It is often assumed that similar domain-specific behavioural impairments found in cases of adult brain damage and developmental disorders correspond to similar underlying causes, and can serve as convergent evidence for the modular structure of the normal adult cognitive system. We argue that this correspondence is contingent on an unsupported assumption that atypical development can produce selective deficits while the rest of the system develops normally (Residual Normality), and that this assumption tends to bias data collection in the (...) field. Based on a review of connectionist models of acquired and developmental disorders in the domains of reading and past tense, as well as on new simulations, we explore the computational viability of Residual Normality and the potential role of development in producing behavioural deficits. Simulations demonstrate that damage to a developmental model can produce very different effects depending on whether it occurs prior to or following the training process. Because developmental disorders typically involve damage prior to learning, we conclude that the developmental process is a key component of the explanation of endstate impairments in such disorders. Further simulations demonstrate that in simple connectionist learning systems, the assumption of Residual Normality is undermined by processes of compensation or alteration elsewhere in the system. We outline the precise computational conditions required for Residual Normality to hold in development, and suggest that in many cases it is an unlikely hypothesis. We conclude that in developmental disorders, inferences from behavioural deficits to underlying structure crucially depend on developmental conditions, and that the process of ontogenetic development cannot be ignored in constructing models of developmental disorders. Key Words: Acquired and developmental disorders; connectionist models; modularity; past tense; reading. (shrink)

For the last thirty years, cognitive scientists have attempted to describe the cognitive architecture of typically developing human beings, using, among other sources of evidence, the dissociations that result from developmental psychopathologies such as autism spectrum disorders, Williams syndrome, and Down syndrome. Thus, in his recent defense of the massive modularity hypothesis, Steven Pinker insists on the importance of such dissociations to identify the components of the typical cognitive architecture (2005, 4; my emphasis): This kind of faculty psychology (...) has numerous advantages (...). It is supported by the existence of neurological and genetic disorders that target these faculties unevenly, such as a difficulty in recognizing faces (and facelike shapes) but not other objects, or a difficulty in reasoning about minds but not about objects or pictures. Similarly, Simon Baron-Cohen writes (1998, 335; my emphasis; see also Temple, 1997): I suggest that the study of mental retardation would profit from the application of the framework of cognitive neuropsychology (…). In cognitive neuropsychology, one key question running through the investigator’s mind is “Is this process or mechanism intact or impaired in this person?” When cognitive neuropsychology is done well, a patient’s cognitive system is examined with specific reference to a model of the normal cognitive system. And, not infrequently, evidence from the patient’s cognitive deficits leads to a revision of the model of the normal system. However, in recent years, the use of developmental psychopathologies to identify the components of the typical cognitive architecture has come under heavy fire. In a series of influential articles, neuropsychologist Annette Karmiloff-Smith has argued that findings about the pattern of impairments and preserved capacities in people with developmental psychopathologies say nothing about the cognitive architecture of.. (shrink)

These two companion volumes provide a comprehensive review and critical evaluation of the major DSM-III and DSM-III-R child disorders. Their major goal is to provide diagnostic and assessment guidelines that are based on scientific literature in specific clinical domains. Each chapter contains a discussion of the historical background of a particular diagnosis, definitional issues, a critical but selective review of the literature addressing the diagnosis in question, proposed changes in the diagnostic criteria based on the available literature, and proposed (...) assessment models and methods based on the designated criteria. Given the scientific bases for many of these discussions of diagnostic criteria, these two volumes will serve professionals and graduate students in a wide variety of fields: clinical child psychology, child psychiatry, pediatrics, pediatric and school psychology, special education, social work, and other child mental health specialties. (shrink)

