1. {{Association of estrogen receptor alpha polymorphisms with symptoms of autism among Chinese Han children}}. {Neuro Endocrinol Lett};2016 (Nov 19);37(6):439-444.
OBJECTIVES: Autism has a significant sex difference. This implies that the sex hormones might have effect on autism. Estrogens play an important role in early nervous system development and sex differentiation through estrogen receptors in brain. Thus, we tested the hypothesis that estrogen receptor alpha (ESR1) gene affects the pathogenesis of autism and related symptoms. METHODS: Genotypes of rs11155819 and rs2234693 were determined in boys with autism and normal boys from Chinese Han population. A case-control study was performed to explore the association between polymorphisms in ESR1 gene and autism susceptibility. Assessment tool was used to evaluate the neuropsychological developmental level of autistic children. Finally, we analyzed the association of these single nucleotide polymorphisms (SNPs) with specific symptoms. RESULTS: The results showed no significant differences between cases and controls in the distribution of genotypes and allele frequencies of the two SNPs. However, rs11155819 TT genotype showed a lower neuropsychological development level among autistic children, especially in the aspects of fine motor and adaptation ability (p=0.028; p=0.042). CONCLUSION: Polymorphisms of ESR1 are relevant to autism symptoms in Chinese Han children.
2. de Vries M, Verdam MG, Prins PJ, Schmand BA, Geurts HM. {{Exploring possible predictors and moderators of an executive function training for children with an autism spectrum disorder}}. {Autism};2017 (Mar 01):1362361316682622.
Previously, a total of 121 children with an autism spectrum disorder (ASD) performed an adaptive working memory (WM)-training, an adaptive flexibility-training, or a non-adaptive control (mock)-training. Despite overall improvement, there were minor differences between the adaptive and mock-training conditions. Moreover, dropout was relatively high (26%). In the current study we explored potential predicting and moderating factors to clarify these findings. The effects of intelligence, autism traits, WM, flexibility, reward sensitivity and Theory of Mind on dropout, improvement during training, and improvement in everyday executive functioning (EF), ASD-like behavior, and Quality of Life (QoL) were studied. None of the predictors influenced dropout or training improvement. However, 1) more pre-training autism traits related to less improvement in EF and QoL, and 2) higher reward sensitivity was related to more improvement in QoL and ASD-like behavior. These findings suggest that these EF-training procedures may be beneficial for children with fewer autism traits and higher reward sensitivity. However, the exploratory nature of the analyses warrant further research before applying the findings clinically.
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3. Ellis SE, Gupta S, Moes A, West AB, Arking DE. {{Exaggerated CpH methylation in the autism-affected brain}}. {Mol Autism};2017;8:6.
BACKGROUND: The etiology of autism, a complex, heritable, neurodevelopmental disorder, remains largely unexplained. Given the unexplained risk and recent evidence supporting a role for epigenetic mechanisms in the development of autism, we explored the role of CpG and CpH (H = A, C, or T) methylation within the autism-affected cortical brain tissue. METHODS: Reduced representation bisulfite sequencing (RRBS) was completed, and analysis was carried out in 63 post-mortem cortical brain samples (Brodmann area 19) from 29 autism-affected and 34 control individuals. Analyses to identify single sites that were differentially methylated and to identify any global methylation alterations at either CpG or CpH sites throughout the genome were carried out. RESULTS: We report that while no individual site or region of methylation was significantly associated with autism after multi-test correction, methylated CpH dinucleotides were markedly enriched in autism-affected brains (~2-fold enrichment at p < 0.05 cutoff, p = 0.002). CONCLUSIONS: These results further implicate epigenetic alterations in pathobiological mechanisms that underlie autism. Lien vers le texte intégral (Open Access ou abonnement)
4. Endres D, Tebartz van Elst L, Meyer SA, Feige B, Nickel K, Bubl A, Riedel A, Ebert D, Lange T, Glauche V, Biscaldi M, Philipsen A, Maier SJ, Perlov E. {{Glutathione metabolism in the prefrontal brain of adults with high-functioning autism spectrum disorder: an MRS study}}. {Mol Autism};2017;8:10.
