Reading and Spelling Disabilities in Children with and Without a History of Early Language Delay: A Neuropsychological and Linguistic Study

Language delay is a frequent antecedent of literacy problems, and both may be linked to phonological impairment. Studies on developmental dyslexia have led to contradictory results due to the heterogeneity of the pathological samples. The present study investigated whether Italian children with dyslexia showed selective phonological processing deficits or more widespread linguistic impairment and whether these deficits were associated with previous language delay. We chose 46 children with specific reading deficits and divided them into two groups based on whether they had language delay (LD) or not (NoLD). LD and NoLD children showed similar, severe deficits in reading and spelling decoding, but only LD children showed a moderate impairment in reading comprehension. LD children were more impaired in phonological working memory and phonological fluency, as well as in semantic fluency, grammatical comprehension, and verbal IQ. These findings indicate the presence of a moderate but widespread linguistic deficit (not limited to phonological processing) in a subset of dyslexic children with previous language delay that does not generalize to all children with reading difficulties.     

Developmental cognitive genetics: how psychology can inform genetics and vice versa

Developmental neuropsychology is concerned with uncovering the underlying basis of developmental disorders such as specific language impairment (SLI), developmental dyslexia, and autistic disorder. Twin and family studies indicate that genetic influences play an important part in the aetiology of all of these disorders, yet progress in identifying genes has been slow. One way forward is to cut loose from conventional clinical criteria for diagnosing disorders and to focus instead on measures of underlying cognitive mechanisms. Psychology can inform genetics by clarifying what the key dimensions are for heritable phenotypes. However, it is not a one-way street. By using genetically informative designs, one can gain insights about causal relationships between different cognitive deficits. For instance, it has been suggested that low-level auditory deficits cause phonological problems in SLI. However, a twin study showed that, although both types of deficit occur in SLI, they have quite different origins, with environmental factors more important for auditory deficit, and genes more important for deficient phonological short-term memory. Another study found that morphosyntactic deficits in SLI are also highly heritable, but have different genetic origins from impairments of phonological short-term memory. A genetic perspective shows that a search for the underlying cause of developmental disorders may be misguided, because they are complex and heterogeneous and are associated with multiple risk factors that only cause serious disability when they occur in combination.     

Developmental cognitive genetics: How psychology can inform genetics and vice versa

Developmental neuropsychology is concerned with uncovering the underlying basis of developmental disorders such as specific language impairment (SLI), developmental dyslexia, and autistic disorder. Twin and family studies indicate that genetic influences play an important part in the aetiology of all of these disorders, yet progress in identifying genes has been slow. One way forward is to cut loose from conventional clinical criteria for diagnosing disorders and to focus instead on measures of underlying cognitive mechanisms. Psychology can inform genetics by clarifying what the key dimensions are for heritable phenotypes. However, it is not a one-way street. By using genetically informative designs, one can gain insights about causal relationships between different cognitive deficits. For instance, it has been suggested that low-level auditory deficits cause phonological problems in SLI. However, a twin study showed that, although both types of deficit occur in SLI, they have quite different origins, with environmental factors more important for auditory deficit, and genes more important for deficient phonological short-term memory. Another study found that morphosyntactic deficits in SLI are also highly heritable, but have different genetic origins from impairments of phonological short-term memory. A genetic perspective shows that a search for the underlying cause of developmental disorders may be misguided, because they are complex and heterogeneous and are associated with multiple risk factors that only cause serious disability when they occur in combination.     

获得性阅读障碍的“主要系统”假说

认知神经心理学为阅读机制的探讨提供了大量的证据,认为不同阅读障碍是不同加工通道选择性受损的结果。近年来,基于联结主义的三角模型理论,研究者提出了主要系统假说（primary system hypothesis）,认为阅读障碍是主要的认知系统（如视觉、语义和语音系统）受损导致的：表层障碍是因为语义系统受损导致的阅读困难,语音和深层障碍是语音和语义系统同时受损时综合症状的连续体。该理论认为各主要系统可能同时是多个认知活动的加工成分,一个系统的受损会影响所有与之相关的认知过程,从而把阅读障碍与其它认知功能障碍联系起来。统一的主要系统受损下对各种获得性阅读障碍形成机制在文中得到详细的解释     

Are developmental disorders like cases of adult brain damage? Implications from connectionist modelling

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.     

