Annemie Ploeger

Identification of Everyday Objects on the Basis of Silhouette and Outline Versions

Line drawings of everyday objects were modified into silhouettes by filling-in the complete area enclosed by boundary contours, and outline versions were created by extracting the contours from the silhouettes. A large number of participants was asked to try to identify these silhouette and outline versions in experiment 1. Identifiability ranged from 0% to 100% correct responses with a large range in-between. Several kinds of errors and several reasons for difficulties with identification emerged in our data set. In experiment 2, we compared the original identification rates to those of inverted silhouettes (white figures on a black background), and in experiment 3 we compared the original identification rates of objects with filled-in holes or background parts to those of versions without filling-in. These stimuli and identification norms are useful for additional research on priming and context effects of object identification, neuropsychological deficits of object identification, and all kinds of studies with silhouettes where the role of top down knowledge could be of interest.

The Association Between Autism and Errors in Early Embryogenesis: What Is the Causal Mechanism?

The association between embryonic errors and the development of autism has been recognized in the literature, but the mechanism underlying this association remains unknown. We propose that pleiotropic effects during a very early and specific stage of embryonic development-early organogenesis-can explain this association. In humans early organogenesis is an embryonic stage, spanning Day 20 to Day 40 after fertilization, which is characterized by intense interactivity among body parts of the embryo. This implies that a single mutation or environmental disturbance affecting development at this stage can have several phenotypic effects (i.e., pleiotropic effects). Disturbances during early organogenesis can lead to many different anomalies, including limb deformities, craniofacial malformations, brain pathology, and anomalies in other organs. We reviewed the literature and found ample evidence for the association between autism and different kinds of physical anomalies, which agrees with the hypothesis that pleiotropic effects are involved in the development of autism. The proposed mechanism integrates findings from a variety of studies on autism, including neurobiological studies and studies on physical anomalies and prenatal influences on neurodevelopmental outcomes. The implication is that the origin of autism can be much earlier in embryologic development than has been frequently reported.

Cognition and the Evolution of Music: Pitfalls and Prospects

What was the role of music in the evolutionary history of human beings? We address this question from the point of view that musicality can be defined as a cognitive trait. Although it has been argued that we will never know how cognitive traits evolved (Lewontin, 1998), we argue that we may know the evolution of music by investigating the fundamental cognitive mechanisms of musicality, for example, relative pitch, tonal encoding of pitch, and beat induction. In addition, we show that a nomological network of evidence (Schmitt & Pilcher, 2004) can be built around the hypothesis that musicality is a cognitive adaptation. Within this network, different modes of evidence are gathered to support a specific evolutionary hypothesis. We show that the combination of psychological, medical, physiological, genetic, phylogenetic, hunter-gatherer, and cross-cultural evidence indicates that musicality is a cognitive adaptation.

Stochastic catastrophe analysis of switches in the perception of apparent motion.

Dynamical phenomena such as bistability and hysteresis have been found in a number of studies on perception of apparent motion. We show that new developments in stochastic catastrophe theory make it possible to test models of these phenomena empirically. Catastrophe theory explains discontinuous changes in responses caused by continuous changes in experimental parameters. We propose catastrophe models for two experimental paradigms on perception of apparent motion and present experiments that support these models. We test these models by using an algorithm for fitting stochastic catastrophe models. We derive from catastrophe theory the prediction that a dynamical phenomenon calleddivergence is necessary when hysteresis is found. This new prediction is supported by the data.

Nonlinear epigenetic variance: review and simulations

We present a review of empirical evidence that suggests that a substantial portion of phenotypic variance is due to nonlinear (epigenetic) processes during ontogenesis. The role of such processes as a source of phenotypic variance in human behaviour genetic studies is not fully appreciated. In addition to our review, we present simulation studies of nonlinear epigenetic variance using a computational model of neuronal network development. In each simulation study, time series for monozygotic and dizygotic twins were generated and analysed using conventional behaviour genetic modelling. In the results of these analyses, the nonlinear epigenetic variance was subsumed under the non-shared environmental component. As is commonly found in behaviour genetic studies, observed heritabilities and unique environmentabilities increased with time, whereas common environmentabilities decreased. The fact that the phenotypic effects of nonlinear epigenetic processes appear as unsystematic variance in conventional twin analyses complicates the identification and quantification of the ultimate genetic and environmental causes of individual differences. We believe that nonlinear dynamical system theories provide a challenging perspective on the development of individual differences, which may enrich behaviour genetic studies.