BACKGROUND: Autism spectrum disorder (ASD) is a neurodevelopmental disease characterized by difficulties in social communication, unusually restricted, repetitive behavior and interests, and specific abnormalities in language and perception. The precise etiology of ASD is still unknown and probably heterogeneous. In a subgroup of patients, toxic environmental exposure might lead to an imbalance between oxidative stress and anti-oxidant systems. Previous serum and postmortem studies measuring levels of glutathione (GSH), the main cellular free radical scavenger in the brain, have supported the hypothesis that this compound might play a role in the pathophysiology of autism. METHODS: Using the method of single-voxel proton magnetic resonance spectroscopy (MRS), we analyzed the GSH signal in the dorsal anterior cingulate cortex (dACC) and the dorsolateral prefrontal cortex (DLPFC) of 24 ASD patients with normal or above average IQs and 18 matched control subjects. We hypothesized that we would find decreased GSH concentrations in both regions. RESULTS: We did not find overall group differences in neurometabolites including GSH, neither in the dorsal ACC (Wilks’ lambda test; p = 0.429) nor in the DLPFC (p = 0.288). In the dACC, we found a trend for decreased GSH signals in ASD patients (p = 0.076). CONCLUSIONS: We were unable to confirm our working hypothesis regarding decreased GSH concentrations in the ASD group. Further studies combining MRS, serum, and cerebrospinal fluid measurements of GSH metabolism including other regions of interest or even whole brain spectroscopy are needed.
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5. Garipardic M, Dogan M, Bala KA, Mutluer T, Kaba S, Aslan O, Ustyol L. {{Association of Attention Deficit Hyperactivity Disorder and Autism Spectrum Disorders with Mean Platelet Volume and Vitamin D}}. {Med Sci Monit};2017 (Mar 20);23:1378-1384.
BACKGROUND The purpose of this study was to assess the values of the mean platelet volume (MPV) in children with attention deficit hyperactivity disorder (ADHD) and with autism spectrum disorders (ASDs) to determine the risk of cardiovascular disease in these 2 disorder groups. MATERIAL AND METHODS The study included a total of 79 patients with ADHD or ASDs and controls in the Van region of Turkey. The control group included subjects of matching age and sex with no ADHD, ASDs, or chronic disease and taking no vitamins. The hematological parameters of the patients, including MPV, vitamin B12, and vitamin D, were assessed. RESULTS The study included a total of 79 children and adolescents aged 2-18 years (32 females and 47 males). Of the patients, 36 were in the ADHD group, 18 in the ASDs group, and 25 in the control group. There was no statistically significant difference in hematological parameters between the groups, but there were significant differences in terms of vitamin D and vitamin B12. The patient groups showed lower levels of vitamin B12 and vitamin D. In the ADHD group, there was a negative correlation between both vitamins and MPV (p<0.05). Partial correlation analysis of the ADHD group showed that MPV in particular was negatively correlated to vitamin D, and not to vitamin B12 (p: 0.03). CONCLUSIONS Both ADHD and ASDs may accompany increased risk for cardiovascular disease due to the presence of vitamin B12 and D deficiency and their own characteristics. Therefore, these disorders should be closely followed up. Lien vers Pubmed
6. Liu X, Li Z, Fan C, Zhang D, Chen J. {{Genetics implicate common mechanisms in autism and schizophrenia: synaptic activity and immunity}}. {J Med Genet};2017 (Mar 17)
The diagnosis of debilitating psychiatric disorders like autism spectrum disorder (ASD) and schizophrenia (SCHZ) is on the rise. These are severe conditions that lead to social isolation and require lifelong professional care. Improved diagnosis of ASD and SCHZ provides early access to medication and therapy, but the reality is that the mechanisms and the cellular pathology underlying these conditions are mostly unknown at this time. Although both ASD and SCHZ have strong inherited components, genetic risk seems to be distributed in hundreds of variants, each conferring low risk. The poor understanding of the genetics of ASD and SCHZ is a significant hurdle to developing effective treatments for these costly conditions. The recent implementation of next-generation sequencing technologies and the creation of large consortia have started to reveal the genetic bases of ASD and SCHZ. Alterations in gene expression regulation, synaptic architecture and activity and immunity seem to be the main cellular mechanisms contributing to both ASD and SCHZ, a surprising overlap given the distinct phenotypes and onset of these conditions. These diverse pathways seem to converge in aberrant synaptic plasticity and remodelling, which leads to altered connectivity between relevant brain regions. Continuous efforts to understand the genetic basis of ASD and SCHZ will soon lead to significant progress in the mechanistic understanding of these prominent psychiatric disorders and enable the development of disease-modifying therapies for these devastating conditions.
