parallel group design: (i) placebo; (ii) the NE-reuptake inhibitor reboxetine (4 mg); (iii) hydrocortisone (synthetic CORT) (30 mg); or (iv) both agents in combination.

Differential drug effects were found in the left hippocampus, whereas hydrocortisone alone selectively decreased hippocampal responses to emotional relative to neutral stimuli, reboxetine potentiated hippocampal responses to these stimuli. Importantly, the inhibitory influence of hydrocortisone was reversed by co-administration of reboxetine.

Our results imply that stress levels of CORT alone attenuate hippocampal responses to emotional stimuli, an effect possibly related to a regulatory negative feedback loop. However, when simultaneously elevated to stress levels, NE and CORT act together to synergistically enhance hippocampal activity during encoding of emotional stimuli, a mechanism that may turn maladaptive under circumstances of traumatic stress.

Three cognitive constructs are risk factors for eating disorders: undue influence of weight and shape, concern about weight and shape, and body dissatisfaction (BD). Undue influence, a diagnostic criterion for eating disorders, is postulated to be closely associated with self-esteem whereas BD is postulated to be closely associated with body mass index (BMI). We understand less about the relationships with concern about weight and shape. The aim of the current investigation was examine the degree of overlap across these five phenotypes in terms of latent genetic and environmental risk factors in order to draw some conclusions about the similarities and differences across the three cognitive variables.

A sample of female Australian twins (n=1056, including 348 complete pairs), mean age 35 years (s.d.=2.11, range 28–40), completed a semi-structured interview about eating pathology and self-report questionnaires. An independent pathways model was used to investigate the overlap of genetic and environmental risk factors for the five phenotypes.

In terms of variance that was not shared with other phenotypes, self-esteem emerged as being separate, with 100% of its variance unshared with the other phenotypes, followed by undue influence (51%) and then concern (34%), BD (28%) and BMI (32%).

In terms of shared genetic risk, undue influence and concern were more closely related than BD, whereas BMI and BD were found to share common sources of risk. With respect to environmental risk factors, concern, BMI and BD were more closely related to each other than to undue influence.

Military service can lead to profound changes in identity, both in servicemen's perception of themselves and in their relationship to the world, but the significance of these changes for psychopathology is unclear. We investigated whether the extent and valence of identity change was related to the degree of military trauma exposure or to post-traumatic stress disorder (PTSD) and suicide attempts. We further sought to describe the nature of such changes using qualitative analysis.

A total of 153 veterans in receipt of a war pension for PTSD or physical disability were identified. Interviews established retrospectively DSM-IV diagnoses of PTSD and reports of suicidal ideation or behaviour since enlistment were examined.

Trauma exposure alone was unrelated to any measure of identity change. By contrast, PTSD was associated with a relationship to the world that had changed in a negative direction. It was also associated with a changed perception of self, which could be either positive or negative. After controlling for trauma exposure and PTSD, suicidal behaviours were associated with more negative perceptions of the world. These perceptions of the world included disillusionment about human nature and a more specific rejection of civilian life.

PTSD and suicidal behaviours in veterans seem not to be associated with significantly more negative views of the self but rather with more alienation from civilian life. This has serious consequences for engaging veterans in National Health Service (NHS) mental health services and for the provision of effective treatment.

The expanded suffocation false alarm theory (SFA) hypothesizes that dysfunction in endogenous opioidergic regulation increases sensitivity to CO2, separation distress and panic attacks. In panic disorder (PD) patients, both spontaneous clinical panics and lactate-induced panics markedly increase tidal volume (TV), whereas normals have a lesser effect, possibly due to their intact endogenous opioid system. We hypothesized that impairing the opioidergic system by naloxone could make normal controls parallel PD patients' response when lactate challenged. Whether actual separations and losses during childhood (childhood parental loss, CPL) affected naloxone-induced respiratory contrasts was explored. Subjective panic-like symptoms were analyzed although pilot work indicated that the subjective aspect of anxious panic was not well modeled by this specific protocol.

