There is disagreement in the literature about the exact nature of the phenomenon of empathy. There are emotional, cogni- tive, and conditioning views, applying in varying degrees across species. An adequate description of the ultimate and proximate mecha- nism can integrate these views. Proximately, the perception of an object's state activates the subject's corresponding representations, which in turn activate somatic and autonomic responses. This mechanism supports basic behaviors (e.g., alarm, social facilitation, vicar- iousness of emotions, mother-infant responsiveness, and the modeling of competitors and predators) that are crucial for the reproduc- tive success of animals living in groups. The Perception-Action Model (PAM), together with an understanding of how representations change with experience, can explain the major empirical effects in the literature (similarity, familiarity, past experience, explicit teach- ing, and salience). It can also predict a variety of empathy disorders. The interaction between the PAM and prefrontal functioning can also explain different levels of empathy across species and age groups. This view can advance our evolutionary understanding of empa- thy beyond inclusive fitness and reciprocal altruism and can explain different levels of empathy across individuals, species, stages of de- velopment, and situations.

/pdf/empathy-its-ultimate-and-proximate-bases-3gnr9okjki.pdf

Empathy: Its ultimate and proximate bases.

Autism is a severe neurobehavioral syndrome, arising largely as an inherited disorder, which can arise from several diseases. Despite recent advances in identifying some genes that can cause autism, its underlying neurological mechanisms are uncertain. Autism is best conceptualized by considering the neural systems that may be defective in autistic individuals. Recent advances in understanding neural systems that process sensory information, various types of memories and social and emotional behaviors are reviewed and compared with known abnormalities in autism. Then, specific genetic abnormalities that are linked with autism are examined. Synthesis of this information leads to a model that postulates that some forms of autism are caused by an increased ratio of excitation/inhibition in sensory, mnemonic, social and emotional systems. The model further postulates that the increased ratio of excitation/inhibition can be caused by combinatorial effects of genetic and environmental variables that impinge upon a given neural system. Furthermore, the model suggests potential therapeutic interventions.

https://onlinelibrary.wiley.com/doi/epdf/10.1034/j.1601-183X.2003.00037.x

Model of autism: increased ratio of excitation/inhibition in key neural systems

Autism spectrum disorders are not rare; many primary care pediatricians care for several children with autism spectrum disorders. Pediatricians play an important role in early recognition of autism spectrum disorders, because they usually are the first point of contact for parents. Parents are now much more aware of the early signs of autism spectrum disorders because of frequent coverage in the media; if their child demonstrates any of the published signs, they will most likely raise their concerns to their child's pediatrician. It is important that pediatricians be able to recognize the signs and symptoms of autism spectrum disorders and have a strategy for assessing them systematically. Pediatricians also must be aware of local resources that can assist in making a definitive diagnosis of, and in managing, autism spectrum disorders. The pediatrician must be familiar with developmental, educational, and community resources as well as medical subspecialty clinics. This clinical report is 1 of 2 documents that replace the original American Academy of Pediatrics policy statement and technical report published in 2001. This report addresses background information, including definition, history, epidemiology, diagnostic criteria, early signs, neuropathologic aspects, and etiologic possibilities in autism spectrum disorders. In addition, this report provides an algorithm to help the pediatrician develop a strategy for early identification of children with autism spectrum disorders. The accompanying clinical report addresses the management of children with autism spectrum disorders and follows this report on page 1162 [available at www.pediatrics.org/cgi/content/full/120/5/1162]. Both clinical reports are complemented by the toolkit titled "Autism: Caring for Children With Autism Spectrum Disorders: A Resource Toolkit for Clinicians," which contains screening and surveillance tools, practical forms, tables, and parent handouts to assist the pediatrician in the identification, evaluation, and management of autism spectrum disorders in children.

/pdf/identification-and-evaluation-of-children-with-autism-47d21l77u4.pdf

Identification and Evaluation of Children With Autism Spectrum Disorders

Summary The brain activation of a group of high-functioning autistic participants was measured using functional MRI during sentence comprehension and the results compared with those of a Verbal IQ-matched control group. The groups differed in the distribution of activation in two of the key language areas. The autism group produced reliably more activation than the control group in Wernicke’s (left laterosuperior temporal) area and reliably less activation than the control group in Broca’s (left inferior frontal gyrus) area. Furthermore, the functional connectivity, i.e. the degree of synchronization or correlation of the time series of the activation, between the various participating cortical areas was consistently lower for the autistic than the control participants. These findings suggest that the neural basis of disordered language in autism entails a lower degree of information integration and synchronization across the large-scale cortical network for language processing. The article presents a theoretical account of the findings, related to neurobiological foundations of underconnectivity in autism.