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7. Macari SL, Koller J, Campbell DJ, Chawarska K. {{Temperamental markers in toddlers with autism spectrum disorder}}. {J Child Psychol Psychiatry};2017 (Mar 20)
BACKGROUND: Although temperament has been recognized as an important contributor to childhood psychopathology, its role in emergent autism spectrum phenotypes is not well understood. This study examined whether toddlers with autism spectrum disorder (ASD) display temperamental vulnerabilities compared to toddlers with other developmental challenges, whether these characteristics are distinct from core autism symptoms, if they are stable over time, and if they contribute to social outcomes in preschool. METHODS: Parents of 165 toddlers with ASD, 58 nonverbal ability- and chronological age- (CA) matched developmentally delayed (DD) toddlers, and 92 CA-matched typically developing (TD) toddlers completed the Toddler Behavior Assessment Questionnaire-Supplemental (TBAQ-S) at 26 months (SD = 6; Time 1). TBAQ-S data were also available for a subset of toddlers with ASD (n = 126) at 43 months (SD = 9; Time 2). RESULTS: Compared to the DD and TD groups, toddlers with ASD exhibited vulnerabilities within the Effortful Control domain as well as the Surgency domain. They also displayed greater Negative Emotionality compared to TD peers. In the ASD group, temperamental characteristics were not concurrently related to autism severity or developmental level and individual differences were highly stable over time. Changes in Perceptual Sensitivity, Inhibitory Control, and Low-Intensity Pleasure from age 2 to 3.5 uniquely predicted autism symptom severity and adaptive social skill level at Time 2. CONCLUSIONS: Temperamental vulnerabilities in toddlers with ASD are stable over time and involve attentional and behavioral control as well as affective reactivity. They contribute uniquely to social outcomes in preschool and are likely to signal risk for developing later maladaptive attentional, affective, and behavioral symptoms. Considering biologically based dimensions may shed light on noncore facets of the early ASD phenotype that are potentially relevant to the emergence of comorbid conditions later in childhood.
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8. Meng J, Li Z, Shen L. {{Responses to others’ pain in adults with autistic traits: The influence of gender and stimuli modality}}. {PLoS One};2017;12(3):e0174109.
Individuals with autism-spectrum disorder (ASD) exhibit impairments in response to others’ pain. Evidence suggests that features of autism are not restricted to individuals with ASD, and that autistic traits vary throughout the general population. To investigate the association between autistic traits and the responses to others’ pain in typically developing adults, we employed the Autism-Spectrum Quotient (AQ) to quantify autistic traits in a group of 1670 healthy adults and explored whether 60 participants (30 males and 30 females) with 10% highest AQ scores (High-AQ) would exhibit difficulties in the responses to others’ pain relative to 60 participants (30 males and 30 females) with 10% lowest AQ scores (Low-AQ). This study included a Visual Task and an Auditory Task to test behavioral differences between High-AQ and Low-AQ groups’ responses to others’ pain in both modalities. For the Visual Task, participants were instructed to respond to pictures depicting others’ pain. They were instructed to judge the stimuli type (painful or not), judge others’ pain intensity, and indicate the unpleasantness they personally felt. For the Auditory Task, experimental procedures were identical to the Visual Task except that painful voices were added. Results showed the High-AQ group was less accurate than the Low-AQ group in judging others’ pain. Moreover, relative to Low-AQ males, High-AQ males had significantly longer reaction times in judging others’ pain in the Auditory Task. However, High-AQ and Low-AQ females showed similar reaction times in both tasks. These findings demonstrated identification of others’ pain by healthy adults is related to the extent of autistic traits, gender, and modality.
