1. Dawson G. {{Review: more RCTs on early intensive behavioural intervention for young children with autism spectrum disorders needed}}. {Evid Based Ment Health};2013 (Feb 6)
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2. Hagebeuk EE, Duran M, Abeling NG, Vyth A, Poll-The BT. {{S-adenosylmethionine and S-adenosylhomocysteine in plasma and cerebrospinal fluid in Rett syndrome and the effect of folinic acid supplementation}}. {J Inherit Metab Dis};2013 (Feb 8)
Rett syndrome is a neurodevelopmental disorder characterized by cognitive and locomotor regression and stereotypic hand movements. The disorder is caused by mutations in the X chromosomal MECP2 a gene encoding methyl CpG-binding protein. It has been associated with disturbances of cerebral folate homeostasis, as well as with speculations on a compromised DNA-methylation. Folinic acid is the stable form of folate. Its derived intermediate 5-MTHF supports the conversion of homocysteine to methionine, the precursor of S-adenosylmethionine (SAM). This in turn donates its methyl group to various acceptors, including DNA, thereby being converted to S-adenosylhomocysteine (SAH). The SAM/SAH ratio reflects the methylation potential. The goal of our study was to influence DNA methylation processes and ameliorate the clinical symptoms in Rett syndrome. Therefore we examined the hypothesis that folinic acid supplementation, besides increasing cerebrospinal fluid (CSF) 5-MTHF (p = 0.003), influences SAM and SAH and their ratio. In our randomized, double-blind crossover study on folinic acid supplementation, ten female Rett patients received both folinic acid and placebo for 1 year each. It was shown that both SAM and SAH levels in the CSF remained unchanged following folinic acid administration (p = 0.202 and p = 0.097, respectively) in spite of a rise of plasma SAM and SAH (p = 0.007; p = 0.009). There was no significant change in the SAM/SAH ratio either in plasma or CSF. The apparent inability of Rett patients to upregulate SAM and SAH levels in the CSF may contribute to the biochemical anomalies of the Rett syndrome. Our studies warrant further attempts to promote DNA methylation in the true region of interest, i.e. the brain.
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3. Nuske HJ, Vivanti G, Dissanayake C. {{Are emotion impairments unique to, universal, or specific in autism spectrum disorder? A comprehensive review}}. {Cogn Emot};2013 (Feb 6)
There is widespread belief that individuals with Autism Spectrum Disorders (ASDs) are « emotionally detached » from others. This comprehensive review examines the empirical evidence for this assumption, addressing three critical questions: (1) Are emotion-processing impairments universal in ASD? (2) Are they specific, or can they be explained by deficits in other domains? (3) Is the emotion processing profile seen in ASD unique to these conditions? Upon review of the literature (over 200 studies), we conclude that: (1) emotion-processing impairments might not be universal in ASD, as suggested by variability across participants and across emotion-processing tasks; (2) emotion-processing impairments might not be specific to ASD, as domain-general processes appear to account for some of these impairments; and (3) the specific pattern of emotion-processing strengths and weaknesses observed in ASD, involving difficulties with processing social versus non-social, and complex versus simple emotional information (with impairments more consistently reported on implicit than explicit emotion-processing tasks), appears to be unique to ASD. The emotion-processing profile observed in ASD might be best understood as resulting from heterogeneous vulnerabilities in different components of an « emotional communication system » that, in typical development, emerges from the interplay between domain-general cognitive, social and affective processes.
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4. Russell AJ, Jassi A, Fullana MA, Mack H, Johnston K, Heyman I, Murphy DG, Mataix-Cols D. {{COGNITIVE BEHAVIOR THERAPY FOR COMORBID OBSESSIVE-COMPULSIVE DISORDER IN HIGH-FUNCTIONING AUTISM SPECTRUM DISORDERS: A RANDOMIZED CONTROLLED TRIAL}}. {Depress Anxiety};2013 (Feb 6)
BACKGROUND: High rates of anxiety disorders, particularly obsessive compulsive disorder (OCD) are reported in people with Autism spectrum disorders (ASD). Group cognitive behavioral treatment (CBT) has been found effective for anxiety in young people with ASD but not been OCD specific. One uncontrolled pilot study of individual CBT for OCD for adults with ASD showed good treatment efficacy. METHODS: Forty-six adolescents and adults (mean age 26.9 years, 35 Males) with ASD and comorbid OCD were randomized to CBT for OCD or anxiety management (AM), a plausible control treatment. Treatments were matched in duration (mean of 17.4 sessions CBT; 14.4 sessions AM), the Yale-Brown Obsessive Compulsive Severity Scale (YBOCS) as primary outcome measure and evaluations blind to treatment group. Treatment response was defined as > 25% reduction in YBOCS total severity scores. RESULTS: Both treatments produced a significant reduction in OCD symptoms, within-group effect sizes of 1.01 CBT group and 0.6 for the AM group. There were no statistically significant differences between the two groups at end of treatment, although more responders in the CBT group (45 versus 20%). Effect sizes for self-rated improvement were small (0.33 CBT group; -0.05 AM group). Mild symptom severity was associated with improvement in the AM but not the CBT group. Family/carer factors were important for both groups, in that increased family accommodation was associated with poorer outcome. CONCLUSIONS: Evidence-based psychological interventions, both AM and CBT, were effective in treating comorbid OCD in young people and adults with ASD.
