Evaluation of an adapted version of the International Trauma Questionnaire for use by people with intellectual disabilities.

AIMS: The International Trauma Questionnaire (ITQ) is a novel assessment instrument that is aligned to the ICD-11 diagnoses of post-traumatic stress disorder (PTSD) and complex PTSD (CPTSD). The purpose of this study was to develop and evaluate an adapted version of the ITQ suitable for use by people with intellectual disabilities. METHODS: The ITQ-ID follows the original ITQ, using wording developed in collaboration with a focus group of people with intellectual disabilities The ITQ-ID was administered to 40 people with intellectual disabilities recruited from learning disability forensic and community settings, alongside a Trauma Information Form and the Impact of Event Scale-Intellectual Disabilities (IES-IDs). RESULTS: Most participants reported multiple traumatizing events. Around half of the participants met strict criteria for a diagnosis of PTSD, and around three quarters met looser criteria. Depending on definitions, between 66% and 93% of those who met criteria for PTSD also met criteria for a diagnosis of CPTSD. The ITQ-ID showed a single-component structure, with very good-to-excellent internal consistency, excellent test-retest reliability, and evidence of concurrent, discriminant, and content validity. SIGNIFICANCE: The results support the potential of the ITQ-ID for assessment of PTSD and CPTSD in people with intellectual disabilities in both clinical and research contexts and highlight the need for further validation work.

The experiences of mothers of children and young people with intellectual disabilities during the first COVID-19 lockdown period.

BACKGROUND: Recent COVID-19 lockdown restrictions resulted in reduced access to educational, professional and social support systems for children with intellectual disabilities and their carers. AIM: The aim of this study was to gain insight into the ways mothers of children with intellectual disabilities coped during the first 2020 lockdown period. METHODS: Eight mothers of children with intellectual disabilities were interviewed. The recordings of these interviews were subjected to a thematic analysis. RESULTS: Three main themes were identified: carrying the burden; a time of stress; and embracing change and looking to the future. CONCLUSIONS: All mothers experienced increased burden and stress. However, some also described some positive impact of lockdown conditions on them as well as on their child's well-being and behaviour. These findings are discussed in the light of the (Journal of Applied Research in Intellectual Disabilities, 33, 2020, 1523) survey results on parental coping and suggestions for future service provision during pandemic conditions are proposed.

Effect of the COVID-19 pandemic on the mental health of carers of people with intellectual disabilities.

INTRODUCTION: The measures implemented to manage the COVID-19 pandemic have been shown to impair mental health. This problem is likely to be exacerbated for carers. METHOD: Informal carers (mainly parents) of children and adults with intellectual disabilities, and a comparison group of parents of children without disabilities, completed an online questionnaire. Almost all the data were collected while strict lockdown conditions were in place. RESULTS: Relative to carers of children without intellectual disability, carers of both children and adults with intellectual disability had significantly greater levels of a wish fulfilment coping style, defeat/entrapment, anxiety, and depression. Differences were 2-3 times greater than reported in earlier pre-pandemic studies. Positive correlations were found between objective stress scores and all mental health outcomes. Despite their greater mental health needs, carers of those with intellectual disability received less social support from a variety of sources. CONCLUSIONS: The greater mental health needs of carers in the context of lesser social support raises serious concerns. We consider the policy implications of these findings.

Functional lateralization in the prefrontal cortex of dopaminergic modulation of memory consolidation.

There is increasing evidence of functional lateralization within the rat brain. Here, we have examined the lateralization of dopamine (DA) function in the medial prefrontal cortex (PFC) in relation to memory consolidation in the novel object recognition test (NOR). Male Wistar rats received single bilateral or unilateral injections into prelimbic-PFC of agonists (SKF81297; 0.2 µg, quinpirole; 1 µg, SB277,011; 0.5 µg) and antagonists (SCH23390; 3 µg, L-741,626; 1 µg, 7-OH-DPAT; 3 µg) at DA D1, D2, or D3 receptors, immediately following the exposure trial in the NOR, and were tested either 1 or 24 h later for discrimination between a novel and a familiar object. As previously reported, bilateral injection of a D1 antagonist (SCH23390, 3 µg/side), a D2 antagonist (L-741,626, 1 µg/side) or a D3 agonist (7-OH-DPAT, 3 µg/side) impaired NOR at 1 h, while a D1 agonist (SKF81297, 0.2 µg/side), a D2 agonist (quinpirole, 1 µg/side) or a D3 antagonist (SB277,011, 0.5 µg/side) improved NOR at 24 h. The same effects were seen with left-sided unilateral injections. No effects were seen with right-sided unilateral injections. Endogenous DA release in the prelimbic-PFC promotes memory consolidation in the NOR, but only on the left side of the brain.

Validation of chronic mild stress in the Wistar-Kyoto rat as an animal model of treatment-resistant depression.