Randomized cross-over sequences of intravenous naloxone (2 mg/kg) followed by lactate (10 mg/kg), or saline followed by lactate, were given to 25 volunteers. Respiratory physiology was objectively recorded by the LifeShirt. Subjective symptomatology was also recorded.

Impairment of the endogenous opioid system by naloxone accentuates TV and symptomatic response to lactate. This interaction is substantially lessened by CPL.

Opioidergic dysregulation may underlie respiratory pathophysiology and suffocation sensitivity in PD. Comparing specific anti-panic medications with ineffective anti-panic agents (e.g. propranolol) can test the specificity of the naloxone+lactate model. A screen for putative anti-panic agents and a new pharmacotherapeutic approach are suggested. Heuristically, the experimental unveiling of the endogenous opioid system impairing effects of CPL and separation in normal adults opens a new experimental, investigatory area.

This study aimed to compare ‘cool’ [working memory (WM) and response inhibition] and ‘hot’ (delay aversion) executive functions (EFs) in children with and without attention deficit hyperactivity disorder (ADHD).

A total of 100 ADHD children (45 with family history of ADHD and 55 with no family history) and 100 healthy controls, all medication free, were tested on tasks related to the ‘hot’ (i.e. two choice-delay tasks) and ‘cool’ domains of EF (i.e. Digits backward, Corsi Block Task backward, Go/No-Go Task, Stop-Signal Task, and the Stroop).

Compared with the controls, children with ADHD were found to perform significantly worse on one or more measures of response inhibition, WM, and delay aversion after controlling for co-morbidities and estimated IQ. In addition, comparisons between ADHD children with family history of ADHD and those with no family history found significant differences on measures of response inhibition and WM but not delay aversion. These results are largely supported by results of two logistic regressions.

ADHD was found to be associated with deficits on both cool and hot EFs. There is also evidence to suggest that cool EFs impairment is related to a family history of ADHD. Findings of this study have helped to elucidate the nature and extent of EF deficits in children with ADHD.

It is important for doctors and patients to know what factors help recovery from depression. Our objectives were to predict the probability of sustained recovery for patients presenting with mild to moderate depression in primary care and to devise a means of estimating this probability on an individual basis.

Participants in a randomized controlled trial were identified through general practitioners (GPs) around three academic centres in England. Participants were aged >18 years, with Hamilton Depression Rating Scale (HAMD) scores 12–19 inclusive, and at least one physical symptom on the Bradford Somatic Inventory (BSI). Baseline assessments included demographics, treatment preference, life events and difficulties and health and social care use. The outcome was sustained recovery, defined as HAMD score <8 at both 12 and 26 week follow-up. We produced a predictive model of outcome using logistic regression clustered by GP and created a probability tree to demonstrate estimated probability of recovery at the individual level.

Of 220 participants, 74% provided HAMD scores at 12 and 26 weeks. A total of 39 (24%) achieved sustained recovery, associated with being female, married/cohabiting, having a low BSI score and receiving preferred treatment. A linear predictor gives individual probabilities for sustained recovery given specific characteristics and probability trees illustrate the range of probabilities and their uncertainties for some important combinations of factors.

Sustained recovery from mild to moderate depression in primary care appears more likely for women, people who are married or cohabiting, have few somatic symptoms and receive their preferred treatment.

It is generally accepted that antipsychotics are more effective than placebo. However, it remains unclear whether antipsychotics induce a pattern or trajectory of response that is distinct from placebo. We used a data-driven technique, called growth mixture modelling (GMM), to identify the different patterns of response observed in antipsychotic trials and to determine whether drug-treated and placebo-treated subjects show similar or distinct patterns of response.

We examined data on 420 patients with schizophrenia treated for 6 weeks in two double-blind placebo-controlled trials using haloperidol and olanzapine. We used GMM to identify the optimal number of response trajectories; to compare the trajectories in drug-treated versus placebo-treated patients; and to determine whether the trajectories for the different dimensions (positive versus negative symptoms) were identical or different.

Positive symptoms were found to respond along four distinct trajectories, with the two most common trajectories (‘Partial responder’ and ‘Responder’) accounting for 70% of the patients and seen proportionally in both drug- and placebo-treated. The most striking drug–placebo difference was in the ‘Dramatic responders’, seen only among the drug-treated. The response of negative symptoms was more modest and did not show such distinct trajectories.

