1. Burrows CA, Usher LV, Schwartz CB, Mundy PC, Henderson HA. {{Supporting the Spectrum Hypothesis: Self-Reported Temperament in Children and Adolescents with High Functioning Autism}}. {J Autism Dev Disord};2015 (Nov 20)
This study tested the spectrum hypothesis, which posits that children and adolescents with high functioning autism (HFA) differ quantitatively but not qualitatively from typically developing peers on self-reported temperament. Temperament refers to early-appearing, relatively stable behavioral and emotional tendencies, which relate to maladaptive behaviors across clinical populations. Quantitatively, participants with HFA (N = 104, aged 10-16) self-reported less surgency and more negative affect but did not differ from comparison participants (N = 94, aged 10-16) on effortful control or affiliation. Qualitatively, groups demonstrated comparable reliability of self-reported temperament and associations between temperament and parent-reported behavior problems. These findings support the spectrum hypothesis, highlighting the utility of self-report temperament measures for understanding individual differences in comorbid behavior problems among children and adolescents with HFA.
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2. Ito-Ishida A, Ure K, Chen H, Swann JW, Zoghbi HY. {{Loss of MeCP2 in Parvalbumin-and Somatostatin-Expressing Neurons in Mice Leads to Distinct Rett Syndrome-like Phenotypes}}. {Neuron};2015 (Nov 18);88(4):651-658.
Inhibitory neurons are critical for proper brain function, and their dysfunction is implicated in several disorders, including autism, schizophrenia, and Rett syndrome. These neurons are heterogeneous, and it is unclear which subtypes contribute to specific neurological phenotypes. We deleted Mecp2, the mouse homolog of the gene that causes Rett syndrome, from the two most populous subtypes, parvalbumin-positive (PV+) and somatostatin-positive (SOM+) neurons. Loss of MeCP2 partially impairs the affected neuron, allowing us to assess the function of each subtype without profound disruption of neuronal circuitry. We found that mice lacking MeCP2 in either PV+ or SOM+ neurons have distinct, non-overlapping neurological features: mice lacking MeCP2 in PV+ neurons developed motor, sensory, memory, and social deficits, whereas those lacking MeCP2 in SOM+ neurons exhibited seizures and stereotypies. Our findings indicate that PV+ and SOM+ neurons contribute complementary aspects of the Rett phenotype and may have modular roles in regulating specific behaviors.
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3. Turowetz J, Maynard DW. {{Category attribution as a device for diagnosis: fitting children to the autism spectrum}}. {Sociol Health Illn};2015 (Nov 20)
The practice of medicine involves applying abstract diagnostic classifications to individual patients. Patients present with diverse histories and symptoms, and clinicians are tasked with fitting them into generic categories. They must also persuade patients, or family members, that the diagnosis is appropriate and elicit compliance with prescribed treatments. This can be especially challenging with psychiatric disorders such as autism, for which there are no clear biomarkers. In this paper, we explicate a discursive procedure, which we term category attribution. The procedure juxtaposes a narrative about the child with a claim about members of a clinically relevant category, in this case, either children with autism or typically/normally developing children. The attribution procedure carries the implication that the child does or does not belong to that category. We show that category attributions are organised in a recurrent interactional sequence. Further, we argue that category attributions encode normative expectations about child development, such that the child is rendered typical or atypical relative to clinical and social norms. Accordingly, such categorisation devices have a moral dimension as well as a clinical one.