Evolutionary psychology versus Fodor: Arguments for and against the massive modularity hypothesis

Evolutionary psychologists tend to view the mind as a large collection of evolved, functionally specialized mechanisms, or modules. Cosmides and Tooby (1994) have presented four arguments in favor of this model of the mind: the engineering argument, the error argument, the poverty of the stimulus argument, and combinatorial explosion. Fodor (2000) has discussed each of these four arguments and rejected them all. In the present paper, we present and discuss the arguments for and against the massive modularity hypothesis. We conclude that Cosmides and Toobys arguments have considerable force and are too easily dismissed by Fodor.

Evolutionary psychology and intelligence research cannot be integrated the way Kanazawa (2010) suggested

Evolutionary psychologists search for human universals, differential psychologists for variation around common human themes. So far, evolutionary psychology and differential psychology seem somewhat disparate and unconnected, although Kanazawa (May–June 2010) is certainly not the first to attempt integrating them (see Penke, 2010, and references therein). Kanazawa uses intelligence to elaborate his view of integration. His evolutionary theory of intelligence is based on two assumptions: (1) General intelligence (g) is both an individual-differences variable and a domain-specific adaptation, and (2) the domain to which general intelligence is adapted is evolutionary novelty. Both claims are erroneous. Kanazawa (2010) defended his first assumption by arguing that there are individual differences associated with any adaptation. To use one of his illustrations: Bipedalism is a universal human adaptation, but there are individual differences in running speed. In the same vein, Kanazawa claimed that general intelligence is a universal human adaptation but that there are also individual differences in general intelligence. He then inferred that g, an individual-differences variable, can be used as a “measure” or “indicator” of a general intelligence adaptation. This line of reasoning is troublesome. As Borsboom and Dolan (2006) have spelled out, g is a psychometric construct, reflecting positive correlations between scores on different cognitive tests (i.e., the positive manifold). To interpret g as something other than a psychometric construct is to go far beyond the data. Specifically, in contrast to adaptations such as language acquisition or color perception, g refers exclusively to human individual differences, not to a human universal. Individual differences certainly exist in the efficiency, size, quality, sensitivity, or performance of adaptations, but these differences are not the basis of their existence (Borsboom & Dolan, 2006; Penke, 2010). The existence of g does not indicate that general intelligence is present within every normal human, but that every human occupies one of its levels, which is a completely different statement. In short, g is not an adaptation or causal mechanism, but a variable. A variable is not necessarily associated with just one modular adaptation (or mechanism/process/cause). Running speed is associated with bipedalism, but also with the cardiovascular system, with the achievement motive to train harder, and so forth—arguably adaptations in their own rights. A given variable can indicate parameters of adaptations (Penke, 2010), but the variable is never tantamount to the adaption. In addition, a variable is not the cause of the existence of an adaptation (running speed is not the cause of bipedalism), nor does the existence of an adaptation explain the nature of individual differences (bipedalism is not the cause of differences in running speed). The empirical observation of g in itself tells us nothing about the causal reasons why people show individual differences in g. Kanazawa (2010) assumed that g is the result of a single domain-specific adaptation. If this were true, then different individuals with the same g score (or rank on the dimension described by g) should have this score for the same reasons; that is, g differences reflect differences in the performance of a single coherent adaptation. The available biological evidence, however, points to causal heterogeneity underlying g and thus against the single-intelligence-adaptation hypothesis: Different individuals seem to use their brains differently to solve intelligence tests equally well, and different rare (probably private or family-specific) mutations likely contribute substantially to the genetics of g in different individuals (Deary, Penke, & Johnson, 2010; Penke, 2010). Thus, although one cannot rule out the single-intelligence-adaptation hypothesis a priori, the biological evidence does not support it. We need to keep in mind that the g-factor is just one among many models for describing the actual empirical observation, namely, positive-manifold correlations among cognitive tests. Equally plausible and explanatory models exist: For instance, Godfrey Thomson (1881–1955) presented a “bonds” model based on random sampling of cognitive processes for solving test items, thus positing heterogeneity rather than homogeneity in those cognitive processes (Bartholomew, Deary, & Lawn, 2009). Van der Maas et al. (2006) proposed a second plausible model that explains g by positing mutualistic developmental interactions among distinct cognitive processes. These models are irreconcilable with Kanazawa’s (2010) claim that g reflects a single domain-specific adaptation. Kanazawa’s (2010) second assumption, that general intelligence is a specific adaptation to the domain of evolutionary novelty, is also questionable. “Evolutionary novelty,” which is defined by exclusion (i.e., as everything previously not encountered in our evolutionary past), is not a coherent characterization of an adaptive problem. Selection can only tailor domainspecific adaptations to common problem structures. So which structural feature do lightning, flash floods, television characters, genetically unrelated groups, and electric light have in common? According to Kanazawa, their communality is that they pose problems that are logically solvable. But what is logically correct about being politically liberal when living in unrelated groups or about being slightly more nocturnal when having electric light? Furthermore, there is no coherent computational mechanism that embraces “methods of induction . . . deductive reasoning . . . , analogy, abstraction, and so forth” (Kanazawa, 2010, p. 283) and could thus be called a domain-specific general intelligence adaptation. Finally, novelty violates requirements for rational decision theory (including logic), as by definition relevant information is unknown or has to be estimated from small samples when encountering novelty (Gigerenzer & Brighton, 2009). More plausible evolutionary responses to novelty include simple heuristics (Gigerenzer & Brighton, 2009), open developmental programs (Mayr, 1974), and domain-specific adaptations supporting social/cultural learning (instead of widespread individual reasoning) (Henrich & McElreath, 2003). To conclude, while evolved adaptations can and often do vary in certain parameters, an individual-differences variable need not correspond to a specific underlying adaptation. Because g is an individual-differences variable, it is uninformative about whether a domain-specific adaptation for evolutionary novelty exists. This undermines Kanazawa’s (2010) integration of evolutionary and differential psychology as well as his empirical evidence for his evolutionary theory of intelligence—all based on g—completely. In tapraid4/z2n-amepsy/z2n-amepsy/z2n00811/z2n3794d11z xppws S 1 10/12/11 4:21 Art: 2010-2207

