1. Baker SM. Sidney MacDonald Baker, MD: {{taking a biomedical approach to autism treatment. Interview by Frank Lampe and Suzanne Snyder}}. {Altern Ther Health Med};2008 (Nov-Dec);14(6):60-69.
2. Bland J. {{Autism: asking the right questions to find the right answers}}. {Altern Ther Health Med};2008 (Nov-Dec);14(6):20-21.
3. Blaylock RL. {{A possible central mechanism in autism spectrum disorders, part 1}}. {{Altern Ther Health Med}};2008 (Nov-Dec);14(6):46-53.
The autism spectrum disorders (ASD) are a group of related neurodevelopmental disorders that have been increasing in incidence since the 1980s. Despite a considerable amount of data being collected from cases, a central mechanism has not been offered. A careful review of ASD cases discloses a number of events that adhere to an immunoexcitotoxic mechanism. This mechanism explains the link between excessive vaccination, use of aluminum and ethylmercury as vaccine adjuvants, food allergies, gut dysbiosis, and abnormal formation of the developing brain. It has now been shown that chronic microglial activation is present in autistic brains from age 5 years to age 44 years. A considerable amount of evidence, both experimental and clinical, indicates that repeated microglial activation can initiate priming of the microglia and that subsequent stimulation can produce an exaggerated microglial response that can be prolonged. It is also known that one phenotypic form of microglia activation can result in an outpouring of neurotoxic levels of the excitotoxins, glutamate and quinolinic acid. Studies have shown that careful control of brain glutamate levels is essential to brain pathway development and that excesses can result in arrest of neural migration, as well as dendritic and synaptic loss. It has also been shown that certain cytokines, such as TNF-alpha, can, via its receptor, interact with glutamate receptors to enhance the neurotoxic reaction. To describe this interaction I have coined the term immunoexcitotoxicity, which is described in this article.
4. Bromley RL, Mawer G, Clayton-Smith J, Baker GA, On behalf of the Liverpool and Manchester Neurodevelopment Group. {{Autism Spectrum Disorders Following in Utero Exposure to Antiepileptic Drugs}}. {Neurology};2008 (Dec 2);71(23):1923-1924.
5. Cave SF. {{The history of vaccinations in the light of the autism epidemic}}. {Altern Ther Health Med};2008 (Nov-Dec);14(6):54-57.
Autism has been characterized as a behavioral disorder since it was first described by Leo Kanner in 1943. The number of autistic children has increased over the last decade. The incidence of autism was 1 in 10000 before the 1970s and has steadily increased to 1 in 150 in 2008 with a male:female predominance of 4:1. The cause of this epidemic has remained unknown, but several hypotheses have been studied. Many of these suggest an environmental trigger, such as the ethyl mercury contained in the preservative thimerosal, which has been used in vaccines since 1931. Other possible triggers associated with vaccinations are chemical toxins and live viruses. James has published studies suggesting a genetic predisposition in the families of autistic children, exposing them to a deficiency in glutathione and an inability to detoxify heavy metals. Vargas has shown autism to encompass ongoing inflammation in the brains of autistic children. The Hannah Poling vaccine decision was a landmark case. Poling’s family was awarded funds for ongoing medical care of an autistic child who was found to have mitochondrial dysfunction exacerbated by vaccines that left her with autistic behavior and seizures. Several studies have emerged supporting the fact that a significant number of autistic children do have mitochondrial dysfunction. The impact that the Poling case will have on the ability of parents of autistic children to gain access to funds to enable them to properly care for their children remains to be seen.
6. Field SS. Omega-3 {{Fatty acids, prematurity, and autism}}. {Pediatrics};2008 (Dec);122(6):1416-1417.
7. Fragala-Pinkham M, Haley SM, O’Neil ME. {{Group aquatic aerobic exercise for children with disabilities}}.{ Dev Med Child Neurol};2008 (Nov);50(11):822-827.