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9. Mennella R, Leung RC, Taylor MJ, Dunkley BT. {{Disconnection from others in autism is more than just a feeling: whole-brain neural synchrony in adults during implicit processing of emotional faces}}. {Mol Autism};2017;8:7.
BACKGROUND: Socio-emotional difficulties in autism spectrum disorder (ASD) are thought to reflect impaired functional connectivity within the « social brain ». Nonetheless, a whole-brain characterization of the fast responses in functional connectivity during implicit processing of emotional faces in adults with ASD is lacking. METHODS: The present study used magnetoencephalography to investigate early responses in functional connectivity, as measured by interregional phase synchronization, during implicit processing of angry, neutral and happy faces. The sample (n = 44) consisted of 22 young adults with ASD and 22 age- and sex-matched typically developed (TD) controls. RESULTS: Reduced phase-synchrony in the beta band around 300 ms emerged during processing of angry faces in the ASD compared to TD group, involving key areas of the social brain. In the same time window, de-synchronization in the beta band in the amygdala was reduced in the ASD group across conditions. CONCLUSIONS: This is the first demonstration of atypical global and local synchrony patterns in the social brain in adults with ASD during implicit processing of emotional faces. The present results replicate and substantially extend previous findings on adolescents, highlighting that atypical brain synchrony during processing of socio-emotional stimuli is a hallmark of clinical sequelae in autism.
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10. Taylor MJ, Gillberg C, Lichtenstein P, Lundstrom S. {{Etiological influences on the stability of autistic traits from childhood to early adulthood: evidence from a twin study}}. {Mol Autism};2017;8:5.
BACKGROUND: Autism spectrum disorders (ASD) are persistent and lifelong conditions. Despite this, almost all twin studies focus on childhood. This twin study investigated the stability of autistic traits from childhood to early adulthood and explored the degree to which any stability could be explained by genetic or environmental factors. METHODS: Parents of over 2500 twin pairs completed questionnaires assessing autistic traits when twins were aged either 9 or 12 years and again when twins were aged 18. Bivariate twin analysis assessed the degree of phenotypic and etiological stability in autistic traits across this period. Genetic overlap in autistic traits across development was also tested in individuals displaying a broad ASD phenotype, defined as scoring within the highest 5% of the sample. RESULTS: Autistic traits displayed moderate phenotypic stability (r = .39). The heritability of autistic traits was 76-77% in childhood and 60-62% in adulthood. A moderate degree of genetic influences on childhood autistic traits were carried across into adulthood (genetic correlation = .49). The majority (85%) of the stability in autistic traits was attributable to genetic factors. Genetic influences on autistic traits were moderately stable from childhood to early adulthood at the extremes (genetic correlation = .64). CONCLUSIONS: Broad autistic traits display moderate phenotypic and etiological stability from childhood to early adulthood. Genetic factors accounted for almost all phenotypic stability, although there was some phenotypic and etiological instability in autistic traits. Thus, autistic traits in adulthood are influenced by a combination of enduring and unique genetic factors.
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11. van Schalkwyk GI, Volkmar FR. {{Autism Spectrum Disorders: Challenges and Opportunities for Transition to Adulthood}}. {Child Adolesc Psychiatr Clin N Am};2017 (Apr);26(2):329-339.
Improved outcomes for individuals with autism spectrum disorder (ASD) have opened a range of potential pathways during the transition to adulthood. These include attending college, entering the labor force, and achieving a degree of independent living. Less cognitively able individuals may be eligible for state benefits and may enter supported employment programs. Those attending college require careful support and planning. Practitioners need to be familiar with the unique needs of young adults with ASD. Further research should attempt to define the priorities of individuals and families with ASD making this transition and clarify the value of existing supports and interventions.
