This article is concerned with the use of base-rate information that is derived from experience in classifying examples of a category. The basic task involved simulated medical decision making in which participants learned to diagnose hypothetical diseases on the basis of symptom information. Alternative diseases differed in their relative frequency or base rates of occurrence. In five experiments initial learning was followed by a series of transfer tests designed to index the use of base-rate information. On these tests, patterns of symptoms were presented that suggested more than one disease and were therefore ambiguous. The alternative or candidate diseases on such tests could differ in their relative frequency of occurrence during learning. For example, a symptom might be presented that had appeared with both a relatively common and a relatively rare disease. If participants are using base-rate information appropriately (according to Bayes' theorem), then they should be more likely to predict that the common disease is present than that the rare disease is present on such ambiguous tests. Current classification models differ in their predictions concerning the use of base-rate information. For example, most prototype models imply an insensitivity to base-rate information, whereas many exemplar-based classification models predict appropriate use of base-rate information. The results reveal a consistent but complex pattern. Depending on the category structure and the nature of the ambiguous tests, participants use base-rate information appropriately, ignore base-rate information, or use base-rate information inappropriately (predict that the rare disease is more likely to be present). To our knowledge, no current categorization model predicts this pattern of results. To account for these results, a new model is described incorporating the ideas of property or symptom competition and context-sensitive retrieval.

Category learning theories can be separated into those that expect judgments to be sensitive to configural information and those that expect judgments to be based on a weighted, additive summation of information. Predictions of these two classes of models were investigated in a simulated medical diagnosis task. Subjects learned about a fictitious disease or about two diseases from hypothetical case studies in which some symptoms were correlated with each other and others were independent. Following this initial training, subjects were presented either with pairs of new cases and asked to judge which was more likely to have the disease or with a single case and asked which disease was present. Across four experiments, subjects proved to be sensitive to configural information. When choosing between pairs of new cases, subjects tended to choose the case that preserved the correlation over the case that broke the correlation, even when the case with correlated symptoms contained fewer typical symptoms. When judging which disease was present in a single case, subjects' diagnoses were determined primarily by the correlated symptoms. Implications of these findings to process models of categorization are discussed.Considerable evidence suggests that many natural categories are "fuzzy" and contain no simple set of defining features (for a recent review, see Mervis & Rosen, 1981). Consequently, attention has turned to how different sources of information (i.e., attributes) are integrated in order to make category judgments. When people learn about a category, do they learn about each attribute independently, or do they instead learn about relations that hold between attributes? The problem is of special interest under conditions in which category structure is not directly specified but must instead be based on experience with exemplars of a category.In this study, classification into ill-defined categories was investigated in two types of simulated medical diagnosis tasks. In the single disease task used in Experiments 1-3, subjects learned about a fictitious disease

The Autism Treatment Evaluation Checklist (ATEC) was developed by Bernard Rimland and Stephen M. Edelson of the Autism Research Institute to provide an easy-toadminister, sensitive-to-change, and valid monitoring tool specific to autism spectrum disorders (Autism Research Institute 2016). It has been in use as an objective measure of autism severity since 1999 and is available on the Internet with results e-mailed to a specified address.

No abstract

These preliminary findings support the hypothesis that deep pressure may have a calming effect for persons with autism, especially those with high levels of arousal or anxiety.