The effectiveness and safety of a group aquatic aerobic exercise program on cardiorespiratory endurance for children with disabilities was examined using an A-B study design. Sixteen children (11 males, five females) age range 6 to 11 years (mean age 9y 7mo [SD 1y 4mo]) participated in this twice-per-week program lasting 14 weeks. The children’s diagnoses included autism spectrum disorder, myelomeningocele, cerebral palsy, or other developmental disability. More than half of the children ambulated independently without aids. Children swam laps and participated in relay races and games with a focus of maintaining a defined target heart rate zone. The strengthening component consisted of exercises using bar bells, aquatic noodles, and water resistance. The following outcomes were measured: half-mile walk/run, isometric muscle strength, timed floor to stand 3-meter test, and motor skills. Complaints of pain or injury were systematically collected. Significant improvements in the half-mile walk/run were observed, but not for secondary outcomes of strength or motor skills. The mean program attendance was 80%, and no injury was reported. Children with disabilities may improve their cardiorespiratory endurance after a group aquatic aerobic exercise program with a high adult:child ratio and specific goals to maintain training heart rates.
8. Giunco CT, Moretti-Ferreira D, Silva AE, Rocha SS, Fett-Conte AC. {{MOMO syndrome associated with autism: a case report}}. {Genet Mol Res};2008;7(4):1223-1225.
This is a case report of macrosomia, obesity, macrocephaly and ocular abnormalities (MOMO syndrome) associated with autism. Studies on genetic or environmental syndromes associated with autism can provide genetic markers or uncover relevant events, and are very important for the definition of autism subgroups in future molecular research.
9. Herbert MR. {{Learning from the autism catastrophe: key leverage points}}. {Altern Ther Health Med};2008 (Nov-Dec);14(6):28-30.
10. Hyman MA. {{Autism: is it all in the head?}} {Altern Ther Health Med};2008 (Nov-Dec);14(6):12-15.
11. Kogan MD, Strickland BB, Blumberg SJ, Singh GK, Perrin JM, van Dyck PC. {{A national profile of the health care experiences and family impact of autism spectrum disorder among children in the United States, 2005-2006}}. {Pediatrics};2008 (Dec);122(6):e1149-1158.
OBJECTIVES. We sought to examine the health care experiences of children with autism spectrum disorder and the impact of autism spectrum disorder on the family and to assess whether having a medical home is associated with less family impact. METHODS. We used the 2005-2006 National Survey of Children With Special Health Care Needs to compare 2088 children with special health care needs, aged 3 to 17 years, reported by their parents to have autism spectrum disorder, with children with special health care needs with « other emotional, developmental, or behavioral problems » (excluding autism spectrum disorder; n = 9534) and 26751 other children with special health care needs. We used weighted logistic regression to examine unmet needs for specific health care and support services, delayed care, no usual care source or personal physician, difficulty receiving referrals, and financial, employment, or time problems because of child’s care. RESULTS. Nationally, an estimated 535000 children have special health care needs and autism spectrum disorder, a prevalence of 86 per 10000 children aged 3 to 17 years. Among children with special health care needs, 5.6% have autism spectrum disorder. Compared with other children with special health care needs without emotional, developmental, or behavioral problems, children with special health care needs with autism spectrum disorder were more likely to have unmet needs for specific health care services, family support services, delayed or foregone care, difficulty receiving referrals, and care that is not family centered. Children with special health care needs with autism spectrum disorder were more likely to live in families that report financial problems, need additional income for the child’s medical care, reduce or stop work because of the child’s condition, spend >/=10 hours per week providing or coordinating care, and paid more than $1000 in the previous year for the child’s care. The financial impacts of autism spectrum disorder were significantly more burdensome when children with special health care needs did not have a medical home. CONCLUSIONS. Children with special health care needs with autism spectrum disorder are significantly more likely to have problems regarding access to care and unmet needs, and their families have greater financial, employment, and time burdens compared with other children with special health care needs. Receipt of primary care in a medical home may reduce these burdens.