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12. Vuillermot S, Luan W, Meyer U, Eyles D. {{Vitamin D treatment during pregnancy prevents autism-related phenotypes in a mouse model of maternal immune activation}}. {Mol Autism};2017;8:9.
BACKGROUND: Prenatal exposure to infection is a recognized environmental risk factor for neuropsychiatric disorders of developmental origins such as autism or schizophrenia. Experimental work in animals indicates that this link is mediated by maternal immune activation (MIA) involving interactions between cytokine-associated inflammatory events, oxidative stress, and other pathophysiological processes such as hypoferremia and zinc deficiency. Maternal administration of the viral mimic polyriboinosinic-polyribocytidylic acid (poly(I:C)) in mice produces several behavioral phenotypes in adult offspring of relevance to autism spectrum disorder (ASD) and other neurodevelopmental disorders. METHODS: Here, we investigated whether some of these phenotypes might also present in juveniles. In addition, given the known immunomodulatory and neuroprotective effects of vitamin D, we also investigated whether the co-administration of vitamin D could block MIA-induced ASD-related behaviors. We co-administered the hormonally active form of vitamin D, 1alpha,25 dihydroxy vitamin D3 (1,25OHD), simultaneously with poly(I:C) and examined (i) social interaction, stereotyped behavior, emotional learning and memory, and innate anxiety-like behavior in juveniles and (ii) the levels of the pro-inflammatory cytokines IL-1beta, IL-6 and TNF-alpha in maternal plasma and fetal brains. RESULTS: We show that like adult offspring that were exposed to MIA, juveniles display similar deficits in social approach behavior. Juvenile MIA offspring also show abnormal stereotyped digging and impaired acquisition and expression of tone-cued fear conditioning. Importantly, our study reveals that prenatal administration of 1,25OHD abolishes all these behavioral deficits in poly(I:C)-treated juveniles. However, prenatal administration of vitamin D had no effect on pro-inflammatory cytokine levels in dams or in fetal brains suggesting the anti-inflammatory actions of vitamin D are not the critical mechanism for its preventive actions in this ASD animal model. CONCLUSIONS: This work raises the possibility that early dietary supplementation with vitamin D may open new avenues for a successful attenuation or even prevention of neurodevelopmental disorders following maternal inflammation during pregnancy.
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13. Wang J, Ethridge LE, Mosconi MW, White SP, Binder DK, Pedapati EV, Erickson CA, Byerly MJ, Sweeney JA. {{A resting EEG study of neocortical hyperexcitability and altered functional connectivity in fragile X syndrome}}. {J Neurodev Disord};2017;9:11.
BACKGROUND: Cortical hyperexcitability due to abnormal fast-spiking inhibitory interneuron function has been documented in fmr1 KO mice, a mouse model of the fragile X syndrome which is the most common single gene cause of autism and intellectual disability. METHODS: We collected resting state dense-array electroencephalography data from 21 fragile X syndrome (FXS) patients and 21 age-matched healthy participants. RESULTS: FXS patients exhibited greater gamma frequency band power, which was correlated with social and sensory processing difficulties. Second, FXS patients showed increased spatial spreading of phase-synchronized high frequency neural activity in the gamma band. Third, we observed increased negative theta-to-gamma but decreased alpha-to-gamma band amplitude coupling, and the level of increased theta power was inversely related to the level of resting gamma power in FXS. CONCLUSIONS: Increased theta band power and coupling from frontal sources may represent a mechanism providing compensatory inhibition of high-frequency gamma band activity, potentially contributing to the widely varying level of neurophysiological and behavioral abnormalities and treatment response seen in full-mutation FXS patients. These findings extend preclinical observations and provide new mechanistic insights into brain alterations and their variability across FXS patients. Electrophysiological measures may provide useful translational biomarkers for advancing drug development and individualizing treatments for neurodevelopmental disorders with associated neuronal hyperexcitability.
