scholarly journals The Superior Visual Perception Hypothesis: Neuroaesthetics of Cave Art

2021 ◽  
Vol 11 (6) ◽  
pp. 81
Author(s):  
Per Olav Folgerø ◽  
Christer Johansson ◽  
Linn Heidi Stokkedal

Cave Art in the Upper Paleolithic presents a boost of creativity and visual thinking. What can explain these savant-like paintings? The normal brain function in modern man rarely supports the creation of highly detailed paintings, particularly the convincing representation of animal movement, without extensive training and access to modern technology. Differences in neuro-signaling and brain anatomy between modern and archaic Homo sapiens could also cause differences in perception. The brain of archaic Homo sapiens could perceive raw detailed information without using pre-established top-down concepts, as opposed to the common understanding of the normal modern non-savant brain driven by top-down control. Some ancient genes preserved in modern humans may be expressed in rare disorders. Researchers have compared Cave Art with art made by people with autism spectrum disorder. We propose that archaic primary consciousness, as opposed to modern secondary consciousness, included a savant-like perception with a superior richness of details compared to modern man. Modern people with high frequencies of Neanderthal genes, have notable anatomical features such as increased skull width in the occipital and parietal visual areas. We hypothesize that the anatomical differences are functional and may allow a different path to visual perception.

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Jun Nomura ◽  
Toru Takumi

The development of genetic technologies has led to the identification of several copy number variations (CNVs) in the human genome. Genome rearrangements affect dosage-sensitive gene expression in normal brain development. There is strong evidence associating human psychiatric disorders, especially autism spectrum disorders (ASDs) and schizophrenia to genetic risk factors and accumulated CNV risk loci. Deletions in 1q21, 3q29, 15q13, 17p12, and 22q11, as well as duplications in 16p11, 16p13, and 15q11-13 have been reported as recurrent CNVs in ASD and/or schizophrenia. Chromosome engineering can be a useful technology to reflect human diseases in animal models, especially CNV-based psychiatric disorders. This system, based on the Cre/loxPstrategy, uses large chromosome rearrangement such as deletion, duplication, inversion, and translocation. Although it is hard to reflect human pathophysiology in animal models, some aspects of molecular pathways, brain anatomy, cognitive, and behavioral phenotypes can be addressed. Some groups have created animal models of psychiatric disorders, ASD, and schizophrenia, which are based on human CNV. These mouse models display some brain anatomical and behavioral abnormalities, providing insight into human neuropsychiatric disorders that will contribute to novel drug screening for these devastating disorders.


2020 ◽  
Author(s):  
Amandine Lassalle ◽  
Michael X Cohen ◽  
Laura Dekkers ◽  
Elizabeth Milne ◽  
Rasa Gulbinaite ◽  
...  

Background: People with an Autism Spectrum Condition diagnosis (ASD) are hypothesized to show atypical neural dynamics, reflecting differences in neural structure and function. However, previous results regarding neural dynamics in autistic individuals have not converged on a single pattern of differences. It is possible that the differences are cognitive-set-specific, and we therefore measured EEG in autistic individuals and matched controls during three different cognitive states: resting, visual perception, and cognitive control.Methods: Young adults with and without an ASD (N=17 in each group) matched on age (range 20 to 30 years), sex, and estimated Intelligence Quotient (IQ) were recruited. We measured their behavior and their EEG during rest, a task requiring low-level visual perception of gratings of varying spatial frequency, and the “Simon task” to elicit activity in the executive control network. We computed EEG power and Inter-Site Phase Clustering (ISPC; a measure of connectivity) in various frequency bands.Results: During rest, there were no ASD vs. controls differences in EEG power, suggesting typical oscillation power at baseline. During visual processing, without pre-baseline normalization, we found decreased broadband EEG power in ASD vs. controls, but this was not the case during the cognitive control task. Furthermore, the behavioral results of the cognitive control task suggest that autistic adults were better able to ignore irrelevant stimuli.Conclusions: Together, our results defy a simple explanation of overall differences between ASD and controls, and instead suggest a more nuanced pattern of altered neural dynamics that depend on which neural networks are engaged.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kate McGrath ◽  
Laura Sophia Limmer ◽  
Annabelle-Louise Lockey ◽  
Debbie Guatelli-Steinberg ◽  
Donald J. Reid ◽  
...  