A recent review proposed four criteria for an animal model of treatment-resistant depression (TRD): a phenotypic resemblance to a risk factor for depression; enhanced response to stress; nonresponse to antidepressant drugs and response to treatments effective in TRD, such as deep brain stimulation (DBS) of the prefrontal cortex or ketamine. Chronic mild stress (CMS) provides a valid model of depression; the Wistar-Kyoto (WKY) rat is considered to be nonresponsive to antidepressant drugs. Here, we applied CMS to WKY rats. WKY and Wistar rats were exposed to CMS, then treated with saline, imipramine, citalopram or venlafaxine. After 5 weeks of CMS and 3 weeks of drug treatment, all WKY groups were implanted unilaterally with DBS electrodes in the prefrontal cortex, and examined in sucrose intake, elevated plus maze (EPM; decreased entries and time in the open arms) and novel object recognition (decreased exploration) tests, following 2×2 h of DBS. CMS decreased sucrose intake, open arm entries on the EPM, and object recognition. Relative to Wistars, WKY rats showed evidence of increased emotionality in the EPM and novel object recognition tests, and a greater impact of CMS on body weight gain and open arm entries. Wistars responded to drug treatment with an increase in sucrose intake but WKY were nonresponsive to drug treatment on all three behavioural tests. With one exception, DBS reversed the anhedonic, anxiogenic and dyscognitive effects of CMS in all groups of WKY rats. In a further experiment, subacute ketamine (10 mg/kg) also normalized behaviour on all three tests. We conclude that WKY rats subjected to CMS meet all four criteria for a valid model of TRD, and provide a basis for studying the mechanism of action of DBS.

Effects on brain-derived neurotrophic factor signalling of chronic mild stress, chronic risperidone and acute intracranial dopamine receptor challenges.

We have previously reported the effects of intracranial injections of dopamine D1, D2 and D3 ligands in animals subjected to the Novel Object Recognition (NOR) test following exposure to chronic mild stress (CMS) and chronic treatment with risperidone (RSP). Here, we present some molecular biological data from the same animals. It was predicted that brain-derived neurotrophic factor (BDNF) signalling in the prefrontal cortex (PFC) would reflect behavioural performance, implying an increase following acute administration of a D2 agonist or a D3 antagonist, blockade of this effect by CMS and its restoration by chronic RSP. In separate cohorts, animals were injected within the PFC or the hippocampus (HPC) with either the D1 agonist SKF-81297, the D2 agonist quinpirole or the D3 antagonist SB-277,011, following exposure to control conditions or CMS and chronic treatment with saline or RSP. Intracranial injections followed an exposure trial in the NOR test, with a retention trial 24 h later. Immediately afterwards, the animals were killed and expression of BDNF and TRKß protein, and their respective mRNAs, was measured in PFC and HPC samples. CMS decreased the expression of TRKß in both PFC and HPC. Several effects associated with intracranial injection were noted, but they were inconsistent and unrelated to CMS exposure. The effects of CMS on TRKß are consistent with a decrease in BDNF signalling, albeit that expression of BDNF itself did not change significantly. There was no evidence for an involvement of the BDNF-TRKß system in responses to RSP or dopamine ligands in animals exposed to CMS. However, there was a 24 h delay between the intracranial injection and tissue harvesting, meaning that brief early drug effects could have been missed.

The UK Mental Capacity Act and consent to research participation: asking the right question.

This paper considers the meaning of the term 'intrusive research', as used in the UK Mental Capacity Act 2005 (MCA), in relation to studies in which an informant is asked to provide information about or on behalf of a person who lacks capacity to consent, and who is not otherwise involved in the study. The MCA defines 'intrusive research' as research that would legally require consent if it involved people with capacity. The relevant ethical principles are that consent should be sought from people who would be affected by a piece of research and that this requirement should be implemented proportionately. The critical question, for investigators and research ethics committees, is: would provision of the personal information specified in the research protocol significantly affect a person whose capacity is not impaired? If the answer to this question is 'no', then the study falls outside the definition of 'intrusive research', and the MCA does not apply.

Antidepressant, anxiolytic and procognitive effects of subacute and chronic ketamine in the chronic mild stress model of depression.

Ketamine is the prototype of a new generation of antidepressant drugs, which is reported in clinical studies to be effective in treatment-resistant patients, with an effect that appears within hours and lasts for a few days. Chronic mild stress (CMS) is a well-established and widely used animal model of depression, in which anhedonia, anxiogenesis and cognitive dysfunction can be observed reliably. Studies using acute or brief ketamine treatment following withdrawal from CMS have replicated the clinical finding of a rapid onset of antidepressant action. However, there have been no CMS studies of chronic daily ketamine treatment or continued stress following ketamine treatment, which would have greater translational potential in relation to the long-term maintenance of antidepressant effects. Wistar rats were drug treated following an initial 2 weeks of CMS exposure, which continued alongside daily drug treatment. A first experiment tested a range of chronic (5 weeks) ketamine doses (5-30 mg/kg); a second compared the effects of subacute (3-5 days) and chronic (5 weeks) treatment. CMS-induced anhedonic, anxiogenic and dyscognitive effects, as measured, respectively, by decreased sucrose intake, avoidance of open arms in the elevated plus maze and loss of discrimination in the novel object recognition test. A sustained antidepressant-like effect of ketamine in the sucrose intake test was observed in both experiments, with an onset at around 1 week, faster than imipramine, and an optimum dose of 10 mg/kg. Anxiogenic and dyscognitive effects of CMS, in the elevated plus maze and novel object recognition test, respectively, were fully reversed by both subacute and chronic ketamine treatment. Daily treatment with ketamine in the CMS model causes sustained long-term antidepressant, anxiolytic and procognitive effects. The demonstration of a procognitive effect of ketamine may have particular translational value.