Despite the fact that seizures are commonly associated with autism spectrum disorder (ASD), the effectiveness of treatments for seizures has not been well studied in individuals with ASD. This manuscript reviews both traditional and novel treatments for seizures associated with ASD. Studies were selected by systematically searching major electronic databases and by a panel of experts that treat ASD individuals. Only a few anti-epileptic drugs (AEDs) have undergone carefully controlled trials in ASD, but these trials examined outcomes other than seizures. Several lines of evidence point to valproate, lamotrigine, and levetiracetam as the most effective and tolerable AEDs for individuals with ASD. Limited evidence supports the use of traditional non-AED treatments, such as the ketogenic and modified Atkins diet, multiple subpial transections, immunomodulation, and neurofeedback treatments. Although specific treatments may be more appropriate for specific genetic and metabolic syndromes associated with ASD and seizures, there are few studies which have documented the effectiveness of treatments for seizures for specific syndromes. Limited evidence supports l-carnitine, multivitamins, and N-acetyl-l-cysteine in mitochondrial disease and dysfunction, folinic acid in cerebral folate abnormalities and early treatment with vigabatrin in tuberous sclerosis complex. Finally, there is limited evidence for a number of novel treatments, particularly magnesium with pyridoxine, omega-3 fatty acids, the gluten-free casein-free diet, and low-frequency repetitive transcranial magnetic simulation. Zinc and l-carnosine are potential novel treatments supported by basic research but not clinical studies. This review demonstrates the wide variety of treatments used to treat seizures in individuals with ASD as well as the striking lack of clinical trials performed to support the use of these treatments. Additional studies concerning these treatments for controlling seizures in individuals with ASD are warranted.

This manuscript reviews biological abnormalities shared by autism spectrum disorder (ASD) and epilepsy. Two neuropathological findings are shared by ASD and epilepsy: abnormalities in minicolumn architecture and γ-aminobutyric acid (GABA) neurotransmission. The peripheral neuropil, which is the region that contains the inhibition circuits of the minicolumns, has been found to be decreased in the post-mortem ASD brain. ASD and epilepsy are associated with inhibitory GABA neurotransmission abnormalities including reduced GABAA and GABAB subunit expression. These abnormalities can elevate the excitation-to-inhibition balance, resulting in hyperexcitablity of the cortex and, in turn, increase the risk of seizures. Medical abnormalities associated with both epilepsy and ASD are discussed. These include specific genetic syndromes, specific metabolic disorders including disorders of energy metabolism and GABA and glutamate neurotransmission, mineral and vitamin deficiencies, heavy metal exposures and immune dysfunction. Many of these medical abnormalities can result in an elevation of the excitatory-to-inhibitory balance. Fragile X is linked to dysfunction of the mGluR5 receptor and Fragile X, Angelman and Rett syndromes are linked to a reduction in GABAA receptor expression. Defects in energy metabolism can reduce GABA interneuron function. Both pyridoxine dependent seizures and succinic semialdehyde dehydrogenase deficiency cause GABA deficiencies while urea cycle defects and phenylketonuria cause abnormalities in glutamate neurotransmission. Mineral deficiencies can cause glutamate and GABA neurotransmission abnormalities and heavy metals can cause mitochondrial dysfunction which disrupts GABA metabolism. Thus, both ASD and epilepsy are associated with similar abnormalities that may alter the excitatory-to-inhibitory balance of the cortex. These parallels may explain the high prevalence of epilepsy in ASD and the elevated prevalence of ASD features in individuals with epilepsy.

Prefrontal synthesis (PFS) is defined as the ability to juxtapose mental visuospatial objects at will. Paralysis of PFS may be responsible for the lack of comprehension of spatial prepositions, semantically-reversible sentences, and recursive sentences observed in 30 to 40% of individuals with autism spectrum disorder (ASD). In this report we present data from a three-year-long clinical trial of 6454 ASD children age 2 to 12 years, which were administered a PFS-targeting intervention. Tablet-based verbal and nonverbal exercises emphasizing mental-juxtaposition-of-objects were organized into an application called Mental Imagery Therapy for Autism (MITA). The test group included participants who completed more than one thousand exercises and made no more than one error per exercise. The control group was selected from the rest of participants by a matching procedure. Each test group participant was matched to the control group participant by age, gender, expressive language, receptive language, sociability, cognitive awareness, and health score at first evaluation using propensity score analysis. The test group showed a 2.2-fold improvement in receptive language score vs. control group (p < 0.0001) and a 1.4-fold improvement in expressive language (p = 0.0144). No statistically significant change was detected in other subscales not targeted by the exercises. These findings show that language acquisition improves after training PFS and that a further investigation of the PFS-targeting intervention in a randomized controlled study is warranted.