AbstractEarly life stress disrupts growth and creates horizontal grooves on the tooth surface in humans and other mammals, yet there is no consensus for their quantitative analysis. Linear defects are considered to be nonspecific stress indicators, but evidence suggests that intermittent, severe stressors create deeper defects than chronic, low-level stressors. However, species-specific growth patterns also influence defect morphology, with faster-growing teeth having shallower defects at the population level. Here we describe a method to measure the depth of linear enamel defects and normal growth increments (i.e., perikymata) from high-resolution 3D topographies using confocal profilometry and apply it to a diverse sample of Homo neanderthalensis and H. sapiens anterior teeth. Debate surrounds whether Neanderthals exhibited modern human-like growth patterns in their teeth and other systems, with some researchers suggesting that they experienced more severe childhood stress. Our results suggest that Neanderthals have shallower features than H. sapiens from the Upper Paleolithic, Neolithic, and medieval eras, mirroring the faster growth rates in Neanderthal anterior teeth. However, when defect depth is scaled by perikymata depth to assess their severity, Neolithic humans have less severe defects, while Neanderthals and the other H. sapiens groups show evidence of more severe early life growth disruptions.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lison Martinet ◽  
Cédric Sueur ◽  
Satoshi Hirata ◽  
Jérôme Hosselet ◽  
Tetsuro Matsuzawa ◽  
...  

AbstractTechniques used in cave art suggest that drawing skills emerged long before the oldest known representative human productions (44,000 years bc). This study seeks to improve our knowledge of the evolutionary origins and the ontogenetic development of drawing behavior by studying drawings of humans (N = 178, 3- to 10-year-old children and adults) and chimpanzees (N = 5). Drawings were characterized with an innovative index based on spatial measures which provides the degree of efficiency for the lines that are drawn. Results showed that this index was lowest in chimpanzees, increased and reached its maximum between 5-year-old and 10-year-old children and decreased in adults, whose drawing efficiency was reduced by the addition of details. Drawings of chimpanzees are not random suggesting that their movements are constrained by cognitive or locomotor aspect and we cannot conclude to the absence of representativeness. We also used indices based on colors and time and asked children about what they drew. These indices can be considered relevant tools to improve our understanding of drawing development and evolution in hominids.


2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Domenica Veniero ◽  
Joachim Gross ◽  
Stephanie Morand ◽  
Felix Duecker ◽  
Alexander T. Sack ◽  
...  

AbstractVoluntary allocation of visual attention is controlled by top-down signals generated within the Frontal Eye Fields (FEFs) that can change the excitability of lower-level visual areas. However, the mechanism through which this control is achieved remains elusive. Here, we emulated the generation of an attentional signal using single-pulse transcranial magnetic stimulation to activate the FEFs and tracked its consequences over the visual cortex. First, we documented changes to brain oscillations using electroencephalography and found evidence for a phase reset over occipital sites at beta frequency. We then probed for perceptual consequences of this top-down triggered phase reset and assessed its anatomical specificity. We show that FEF activation leads to cyclic modulation of visual perception and extrastriate but not primary visual cortex excitability, again at beta frequency. We conclude that top-down signals originating in FEF causally shape visual cortex activity and perception through mechanisms of oscillatory realignment.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Yuen Gao ◽  
Natalia Duque-Wilckens ◽  
Mohammad B. Aljazi ◽  
Yan Wu ◽  
Adam J. Moeser ◽  
...  

AbstractAutism spectrum disorder (ASD) is a neurodevelopmental disease associated with various gene mutations. Recent genetic and clinical studies report that mutations of the epigenetic gene ASH1L are highly associated with human ASD and intellectual disability (ID). However, the causality and underlying molecular mechanisms linking ASH1L mutations to genesis of ASD/ID remain undetermined. Here we show loss of ASH1L in the developing mouse brain is sufficient to cause multiple developmental defects, core autistic-like behaviors, and impaired cognitive memory. Gene expression analyses uncover critical roles of ASH1L in regulating gene expression during neural cell development. Thus, our study establishes an ASD/ID mouse model revealing the critical function of an epigenetic factor ASH1L in normal brain development, a causality between Ash1L mutations and ASD/ID-like behaviors in mice, and potential molecular mechanisms linking Ash1L mutations to brain functional abnormalities.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Chloé Stengel ◽  
Marine Vernet ◽  
Julià L. Amengual ◽  
Antoni Valero-Cabré

AbstractCorrelational evidence in non-human primates has reported increases of fronto-parietal high-beta (22–30 Hz) synchrony during the top-down allocation of visuo-spatial attention. But may inter-regional synchronization at this specific frequency band provide a causal mechanism by which top-down attentional processes facilitate conscious visual perception? To address this question, we analyzed electroencephalographic (EEG) signals from a group of healthy participants who performed a conscious visual detection task while we delivered brief (4 pulses) rhythmic (30 Hz) or random bursts of Transcranial Magnetic Stimulation (TMS) to the right Frontal Eye Field (FEF) prior to the onset of a lateralized target. We report increases of inter-regional synchronization in the high-beta band (25–35 Hz) between the electrode closest to the stimulated region (the right FEF) and right parietal EEG leads, and increases of local inter-trial coherence within the same frequency band over bilateral parietal EEG contacts, both driven by rhythmic but not random TMS patterns. Such increases were accompained by improvements of conscious visual sensitivity for left visual targets in the rhythmic but not the random TMS condition. These outcomes suggest that high-beta inter-regional synchrony can be modulated non-invasively and that high-beta oscillatory activity across the right dorsal fronto-parietal network may contribute to the facilitation of conscious visual perception. Our work supports future applications of non-invasive brain stimulation to restore impaired visually-guided behaviors by operating on top-down attentional modulatory mechanisms.