Although the field of psychiatry has witnessed the proliferation of studies on Gene x Environment (GxE) interactions, still limited is the knowledge we possess of GxE interactions regarding developmental disorders. In this perspective paper, we discuss why GxE interaction studies are needed to broaden our knowledge of developmental disorders. We also discuss the different roles of hazardous versus self-generated environmental factors and how these types of factors may differentially engage with an individual’s genetic background in predicting (...) a resulting phenotype. Then, we present exemplar studies that highlight the role of GxE in predicting atypical developmental trajectories as well as provide insight regarding treatment outcomes. Supported by these examples, we explicate the need to move beyond merely examining statistical interactions between genes and the environment, and to investigate specific genetic susceptibility and environmental contexts that drive developmental disorders. We propose that further parsing of genetic and environmental components is required to fully understand the unique contribution of each factor to the etiology of developmental disorders. Finally, with a greater appreciation of the complexities of GxE interaction, this discussion will converge upon the potential implications for clinical and translational research. (shrink)

Lewis’ neurodevelopmental model provides a plausible alternative to the brain disease model of addiction that is a dominant perspective in the USA. We disagree with Lewis’ claim that the BDMA is unchallenged within the addiction field but we agree that it provides unduly pessimistic prospects of recovery. We question the strength of evidence for the BDMA provided by animal models and human neuroimaging studies. We endorse Lewis’ framing of addiction as a developmental process underpinned by reversible forms of neuroplasticity. (...) His view is consistent with epidemiological evidence of addicted individuals ‘maturing out’ and recovering from addiction. We do however hold some reservations about Lewis’ model. We do not think that his analysis of the neurobiological evidence is clearly different from that of the BDMA or that his neurodevelopmental model provides a more rigorous interpretation of the evidence than the BDMA. We believe that our understanding of the neurobiology of drug use is too immature to warrant the major role given to it in the BDMA. Our social research finds very mixed support for the BDMA among addicted people and health professionals in Australia. Lewis’ account of addiction requires similar empirical evaluation of its real-world implications. (shrink)

This commentary discusses the logic of inferring modularity or the lack of modularity from observed patterns of developmental disorders.

Evidence from various subtypes of Specific Language Impairment and developmental peripheral dyslexias is presented to support the idea that even developmental disorders can be modular. However, in developmental letter position dyslexia and neglect dyslexia we show that additional errors can occur because of insufficient orthographic-lexical knowledge.

What is attention? How does it go wrong? Do attention deficits arise from genes or from the environment? Can we cure it with drugs or training? Are there disorders of attention other than deficit disorders? The past decade has seen a burgeoning of research on the subject of attention. This research has been facilitated by advances on several fronts: New methods are now available for viewing brain activity in real time, there is expanding information on the complexities of (...) the biochemistry of neural activity, individual genes can be isolated and their functions identified, analysis of the component processes included under the broad umbrella of "attention" has become increasingly sophisticated, and ingenious methods have been devised for measuring typical and atypical development of these processes, from infancy into childhood, and then into adulthood. In this book, Kim Cornish and John Wilding are concerned with attention and its development, both typical and atypical, particularly in disorders with a known genetic etiology or assumed genetic linkage. Tremendous advances across seemingly diverse disciplines - molecular genetics, pediatric neurology, child psychiatry, developmental cognitive neuroscience, and education - have culminated in a wealth of new methods for elucidating disorders at multiple levels, possibly paving the way for new treatment options. Cornish and Wilding use three specific-yet-interlinking levels of analysis: genetic blueprint, the developing brain, and the behavioral-cognitive outcomes, as the basis for charting the attention profiles of six well-documented neurodevelopmental disorders: ADHD, autism, fragile X syndrome, Down syndrome, Williams syndrome, and 22q11 deletion syndrome. Their overarching aim in this book is to provide the most authoritative and extensive account to date of disorder-specific attention profiles and their development from infancy through adolescence. (shrink)