12. Lind SE, Bowler DM. {{Delayed Self-recognition in Children with Autism Spectrum Disorder}}. {J Autism Dev Disord};2008 (Dec 3)
This study aimed to investigate temporally extended self-awareness (awareness of one’s place in and continued existence through time) in autism spectrum disorder (ASD), using the delayed self-recognition (DSR) paradigm (Povinelli et al., Child Development 67:1540-1554, 1996). Relative to age and verbal ability matched comparison children, children with ASD showed unattenuated performance on the DSR task, despite showing significant impairments in theory-of-mind task performance, and a reduced propensity to use personal pronouns to refer to themselves. The results may indicate intact temporally extended self-awareness in ASD. However, it may be that the DSR task is not an unambiguous measure of temporally extended self-awareness and it can be passed through strategies which do not require the possession of a temporally extended self-concept.
13. Lindell AK, Notice K, Withers K. {{Reduced language processing asymmetry in non-autistic individuals with high levels of autism traits}}. {Laterality};2008 (Dec 3):1-16.
In the normal population the left hemisphere’s predominance for language processing is well established. However, in disorders such as autism atypical patterns of hemispheric lateralisation are common. Given increasing recognition of the idea that autism represents a continuum, we investigated whether the reduced/absent hemispheric asymmetry for language processing extended into the normal population at the upper end of the autism spectrum. A total of 51 participants completed the AQ questionnaire (Baron-Cohen et al., 2001), and a lateralised lexical decision task assessing identification of concrete and abstract words. Based on the clinical finding of decreased hemispheric asymmetry in people with autism, we anticipated reduced hemispheric lateralisation in non-autistic people with higher levels of autism traits. Consistent with prediction, whereas people with lower AQ scores showed a clear right visual field (left hemisphere) advantage for word/nonword discrimination, people with higher AQ scores showed equivalent performance for the left and right visual fields. Our data indicate reduced left hemisphere language dominance in people with higher levels of autism traits, just as people with a clinical diagnosis of autism show atypical lateralisation. Moreover, the data offer further support for the notion that autism is a continuum, rather than a categorical diagnosis, with atypical patterns of hemispheric asymmetry being characteristic of people at the upper end of the spectrum.
14. Mayor-Dubois C, Maeder-Ingvar M, Deonna T, Roulet-Perez E. {{The role of epilepsy in early language development in a child with a congenital lesion in the right hemisphere}}. {Dev Med Child Neurol};2008 (Nov);50(11):870-875.
Early epilepsy is known to worsen the developmental prognosis of young children with a congenital focal brain lesion, but its direct role is often very difficult to delineate from the other variables. This requires prolonged periods of follow-up with simultaneous serial electrophysiological and developmental assessments which are rarely obtained. We studied a male infant with a right prenatal infarct in the territory of the right middle cerebral artery resulting in a left spastic hemiparesis, and an epileptic disorder (infantile spasms with transient right hemihypsarrhythmia and focal seizures) from the age of 7 months until the age of 4 years. Pregnancy and delivery were normal. A dissociated delay of early language acquisition affecting mainly comprehension without any autistic features was documented. This delay was much more severe than usually expected in children with early focal lesions, and its evolution, with catch-up to normal, was correlated with the active phase of the epilepsy. We postulate that the epilepsy specifically amplified a pattern of delayed language emergence, mainly affecting lexical comprehension, reported in children with early right hemisphere damage.
