Self-injury, aggression and destruction in children with severe intellectual disability: Incidence, persistence and novel, predictive behavioural risk markers.

BACKGROUND: A risk informed, early intervention strategy for self-injurious, aggressive and destructive behaviours in children with severe intellectual disability is gaining support. The aims of this study were to establish the cumulative incidence and persistence of self-injury, aggression and destruction and the relationship between these behaviours and two potentially predictive behavioural risk markers (repetitive behaviour, and impulsivity and overactivity) in children at high risk. METHODS: In a longitudinal design self-injury, aggression and destruction were assessed by teachers of 417 children with severe intellectual disability on two occasions separated by 15-18 months. RESULTS: Aggression, destruction and self-injury were persistent (69%, 57% and 58% respectively). Repetitive and restricted behaviours and interests (RRBI) and overactivity/impulsivity (O/I) were significantly associated with aggression (O/I OR=1.291, p<.001), destruction (RRBI OR 1.201, p=.013; O/I OR 1.278, p<.001) and/or self-injury (RRBI, OR 1.25, p=.004; O/I OR=1.117, p<.001). The relative risk of the cumulative incidence of self-injury, aggression and destruction was significantly increased by repetitive and restricted behaviours and interests (self-injury 2.66, destruction 2.16) and/or overactivity/impulsivity (aggression 2.42, destruction 2.07). CONCLUSIONS: The results provide evidence that repetitive and restricted behaviours and interests, and overactivity/impulsivity, are risk markers for the onset of self-injury, aggression and destruction within the already high risk group of children with severe intellectual disability.

Correlates of self-injurious, aggressive and destructive behaviour in children under five who are at risk of developmental delay.

AIM: Several behavioural correlates of self-injury, aggression and destructive behaviour have been identified in children and young adults with intellectual disabilities. This cross-sectional study aimed to further explore these correlates in very young children with developmental delay. METHODS: Parents of 56 children (40 male) under the age of five years (mean age 2 years 10 months) completed a questionnaire about their child's behaviour and the presence of behavioural correlates, including repetitive, over-active or impulsive behaviour and more severe developmental delay. RESULTS: Parents reported very high prevalence of self-injurious, aggressive and destructive behaviour: 51%, 64% and 51%, respectively. A binary logistic regression revealed that a higher score on a measure of overactive and impulsive behaviour significantly predicted the presence of destructive behaviour. A multiple linear regression revealed that both repetitive behaviour and number of health problems approached significance as independent predictors of severe self-injurious behaviour. INTERPRETATION: Despite the very small sample, several factors emerged as potential predictors of self-injurious, aggressive and destructive behaviour. These findings support the need for further investigation in a larger sample. Confirmation in this age group could help guide the development of targeted early intervention for these behaviours by identifying behavioural risk markers.

The influence of genetic explanations of type 2 diabetes on patients' attitudes to prevention, treatment and personal responsibility for health.

BACKGROUND/AIMS: It is widely accepted that type 2 diabetes is caused by an interaction of both lifestyle and genetic factors. However, the impact of explaining disease aetiology as primarily genetic or environmental is relatively unexplored for common chronic multi-factorial conditions. This study investigates whether perceiving the cause of type 2 diabetes as primarily genetic or environmental influences attitudes towards the controllability of the condition. METHODS: Using a between-participants vignette-based experimental survey design, 200 participants aged 40 years and above from a primary care setting responded to a vignette which implied the cause of diabetes as being predominantly genetic or environmental. Attitudes towards personal responsibility, prevention and treatment were measured using an attitude questionnaire. RESULTS: There was a significant interaction effect between perceived aetiology and family history on attitude to treatment; participants with a family history of type 2 diabetes perceived treatment as less effective if they read the genetic vignette, but those without a family history did not (p < 0.05). The findings also indicated that an individual was perceived as less responsible for the development of type 2 diabetes (p < 0.05) when participants (regardless of family history) read a vignette with an implied genetic causation. CONCLUSION: Awareness by health professionals of the impact of genetic attributions in disease aetiology is fundamental when encouraging positive attitudes to personal responsibility for lifestyle change and treatment for the condition. These findings may impact the way preventative health messages are tailored to people depending on their family history of diabetes.

The role of the pedunculopontine region in basal-ganglia mechanisms of akinesia.

The akinesia of Parkinsonism is relieved by pallidotomy and subthalamic nucleotomy, but not by thalamotomy. Therefore, this disabling symptom probably depends upon connections other than the pallidalthalamocortical tracts, possibly efferents of the medial pallidum descending to the upper brainstem. We have previously demonstrated akinesia in the normal monkey following radiofrequency lesioning in the region of the pedunculopontine nucleus (PPN), one of the primary targets for descending pallidal outflow. Here, we confirm that selectively destroying neurones in the PPN area, whilst sparing fibres of passage, results in an akinetic state in normal macaques.

Lateral pallidotomy exacerbates akinesia in the Parkinsonian patient.

Despite the recent resurgence of interest in the use of pallidotomy for the treatment of Parkinson's disease, there remains considerable debate about the optimal lesion site. Although the current understanding of the neural mechanisms underlying Parkinsonism would suggest that the medial pallidum is the logical site for alleviation of symptoms, some surgeons still advocate lesions in the lateral pallidum. We report the case of such a lesion placement verified pathologically, which resulted in exacerbation of akinesia postoperatively. This demonstrates that accurate targeting in the pallidum is critical to avoid exacerbation of symptoms by lesioning the lateral pallidum.

The pallidotomy debate.

It has been suggested that image-guidance and macro-stimulation alone are not sufficiently accurate to result in safe and effective lesion localization in pallidotomy for Parkinson's disease when compared with micro-electrode recording. This review analyses the data in the series published to date, and compares the safety and efficacy of the two techniques, finding no evidence to support this claim. In addition, evidence regarding the necessary accuracy of lesion placement is reviewed.