Review articleEfficacy of beta blockers in the management of problem behaviours in people with intellectual disabilities: A systematic review
Introduction
A high proportion of people with intellectual disabilities (ID) manifest problem behaviours (PB) (Deb, Thomas, & Bright, 2001) which can lead to significant levels of risk and distress for both service users and carers. Aggression to others, property damage, overactivity/impulsivity, stereotyped behaviour and self injuries (SIB) are amongst the commonest behavioural presentations and can be challenging to manage. Thorough assessment and formulation to identify underlying physical/mental illness or environmental precipitants is essential before proceeding to prescribe medication for PBs and pharmacological strategies should be used in conjunction with behavioural management strategies (Deb et al., 2009).
Many PBs are associated with the presence of autistic spectrum disorder (ASD) which occurs in approximately 30% of adults with ID (Morgan et al., 2002). It has been postulated that anxiety is a possible mediating factor in the aetiology of PBs, particularly in people with ID with comorbid ASD (Bradley, Ames, & Bolton, 2011), and various psychotropic medications are widely used to target underlying anxiety and/or irritability. Although low dose antipsychotics such as risperidone are the most favoured pharmacological interventions (Deb, 2013), followed by new generation antidepressants and mood stabilisers, beta blockers are also frequently used in the management of PBs in people with ID, particularly where other drugs have failed (Unwin & Deb, 2008).
Beta-adrenoceptor blocking drugs (beta blockers) are competitive antagonists of noradrenaline and adrenaline action at beta-adrenergic receptor sites. These receptors are present in the peripheral as well as the central nervous system, where cardiac activity and broncho-/vaso- dilation are mediated by beta 1 and beta 2 receptors respectively. Beta blockers differ in their selectivity, with propanolol and nadolol acting on both Beta 1 and Beta 2 receptors and Atenolol and metoprolol selectively acting on beta 1 sites.
Because beta-blockers carry no risk of pharmacological dependence their use has been preferred to many other anti-anxiety drugs (Morgan & Tyrer, 1994). There is some evidence to support the efficacy of beta blockers in the management of generalised anxiety, particularly when associated with physical symptoms of anxiety such as sweating, termor and fast heart rate, and acute stress in the general population (Lader, 1988) although the precise mechanism of action is unknown. A number of hypotheses have been put forward to explain the efficacy of beta blockers in decreasing aggression in patients with psychiatric disorderss. These include central CNS beta blockade in decreasing noradrenergic function (Baumeister & Sevin, 1990), peripheral blockade of overarousal in sympathetic activity (Connor, 1994, Connor et al., 1997, Polakoff et al., 1986), or a combination of the two (Ratey et al., 1992). A role for the use of beta blockers in management of treatment resistant attention-deficit hyperactivity disorder (ADHD) has been suggested and Ratey, Greenberg, and Lindem (1991) reported immediate improvement in symptoms of overarousal, impulsivity, hyperactivity and temper volatility when a beta blocker was added to stimulant medication in three adults with residual ADHD.
There is very limited evidence with regard to the the effectiveness of beta blockers in people with ID (Deb, 2009), and little evaluation of adverse effects when they are prescribed for the management of PBs. Ruedrich and Erhardt (1999) reported that beta blockers are generally effective and well-tolerated in individuals with ID but that they are best used as an adjunct to other psychotropic medications, and should not be considered treatments of choice as monotherapy. Haspel (1995) reviewed the usefulness of beta blockers in the treatment of aggression in a wide range of neurological and psychiatric conditions including profound mental retardation and autism. It was concluded that beta blockers appeared to be effective in reducing the frequency and intensity of aggressive outbursts. Positive effects on rage and violent behaviour in people with organic brain dysfunction have been reported (Greendyke et al., 1986, Sadavoy et al., 2008, Williams et al., 1982).
The objective of the current systematic review was to identify the evidence base regarding the use of beta blockers for the management of PBs in individuals with ID, both with and without ASD. As far as the authors are aware this is the first systematic review examining the use of beta blockers for these indications.
Section snippets
Search strategy
Four electronic databases, namely PsycInfo, MEDLINE, Cochrane, and Embase, were searched for relevant journal articles. The search terms consisted of broad expressions used to describe ID and ASD as well as terms relating to beta blockers and specific beta blocking medications (see Appendix 1). Each database was searched up to September 2012 with no restrictions on the date of publication.
In addition, cross-referencing of pertinent reviews and a hand search for relevant literature were
Results
Of a total of 202 citations, 14 articles met the inclusion criteria (see Fig. 1). Fifty seven studies were excluded on the grounds that these were duplicates; nine were animal studies and eight non-English. Of the subsequent 140 citations, 116 were excluded on abstracts and 10 on full texts. Many of the irrelevant titles were studies involving participants with dementia rather than developmental disorders. Another common reason for exclusion was that target symptoms were physical, in particular
Discussion
Heterogeneity in the characteristics of the populations included and in the methodology used makes it difficult to establish the overall effects of beta blockers. However on the whole many had positive outcomes. The overall quality of research addressing the use of beta blockers for this indication is poor as is reflected in the low quality index scores. No randomised controlled trials (RCTs) were identified and only one of the studies was blinded (Cohen et al., 1991). This was a single case
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