1. Bass MM, Duchowny CA, Llabre MM. {{The Effect of Therapeutic Horseback Riding on Social Functioning in Children with Autism}}. {J Autism Dev Disord};2009 (Apr 7)
This study evaluated the effects of therapeutic horseback riding on social functioning in children with autism. We hypothesized that participants in the experimental condition (n = 19), compared to those on the wait-list control (n = 15), would demonstrate significant improvement in social functioning following a 12-weeks horseback riding intervention. Autistic children exposed to therapeutic horseback riding exhibited greater sensory seeking, sensory sensitivity, social motivation, and less inattention, distractibility, and sedentary behaviors. The results provide evidence that therapeutic horseback riding may be a viable therapeutic option in treating children with autism spectrum disorders.
2. Senecky Y, Chodick G, Diamond G, Lobel D, Drachman R, Inbar D. {{Time trends in reported autistic spectrum disorders in Israel, 1972-2004}}. {Isr Med Assoc J};2009 (Jan);11(1):30-33.
BACKGROUND: Studies from many countries have reported an increasing prevalence of autistic spectrum disorder in childhood. No comprehensive epidemiological studies of ASD have been performed in Israel. OBJECTIVES: To describe time trends in the reported number of patients with ASD in Israel and to characterize the demographic features of the reported patients. METHODS: We reviewed the charts of the National Insurance Institute of Israel from 1972 to 2004 for all children with a diagnosis of ASD receiving disability benefits. RESULTS: A total of 3509 children met the study criteria. Eighty percent were boys and 98% were Jewish. The incidence data showed an increase in the number of cases from zero in 1982-84 and 2 (1.2 per million capita under 18 years) in 1985 to a high of 428 cases in 2004 (190 per million). CONCLUSIONS: This is the first comprehensive study of the incidence of ASD in Israel. According to data derived from official health records, the rate of occurrence of ASD has substantially increased in the last 20 years. Further studies are needed to determine if this is a true increase or if the findings were confounded by external factors, such as recent improvements in diagnostic measures and social stigmas.
3. Zeev BB, Bebbington A, Ho G, Leonard H, de Klerk N, Gak E, Vecksler M, Christodoulou J. {{The common BDNF polymorphism may be a modifier of disease severity in Rett syndrome}}. {Neurology};2009 (Apr 7);72(14):1242-1247.
BACKGROUND: Rett syndrome (RTT) is caused by mutations in the transcriptional repressor methyl CpG-binding protein 2 (MECP2). Brain-derived neurotrophic factor (BDNF) is a neurotrophic factor playing a major role in neuronal survival, neurogenesis, and plasticity, and it has been shown that BDNF expression is regulated by MeCP2 through a complex interaction. A common polymorphism of BDNF (Val66Met [p.V66M]) has been found to correlate with severity and course of several neuropsychiatric disorders. METHODS: We examined the association between disease severity score, assessed by the modified Percy score, and BDNF polymorphism, using regression methods, in 125 mutation-positive patients with RTT from the Australian Rett Syndrome Database and an Israeli cohort. RESULTS: Those who were heterozygous (Val/Met) had slightly more severe disease than those who were homozygous for the wild-type (Val/Val) BDNF polymorphism (increased severity score 2.1, p = 0.09). In those with p.R168X, a commonly occurring MECP2 mutation in RTT, there was a 6-point increase in severity score for those who were heterozygous for the BDNF polymorphism, both unadjusted (p = 0.02) and adjusted for age (p = 0.03). Individuals with the p.R168X mutation and heterozygous for the BDNF polymorphism were also at an increased risk of seizure onset (hazard ratio 5.3, 95% confidence interval 1.6-17.7) compared with those homozygous for the wild-type BDNF allele. CONCLUSIONS: In addition to mutation type and degree of X-chromosome skewing, the common brain-derived neurotrophic factor (BDNF) polymorphism appears to be another genetic modifier of Rett syndrome (RTT) severity. This suggests that BDNF function may play a significant role in the pathogenesis of RTT.