This chapter seeks to recover an approach to consciousness from a general theory of brain function, namely the prediction error minimization theory. The way this theory applies to mental and developmental disorder demonstrates its relevance to consciousness. The resulting view is discussed in relation to a contemporary theory of consciousness, namely the idea that conscious perception depends on Bayesian metacognition; this theory is also supported by considerations of psychopathology. This Bayesian theory is first disconnected from the higher-order thought theory, (...) and then, via a prediction error conception of action, connected instead to the global neuronal workspace theory. Considerations of mental and developmental disorder therefore show that a very general theory of brain function is relevant to explaining the structure of conscious perception; furthermore, this theory can subsume and unify two contemporary approaches to consciousness, in a move that seeks to elucidate the fundamental mechanism for selection of representational content into consciousness. (shrink)

Either genetically specified modular cognitive architecture for syntactic processing does not exist (neuroconstructivism), or there is a module but its development is so abnormal in Williams syndrome (WS) that no conclusion can be drawn about its normal architecture (moderate nativism). Radical nativism, which holds that WS is a case of intact syntax, is untenable. Specific Language Impairment and WS create a dilemma that radical nativism cannot accommodate.

Grammatical markers are not uniformly impaired across speakers of different languages, even when speakers share a diagnosis and the marker in question is grammaticalized in a similar way in these languages. The aim of this work is to demarcate, from a cross-linguistic perspective, the linguistic phenotype of three genetically heterogeneous developmental disorders: specific language impairment, Down syndrome, and autism spectrum disorder. After a systematic review of linguistic profiles targeting mainly English-, Greek-, Catalan-, and Spanish-speaking populations with developmental (...) disorders (n = 880), shared loci of impairment are identified and certain domains of grammar are shown to be more vulnerable than others. The distribution of impaired loci is captured by the Locus Preservation Hypothesis which suggests that specific parts of the language faculty are immune to impairment across developmental disorders. Through the Locus Preservation Hypothesis, a classical chicken and egg question can be addressed: Do poor conceptual resources and memory limitations result in an atypical grammar or does a grammatical breakdown lead to conceptual and memory limitations? Overall, certain morphological markers reveal themselves as highly susceptible to impairment, while syntactic operations are preserved, granting support to the first scenario. The origin of resilient syntax is explained from a phylogenetic perspective in connection to the “syntax-before-phonology” hypothesis. (shrink)

Cognitive developmental disorders cannot be properly understood without due attention to the developmental process, and we commend the authors’simulations in this regard. We note the contribution of these simulations to the nascent field of connectionist modeling of developmental disorders and outline a set of criteria for assessing individual models in the hope of furthering future modeling efforts.

Thomas & Karmiloff- Smith provide evidence from computational modeling against modular assumptions of “Residual Normality” in developmental disorders. Even though I agree with their criticism, I find their choice of empirical evidence disappointing. Cognitive neuroscience cannot as yet provide a complete understanding of most developmental disorders, but what is known is more than enough to debunk the idea of RN.

Using connectionist modelling, Thomas & Karmiloff-Smith (T&K-S) claim that developmental disorders in children are characterised by atypical trajectories and an ultimate functional architecture that is fundamentally different from normal. We argue that there is no empirical evidence for these claims in any developmental disorder and that the available evidence provides support for Residual Normality in both developmental and acquired disorders. We also refute the claim that modular accounts cannot encompass developmental trajectories in children with (...) developmental disorders. (shrink)