15. Nijmeijer JS, Hoekstra PJ, Minderaa RB, Buitelaar JK, Altink ME, Buschgens CJ, Fliers EA, {{Rommelse NN, Sergeant JA, Hartman CA. PDD Symptoms in ADHD, an Independent Familial Trait?}} {J Abnorm Child Psychol};2008 (Dec 3)
The aims of this study were to investigate whether subtle PDD symptoms in the context of ADHD are transmitted in families independent of ADHD, and whether PDD symptom familiality is influenced by gender and age. The sample consisted of 256 sibling pairs with at least one child with ADHD and 147 healthy controls, aged 5-19 years. Children who fulfilled criteria for autistic disorder were excluded. The Children’s Social Behavior Questionnaire (CSBQ) was used to assess PDD symptoms. Probands, siblings, and controls were compared using analyses of variance. Sibling correlations were calculated for CSBQ scores after controlling for IQ, ADHD, and comorbid anxiety. In addition, we calculated cross-sibling cross-trait correlations. Both children with ADHD and their siblings had higher PDD levels than healthy controls. The sibling correlation was 0.28 for the CSBQ total scale, with the CSBQ stereotyped behavior subscale showing the strongest sibling correlation (r = 0.35). Sibling correlations remained similar in strength after controlling for IQ and ADHD, and were not confounded by comorbid anxiety. Sibling correlations were higher in female than in male probands. The social subscale showed stronger sibling correlations in elder than in younger sibling pairs. Cross-sibling cross-trait correlations for PDD and ADHD were weak and not-significant. The results confirm that children with ADHD have high levels of PDD symptoms, and further suggest that the familiality of subtle PDD symptoms in the context of ADHD is largely independent from ADHD familiality.
16. O’Hara NH, Szakacs GM. {{The recovery of a child with autism spectrum disorder through biomedical interventions}}. {Altern Ther Health Med};2008 (Nov-Dec);14(6):42-44.
17. Pagnamenta AT, Wing K, Akha ES, Knight SJ, Bolte S, Schmotzer G, Duketis E, Poustka F, Klauck SM, Poustka A, Ragoussis J, Bailey AJ, Monaco AP. {{A 15q13.3 microdeletion segregating with autism}}. {Eur J Hum Genet};2008 (Dec 3)
Autism and mental retardation (MR) show high rates of comorbidity and potentially share genetic risk factors. In this study, a rare approximately 2 Mb microdeletion involving chromosome band 15q13.3 was detected in a multiplex autism family. This genomic loss lies between distal break points of the Prader-Willi/Angelman syndrome locus and was first described in association with MR and epilepsy. Together with recent studies that have also implicated this genomic imbalance in schizophrenia, our data indicate that this CNV shows considerable phenotypic variability. Further studies should aim to characterise the precise phenotypic range of this CNV and may lead to the discovery of genetic or environmental modifiers.European Journal of Human Genetics advance online publication, 3 December 2008; doi:10.1038/ejhg.2008.228.
18. Parner ET, Schendel DE, Thorsen P. {{Autism prevalence trends over time in denmark: changes in prevalence and age at diagnosis}}. {Arch Pediatr Adolesc Med};2008 (Dec);162(12):1150-1156.
OBJECTIVE: To examine the effect of changing age at diagnosis on the diagnosed prevalence of autism among different birth cohorts. DESIGN: Population-based cohort study. SETTING: Children were identified in the Danish Medical Birth Registry and psychiatric outcomes were obtained via linkage with the Danish National Psychiatric Register. PARTICIPANTS: All children born in Denmark from January 1, 1994, through December 31, 1999 (N = 407 458). MAIN OUTCOME MEASURES: The age-specific prevalence, hazard ratio, and relative risk by age. RESULTS: Statistically significant shifts in age at diagnosis were observed for autism spectrum disorder; children diagnosed before age 9 years in the cohorts born between January 1, 1994, and December 31, 1995, between January 1, 1996, and December 31, 1997, and between January 1, 1998, and December 31, 1999, were on average diagnosed at ages 5.9 (95% confidence interval [CI], 5.8-6.0), 5.8 (95% CI, 5.7-5.9), and 5.3 (95% CI, 5.2-5.4) years, respectively. The relative risk comparing the 1996-1997 birth cohort with the 1994-1995 birth cohort at age 3 years was 1.20 (95% CI, 0.86-1.67), which decreased to 1.10 (95% CI, 1.00-1.20) at age 11 years. Similarly, the relative risk comparing the 1998-1999 birth cohort with the 1994-1995 birth cohort at age 3 years was 1.69 (95% CI, 1.24-2.31), which decreased to 1.23 (95% CI, 1.11-1.37) at age 11 years. Similar results were observed for childhood autism. CONCLUSIONS: Shifts in age at diagnosis inflated the observed prevalence of autism in young children in the more recent cohorts compared with the oldest cohort. This study supports the argument that the apparent increase in autism in recent years is at least in part attributable to decreases in the age at diagnosis over time.
