1. Akhondzadeh S, Fallah J, Mohammadi MR, Imani R, Mohammadi M, Salehi B, Ghanizadeh A, Raznahan M, Mohebbi-Rasa S, Rezazadeh SA, Forghani S. {{Double-blind placebo controlled trial of pentoxifylline added to risperidone: Effects on aberrant behavior in children with autism}}. {Prog Neuropsychopharmacol Biol Psychiatry};2009 (Sep 19)
BACKGROUND: There are several lines of evidence to indicate that the immune system plays an important role in the pathophysiology of autism. The objective of this study was to access the effects of pentoxifylline plus risperidone in the treatment of autistic disorder. METHODS: Forty children between the ages four and 12years with a DSM IV-TR clinical diagnosis of autism were recruited. The children presented with a chief complaint of severely disruptive symptoms related to autistic disorder. Patients were randomly allocated to pentoxifylline+risperidone or placebo+risperidone for a 10-week, double-blind, placebo-controlled study. The dose of risperidone was titrated up to 3mg/day, pentoxifylline was titrated to 600mg/day. Patients were assessed at baseline and after 2, 4, 6, 8 and 10weeks of starting medication. The measure of the outcome was the Aberrant Behavior Checklist-Community (ABC-C). RESULTS: The difference between the two protocols was significant as the group that received pentoxifylline had greater reduction in ABC-C subscale scores for Irritability, Lethargy/Social Withdrawal, Stereotypic Behavior, Hyperactivity/Noncompliance and Inappropriate Speech. CONCLUSION: The results suggest that combination of atypical antipsychotic medications and pentoxifylline might have synergistic effects in treatment of behavioral problems of children with autism.
2. Blatt J, Deal AM, Mesibov G. {{Autism in children and adolescents with cancer}}. {Pediatr Blood Cancer};2009 (Sep 22)
BACKGROUND: The causes of autistic disorders (AD) are not known. Abnormalities of tumor suppressor genes have suggested that these genes may be important to the development of autism in some cases, and result in an increased risk of developing cancer or other neoplasms. We explore possible associations between AD and childhood cancer. PROCEDURE: We reviewed our institutional pediatric cancer database for all new cancer diagnoses 1997-2007. Medical records from patients older than 2 years at last visit were reviewed for a diagnosis of AD. The prevalence of AD was estimated for neoplasms overall and for specific tumor types, and compared with that in the general pediatric population. RESULTS: Of 702 eligible patients, 7 (1%; 95% CI: (0.4%, 2.04%)) were labeled as AD, not different than the prevalence of AD in North Carolina’s general population (0.65%, P = 0.35). Cancer diagnoses for these 7 children were acute lymphoblastic leukemia (n = 1), acute nonlymphocytic leukemia (n = 2), non-Hodgkin lymphoma (n = 1), Hodgkin Disease (n = 1), brain tumor (n = 1), osteogenic sarcoma (n = 1). CONCLUSIONS: These data do not suggest that there is a high concordance between AD and childhood cancer. However, studies of large rigorously characterized AD cohorts will be needed to definitively address this issue. Pediatr Blood Cancer. (c) 2009 Wiley-Liss, Inc.
3. Crane L, Goddard L, Pring L. {{Brief Report: Self-defining and Everyday Autobiographical Memories in Adults with Autism Spectrum Disorders}}. {J Autism Dev Disord};2009 (Sep 24)
Autobiographical memory impairments in autism spectrum disorders (ASD) have been attributed to a failure in using the self as an effective memory organisational system. To explore this hypothesis, we compared self-defining and everyday memories in adults with and without ASD. Results demonstrated that both groups were able to distinguish between self-defining and everyday memories, although the ASD group generated fewer specific memories overall. Despite qualitative similarities between the narratives of the two groups, the adults with ASD extracted less meaning from their narratives. Difficulties in eliciting meaning from memories suggests a failure in using past experiences to update the self. We therefore propose that the self-memory relationship might be static, rather than dynamic, in ASD.