PurposeTo evaluate the prevalence and treatment patterns of speech and language disorders in Germany.MethodsA retrospective analysis of data collected from 32% of the German population, insured by the statutory German health insurance. We used The International Statistical Classification of Diseases and Related Health Problems, 10th revision, German Modification codes for stuttering, cluttering, and developmental disorders of speech and language to identify prevalent and newly diagnosed cases each year. Prescription and speech therapy reimbursement data were used to evaluate (...) treatment patterns.ResultsIn 2017, 27,977 patients of all ages were diagnosed with stuttering. Stuttering prevalence peaks at age 5 years. Cluttering was diagnosed in 1,800 patients of all ages. Developmental disorders of speech and language were identified in 555,774 AOK-insurants. Treatment data indicate a substantial proportion newly diagnosed stuttering individuals receive treatment, with slightly fewer than 20 sessions per year, on average. We confirmed a previous study showing increased rates of atopic disorders and neurological and psychiatric comorbidities in individuals with stuttering, cluttering, and developmental disorders of speech and language.ConclusionThis is the first nationwide study using health insurance data to analyze the prevalence and newly diagnosed cases of a speech and language disorder. Prevalence and gender ratio data were consistent with the international literature. The crude prevalence of developmental disorders of speech and language increased from 2015 to 2018, whereas the crude prevalence for stuttering remained stable. For cluttering, the numbers were too low to draw reliable conclusions. Proportional treatment allocation for stuttering peaked at 6 years of age, which is the school entrance year, and is later than the prevalence peak of stuttering. (shrink)

The developmental modeling approach to investigating developmental disorders appears highly promising. In this commentary, we question the untapped potential of this approach for supporting insights into particular developmental disorders, developmental processes across the life span, and the viability of traditional theories of developmental disorders.

Models of the architecture of mature cognitive systems can inform the study of normal and disordered cognitive development, if one distinguishes between proximal and distal causes of performance. The assumption of residual normality need not be made in order to apply adult models to performance early in development, because these models can be modified to reflect the results of compensatory processing.

Applying a necessary condition communication theory formalism roughly similar to that of Dretske, but focused entirely on the statistical properties of long sequences of signals emitted by the interacting cognitive modules of human biology, we explore the regularities apparent in comorbid psychiatric and chronic physical disorders using an extension of recent perspectives on autoimmune disease. We find that structured psychosocial stress can literally write a distorted image of itself onto child development, resulting in a life course trajectory to characteristic (...) forms of comorbid mind/body dysfunction affecting both dominant and subordinate populations within a pathogenic social hierarchy. (shrink)

Cognitive frameworks provide important means for uniting concepts of specificity, cognition, and dynamic change in development. Two points are challenged by evidence from special populations: (1) that boundary constraints such as Residual Normality and a cognitive “endstate” compromise the use of cognitive models; and (2) the developmental process itself automatically rejects either Residual Normality or residual deviance from typical development.

We raise the new possibility that people diagnosed with developmental dyslexia (DD) are specialized in explorative cognitive search, and rather than having a neurocognitive disorder, play an essential role in human adaptation. Most DD research has studied educational difficulties, with theories framing differences in neurocognitive processes as deficits. However, people with DD are also often proposed to have certain strengths – particularly in realms like discovery, invention, and creativity – that deficit-centered theories cannot explain. We investigate whether these strengths (...) reflect an underlying explorative specialization. We re-examine experimental studies in psychology and neuroscience using the framework ofcognitive search, whereby many psychological processes involve a trade-off between exploration and exploitation. We report evidence of an explorative bias in DD-associated cognitive strategies. High DD prevalence and an attendant explorative bias across multiple areas of cognition suggest the existence of explorative specialization. An evolutionary perspective explains the combination of findings and challenges the view that individuals with DD have a disorder. In cooperating groups, individual specialization is favored when features that confer fitness benefits are functionally incompatible. Evidence for search specialization suggests that, as with some other social organisms, humans mediate the exploration–exploitation trade-off by specializing in complementary strategies. The existence of a system of collective cognitive search that emerges through collaboration would help to explain our species’ exceptional adaptiveness. It also aligns with evidence for substantial variability during our evolutionary history and the notion that humans are adapted not to a particular habitat but to variability itself. Specialization creates interdependence and necessitates balancing complementary strategies. Reframing DD therefore underscores the urgency of changing certain cultural practices to ensure we do not inhibit adaptation. Key improvements would remove cultural barriers to exploration and nurture explorative learning in education, academia, and the workplace, as well as emphasize collaboration over competition. Specialization in complementary search abilities represents a meta-adaptation; through collaboration, this likely enables human groups (as a species and as cultural systems) to successfully adapt. Cultural change to support this system of collaborative search may therefore be essential in confronting the challenges humanity now faces. (shrink)