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14. Wojcik S, Bernatsky S, Platt RW, Pineau CA, Clarke AE, Fombonne E, Berard A, Vinet E. {{Risk of autism spectrum disorders in children born to mothers with rheumatoid arthritis: A systematic literature review}}. {Arthritis Care Res (Hoboken)};2017 (Mar 20)
OBJECTIVE: Recent evidence suggests in utero exposure to maternal antibodies and cytokines as important risk factors for autism spectrum disorders (ASD). We aimed to systematically review the risk of ASD in children born to mothers with rheumatoid arthritis (RA) compared to children born to mothers without RA. METHODS: We conducted a systematic review of original articles using electronic databases: PubMed, EMBase, and Web of Science. RESULTS: Our literature search identified a total of 70 articles. Of the potentially relevant studies retrieved, 67 were excluded for lack of relevance and/or because they did not report original data. Three studies were included in the final analysis. A case-control study was unable to detect a difference in the prevalence of RA in ASD mothers versus control mothers. Another case-control study showed a statistically significant 8-fold increase in autoimmune disorders, including RA, in mothers of ASD offspring compared to controls. Forty-six percent of ASD offspring had a first-degree relative with RA compared to 26% of controls. Moreover, in a population-based cohort study, investigators observed an increased risk of ASD in children with a maternal history of RA compared to children born to unaffected mothers. These studies had methodological limitations: none controlled for medication exposures, only 1 controlled for obstetrical complications and considered the timing of RA diagnosis in relation to pregnancy, and all but 1 used a case-control study design. CONCLUSION: Observational studies suggest a potentially increased risk of ASD in children born to mothers with RA compared to children born to unaffected mothers, although data are limited. This article is protected by copyright. All rights reserved.
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15. Wolff JJ, Swanson MR, Elison JT, Gerig G, Pruett JR, Jr., Styner MA, Vachet C, Botteron KN, Dager SR, Estes AM, Hazlett HC, Schultz RT, Shen MD, Zwaigenbaum L, Piven J. {{Neural circuitry at age 6 months associated with later repetitive behavior and sensory responsiveness in autism}}. {Mol Autism};2017;8:8.
BACKGROUND: Restricted and repetitive behaviors are defining features of autism spectrum disorder (ASD). Under revised diagnostic criteria for ASD, this behavioral domain now includes atypical responses to sensory stimuli. To date, little is known about the neural circuitry underlying these features of ASD early in life. METHODS: Longitudinal diffusion tensor imaging data were collected from 217 infants at high familial risk for ASD. Forty-four of these infants were diagnosed with ASD at age 2. Targeted cortical, cerebellar, and striatal white matter pathways were defined and measured at ages 6, 12, and 24 months. Dependent variables included the Repetitive Behavior Scale-Revised and the Sensory Experiences Questionnaire. RESULTS: Among children diagnosed with ASD, repetitive behaviors and sensory response patterns were strongly correlated, even when accounting for developmental level or social impairment. Longitudinal analyses indicated that the genu and cerebellar pathways were significantly associated with both repetitive behaviors and sensory responsiveness but not social deficits. At age 6 months, fractional anisotropy in the genu significantly predicted repetitive behaviors and sensory responsiveness at age 2. Cerebellar pathways significantly predicted later sensory responsiveness. Exploratory analyses suggested a possible disordinal interaction based on diagnostic status for the association between fractional anisotropy and repetitive behavior. CONCLUSIONS: Our findings suggest that restricted and repetitive behaviors contributing to a diagnosis of ASD at age 2 years are associated with structural properties of callosal and cerebellar white matter pathways measured during infancy and toddlerhood. We further identified that repetitive behaviors and unusual sensory response patterns co-occur and share common brain-behavior relationships. These results were strikingly specific given the absence of association between targeted pathways and social deficits.