Contributions of memory circuits to language: the declarative/procedural model

The structure of the brain and the nature of evolution suggest that, despite its uniqueness, language likely depends on brain systems that also subserve other functions. The declarative/procedural (DP) model claims that the mental lexicon of memorized word-specific knowledge depends on the largely temporal-lobe substrates of declarative memory, which underlies the storage and use of knowledge of facts and events. The mental grammar, which subserves the rule-governed combination of lexical items into complex representations, depends on a distinct neural system. This system, which is composed of a network of specific frontal, basal-ganglia, parietal and cerebellar structures, underlies procedural memory, which supports the learning and execution of motor and cognitive skills, especially those involving sequences. The functions of the two brain systems, together with their anatomical, physiological and biochemical substrates, lead to specific claims and predictions regarding their roles in language. These predictions are compared with those of other neurocognitive models of language. Empirical evidence is presented from neuroimaging studies of normal language processing, and from developmental and adult-onset disorders. It is argued that this evidence supports the DP model. It is additionally proposed that "language" disorders, such as specific language impairment and non-fluent and fluent aphasia, may be profitably viewed as impairments primarily affecting one or the other brain system. Overall, the data suggest a new neurocognitive framework for the study of lexicon and grammar.     

The neural underpinnings of prosody in autism

This study examines the processing of prosodic cues to linguistic structure and to affect, drawing on fMRI and behavioral data from 16 high-functioning adolescents with autism spectrum disorders (ASD) and 11 typically developing controls. Stimuli were carefully matched on pitch, intensity, and duration, while varying systematically in conditions of affective prosody (angry versus neutral speech) and grammatical prosody (questions versus statement). To avoid conscious attention to prosody, which normalizes responses in young people with ASD, the implicit comprehension task directed attention to semantic aspects of the stimuli. Results showed that when perceiving prosodic cues, both affective and grammatical, activation of neural regions was more generalized in ASD than in typical development, and areas recruited reflect heightened reliance on cognitive control, reading of intentions, attentional management, and visualization. This broader recruitment of executive and "mind-reading" brain areas for a relative simple language-processing task may be interpreted to suggest that speakers with high-functioning autism (HFA) have developed less automaticity in language processing and may also suggest that "mind-reading" or theory of mind deficits are intricately bound up in language processing. Data provide support for both a right-lateralized as well as a bilateral model of prosodic processing in typical individuals, depending upon the function of the prosodic information.     

Genes, language development, and language disorders

Genetic factors are important contributors to language and learning disorders, and discovery of the underlying genes can help delineate the basic neurological pathways that are involved. This information, in turn, can help define disorders and their perceptual and processing deficits. Initial molecular genetic studies of dyslexia, for example, appear to converge on defects in neuronal and axonal migration. Further study of individuals with abnormalities of these genes may lead to the recognition of characteristic cognitive deficits attributable to the neurological dysfunction. Such abnormalities may affect other disorders as well, and studies of co-morbidity of dyslexia with attention deficit disorder and speech sound disorder are helping to define the scope of these genes and show the etiological and cognitive commonalities between these conditions. The genetic contributions to specific language impairment (SLI) are not as well defined at this time, but similar molecular approaches are being applied to identify genes that influence SLI and comorbid disorders. While there is co-morbidity of SLI with dyslexia, it appears that most of the common genetic effects may be with the language characteristics of autism spectrum disorders rather than with dyslexia and related disorders. Identification of these genes and their neurological and cognitive effects should lay out a functional network of interacting genes and pathways that subserve language development. Understanding these processes can form the basis for refined procedures for diagnosis and treatment.     

Mechanisms of verbal memory impairment in four neurodevelopmental disorders

Profiles of verbal learning and memory performance were compared for typically developing children and for four developmental disorders characterized by different patterns of language functioning: specific language impairment, early focal brain damage, Williams Syndrome, and Down Syndrome. A list-learning task was used that allowed a detailed examination of the process of verbal learning, recall, and recognition (California Verbal Learning Test--Children's Version). Distinct patterns of performance characterized the four disorders. These patterns were consistent with the language deficits typically seen in the disorders, with the exception of a dissociation seen in Williams Syndrome.     