4. Currenti SA. {{Understanding and Determining the Etiology of Autism}}. {Cell Mol Neurobiol};2009 (Sep 23)
Worldwide, the rate of autism has been steadily rising. There are several environmental factors in concert with genetic susceptibilities that are contributing to this rise. Impaired methylation and mutations of mecp2 have been associated with autistic spectrum disorders, and related Rett syndrome. Genetic polymorphisms of cytochrome P450 enzymes have also been linked to autism, specifically CYP27B1 that is essential for proper vitamin D metabolism. Vitamin D is important for neuronal growth and neurodevelopment, and defects in metabolism or deficiency have been implicated in autistic individuals. Other factors that have been considered include: maternally derived antibodies, maternal infection, heavy metal exposure, folic acid supplementation, epigenetics, measles, mumps, rubella vaccination, and even electromagnetic radiation. In each case, the consequences, whether direct or indirect, negatively affect the nervous system, neurodevelopment, and environmental responsive genes. The etiology of autism is a topic of controversial debate, while researchers strive to achieve a common objective. The goal is to identify the cause(s) of autism to understand the complex interplay between environment and gene regulation. There is optimism that specific causes and risk factors will be identified. The results of future investigations will facilitate enhanced screening, prevention, and therapy for « at risk » and autistic patients.
5. Gupta S, Rossignol DA. {{Autism spectrum disorders: navigating in uncharted waters}}. {Ann Clin Psychiatry};2009 (Jul-Sep);21(3):129-130.
6. Hammerschlag CA. {{Autistic rider}}. {Caring};2009 (Aug);28(8):62.
7. Kirby RS, Lane JB, Childers J, Skinner SA, Annese F, Barrish JO, Glaze DG, Macleod P, Percy AK. Longevity in Rett Syndrome: Analysis of the North American Database. J Pediatr;2009 (Sep 19)
OBJECTIVE: To determine longevity in Rett syndrome (RTT) from a large cohort. STUDY DESIGN: The North American RTT Database allows the examination of longevity in a large cohort of individuals with RTT from the United States and Canada. This database contains information on 1928 individuals, 85.5% with typical RTT, 13.4% with atypical RTT, and 1.1% with a mutation in the methyl-CpG-binding protein 2 gene (MECP2) but not RTT. Kaplan-Meier analyses were performed to assess longevity. RESULTS: Earlier decennial cohorts exhibited better survival than recent cohorts, with most participants surviving into middle age. Comparing overall survival in persons with typical RTT and atypical RTT revealed greater mortality in typical RTT across the observed lifespan (P < .0001). Comparing survival in persons with RTT and identified MECP2 mutations and persons with unknown MECP2 status demonstrated greater mortality in the latter group (P < .0001, log-rank test). CONCLUSIONS: This analysis provides strong evidence for significant longevity in RTT and indicates the need for careful planning for long-term care of these women. The disproportionately greater survival seen in earlier time periods and in persons with atypical RTT may be attributed to more severely affected individuals dying before diagnosis in the former and to greater numbers with milder variants (ie, preserved speech and delayed onset) in the latter.
8. Shoffner J, Hyams L, Niedziela-Langley G, Cossette S, Mylacraine L, Dale J, Ollis L, Kuoch S, Bennett K, Aliberti A, Hyland K. {{Fever Plus Mitochondrial Disease Could Be Risk Factors for Autistic Regression}}. {J Child Neurol};2009 (Sep 22)
Autistic spectrum disorders encompass etiologically heterogeneous persons, with many genetic causes. A subgroup of these individuals has mitochondrial disease. Because a variety of metabolic disorders, including mitochondrial disease show regression with fever, a retrospective chart review was performed and identified 28 patients who met diagnostic criteria for autistic spectrum disorders and mitochondrial disease. Autistic regression occurred in 60.7% (17 of 28), a statistically significant increase over the general autistic spectrum disorder population (P < .0001). Of the 17 individuals with autistic regression, 70.6% (12 of 17) regressed with fever and 29.4% (5 of 17) regressed without identifiable linkage to fever or vaccinations. None showed regression with vaccination unless a febrile response was present. Although the study is small, a subgroup of patients with mitochondrial disease may be at risk of autistic regression with fever. Although recommended vaccinations schedules are appropriate in mitochondrial disease, fever management appears important for decreasing regression risk.
