Behavioural and cognitive behavioural therapy for obsessive compulsive disorder (OCD) in individuals with autism spectrum disorder (ASD).

BACKGROUND: Autistic spectrum disorder (ASD) is an increasingly recognised neurodevelopmental condition; that is, a neurologically-based condition which interferes with the acquisition, retention or application of specific skills. ASD is characterised by challenges with socialisation and communication, and by stereotyped and repetitive behaviours. A stereotyped behaviour is one which is repeated over and over again and which seems not to have any useful function. ASD often co-occurs with mental health disorders, including obsessive compulsive disorder (OCD). People with ASD may show certain cognitive differences (i.e. differences in ways of thinking) which influence their response to therapies. Thus, there is a need for evidence-based guidelines to treat mental health issues in this group. OCD, a common condition characterised by repeated obsessional thoughts and compulsive acts, occurs with greater frequency in persons with ASD than in the general population. Genetic, anatomic, neurobiological and psychological factors have been proposed to explain this co-occurrence. However, care should be taken to distinguish stereotyped and repetitive behaviours characteristic of ASD from obsessive compulsive acts in OCD. Cognitive behavioural therapy (CBT) is the recommended treatment for OCD, but studies have suggested that this treatment may be less effective in those with OCD co-occurring with ASD. Hence, modifications to CBT treatment may be helpful when treating OCD co-occurring with ASD to optimise outcomes. OBJECTIVES: To assess the effectiveness of behavioural and cognitive behavioural therapy for obsessive compulsive disorder (OCD) in children and adults with autism spectrum disorder (ASD). SEARCH METHODS: We searched for studies in the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, Embase, PsycINFO, five other bibliographic databases, international trial registries and other sources of grey literature (to 24 August 2020). We checked the reference lists of included studies and relevant systematic reviews to identify additional studies missed from the original electronic searches. We contacted subject experts for further information when needed. SELECTION CRITERIA: We included randomised controlled trials (RCTs), cross-over, cluster- and quasi-randomised controlled trials involving both adults and children with diagnoses of OCD and ASD. We included studies of participants with co-occurring conditions (i.e. those experiencing other mental illnesses or neurodevelopmental conditions at the same time), but we did not include individuals who had a co-occurring global learning difficulty. Treatment could be in any setting or format and include behavioural therapy (BT) and cognitive behavioural therapy (CBT), which may have been adapted for those with ASD. Comparator interventions included no treatment, waiting list, attention placebo (where the control group receives non-specific aspects of therapy, but not the active ingredient) and treatment as usual (TAU, where the control group receives the usual treatment, according to accepted standards). DATA COLLECTION AND ANALYSIS: Three review authors independently screened studies for inclusion. The authors extracted relevant data from the one eligible study, assessed the risk of bias and certainty of evidence (GRADE). Outcomes of interest were changes in OCD symptoms and treatment completion (primary outcome), and severity of depressive symptoms, anxiety symptoms and behavioural difficulties, as well as degree of family accommodation (secondary outcomes). We did not conduct meta-analyses as only one study met the selection criteria. MAIN RESULTS: We included only one RCT of 46 participants in our analysis. This study compared CBT for OCD in persons with high-functioning ASD with a control group who received anxiety management only. There were no differences in rates of treatment completion between the CBT (87%) and anxiety management (87%) groups (risk ratio (RR) 1.00, 95% confidence interval (CI) 0.80 to 1.25; low-certainty evidence). Behavioural difficulties were not included as an outcome measure in the study. This study showed that there may be a benefit at the end of treatment favouring CBT compared with anxiety management in OCD symptoms (mean difference (MD) -3.00, 95% CI -8.02 to 2.02), depression symptoms (MD -1.80, 95% CI -11.50 to 7.90), anxiety symptoms (MD -3.20, 95% CI -11.38 to 4.98), and quality of life (MD 5.20, 95% CI -1.41 to 11.81), but the evidence was of low certainty.  AUTHORS' CONCLUSIONS: Evidence is limited regarding the efficacy of CBT for treatment of OCD in ASD. There is much scope for future study, not only examining the efficacy of CBT for OCD in ASD, but also the particular ways that OCD manifests in and affects people with ASD and the role of the family in treatment response.

Early detection of subclinical left ventricular myocardial dysfunction in patients with chronic kidney disease.

AIMS: To identify subclinical left ventricular (LV) myocardial dysfunction using speckle tracking echocardiography (STE) in patients with chronic kidney disease (CKD), preserved LV ejection fraction (LVEF), and no cardiovascular history or symptoms. METHODS AND RESULTS: Cross-sectional comparisons of conventional and STE parameters were performed between controls and patients with different stages of CKD. CKD patients were followed up for major adverse cardiovascular events (MACEs). We recruited 106 CKD patients and 38 controls. Mean age was 54.4 ± 15.1 and 36.9 ± 11.5 years, respectively (P < 0.001), with 49.1 vs. 52.6% being female (P = 0.705). There were 29 (27.4%) patients with CKD stages 1/2, 38 (35.8%) with stage 3, and 39 (36.8%) with stages 4/5. Global longitudinal strain (GLS) was more impaired when moving from controls to CKD stages 4/5 (-20.67 ± 3.06, -20.39 ± 2.29, -18.33 ± 3.81, -18.01 ± 2.64, controls vs. CKD stages 1/2, vs. CKD stage 3, vs. CKD stages 4/5, respectively, Padjusted = 0.016), whereas LV twist (16.2 ± 4.8, 18.51 ± 4.36, 19.91 ± 5.35, 24.6 ± 5.35, Padjusted < 0.001) and LV twist rate (101.7 ± 30.3, 110.4 ± 30.1, 121 ± 31.4, 154.8 ± 36.7, Padjusted < 0.001) increased. Risk factor-adjusted GLS (standardized beta ß = -0.245, P = 0.025), strain rate (SR) [global longitudinal strain rates (GLSRs); ß = -0.236, P = 0.019], and early diastolic longitudinal strain rate (GLSRe; ß = 0.247, P = 0.019) were significantly associated with estimated glomerular filtration rate (eGFR), whereas LV twist (ß = -0.432, P < 0.001), LV twist rate (ß = -0.433, P < 0.001), and number of segments with diastolic dysfunction (ß = -340, P < 0.001) were inversely and independently associated with eGFR. Impaired GLS (more than -16%) was observed in almost a quarter of CKD patients and associated with a reduced estimated MACE-free survival at 12-month follow-up (88.5 vs 93.7%, Plogrank = 0.038). CONCLUSION: In CKD patients with no cardiovascular symptoms or history and preserved LVEF, STE can identify subclinical abnormalities of both systolic (decreased GLS and GLSR, increased LV twist, and twist rate) and diastolic (decreased GLSRe and increased number of segments with diastolic dysfunction) LV function.