Mental rotation under head tilt: Factors influencing the location of the subjective reference frame

We report five experiments on the effect of head tilt on the mental rotation of patterns to the “upright.” In Experiment 1, subjects rotated alphanumeric characters, displayed within a circular surround. Experiment 2 was similar except that the character was an unfamiliar letter-like symbol. In Experiment 3, subjects again rotated alphanumeric characters, but they were displayed within a rectangular frame tilted 60° to the right. Experiment 4 was similar, except that the subjects were instructed to rotate the characters to the “upright” defined by the tilted frame. In all four experiments, the subjects performed the task with their heads either upright or tilted 60°. In Experiment 5, subjects had their heads and bodies tilted 90°, and rotated alphanumeric characters displayed within a circular surround. In all except Experiment 4, analysis of response latencies revealed that the subjective vertical lay closer to the gravitational than to the retinal vertical, although it was somewhat displaced in the direction of the head tilt—more so in Experiments 2 and 3 than in Experiment 1, and more so still in Experiment 5. In Experiment 4, instructions to adopt the axes of the frame land thus of the retina) succeeded in bringing the subjective vertical closer to the retinal than to the gravitational vertical, although the subjective vertical was still some 20° on average from the gravitational vertical. The results show that the subjective reference frame is distinct from both gravitational and the retinal frames, and that the gravitational frame exerts the stronger influence. They also argue against the primacy of a “retinal factor” in the perception of orientation.     

The Ontogenesis of Language Impairment in Autism: A Neuropsychological Perspective

Autistic Disorder (AD) is a phenotypically heterogeneous condition characterized by impairments in social interaction, communication, and the presence of repetitive behavior and restricted interests. It is a model syndrome to investigate neural interaction and integration at the nexus of language and social cognition. This paper considers the problems of language acquisition in AD from an evolutionary and ontogenetic context. Following a review of normal language development during the formative years of brain development, we examine what is known about infant linguistic and nonlinguistic precursors of language acquisition in AD and examine how anomalies of several processes relate to language abnormalities manifest by the early elementary school years. Population heterogeneity and practical limitations inherent to the study of children currently limit a comprehensive understanding of the significance of specific neurological abnormalities in relation to observed deficits. However, convergent evidence implicates anomalies of a widely distributed neural network, involving superior temporal sulcus, superior temporal gyrus, supramarginal gyrus, insula, inferior frontal gyrus, hippocampus, amygdala and cerebellum. These anomalies reflect the cumulative effects of genetic, epigenetic and environmental influences. Neuropsychological studies of language in AD provide an important means to define the phenotypic variation resulting from alterations in neural architecture. By mapping broad relationships between key symptoms, neuropsychological impairment and neural substrate, information derived from these studies enable a level of analysis that bridges the gap between the genome and the syndrome. Further study of children during the critical first 2 years of life using behavioral, electrophysiological, and functional neuroimaging methods is essential.     

Acquired epileptiform aphasia: a dimensional view of Landau-Kleffner syndrome and the relation to regressive autistic spectrum disorders.

Acquired epileptiform aphasia (AEA) is characterized by deterioration in language in childhood associated with seizures or epileptiform electroencephalographic abnormalities. Despite an extensive literature, discrepancies and contradictions surround its definition and nosological boundaries. This paper reviews current conceptions of AEA and highlights variations in the aphasic disturbance, age of onset, epileptiform EEG abnormalities, temporal course, and long-term outcome. We suggest that AEA, rather than being a discrete entity, is comprised of multiple variants that have in common the features of language regression and epileptiform changes on EEG. Viewed this way, we argue that AEA can be conceptualized on a spectrum with other epileptiform neurocognitive disorders that may share pathophysiological features. The implications of this viewpoint are discussed, with emphasis on parallels between the AEA variants and regressive autistic spectrum disorders.     

Regression in Autistic Spectrum Disorders

A significant proportion of children diagnosed with Autistic Spectrum Disorder experience a developmental regression characterized by a loss of previously-acquired skills. This may involve a loss of speech or social responsitivity, but often entails both. This paper critically reviews the phenomena of regression in autistic spectrum disorders, highlighting the characteristics of regression, age of onset, temporal course, and long-term outcome. Important considerations for diagnosis are discussed and multiple etiological factors currently hypothesized to underlie the phenomenon are reviewed. It is argued that regressive autistic spectrum disorders can be conceptualized on a spectrum with other regressive disorders that may share common pathophysiological features. The implications of this viewpoint are discussed.     

Etiologic Subtypes of Attention-Deficit/Hyperactivity Disorder: Brain Imaging, Molecular Genetic and Environmental Factors and the Dopamine Hypothesis

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.     

Attention-Deficit/Hyperactivity Disorder: A Neuropsychological Perspective Towards DSM-V

Neuropsychological methods and techniques have much to offer in the evaluation of the individual suspected as having Attention-Deficit/Hyperactivity Disorder (ADHD). After a review of the historical evolution of the ADHD concept, incidence and prevalence, and DSM-IV criteria for diagnosis, especially as regards omission related to gender differences, and other associated cultural, familial, socioenvironmental, and subject influences, this paper describes a number of dilemmas and obstacles encountered in clinical practice. Included are the confounds associated with the wide range of possible comorbidities, the insufficiency of current DSM-IV criteria, the emergence of subtype differentiation and its impact on diagnosis and treatment. The complex relationship between neuropsychological constructs and ADHD, and obstacles to valid assessment are also addressed. The complexities associated with a thorough ADHD evaluation are viewed within an impressive and expansive existing scientific framework and recommendations are made for future directions.