1. Antonio N, Costanza C, Paolo FP, Umberto B, Filippo M. {{Non- Pharmacological Treatments in Autism Spectrum Disorders: An Overview on Early Interventions for Pre-schoolers}}. {Curr Clin Pharmacol}. 2013.
This paper evaluates the current literature on non-pharmacological early interventions [behavior behavioral, developmental and educational approaches] for pre-schoolers [aged 24-71 months] with autism spectrum disorders. Although there lies a significant heterogeneity among the available studies, the present review emphasizes the importance of considering the wide range of interventions through behavioral [behavioral or developmental interventions] and educational continuum according to the suggestions of the recent literature in this field. Furthermore, the present review: 1] outlines the issues about the scientific validity of the treatment outcome studies; 2] describes the findings of different parent-mediated interventions; 3] highlights the importance to use the same outcome measures through the studies to compare findings of different literature contributes; and 4] focuses on the importance to consider pre-treatment variables to identify children who will have better outcomes. Furthermore, some evidence-based guidelines about clinical management and treatment have also been outlined and summarized in this review. Finally, the review concludes on providing a number of practical recommendations to clinicians working in the field suggesting both the presence of a specialized team and role of an active collaboration of the family to treatment as core milestones for the clinical management.
2. Carigi T, Muratori F, Termine C, Veggiotti P, Derhemi L, Nardo RD, Rossi G, Poli PF, Balottin U. {{Diagnostic Boundaries of Autism Disorder Vs Pervasive Developmental Disorder Nos: Comparative Observational Study and Literature Review}}. {Curr Clin Pharmacol}. 2013.
Diagnosis of pervasive developmental disorders (PDDs), and above all diagnosis of the different PDD subtypes, is an ongoing challenge in psychopathology. Application of categorical criteria is complex and problematic in the clinical field where the boundaries dividing some of the PDD entities are blurred, creating particular problems for the clinician. A dimensional clinical approach, considering autistic symptom severity, level of functioning, developmental characteristics and symptoms other than the ones typically observed in autism, may be a more suitable approach in the clinical field and could provide the clinician treating these disorders with empirical guidance. To identify the clinical features that might differentiate the PDD subtypes, we conducted a comparative study in a clinical sample of children affected by autism disorder (AD) or pervasive developmental disorders not otherwise specified (PDD-NOS) and a mini critical review of the available literature addressing clinical and psychopathological differences between the two subtypes. The results of both our study and our literature review seem to show little support for the current PDD subtypes. In such a framework, the most significant element in clinical practice appears to be a deep knowledge of the characteristics of the individual in question. By adopting a broad and multi-faceted perspective, it becomes possible to define the most effective rehabilitation treatment. This applies particularly to the pharmacological treatment, since, to date, no specific therapies for PDDs are known and the choice of pharmacotherapy can be decided only on the basis of the patient’s general profile and specific features.
3. Chapleau CA, Lane J, Pozzo-Miller L, Percy AK. {{Evaluation of current pharmacological treatment options in the management of Rett syndrome: From the present to future therapeutic alternatives}}. {Curr Clin Pharmacol}. 2013.
Neurodevelopmental disorders are a large family of conditions of genetic or environmental origin that are characterized by deficiencies in cognitive and behavioral functions. The therapeutic management of individuals with these disorders is typically complex and is limited to the treatment of specific symptoms that characterize each disorder. The neurodevelopmental disorder Rett syndrome (RTT) is the leading cause of severe intellectual disability in females. Mutations in the gene encoding the transcriptional regulator methyl-CpG-binding protein 2 (MECP2), located on the X chromosome, have been confirmed in more than 95% of individuals meeting diagnostic criteria for classical RTT. RTT is characterized by an uneventful early infancy followed by stagnation and regression of growth, motor, language, and social skills later in development. This review will discuss the genetics, pathology, and symptoms that distinguish RTT from other neurodevelopmental disorders associated with intellectual disability. Because great progress has been made in the basic and clinical science of RTT, the goal of this review is to provide a thorough assessment of current pharmacotherapeutic options to treat the symptoms associated with this disorder. Furthermore, we will highlight recent discoveries made with novel pharmacological interventions in experimental preclinical phases, and which have reversed pathological phenotypes in mouse and cell culture models of RTT and may result in clinical trials.
4. Erickson CA, Wink LK, Early MC, Stiegelmeyer E, Mathieu-Frasier L, Patrick V, McDougle CJ. {{Brief Report: Pilot Single-Blind Placebo Lead-In Study of Acamprosate in Youth with Autistic Disorder}}. {J Autism Dev Disord}. 2013.
RATIONALE: An excitatory/inhibitory (E:I) imbalance marked by enhanced glutamate and deficient gamma-aminobutyric acid (GABA) neurotransmission may contribute to the pathophysiology of autism spectrum disorders (ASD). OBJECTIVES: We report on the first single-blind placebo lead-in trial of acamprosate, a drug with putative mechanisms restoring E:I imbalance, in twelve youth with ASD. MATERIALS AND METHODS: We conducted a 12-week single-blind, placebo lead-in study of acamprosate in youth age 5-17 years with autistic disorder. RESULTS: Six of nine subjects who received active drug treatment were deemed treatment responders (defined by a score at final visit of « very much improved » or « much improved » on the Clinical Global Impressions Improvement scale) and >/=25 % improvement on the Aberrant Behavior Checklist Social Withdrawal subscale. CONCLUSION: Future larger-scale dose finding studies of acamprosate in ASD may be warranted given this preliminary indication of benefit.