认知神经心理学简介

认知神经心理学是认知心理学的一个分支。它的目的是探讨当人们执行认知活动的时候,心理信息加工过程是怎样的,所采用的手段是研究这些认知功能受损的病人。它与认知神经科学的不同在于：认知神经心理学关注的是心理（mind）,而认知神经科学关注的是大脑（特别是关注与认知有关的大脑机制）。研究认知神经心理学的方法也可以用于研究发展性认知障碍,如阅读障碍,或者特殊的语言损伤,这就是发展性认知神经心理学。这些方法还可以用于高级认知发面的研究,如信念形成和心理理论。这些高级认知方面的障碍是精神病学的范畴,因此这类研究错觉、幻想或虚构等的认知神经心理学叫做认知神经精神病学。认知神经心理学的典型特征有：1）研究症状,而不是并发症;2）采用个案研究,而不是群体研究;3）主要数据来源是症状间的双分离;4）致力于模块化认知模型的建立。     

Speech perception and short-term memory deficits in persistent developmental speech disorder

Children with developmental speech disorders may have additional deficits in speech perception and/or short-term memory. To determine whether these are only transient developmental delays that can accompany the disorder in childhood or persist as part of the speech disorder, adults with a persistent familial speech disorder were tested on speech perception and short-term memory. Nine adults with a persistent familial developmental speech disorder without language impairment were compared with 20 controls on tasks requiring the discrimination of fine acoustic cues for word identification and on measures of verbal and nonverbal short-term memory. Significant group differences were found in the slopes of the discrimination curves for first formant transitions for word identification with stop gaps of 40 and 20 ms with effect sizes of 1.60 and 1.56. Significant group differences also occurred on tests of nonverbal rhythm and tonal memory, and verbal short-term memory with effect sizes of 2.38, 1.56, and 1.73. No group differences occurred in the use of stop gap durations for word identification. Because frequency-based speech perception and short-term verbal and nonverbal memory deficits both persisted into adulthood in the speech-impaired adults, these deficits may be involved in the persistence of speech disorders without language impairment.     

Verbal Declarative Memory Dysfunction in Schizophrenia: From Clinical Assessment to Genetics and Brain Mechanisms

The recent literature on the neuropsychology of schizophrenia has emphasized memory deficits as a key area of impairment. Abnormalities in the medial temporal lobe, a brain region crucial for long-term memory formation, have also consistently been reported. We conducted a comprehensive review of verbal declarative memory (VDM) in schizophrenia with the aim of systematically addressing the nature of this impairment. We conclude that verbal declarative memory is significantly impaired in schizophrenia and is largely accounted for by deficits in the encoding stage. Subtle impairments in increased rates of forgetting are present, but are mild compared with those in amnestic disorders. Impairment in other cognitive domains studied thus far (e.g., attention), medication effects, or fluctuations in symptoms do not completely account for the deficit. VDM is among the most impaired neurocognitive domains in schizophrenia (along with attention and executive functions). Milder encoding deficits are present in high-risk subjects and non-psychotic relatives of individuals with schizophrenia suggesting that components of the deficit are associated with a genetic vulnerability to the illness, and are independent of the frank psychotic illness. Furthermore, VDM is observed in individuals experiencing their first-psychotic episode and it remains fairly consistent over time. Preliminary imaging studies and other work suggest abnormalities in prefrontal-hippocampal processing networks. Future work should emphasize delineating specific information processing components contributing to the deficit. This would allow imaging studies to determine which brain regions contribute to specific information processing deficits in schizophrenia.     

Specific language impairment in children: A cross-linguistic study

A common profile in English-speaking specifically language-impaired children is a moderate deficit across a broad range of linguistic features and a more marked, selective impairment in using bound morphemes and components of the verb system. To gain a clearer understanding of the nature of these more serious problems, we examined the speech of monolingual Italian-speaking as well as English-speaking children with specific language impairment. The evidence suggested that phonological factors contributed significantly to these children's extraordinary problems with particular linguistic features. Contrary to expectations, other marked deficits seemed more related to the opacity of the rules involved and homonymity with other morphemes than to problems with formal grammatical devices in general or components of the verb system in particular.     

Domain-specific cognitive systems: insight from Grammatical-SLI

Specific language-impairment (SLI) is a disorder of language acquisition in children who otherwise appear to be normally developing. Controversy surrounds whether SLI results from impairment to a "domain-specific" system devoted to language itself or from some more "domain-general" system. I compare these two views of SLI, and focus on three components of grammar that are good candidates for domain-specificity: syntax, morphology and phonology. I argue that the disorder is heterogeneous, and that deficits of different subgroups potentially stem from different underlying causes. Interestingly, although poor sensory or non-verbal abilities often co-occur with SLI, there is no evidence that these impairments cause the grammatical deficits found in SLI. Moreover, evidence suggests that impairment in at least one subgroup is specific to grammar.     