Cortical activation and synchronization during sentence comprehension in high-functioning autism: evidence of underconnectivity

https://www.cell.com/trends/neurosciences/pdf/S0166-2236(08)00038-6.pdf

Neuroanatomy of autism

Objective: To determine whether differences exist in the configuration of minicolumns between the brains of autistic and control patients. Background: Autism is a severe and pervasive developmental disturbance of childhood characterized by disturbances in both social interactions and communication, as well as stereotyped patterns of interests, activities, and behaviors. Postmortem neuropathologic studies remain inconclusive. Methods: The authors used a computerized imaging program to measure details of cell column morphologic features in area 9 of the prefrontal cortex and areas 21 and posterior 22 (Tpt) within the temporal lobe of nine brains of autistic patients and controls. Results: The authors found significant differences between brains of autistic patients and controls in the number of minicolumns, in the horizontal spacing that separates cell columns, and in their internal structure, that is, relative dispersion of cells. Specifically, cell columns in brains of autistic patients were more numerous, smaller, and less compact in their cellular configuration with reduced neuropil space in the periphery. Conclusions: In autism, there are minicolumnar abnormalities in the frontal and temporal lobes of the brain.

Minicolumnar pathology in autism.

Gross analyses of large brain areas, as in MRI studies of macroanatomical structures, average subtle alterations in small regions, inadvertently missing significant anomalies. We developed a computeri

Lateralization of minicolumns in human planum temporale is absent in nonhuman primate cortex.

Although neuropathologic studies have centered on small samples, it is accepted that brains of autistic individuals tend to be large, on average. Knowledge regarding the cause of this macrocephaly is limited. Postmortem studies reveal little in terms of cortical dysplasia. Some of these studies suggest increased cell-packing density in subcortical structures. These neuronomorphometric studies have been subjective or based their conclusions on measures of neuronal density. Our study sought the possible presence of increased cell-packing density by using the Gray Level Index. The Gray Level Index is defined as the ratio of the area covered by Nissl-stained elements to unstained area in postmortem samples. Analyzed images included Brodmann's cortical areas 9, 21, and 22 of 9 autistic patients (7 males, 2 females; mean age of 12 years, with a range of 5 to 28 years) and 11 normal controls (7 males, 4 females; mean age of 14 years, with a range of 3 to 25 years). The overall multivariate test revealed significant differences both between autistic patients and controls (P = .001) and between hemispheres (P = .025). Follow-up univariate tests showed significant diagnosis-dependent effects in feature distance (P = .005), the standard deviation in distance (P = .016), and feature amplitude (P = .001). The overall mean Gray Level Index was 19.4% in controls and 18.7% in autism (P = .724). In autism, an increased number of minicolumns, combined with fewer cells per column (or their greater dispersion), results in no global difference in neuronal density.

Neuronal density and architecture (Gray Level Index) in the brains of autistic patients.

Asperger's disorder or syndrome is characterized by impaired social interaction, normal intelligence, and adequate language skills in the areas of grammar and vocabulary. The symptoms are pervasive in nature and usually manifested in childhood. Despite the gravity and chronicity of the condition, the medical literature remains sparse and offers no information about possible neuropathologic underpinnings. The present study is a case report on two patients with Asperger's syndrome. Neuropathologic examination revealed no degenerative changes or gliosis. A more detailed assessment with computerized image analysis indicated abnormalities in the minicolumnar organization of the three areas examined (9, 21, 22) (P = .032). Specifically, minicolumns were smaller, and their component cells were more dispersed than normal. A similar neuropathology has recently been reported for autism and disputes the uniqueness of these findings. The minicolumnar changes provide a possible link to receptive field abnormalities and a useful clinicopathologic correlate to Asperger's syndrome.

Asperger's syndrome and cortical neuropathology.

The minicolumn is an anatomical and functional unit of the brain whose genesis accrues from germinal cell divisions in the ventricular zone of the brain. Disturbances in the morphometry of minicolumns have been demonstrated recently for both autism and Down's syndrome. We report minicolumnar abnormalities in the brain of a dyslexic patient. The corresponding developmental disturbance (ie, large minicolumns) could account for the perceptual errors observed in dyslexia.

Emil Roy

Papers

Minicolumnar pathology in autism.

Lateralization of minicolumns in human planum temporale is absent in nonhuman primate cortex.

Neuronal density and architecture (Gray Level Index) in the brains of autistic patients.

Asperger's syndrome and cortical neuropathology.

Minicolumnar pathology in dyslexia