This focused review is based on earlier studies which have shown that both children and adults diagnosed as having developmental coordination disorder (DCD), benefited from sensorimotor therapy according to the method Retraining for Balance (RB). Different approaches and assessments for children and adults in regard to DCD are scrutinized and discussed in comparison to RB which mainly includes (a) vestibular assessment and stimulation (b) assessment and integration of aberrant primary reflexes and (c) assessment and stimulation of auditory and visual (...) perception. Earlier results indicate that the process of sensorimotor therapy using RB techniques could be described according to a conceptual Kinesthetic-Vestibular Developmental Model (KVDM) whereby the training elicited temporary physical and psychological regressions followed by transformations i.e. positive physical and psychological development. We have also seen that this recurring pattern is similar for children and adults. In our conceptual model vestibular stimulation (perceptual priming) stimulates the nervous system, which might enhance object-related priming. This perceptual priming will also assist the suppression of persistent aberrant primary reflexes. In order to develop effective methods for assessment and intervention of DCD over the life span the importance of primary reflex inhibition and vestibular stimulation as well as a combination of bottom-up and top-down approaches have to be considered. (shrink)

A new etiological model is proposed for schizophrenia that combines variability‐enhancing nonspecific factors acting during development with more specific risk factors. This model is better suited than the current etiological models of schizophrenia, based on the risk factors paradigm, for predicting and/or explaining several important findings about schizophrenia: high co‐morbidity rates, low specificity of many risk factors, and persistence in the population of the associated genetic polymorphisms. Compared with similar models, e.g., de‐canalization, common psychopathology factor, sexual‐selection, or differential sensitivity to (...) the environment, this proposal is more general and integrative. Recently developed research methods have proven the existence of genetic and environmental factors that enhance developmental variability. Applying such methods to newly collected or already available data can allow for testing the hypotheses upon which this model is built. If validated, this model may change the understanding of the etiology of schizophrenia, the research models, and preventionbrk paradigms. (shrink)

Children with developmental language disorder (DLD) served as a test case for determining the role of extant vocabulary knowledge, endogenous attention, and phonological working memory abilities in cross-situational word learning. First-graders (Mage = 7 years; 3 months), 44 with typical development (TD) and 28 with DLD, completed a cross-situational word-learning task comprised six cycles, followed by retention tests and independent assessments of attention, memory, and vocabulary. Children with DLD scored lower than those with TD on all measures of learning (...) and retention, a performance gap that emerged in the first cycle of the cross-situational protocol and that we attribute to weaknesses in initial encoding. Over cycles, children with DLD learned words at a similar rate as their TD peers but they were less flexible in their strategy use, demonstrating a propose-but-verify approach but never a statistical aggregation approach. Also, they drew upon different mechanisms to support their learning. Attention played a greater role for the children with DLD, whereas extant vocabulary size played a greater role for the children with TD. Children navigate the problem space of cross-situational learning via varied routes. This conclusion is offered as motivation for theorists to capture all learners, not just the most typical ones. (shrink)