19. Paylor R, Yuva-Paylor LA, Nelson DL, Spencer CM. {{Reversal of sensorimotor gating abnormalities in Fmr1 knockout mice carrying a human Fmr1 transgene}}. {Behav Neurosci};2008 (Dec);122(6):1371-1377.
Fragile X syndrome is caused by a CGG trinucleotide repeat expansion of the FMR1 gene. Individuals with fragile X display several behavioral abnormalities including hyperactivity, social anxiety, autistic-like features, impaired cognitive processing, and impaired sensorimotor gating. The Fmr1KO mouse model of fragile X exhibits several related behavioral phenotypes such as increased activity and altered social interactions. Individuals with fragile X also have impaired sensorimotor gating as measured using the prepulse inhibition of startle response. The authors have recently shown that Fmr1KO mice with a yeast artificial chromosome containing the human FMR1 gene have corrected or overcorrected abnormal behaviors including hyperactivity and altered social interactions. Here the authors present results from a study examining abnormal sensorimotor gating in Fmr1KO mice. Consistent with previous findings, Fmr1KO mice have increased prepulse inhibition. The KO mice with the yeast artificial chromosome containing the human FMR1 gene had levels of prepulse inhibition comparable to WT mice, indicating not only a correction of this phenotype, but also clearly demonstrating that in mice levels of the fragile X mental retardation protein regulate sensorimotor gating. (PsycINFO Database Record (c) 2008 APA, all rights reserved).
20. Ramelli GP, Silacci C, Ferrarini A, Cattaneo C, Visconti P, Pescia G. {{Microduplication 22q11.2 in a child with autism spectrum disorder: clinical and genetic study}}. {Dev Med Child Neurol};2008 (Dec);50(12):953-955.
Microduplication of the 22q11.2 chromosomal region has been recognized since 1999 and has been associated with a highly variable phenotype. Neurodevelopmental impairment and behavioural problems are very common in patients with 22q11.2 duplication. Autism spectrum disorders (ASDs) have previously been reported in only two patients with 22q11.2 duplication and striking dysmorphic features. We report here on a 4-year-old male of healthy consanguineous parents presenting with ASD according to DSMIV, revised, criteria as a primary manifestation. The child walked at 16 months and started to say one word and some sounds. Parents noticed a subsequent developmental arrest. At 4 years his functional development age, evaluated by the Psychoeducational Profile, was roughly 6 months. Mild non-specific facial dysmorphism was noted. Genetic analyses of the child demonstrated a de novo microduplication of the 22q11.2 chromosomal region. This genetic anomaly was best seen in interphases of blood lymphocytes and in buccal smear nuclei. Our case illustrates once again the clinical heterogeneity of the 22q11.2 duplication as well as the wide genetic complexity of ASD. We suggest that genetic evaluation of ASD should include fluorescence in-situ hybridization analysis of the 22q11.2 chromosomal region.
21. Towle PO, Visintainer PF, O’Sullivan C, Bryant NE, Busby S. {{Detecting Autism Spectrum Disorder from Early Intervention Charts: Methodology and Preliminary Findings}}. {J Autism Dev Disord};2008 (Dec 2)
22. Williams ME, Atkins M, Soles T. {{Assessment of Autism in Community Settings: Discrepancies in Classification}}. {J Autism Dev Disord};2008 (Dec 3)
Review of 78 evaluations for 29 young children examined practices used in assessment of autism spectrum disorders in three settings: public schools, developmental disabilities eligibility determinations, and our hospital-based early childhood mental health program. While similar rates of classification of autism spectrum disorders were found across sites, the rate of agreement by different evaluators for individual children was only 45%. Further, most community evaluators did not follow best practice guidelines nor use autism diagnostic tools with established psychometric properties. In this sample of primarily Latino, Spanish-speaking children, most community evaluators did not document assessment of the child in their native language, nor address the impact of language in their assessments.