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16. Wongpakaran R, Suansanae T, Tan-Khum T, Kraivichian C, Ongarjsakulman R, Suthisisang C. {{Impact of providing psychiatry specialty pharmacist intervention on reducing drug-related problems among children with autism spectrum disorder related to disruptive behavioural symptoms: A prospective randomized open-label study}}. {J Clin Pharm Ther};2017 (Mar 20)
WHAT IS KNOWN AND OBJECTIVES: Psychopharmacologic therapy has so far focused on ameliorating disruptive behaviours to improve patient’s function and quality of life. Due to the complicated neurobiological aetiology of autism spectrum disorder (ASD), a traditional pharmacist intervention may be insufficient to initiate the optimal care for this vulnerable population. We evaluate the impact of providing specialty psychiatry (PS) pharmacist intervention in identifying and resolving drug-related problems (DRPs) among children with ASD associated with disruptive behaviours. METHODS: An eight-week-long, prospective, randomized open-label study was conducted. Children between 2.5 and 12 years of age with ASD and showing disruptive behaviours were included. They were randomly assigned to an intervention or a control group. Patients in the intervention group received pharmacist interventions delivered by a PS pharmacist, while those in control group were cared by a hospital pharmacist. The primary outcome was the number of patients who resolved of at least one DRP by the end of the study. The secondary outcome was to compare the mean Aberrant Behavior Checklist-Irritability (ABC-I) scores between the two groups. RESULTS: Twenty-five patients were randomly assigned to either an intervention or control group. At week 8, the total number of patients who resolved of at least one DRP was 13 (52%) in the intervention group and 4 (16%) in the control group, respectively (P=.016). Improper drug selection, medication non-adherence and subtherapeutic dosage were the most common DRPs. Mean ABC-I scores improved in the intervention group more than in the control group (9.8+/-5.6 vs 17.7+/-7.9; P<.001). WHAT IS NEW AND CONCLUSION: To the best of our knowledge, this is the first study which demonstrated that PS pharmacist intervention is an effective strategy to resolve DRPs in patient with ASD. The reduction in common DRPs mostly resulted from the PS pharmacist interventions, including selection of antipsychotic agent, adjustment of dosage based on ABC-I scores and provision of individualized drug counselling. Reducing DRPs led to the improvement of any disruptive behaviour. In addition, multidisciplinary team should develop drug therapy protocols to promote the role of pharmacists in this setting. Lien vers le texte intégral (Open Access ou abonnement)
17. Yamamuro K, Tsujii N, Ota T, Kishimoto T, Iida J. {{Pharmacotherapy for the treatment of aggression in pediatric and adolescent patients with autism spectrum disorder comorbid attention-deficit/hyperactivity disorder: a questionnaire survey of 571 psychiatrists}}. {Psychiatry Clin Neurosci};2017 (Mar 20)
AIMS: Both attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) are frequently accompanied by serious aggression that requires psychiatric treatment. However, little is known about the experiences psychiatrists have had using pharmacotherapy to treat aggression in patients who have both ASD and ADHD (ASD/ADHD). The purpose of this study was to examine the experiences of Japanese child and adolescent psychiatrists in prescribing medication for aggression in patients with ASD/ADHD. METHODS: A prospective questionnaire was mailed to 2,001 psychiatrists affiliated with the Japanese Society for Child and Adolescent Psychiatry. Multivariate logistic regression analysis was used to identify factors predicting the outcome of pharmacotherapeutic treatment of aggression in pediatric and adolescent patients with ASD/ADHD. RESULTS: Of 2,001 psychiatrists, 571 (28.5%) completed the full questionnaire (final sample). Of these, 488 (85.4%) prescribed psychotropic medication in treating pediatric and adolescent patients with ASD/ADHD, 299 (61.3%) of them doing so to treat aggression. Prescribers’ duration of practice (odds ratio [OR]: 1.055; P = 0.038) and patient symptoms of residual impulsivity (OR, 2.479; P = 0.039) increased the odds of prescribing psychotropic medications to treat aggression in these patients. The respondents reported a similar effect for patients with ADHD/ASD compared with those with ADHD only in treating aggression. CONCLUSIONS: Japanese psychiatrists tended to prescribe psychotropic medication for aggression in pediatric and adolescent patients with ASD/ADHD. Future studies examining aggression in pediatric and adolescent patients with ASD/ADHD should aim to accumulate evidence for the use of psychotropic medications, which could help clinicians make better decisions.
