The AQ appears to be sensitive to the broad phenotype, provided attention is restricted to the social skills and communication scales.

Non-autistic relatives of people with autistic disorder have an increased risk of social and communicative difficulties: this is known as the "broad phenotype." Better methods for characterizing the broad phenotype are needed to facilitate identification of risk genes for autism. 29 siblings of 20 children with autistic disorder, 13 siblings of 9 children with PDDNOS, and 46 typically developing control children from 26 families were assessed by parental report using the Children's Communication Checklist-2 (CCC-2). Groups were matched on age and IQ and siblings with autism were excluded. Group mean scores on the CCC-2 differed on only one subscale, syntax. However, siblings of children with autism or PDDNOS were over-represented in the tails of the distributions of several scales, and 10 (24%) scored more than 2 SD below the control mean on a total score based on all 10 subscales. Only two of these 10 children scored above threshold on one or more scales of the Autism Diagnostic Interview-Revised (ADI-R). Children with abnormal scores on the CCC-2 total were characterized by low-verbal IQ and their fathers tended to score high on the social and communication scales of the Autism Quotient, a measure of the broad phenotype in adults. The CCC-2 shows promise as a quick screening device for the broad phenotype in non-autistic siblings of children with autism.

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The AQ appears to be sensitive to the broad phenotype, provided attention is restricted to the social skills and communication scales.

The objective of this study was to evaluate the effectiveness of individual cognitive behavioural therapy (CBT) for post-stroke fatigue and sleep disturbance compared to treatment as usual (TAU). In a parallel two-group pilot randomised controlled trial of 15 participants, nine were allocated to eight weekly sessions of adapted CBT and six continued usual care rehabilitation. The primary outcome was the Fatigue Severity Scale (FSS-7) at two and four months from baseline. Secondary outcomes included measures of sleep, mood and quality of life. Outcomes were assessed by a rater who was blind to group membership. At the four-month endpoint, the CBT group demonstrated significantly reduced fatigue relative to TAU (FSS-7 mean difference: 1.92, 95% CI: 0.24 to 3.60). Significant group differences also emerged for sleep quality and depression, favouring the CBT group. Insomnia and physical quality of life improved immediately post-therapy but were no longer superior to TAU at follow-up. Overall, CBT is a promising treatment for improving post-stroke fatigue, sleep quality and depression. Gains were maintained for two months after therapy cessation and represented large treatment effects. These findings highlight the feasibility of the intervention and warrant extension to a phase III clinical trial.

Although cognitive-behavioural therapy (CBT) is the treatment of choice for anxiety, its delivery needs to be adapted for individuals with traumatic brain injury (TBI). It also requires clients' active engagement for maximum benefit. This study was a pilot randomised controlled trial involving an anxiety treatment programme adapted for people with TBI, based on CBT and motivational interviewing (MI). Twenty-seven participants with moderate/severe TBI (aged 21-73 years, 78% males) recruited from a brain injury rehabilitation hospital were randomly allocated to receive MI + CBT (n = 9), non-directive counselling (NDC) + CBT (n = 10) and treatment-as-usual (TAU) (n = 8). CBT and MI were manualised and delivered in 12 weekly individual sessions. Primary outcome was self-reported anxiety symptoms assessed at baseline, at the end of NDC/MI and immediately following CBT. Assessment was conducted by assessors blinded to group assignment. Intention-to-treat analyses showed that the two active treatment groups demonstrated significantly greater anxiety reduction than TAU. Participants receiving MI showed greater response to CBT, in terms of reduction in anxiety, stress and non-productive coping, compared to participants who received NDC. The results provided preliminary support for the adapted CBT programme, and the potential utility of MI as treatment prelude. Longer follow-up data are required to evaluate the maintenance of treatment effects.

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Two tests of phonological processing, nonword repetition, and nonsense passage reading, were administered to 80 probands with autistic disorder or PDDNOS (index cases) and 59 typically developing controls, together with their parents and siblings. In addition, parents completed a questionnaire about history of language and literacy problems, and all participants were given tests of verbal (VIQ) and performance IQ (PIQ). Parents also completed the Autism-Spectrum Quotient, which was used to index the broad autism phenotype. Index probands scored well below control probands on the two phonological tests. However, on neither phonological measure did index relatives differ from control relatives. Within the index group, there was no relationship between the proband's level of VIQ, or age at achieving phrase speech, and phonological score of relatives. VIQ was the only measure to show any familiality within the index group. Reported history of language and literacy problems did not differentiate index parents from control parents overall, but those who were categorized as cases of the broad phenotype reported more history of language and literacy problems than did other index parents. However, they did not have poorer scores on the phonological measures. It is concluded that phonological processing deficits are not part of the broad autism phenotype.