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5. Marti LF. {{Dietary Interventions in Children with Autism Spectrum Disorders- An Updated Review of The Research Evidence}}. {Curr Clin Pharmacol}. 2013.
Autism Spectrum Disorders (ASD) is a group of life-long neurodevelopmental disorders, with onset before 3 years of age. They are characterized by qualitative impairment in social interactions, absent or impaired language and communication skills, and present with a wide range of stereotyped, repetitive behaviors. Function and outcome is affected not only by core deficits but by associated behaviors such as hyperactivity, aggression, anxiety, and depression. Increasing evidence indicates that autism is a complex, multifactorial disorder involving the brain and the body, a result of genetic vulnerabilities interacting with environmental factors. Although genetics play a role, the fact, that the incidence of autism in identical twins is not a 100% points to external or environmental factors as contributors 77. No etiology – based treatment has yet been developed. During the last two decades many educational, psychosocial and pharmacological interventions had been utilized and claimed to be effective and even « curative ». The word treatment should be used with caution, and should stand for interventions that are aimed to help people with ASD to adjust more effectively to their environment 23. Many studies have indicated that behavioral therapy and medication may be at least partially helpful in the treatment of children with ASD particularly on the symptoms of aggression, hyperactivity and attention. In the light of an approved and well established treatment for ASD, over the past two decades research on the effect of diet and nutrition on autism has been increasing. Particular attention has focused on the role of food additives, refined sugar, food allergies, and fatty acid metabolism. However, the results are conflicting and not conclusive. We present here an updated review summarizing the potentials and limits of the most frequent nutritional and dietary interventions in the treatment of Autism Spectrum Disorders.
6. Rossignol DA, Frye RE. {{Melatonin in Autism Spectrum Disorders}}. {Curr Clin Pharmacol}. 2013.
Melatonin is an endogenous neurohormone produced predominantly in the pineal gland. Recent studies have implicated abnormalities in melatonin physiology and the circadian rhythm in individuals with autism spectrum disorders (ASD). These physiological abnormalities include lower nighttime melatonin or melatonin metabolite concentrations in ASD compared to controls. These abnormalities in melatonin concentrations may be directly attributed to variations in melatonin pathway physiology as both functional and genetic variations in this pathway have been reported in children with ASD. Four studies have observed a correlation between abnormal melatonin concentrations and the severity of autistic behaviors. Twenty clinical studies have reported improvements in sleep parameters with exogenous melatonin supplementation in ASD, including longer sleep duration, less nighttime awakenings and quicker sleep onset. A recent meta-analysis of five randomized, double-blind, placebo-controlled crossover trials examining exogenous melatonin supplementation in ASD reported significant improvements with large effect sizes in total sleep duration and sleep onset latency compared to both baseline and placebo. Six studies reported that the nighttime administration of exogenous melatonin was associated with better daytime behaviors. Four studies reported improvements with exogenous melatonin supplementation when other sleep medications had previously failed. Adverse effects of melatonin were minimal to none in the twenty treatment studies. These studies indicate that the administration of exogenous melatonin for abnormal sleep parameters in ASD is evidence-based. Further studies examining optimal effective dosing and timing of dosing are warranted.
7. Sochocky N, Milin R. {{Second Generation Antipsychotics in Asperger’s Disorder and High Functioning Autism: A Systematic Review of The Literature and Effectiveness Meta-Analysis}}. {Curr Clin Pharmacol}. 2013.
Objective: Second generation antipsychotics (SGA) have gained increased evidence for the treatment of irritability and aggression in children and adolescents with lower functioning autistic disorder. Individuals with Asperger’s Disorder (AD) and High Functioning Autism (HFA) experience significant emotional and behavioural problems and psychiatric comorbidity. There is a need to review the published literature on SGA treatment efficacy in the AD and HFA populations to provide more effective treatment choices for these subgroups. Methods: We conducted a systematic review and meta-analysis of the recent English literature on SGA use in children and adolescents (ages 0-24 years) with AD and HFA using the Medline/PubMed and PsychINFO computerized databases. Key search words were ‘Asperger’, ‘high functioning autism’, ‘autism spectrum disorders (ASD)’, and ‘pervasive developmental disorder (PDD)’ in combination with ‘second generation antipsychotics’, ‘aripiprazole; ‘olanzapine’, ‘quetiapine’, ‘risperidone’, or ‘ziprasidone’. Results: Our search yielded 214 citations, however only open-label or randomized-controlled trials (RCT) with >/=25% of their subjects having an IQ>/=71 were included in our review. Eleven original studies met our inclusion parameters for review; eight studies for the meta-analysis. These studies, although limited in methodological rigor, and the meta-analytic results suggest that SGAs provide improvement in behavioural symptoms associated with AD and HFA. The majority of the studies reported weight gain as a potentially concerning adverse effect. Conclusion: There is a lack of robustly conducted trials on the use of SGAs in the management of AD and HFA. More research in pharmacological and psychosocial treatments is warranted. Clinicians are cautioned to approach pharmacological treatment prudently balancing benefit with potential cardiometabolic risk.