2017 ◽  
Vol 41 (S1) ◽  
pp. S457-S458
Author(s):  
N. Zvereva ◽  
N. Simashkova ◽  
A. Koval-Zaitsev

IntroductionAutism spectrum disorder and early onset schizophrenia have many similar symptoms, however, these are different disorders. It is important to identify the main similarities\differences in the structure of cognitive impairment to define further assistance these children correctly. We distinguished two options for cognitive defect (total and partial) in children with schizophrenia.AimsComparison of cognitive functions at children with autism spectrum disorder and early onset schizophrenia.ObjectivesTwo groups with autism spectrum disorder (ASD1 – 22 patients of MHRC mean age 8.9; ASD2 – 27 pupils of special school mean age 7,4). Two groups with early onset schizophrenia (F20.8 – 16 patients of MHRC mean age 10,2; F21 – 18 patients of MHRC mean age 10.0).MethodsBattery of pathopsychological tests for assessing cognitive functions (memory, attention, thinking), test figures of Leeper for visual perception. Z-scales were used for estimation of cognitive deficit or defect.ResultsPatients demonstrate variety of cognitive functioning. Normal cognitive functioning: ASD1* – 22%, F20.8 – 18%, F21* – 50% (* – P ≤ 0.05); partial cognitive defect: ASD1 – 27%, F20.8 – 18%, F21 – 22%; total cognitive defect: ASD1** – 50%, F20.8 – 64%, F21** – 27% (** – P ≤ 0.01). ASD1 and F20 were the worth in thinking. Children ASD1 and ASD2 demonstrate similar success in recognizing Leeper's figures.ConclusionsThere are some common features of cognitive development in children with severe forms of ASD and early onset schizophrenia, first of all in thinking.No significant differences obtained between severe – mild forms of autistic disorders in visual perception (ASD1 and ASD2).Disclosure of interestThe authors have not supplied their declaration of competing interest.


Brain ◽  
2021 ◽  
Author(s):  
Clara A Moreau ◽  
Armin Raznahan ◽  
Pierre Bellec ◽  
Mallar Chakravarty ◽  
Paul M Thompson ◽  
...  

Abstract Neuroimaging genomic studies of autism spectrum disorder and schizophrenia have mainly adopted a ‘top-down’ approach, starting with the behavioural diagnosis, and moving down to intermediate brain phenotypes and underlying genetic factors. Advances in imaging and genomics have been successfully applied to increasingly large case-control studies. As opposed to diagnostic-first approaches, the bottom-up strategy starts at the level of molecular factors enabling the study of mechanisms related to biological risk, irrespective of diagnoses or clinical manifestations. The latter strategy has emerged from questions raised by top-down studies: Why are mutations and brain phenotypes over-represented in individuals with a psychiatric diagnosis? Are they related to core symptoms of the disease or to comorbidities? Why are mutations and brain phenotypes associated with several psychiatric diagnoses? Do they impact a single dimension contributing to all diagnoses? In the review, we aimed at summarizing imaging genomic findings in autism and schizophrenia as well as neuropsychiatric variants associated with these conditions. Top-down studies of autism and schizophrenia identified patterns of neuroimaging alterations with small effect-sizes and an extreme polygenic architecture. Genomic variants and neuroimaging patterns are shared across diagnostic categories suggesting pleiotropic mechanisms at the molecular and brain network levels. Although the field is gaining traction; characterizing increasingly reproducible results, it is unlikely that top-down approaches alone will be able to disentangle mechanisms involved in autism or schizophrenia. In stark contrast with top-down approaches, bottom-up studies showed that the effect-sizes of high-risk neuropsychiatric mutations are equally large for neuroimaging and behavioural traits. Low specificity has been perplexing with studies showing that broad classes of genomic variants affect a similar range of behavioral and cognitive dimensions, which may be consistent with the highly polygenic architecture of psychiatric conditions. The surprisingly discordant effect sizes observed between genetic and diagnostic first approaches underscore the necessity to decompose the heterogeneity hindering case-control studies in idiopathic conditions. We propose a systematic investigation across a broad spectrum of neuropsychiatric variants to identify putative latent dimensions underlying idiopathic conditions. Gene expression data on temporal, spatial and cell type organization in the brain have also considerable potential for parsing the mechanisms contributing to these dimensions phenotypes. While large neuroimaging genomic datasets are now available in unselected populations, there is an urgent need for data on individuals with a range of psychiatric symptoms and high-risk genomic variants. Such efforts together with more standardized methods will improve mechanistically informed predictive modeling for diagnosis and clinical outcomes.


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