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Individuals with autistic spectrum disorders (ASDs) often experience, describe and exhibit unusual patterns of sensation and attention. These anomalies have been hypothesized to result from overarousal and consequent overfocused attention. Parents of individuals with ASD rated items in three domains, 'sensory overreactivity', 'sensory underreactivity' and 'sensory seeking behaviors', of an expanded version of the Sensory Profile, a 103-item rating scale developed for the present study. Parents also rated symptom severity, overselective attention and exceptional memory, and completed the Vineland Adaptive Behavior Scales. Of 222 rated subjects, 144 had complete data. Cluster analysis showed the predicted overfocused pattern of sensation and attention, comprising overreactivity, perseverative behavior and interests, overfocused attention and exceptional memory in 43 percent of this sample. This pattern was striking in 10 percent. The neurological basis of overreactivity and overfocusing is discussed in relation to the overarousal hypothesis. Attention is drawn to its considerable prevalence in the ASD population.

Multiple theories of Attention-Deficit/Hyper-activity Disorder (ADHD) have been proposed, but one that has stood the test of time is the dopamine deficit theory. We review the narrow literature from recent brain imaging and molecular genetic studies that has improved our understanding of the role of dopamine in manifestation of symptoms of ADHD, performance deficits on neuropsychological tasks, and response to stimulant medication that constitutes the most common treatment of this disorder. First, we consider evidence of the presence of dopamine deficits based on the recent literature that (1) confirms abnormalities in dopamine-modulated frontal-striatal circuits, reflected by size (smaller-than-average components) and function (hypoactivation); (2) clarifies the agonist effects of stimulant medication on dopaminergic mechanisms at the synaptic and circuit level of analysis; and (3) challenges the most-widely accepted ADHD-related neural abnormality in the dopamine system (higher-than-normal dopamine transporter [DAT] density). Second, we discuss possible genetic etiologies of dopamine deficits based on recent molecular genetic literature, including (1) multiple replications that confirm the association of ADHD with candidate genes related to the dopamine receptor D4 (DRD4) and the DAT; (2) replication of differences in performance of neuropsychological tasks as a function of the DRD4 genotype; and (3) multiple genome-wide linkage scans that demonstrate the limitations of this method when applied to complex disorders but implicate additional genes that may contribute to the genetic basis of ADHD. Third, we review possible environmental etiologies of dopamine deficits based on recent studies of (1) toxic substances that may affect the dopamine system in early development and contribute substantially to the etiology of ADHD; (2) fetal adaptations in dopamine systems in response to stress that may alter early development with lasting effects, as proposed by the developmental origins of health and disease hypothesis; and (3) gene-environment interactions that may moderate selective damage or adaptation of dopamine neurons. Based on these reviews, we identify critical issues about etiologic subtypes of ADHD that may involve dopamine, discuss methods that could be used to address these issues, and review old and new theories that may direct research in this area in the future.

We compare the way two models of consciousness treat subjective timing. According to the standard “Cartesian Theater” model, there is a place in the brain where “it all comes together,” and the discriminations in all modalities are somehow put into registration and “presented” for subjective judgment. The timing of the events in this theater determines subjective order. According to the alternative “Multiple Drafts” model, discriminations are distributed in both space and time in the brain. These events do have temporal properties, but those properties do not determine subjective order because there is no single, definitive “stream of consciousness,” only a parallel stream of conflicting and continuously revised contents. Four puzzling phenomena that resist explanation by the Cartesian model are analyzed: (1) a gradual apparent motion phenomenon involving abrupt color change (Kolers & von Grünau 1976), (2) an illusion of an evenly spaced series of “hops” produced by two or more widely spaced series of taps delivered to the skin (Geldard & Sherrick's “cutaneous rabbit” [1972]), (3) backwards referral in time, and (4) subjective delay of consciousness of intention (both reported in this journal by LIbet 1985a; 1987; 1989a). The unexamined assumptions that have always made the Cartesian Theater so attractive are exposed and dismantled. The Multiple Drafts model provides a better account of the puzzling phenomena, avoiding the scientific and metaphysical extravagances of the Cartesian Theater: The temporal order of subjective events is a product of the brain's interpretational processes, not a direct reflection of events making up those processes.

The subjects, 120 college students, sorted cards for 42 sec with instructions to process 0, 1, or 2 bits of information per card (response uncertainty) and then were asked to make an absolute judgement of the interval's duration. Half of the subjects knew this judgement would be required before the interval (prospective paradigm); half did not (retrospective paradigm). Judged time was an inverse linear function of response uncertainty under the prospective paradigm, whereas no significant function was obtained under the retrospective paradigm.

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Although Autism Spectrum Disorders (ASD) are generally assumed to be lifelong, we review evidence that between 3% and 25% of children reportedly lose their ASD diagnosis and enter the normal range of cognitive, adaptive and social skills. Predictors of recovery include relatively high intelligence, receptive language, verbal and motor imitation, and motor development, but not overall symptom severity. Earlier age of diagnosis and treatment, and a diagnosis of Pervasive Developmental Disorder-Not Otherwise Specified are also favorable signs. The presence of seizures, mental retardation and genetic syndromes are unfavorable signs, whereas head growth does not predict outcome. Controlled studies that report the most recovery came about after the use of behavioral techniques. Residual vulnerabilities affect higher-order communication and attention. Tics, depression and phobias are frequent residual co-morbidities after recovery. Possible mechanisms of recovery include: normalizing input by forcing attention outward or enriching the environment; promoting the reinforcement value of social stimuli; preventing interfering behaviors; mass practice of weak skills; reducing stress and stabilizing arousal. Improving nutrition and sleep quality is non-specifically beneficial.

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