Attention-deficit/hyperactivity disorder (ADHD) is currently defined as a cognitive/behavioral developmental disorder where all clinical criteria are behavioral. Inattentiveness, overactivity, and impulsiveness are presently regarded as the main clinical symptoms. The dynamic developmental behavioral theory is based on the hypothesis that altered dopaminergic function plays a pivotal role by failing to modulate nondopaminergic (primarily glutamate and GABA) signal transmission appropriately. A hypofunctioning mesolimbic dopamine branch produces altered reinforcement of behavior and deficient extinction of previously reinforced behavior. This gives rise (...) to delay aversion, development of hyperactivity in novel situations, impulsiveness, deficient sustained attention, increased behavioral variability, and failure to “inhibit” responses (“disinhibition”). A hypofunctioning mesocortical dopamine branch will cause attention response deficiencies (deficient orienting responses, impaired saccadic eye movements, and poorer attention responses toward a target) and poor behavioral planning (poor executive functions). A hypofunctioning nigrostriatal dopamine branch will cause impaired modulation of motor functions and deficient nondeclarative habit learning and memory. These impairments will give rise to apparent developmental delay, clumsiness, neurological “soft signs,” and a “failure to inhibit” responses when quick reactions are required. Hypofunctioning dopamine branches represent the main individual predispositions in the present theory. The theory predicts that behavior and symptoms in ADHD result from the interplay between individual predispositions and the surroundings. The exact ADHD symptoms at a particular time in life will vary and be influenced by factors having positive or negative effects on symptom development. Altered or deficient learning and motor functions will produce special needs for optimal parenting and societal styles. Medication will to some degree normalize the underlying dopamine dysfunction and reduce the special needs of these children. The theory describes how individual predispositions interact with these conditions to produce behavioral, emotional, and cognitive effects that can turn into relatively stable behavioral patterns. Key Words: catecholamine; clumsiness; dopamine; hyperkinesis; hyperkinetic disorder; impulsivity; monoamine; neuromodulator; overactivity; pollutants; reinforcement; reward; verbally governed behavior; soft signs; variability. (shrink)

Opioid use disorder rarely presents as a unitary psychiatric condition, and the comorbid symptoms likely depend upon the diverse risk factors and mechanisms by which OUD can arise. These factors are heterogeneous and include genetic predisposition, exposure to prescription opioids, and environmental risks. Crucially, one key environmental risk factor for OUD is early life adversity. OUD and other substance use disorders are widely considered to derive in part from abnormal reward circuit function, which is likely also implicated in comorbid (...) mental illnesses such as depression, bipolar disorder, and schizophrenia. ELA may disrupt reward circuit development and function in a manner predisposing to these disorders. Here, we describe new findings addressing the effects of ELA on reward circuitry that lead to OUD and comorbid disorders, potentially via shared neural mechanisms. We discuss some of these OUD-related problems in both humans and animals. We also highlight the increasingly apparent, crucial contribution of biological sex in mediating the range of ELA-induced disruptions of reward circuitry which may confer risk for the development of OUD and comorbid neuropsychiatric disorders. (shrink)

Cognitive Science, Volume 46, Issue 2, February 2022.

Developmental Coordination Disorder and Attention-Deficit/Hyperactivity Disorder are unique neurodevelopmental disorders with overlaps in executive functions and motor control. The conditions co-occur in up to 50% of cases, raising questions of the pathological mechanisms of DCD versus ADHD. Few studies have examined these overlaps in adults with DCD and/or ADHD. Therefore, to provide insights about executive functions and motor control between adults with DCD, ADHD, both conditions, or typically developed controls, this study used a stop-signal task and parallel EEG (...) measurement. We assessed executive performance via go accuracy and go reaction time, as well as motor response inhibition via stop-signal reaction time. This was complemented with analysis of event-related potentials. Based on existing investigations of adults with DCD or ADHD, we expected groups would not differ in behavioral performance on stop and go trials, but differences in ERPs, particularly in components N200 and P300 would be evident. The sample included N = 50 adults with DCD, ADHD, DCD + ADHD, and control participants. We replicated that there were no between-group differences for behavioral-level executive performance and motor response inhibition. However, on a physiological level, ERP components N200 and P300 differed between groups, particularly during successful response inhibition. These ERPs reflect potential endophenotypic differences not evident in overt behavior of participants with ADHD and/or DCD. This suggests a disorder specific employment of inhibition or general executive functions in groups of adults with DCD, DCD + ADHD, ADHD, or control participants. (shrink)