ADHD and DCD: a relationship in need of research

Although the connection between attention deficit hyperactivity disorder (ADHD) and developmental coordination disorder (DCD) has been recognized for several decades, little research has examined the relationship between these two disorders. This paper draws attention to the contribution the cognitive-energetic model (CEM) can make in determining the specific nature of these two disorders. An information processing approach such as the CEM is a useful model to identify specific and overlapping mechanisms that are disrupted in these two disorders. This paper describes the CEM and reviews the research so-far in relation to the model. The CEM has several advantages over other models: First, it predicts which task variables will be independent or may interact, thus enabling the investigator to determine the success/failure of the task manipulation(s) and identify spurious findings. Second, the CEM links energetic factors to task variables and predicts both additive and interactive effects. Third, the CEM enables executive processes such as selective attention, working memory and inhibition to be related to both energetic and lower level processes. Fourth, by employing the CEM in clinical research, taxonomy of deficits can be derived enabling further insight into the nature of the disorders and their specific neuropsychological dysfunction. Suggestions are made for future research into the neuropsychological deficits associated with ADHD and DCD.     

Genetic influences on language impairment and phonological short-term memory

It has been known for some years that specific language impairment (SLI), an unexpected failure to acquire age-appropriate language skills, is highly heritable. However, molecular genetic studies have been hampered by the heterogeneity of the disorder and the predominant lack of clear genotype-phenotype relationships. We review recent studies suggesting that a better understanding of the genetics of SLI might emerge if we move away from clinical criteria for diagnosis to look instead at a theoretically based quantitative and cognitive measure of the phenotype: a test of phonological short-term memory (STM). Deficient phonological STM has been linked to specific genetic loci, and might play a role in determining some types of reading impairment as well as SLI. Identifying those cognitive deficits that work best as indices of heritable phenotypes will help us to uncover the aetiology of developmental disorders.     

Cognitive deficits in developmental disorders

The existence of specific developmental disorders such as dyslexia and autism raises interesting issues about the structure of the normally developing mind. In these disorders distinct cognitive deficits can explain a range of behavioural impairments and have the potential to be linked to specific brain abnormalities. One possibility is that there are specific mechanisms dedicated to particular types of information processing. These mechanisms may function independently of more general information processing systems and may have a distinct anatomical basis in the brain.     

The neural underpinnings of prosody in autism

This study examines the processing of prosodic cues to linguistic structure and to affect, drawing on fMRI and behavioral data from 16 high-functioning adolescents with autism spectrum disorders (ASD) and 11 typically developing controls. Stimuli were carefully matched on pitch, intensity, and duration, while varying systematically in conditions of affective prosody (angry versus neutral speech) and grammatical prosody (questions versus statement). To avoid conscious attention to prosody, which normalizes responses in young people with ASD, the implicit comprehension task directed attention to semantic aspects of the stimuli. Results showed that when perceiving prosodic cues, both affective and grammatical, activation of neural regions was more generalized in ASD than in typical development, and areas recruited reflect heightened reliance on cognitive control, reading of intentions, attentional management, and visualization. This broader recruitment of executive and “mind-reading” brain areas for a relative simple language-processing task may be interpreted to suggest that speakers with high-functioning autism (HFA) have developed less automaticity in language processing and may also suggest that “mind-reading” or theory of mind deficits are intricately bound up in language processing. Data provide support for both a right-lateralized as well as a bilateral model of prosodic processing in typical individuals, depending upon the function of the prosodic information.     

The effect of communication deficits on anxiety symptoms in infants and toddlers with autism spectrum disorders

Autism spectrum disorders (ASDs) are life-long developmental disorders characterized by impairments in the development of reciprocal social and communication skills, abnormal language development, and a restricted repertoire of behaviors and interests. While it has been known for some time that children with ASD can evince elevated rates of anxiety symptoms, little research has been conducted on whether deficits in communication skills affect the range of anxiety symptoms in infants and toddlers with ASD. This study represents a first attempt to determine whether deficits in communication skills have an effect on the expression of anxiety in infants and toddlers with autistic disorder and pervasive developmental disorder-not otherwise specified. Seven hundred thirty-five infants were evaluated with respect to the nature and extent of anxiety symptoms and developmental functioning. Both receptive and expressive communication skills appeared to play a significant role in the manifestation of anxiety symptoms.