Trajectory models of response, rather than the simple responder/non-responder dichotomy, provide a better statistical account of how antipsychotics work. The ‘Dramatic responders’ (those showing >70% response) were seen only among the drug-treated and make a significant contribution to the overall drug–placebo difference. Identifying and studying this subset may provide specific insight into antipsychotic action.

Few data exist examining the longer-term outcome of bulimia nervosa (BN) following treatment with cognitive behavioral therapy (CBT) and exposure with response prevention (ERP).

One hundred and thirty-five women with purging BN received eight sessions of individual CBT and were then randomly assigned to either relaxation training (RELAX) or one of two ERP treatments, pre-binge (B-ERP) or pre-purge cues (P-ERP). Participants were assessed yearly following treatment and follow-up data were recorded.

Eighty-one per cent of the total sample attended long-term follow-up. At 5 years, abstinence rates from binging were significantly higher for the two exposure treatments (43% and 54%) than for relaxation (27%), with no difference between the two forms of exposure. Over 5 years, the frequency of purging was lower for the exposure treatments than for relaxation training. Rates of recovery varied according to definition of recovery. Recovery continued to increase to 5 years. At 5 years, 83% no longer met DSM-III-R criteria for BN, 65% received no eating disorder diagnosis, but only 36% had been abstinent from bulimic behaviors for the past year.

This study provides possible evidence of a conditioned inoculation from exposure treatment compared with relaxation training in long-term abstinence from binge eating at 5 years, and the frequency of purging over 5 years, but not for other features of BN. Differences among the groups were not found prior to 5 years. CBT is effective for BN, yet a substantial group remains unwell in the long term. Definition of recovery impacts markedly on recovery rates.

Numerous longitudinal studies have identified risk factors for the onset of most eating disorders (EDs). Identifying women at highest risk within a high-risk sample would allow for focusing of preventive resources and also suggests different etiologies.

A longitudinal cohort study over 3 years in a high-risk sample of 236 college-age women randomized to the control group of a prevention trial for EDs. Potential risk factors and interactions between risk factors were assessed using the methods developed previously. Main outcome measures were time to onset of a subthreshold or full ED.

At the 3-year follow-up, 11.2% of participants had developed a full or partial ED. Seven of 88 potential risk factors could be classified as independent risk factors, seven as proxies, and two as overlapping factors. Critical comments about eating from teacher/coach/siblings and a history of depression were the most potent risk factors. The incidence for participants with either or both of these risk factors was 34.8% (16/46) compared to 4.2% (6/144) for participants without these risk factors, with a sensitivity of 0.75 and a specificity of 0.82.

Targeting preventive interventions at women with high weight and shape concerns, a history of critical comments about eating weight and shape, and a history of depression may reduce the risk for EDs.

Whether traumatic brain injury (TBI) is an independent risk factor for the subsequent development of schizophrenia has evoked considerable controversy. No evidence has been previously reported from Asia. This study estimated the risk of schizophrenia during a 5-year period following hospital admission for TBI relative to a comparison group of non-TBI patients during the same period in Taiwan.

Two datasets were linked: the Traumatic Brain Injury Registry and the Taiwan National Health Insurance Research Dataset. A total of 3495 patients hospitalized with a diagnosis of TBI from 2001 to 2002 were included, together with 17 475 non-TBI patients as the comparison group, matched on sex, age, and year of TBI hospitalization. Each individual was followed for 5 years to identify any later diagnosis of schizophrenia. Cox proportional hazard regressions were performed for analysis.

During the 5-year follow-up period, patients who had suffered TBI were independently associated with a 1.99-fold (95% confidence interval 1.28–3.08) increased risk of subsequent schizophrenia, after adjusting for monthly income and residential geographical location. The severity and type of TBI was not associated with the subsequent development of schizophrenia.

Our findings add important evidence from Asia and suggest a potential link between TBI and schizophrenia. Our study suggests that clinicians and family members should be alert to possible neuropsychiatric conditions following TBI.