Differential activation solution to the

The correspondence problem arises in motion perception when more than one motion path is possible for discontinuously presented visual elements. Ullman’s (1979) “minimal mapping” solution to the correspondence problem, for which costs are assigned to competing motion paths on the basis of element affinities (e.g., greater affinity for elements that are closer together), is distinguished from a solution based on the differential activation of directionally selective motion detectors. The differential activation account was supported by evidence that path length affects detector activation in a paradigm for which motion correspondence is not a factor. Effects on detector activation in this paradigm also were the basis for the successful prediction of path luminance effects on solutions to the motion correspondence problem. Finally, the differential activation account was distinguished from minimal mapping theory by an experiment showing that the perception of an element moving simultaneously in two directions does not depend on whether the two motions are matched in path-length determined affinity; it is sufficient that the activation of detectors responding to each of the two motion directions is above the threshold level required for the motions to be perceived. Implications of the differential activation solution are discussed for the stability of perceived motions once they are established, and the adaptation of perceived andunperceived motions.

The dot-probe task to measure emotional attention: A suitable measure in comparative studies?

For social animals, attending to and recognizing the emotional expressions of other individuals is of crucial importance for their survival and likely has a deep evolutionary origin. Gaining insight into how emotional expressions evolved as adaptations over the course of evolution can be achieved by making direct cross-species comparisons. To that extent, experimental paradigms that are suitable for investigating emotional processing across species need to be developed and evaluated. The emotional dot-probe task, which measures attention allocation toward emotional stimuli, has this potential. The task is implicit, and subjects need minimal training to perform the task successfully. Findings in nonhuman primates, although scarce, show that they, like humans, have an attentional bias toward emotional stimuli. However, the wide literature on human studies has shown that different factors can have important moderating effects on the results. Due to the large heterogeneity of this literature, these moderating effects often remain unnoticed. We here review this literature and show that subject characteristics and differences in experimental designs affect the results of the dot-probe task. We conclude with specific recommendations regarding these issues that are particularly relevant to take into consideration when applying this paradigm to study animals.

Why did the savant syndrome not spread in the population? A psychiatric example of a developmental constraint.

A developmental constraint is a mechanism that limits the possibility of a phenotype to evolve. There is growing evidence for the existence of developmental constraints in the biological literature. We hypothesize that a developmental constraint prevents the savant syndrome, despite its positive aspects, from spreading in the population. Here, the developmental constraint is the result of the high interactivity among body parts in an early stage in embryological development, namely early organogenesis or the phylotypic stage. The interactivity during this stage involves all components of the embryo, and as a result mutations that affect one part of the embryo also affect other parts. We hypothesize that a mutation, which gives rise to the development of the positive aspects of the savant syndrome (e.g., an impressive memory capacity), will virtually always have a deleterious effect on the development of other phenotypic traits (e.g., resulting in autism and/or impaired motor coordination). Thus, our hypothesis states that the savant syndrome cannot spread in the population because of this developmental constraint. The finding that children with savant syndrome often have autism and physical anomalies, which are known to be established during early organogenesis, supports our hypothesis.