The elaborated Reichardt detector (ERD) proposed by van Santen and Sperling [J. Opt. Soc. Am. A 1, 451 (1984)], based on Reichardt's motion detector [Z. Naturforsch. Teil B 12, 447 (1957)], is an opponent system of two mirror-image subunits. Each subunit receives inputs from two spatiotemporal filters (receptive fields), multiplies the filter outputs, and temporally integrates the product. Subunit outputs are algebraically subtracted to yield ERD output. ERD's can correctly indicate direction of motion of drifting sine waves of any spatial and temporal frequency. Here we prove that with a careful choice of either temporal or spatial filters, the subunits can themselves become quite similar or equivalent to the whole ERD; with suitably chosen filters, the ERD is equivalent to an elaborated version of a motion detector proposed by Watson and Ahumada [NASA Tech. Memo. 84352 (1983)]; and for every choice of filters, the ERD is fully equivalent to the detector proposed by Adelson and Bergen [J. Opt. Soc. Am. A 2, 284-299 (1985)]. Some equivalences between the motion detection (in x, t) by ERD's and spatial pattern detection (in x, y) are demonstrated. The responses of the ERD and its variants to drifting sinusoidal gratings, to other sinusoidally modulated stimuli (on-off gratings, counterphase flicker), and to combinations of sinusoids are derived and compared with data. ERD responses to two-frame motion displays are derived, and several new experimental predictions are tested experimentally.(ABSTRACT TRUNCATED AT 250 WORDS)

We propose a model of direction-sensitive units in human vision. It is a modified and elaborated version of a model by Reichardt [Z. Naturforsch. Teil B 12, 447 (1957)]. The model is applied to threshold experiments in which subjects view adjacent vertical bars with independently (typically sinusoidally), temporally modulated luminances.The subject must report whether the patterns moved to the left or to the right. According to the model, a basic motion-detecting unit consists of two subunits tuned to opposite directions. Each performs a spatial and temporal linear filtering of its input; outputs of the filters are multiplied, and the multiplied output is integrated (for a time that is long relative to the modulation period). The model's output consists of the difference between the subunit outputs. Direction of movement is indicated by the sign of the model output. Mathematical analysis of the model yielded several predictions that were confirmed experimentally.Specifically, we found that (1) performance with complex patterns can be predicted by spatiotemporal Fourier analysis that results in the segregation and linear addition in the output for different temporal frequencies; (2) under special conditions, performance depends on the product of adjacent bar amplitudes, offering strong support for the multiplication principle; (3) performance is unaffected by addition of stationary patterns; and (4) addition of homogeneous flicker normally produces no effect but under special conditions reverses perceived direction. These and other results confirm our model and reject several other models, including Reichardt's original model.

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In a sample of 46 children aged 4 to 7 years with Autism Spectrum Disorder (ASD) and intelligible speech, there was no statistical support for the hypothesis of concomitant Childhood Apraxia of Speech (CAS). Perceptual and acoustic measures of participants' speech, prosody, and voice were compared with data from 40 typically-developing children, 13 preschool children with Speech Delay, and 15 participants aged 5 to 49 years with CAS in neurogenetic disorders. Speech Delay and Speech Errors, respectively, were modestly and substantially more prevalent in participants with ASD than reported population estimates. Double dissociations in speech, prosody, and voice impairments in ASD were interpreted as consistent with a speech attunement framework, rather than with the motor speech impairments that define CAS. Key Words: apraxia, dyspraxia, motor speech disorder, speech sound disorder A continuing question about persons with Autism Spectrum Disorder (ASD) is whether reported diminished abilities in gross, fine, and oral motor control are causally associated with reported deficits in speech acquisition and performance. The classification term for the speech deficit in question, recently adapted by the American Speech-Language-Hearing Association (ASHA;2007a, 2007b, is Childhood Apraxia of Speech (CAS). Medical literatures and speech literatures in other countries continue to prefer several other classificatory terms for this disorder, including dyspraxia and developmental verbal dyspraxia. "Childhood" apraxia of speech differentiates congenital and early acquired forms of apraxia of speech from adult acquired forms, but creates a nosological problem because childhood apraxia of speech generally persists into adulthood. We will use the ASHA (2007a) recommended term-CAS.The strong form of the hypothesis in the title of this paper, hereafter, the 'CAS-ASD' hypothesis, is that CAS is a sufficient cause of lack of speech development in at least some children classified as nonverbal ASD. The weak form of the CAS-ASD hypothesis is that CAS contributes to the inappropriate speech, prosody, and/or voice features reported in some children and adults with verbal ASD. Although the present report addresses only the weak form of the hypotheses, the conceptual framework and implications for treatment NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript apply to both forms of the hypothesis. Forthcoming research addresses the strong form of the hypothesis. The following sections provide (a) rationales for the CAS-ASD hypothesis, (b) an overview of idiopathic speech sound disorders, and (c) a summary of speech, prosody, and voice findings in verbal ASD. Rationales for the CAS-ASD HypothesisThe American Speech-Language-Hearing Association Position Statement recommends the following definition of CAS:Childhood apraxia of speech (CAS) is a neurological childhood (pediatric) speech sound disorder in which the precision and consistency of movements underlying speech are impaired in the absence of neuromuscula...

Aggressive behavior problems (ABP) are frequent yet poorly understood in children with Autism Spectrum Disorders (ASD) and are likely to co-vary significantly with comorbid problems. We examined the prevalence and sociodemographic correlates of ABP in a clinical sample of children with ASD (N = 400; 2–16.9 years). We also investigated whether children with ABP experience more intensive medical interventions, greater impairments in behavioral functioning, and more severe comorbid problems than children with ASD who do not have ABP. One in four children with ASD had Child Behavior Checklist scores on the Aggressive Behavior scale in the clinical range (T-scores ≥ 70). Sociodemographic factors (age, gender, parent education, race, ethnicity) were unrelated to ABP status. The presence of ABP was significantly associated with increased use of psychotropic drugs and melatonin, lower cognitive functioning, lower ASD severity, and greater comorbid sleep, internalizing, and attention problems. In multivariate models, sleep, internalizing, and attention problems were most strongly associated with ABP. These comorbid problems may hold promise as targets for treatment to decrease aggressive behavior and proactively identify high-risk profiles for prevention.