1. Akdemir D, Pehlivanturk B, Unal F, Ozusta S. {{[Comparison of attachment-related social behaviors in autistic disorder and developmental disability.]}}. {Turk Psikiyatri Derg};2009 (Summer);20(2):105-117.Otistik Bozukluk ve Gelisim Geriliginde Baglanmaya Yonelik Sosyal Davranislarin Karsilastirilmasi.
OBJECTIVE: This study examined social behaviors related to attachment in children with autistic disorder and the differences in these behaviors from those observed in developmentally disabled children. Additionally, we aimed to investigate the relationship between attachment behaviors and clinical variables, such as age, cognitive development, severity of autism, language development, and mothers’ attachment styles. METHOD: The study group consisted of 19 children with autistic disorder (mean age: 37.9 +/- 6.8 months) and the control group consisted of 18 developmentally disabled children without autistic disorder that were matched with respect to age, gender, and cognitive development. The Childhood Autism Rating Scale (CARS) was administered to all the children by two child psychiatrists. Mothers completed the Relationships Scale Questionnaire (RSQ). Cognitive development of the children was assessed with the Stanford-Binet intelligence scale. Attachment behaviors of the children were evaluated with a modified Strange Situation Procedure (SSP). RESULTS: Attachment behaviors in the children with autistic disorder and in the children with developmental disabilities were similar. In contrast to the developmentally disabled group, the children with autistic disorder stayed closer toward their mothers compared with their responses to strangers. In the autistic disorder group, attachment behaviors were not associated with age, intelligence quotient, or mothers’ attachment styles; however, a significant relationship between the severity of autism and the presence of speech was observed. CONCLUSION: Parents’ understanding of the attachment needs and the attachment behaviors of their autistic children in the early stages of the disorder may lead to more secure attachment relationships and improved social development.
2. Atkinson AP. {{Impaired recognition of emotions from body movements is associated with elevated motion coherence thresholds in autism spectrum disorders}}. {Neuropsychologia};2009 (Jun 2)
Recent research has confirmed that individuals with Autism Spectrum Disorder (ASD) have difficulties in recognizing emotions from body movements. Difficulties in perceiving coherent motion are also common in ASD. Yet it is unknown whether these two impairments are related. Thirteen adults with ASD and 16 age- and IQ-matched typically developing (TD) adults classified basic emotions from point-light and full-light displays of body movements and discriminated the direction of coherent motion in random-dot kinematograms. The ASD group was reliably less accurate in classifying emotions regardless of stimulus display type, and in perceiving coherent motion. As predicted, ASD individuals with higher motion coherence thresholds were less accurate in classifying emotions from body movements, especially in the point-light displays; this relationship was not evident for the TD group. The results are discussed in relation to recent models of biological motion processing and known abnormalities in the neural substrates of motion and social perception in ASD.
3. Ulay HT, Ertugrul A. {{[Neuroimaging findings in autism: a brief review.]}}. {Turk Psikiyatri Derg};2009 (Summer);20(2):164-174.Otizmde Beyin Goruntuleme Bulgulari: Bir Gozden Gecirme.
OBJECTIVE: Many structural and functional neuroimaging studies have investigated the neuroanatomical changes and possible pathophysiological pathways in autism. In this review the objective was to assess, with an integrative perspective, recent neuroimaging studies that have contributed to the explanation of the possible pathophysiological pathways in autism. METHOD: Relevant attainable studies published between 1997 and 2007 were included in this retrospective literature review. The PubMed search engine and the keywords, autism, autistic spectrum disorders, neuroimaging, computerized tomography, magnetic resonance imaging, functional magnetic resonance imaging, magnetic resonance spectroscopy, positron emission tomography, single photon emission computed tomography, and diffusion tensor imaging were used. RESULTS: Structural neuroimaging studies reported an increase in total cerebral volume, both in grey and white matter, mostly in the frontal, temporal and parietal lobes. These global volumetric changes are suggested to indicate a diffuse disturbance in neural networks during early development. In functional neuroimaging studies, activation abnormalities were observed in the temporal lobes and amygdala, which are involved in language and social cognition. An increase in visual activity cortex was also reported. CONCLUSION: Clinical observations and results from neuroimaging studies were gathered to hypothize and explain the pathophysiology of autism. Yet, it is still very early to conclude with certainty the neurobiological process responsible for autism.
4. Zhao Y, Fung C, Shin D, Shin BC, Thamotharan S, Sankar R, Ehninger D, Silva A, Devaskar SU. {{Neuronal glucose transporter isoform 3 deficient mice demonstrate features of autism spectrum disorders}}. {Mol Psychiatry};2009 (Jun 9)
Neuronal glucose transporter (GLUT) isoform 3 deficiency in null heterozygous mice led to abnormal spatial learning and working memory but normal acquisition and retrieval during contextual conditioning, abnormal cognitive flexibility with intact gross motor ability, electroencephalographic seizures, perturbed social behavior with reduced vocalization and stereotypies at low frequency. This phenotypic expression is unique as it combines the neurobehavioral with the epileptiform characteristics of autism spectrum disorders. This clinical presentation occurred despite metabolic adaptations consisting of an increase in microvascular/glial GLUT1, neuronal GLUT8 and monocarboxylate transporter isoform 2 concentrations, with minimal to no change in brain glucose uptake but an increase in lactate uptake. Neuron-specific glucose deficiency has a negative impact on neurodevelopment interfering with functional competence. This is the first description of GLUT3 deficiency that forms a possible novel genetic mechanism for pervasive developmental disorders, such as the neuropsychiatric autism spectrum disorders, requiring further investigation in humans.Molecular Psychiatry advance online publication, 9 June 2009; doi:10.1038/mp.2009.51.