Sleep does not cause false memories on a story-based test of suggestibility.

Sleep contributes to the consolidation of memories. This process may involve extracting the gist of learned material at the expense of details. It has thus been proposed that sleep might lead to false memory formation. Previous research examined the effect of sleep on false memory using the Deese-Roediger-McDermott (DRM) paradigm. Mixed results were found, including increases and decreases in false memory after sleep relative to wake. It has been questioned whether DRM false memories occur by the same processes as real-world false memories. Here, the effect of sleep on false memory was investigated using the Gudjonsson Suggestibility Scale. Veridical memory deteriorated after a 12-h period of wake, but not after a 12-h period including a night's sleep. No difference in false memory was found between conditions. Although the literature supports sleep-dependent memory consolidation, the results here call into question extending this to a gist-based false memory effect.

CBT in a Caribbean Context: A Controlled Trial of Anger Management in Trinidadian Prisons.

BACKGROUND: Anger causes significant problems in offenders and to date few interventions have been described in the Caribbean region. AIM: To evaluate a package of CBT-based Anger Management Training provided to offenders in prison in Trinidad. METHOD: A controlled clinical trial with 85 participants who participated in a 12-week prison-based group anger management programme, of whom 57 (67%: 16 control, 41 intervention) provided pretrial and posttrial outcome data at Times 1 and 2. RESULTS: Intervention and control groups were not directly comparable so outcome was analysed using t-tests. Reductions were noted for state and trait anger and anger expression, with an increase in coping skills for the intervention group. No changes were noted in the control group. The improvements seen on intervention were maintained at 4 month follow-up for a sub-group of participants for whom data were available. Several predictors of outcomes were identified.

Assessment of Anger-Related Cognitions of People with Intellectual Disabilities.

BACKGROUND: Interventions for anger represent the largest body of research on the adaptation of cognitive behavioural therapy (CBT) for people with intellectual disabilities. The extent to which the effectiveness of these interventions reflects the behavioural or cognitive components of CBT is uncertain. This arises in part because there are few measures of anger-related cognitions. METHOD: The Profile of Anger-related Cognitions (PAC) is built around interpersonal scenarios that the participant identifies as personally anger-provoking, and was designed as an extension of the Profile of Anger Coping Skills (PACS). A conversational presentational style is used to approach ratings of anger experienced in those situations and of four relevant cognitive dimensions: attribution of hostile intent, unfairness, victimhood, and helplessness. The PAC, and other measures, including the PACS, was administered to (i) people with ID identified as having problems with anger control (n = 12) and (ii) university students (n = 23); its psychometric properties were investigated and content analyses were conducted of participants' verbal responses. In a third study, clinicians (n = 6) were surveyed for their impression of using the PAC in the assessment of clients referred for help with anger problems. RESULTS: The PAC had good consistency and test-retest reliability, and the total score on the four cognitive dimensions correlated significantly with anger ratings but not with impersonal measures of anger disposition. The predominant cognitions reported were perceptions of unfairness and helplessness. People with ID and university students were in most respects very similar in both the psychometric analyses and the content analyses of their verbal responses. The PAC had high acceptability both to people with ID and to clinicians. CONCLUSIONS: The PAC may be a useful instrument for both clinical and research purposes. Personal relevance and the conversational mode of administration are particular strengths.

The neurobiology of aggression: implications for the pharmacotherapy of aggressive challenging behaviour by people with intellectual disabilities.

AIM: The aim of this review is to summarise current understanding of the neurobiology of aggression and within this context to consider the evidence base for the pharmacotherapy of aggressive challenging behaviour by people with intellectual disabilities (ID). EVIDENCE: Aggressive encounters involve a variety of psychological processes and progress has been made in understanding the brain mechanisms involved. However, the role in aggression of the neurotransmitters serotonin, dopamine and γ-aminobutyric acid is no longer as clear as it once appeared, with the result that predictions cannot be made with confidence about drug effects on aggression. There have been relatively few controlled trials of pharmacotherapy for aggression in people with ID, or, indeed, in the general population, and their outcomes have largely been negative. CONCLUSION: With the possible exception of risperidone, there is no reliable evidence that antidepressant, neuroleptic or anticonvulsant drugs are effective treatments for aggression by people with ID.