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Frontal lobe function may not universally explain all forms of ADHD, the frontal lobe hypothesis described supports an internally consistent model for integrating the numerous behaviors associated with ADHD. The paper examines the developmental trajectories of frontal and prefrontal lobe development framing ADHD as maturational dysfunction concluding that the cognitive, motor and behavioral abilities of the presumptive majority of the ADHD child may not primarily be disordered or dysfunctional but reflect maturational delays that are inconsistent with the psychomotor and cognitive expectations for the child's chronological and mental age. ADHD children demonstrate decreased activation of the right and middle prefrontal cortex. Prefrontal and frontal lobe regions have an exuberant network of shared pathways with the diencephalic region, also having a regulatory function in arousal as well as with the ascending reticular formation which has a capacity for response suppression to task-irrelevant stimuli. Prefrontal lesions oftentimes are associated with the regulatory breakdown of goal-directed activity and impulsivity. In conclusion, a presumptive majority of childhood ADHD may result from maturational delays of the frontal lobes with effects on the direct, indirect and/or, hyperdirect pathways.

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition that manifests in early childhood and persists throughout an individual’s life. Characterized by a range of symptoms affecting social interaction, communication, and behavior, ASD presents a spectrum of varying degrees of severity and presentation. Recent research emphasizes the importance of understanding the diverse manifestations of ASD across different populations. Core features include social communication differences and restricted and repetitive behaviors (RRBs), often linked to co-occurring conditions such as anxiety and ADHD. The study of ASD has evolved significantly, highlighting the need for individualized approaches to diagnosis and intervention. This paper explores current knowledge on ASD, examining the latest research findings and discussing future directions for improving the lives of those affected by the disorder. The purpose is to present a map of the field and an evidence-strength framing of what is known and unknown, and where the evidence is equivocal. Key areas of focus include behavioral, psychological, genetic, metabolic, immunological, and neurological features, as well as developmental and maturational factors. The aim is to provide a comprehensive overview of what is known, what remains unclear, and where future research should be directed.

Background: Adolescents with autism spectrum disorder (ASD) display distinct neurodevelopmental trajectories marked by atypical neural activation and white matter maturation compared to neurotypical peers. Introduction: While improvements in face recognition and cognitive skills occur during childhood and adolescence, individuals with ASD often experience a plateau in these areas as they transition to adulthood, impacting daily living, executive function, social cognition, and emotional awareness. Results: Neuroimaging studies reveal altered white matter growth and connectivity in brain regions associated with social processing, which may underlie these functional challenges. Intellectual disability further compounds developmental difficulties by limiting foundational abilities and slowing progress. Discussion: The multifaceted and persistent service needs spanning legal, educational, vocational, health, and psychosocial domains highlight the necessity for coordinated, individualized, and family-centered approaches, particularly during the transition to adulthood. Advances in research integrating genetic, neurobiological, and behavioral data hold potential for refining diagnostic subgroups and personalizing interventions. Conclusion: Continued advocacy and innovation in service delivery are essential to address gaps in adult support systems and enhance long-term outcomes for individuals with ASD.

Background: Autism Spectrum Disorder (ASD) can be identified by a general tendency toward a reduction in the expression of low-band, widely dispersed integrative activities, which is made up for by an increase in localized, high-frequency, regionally dispersed activity. The study assessed ASD children and adults all possessing retained primitive reflexes (RPRs) compared with a control group that did not attempt to reduce or remove those RPRs and then examined the effects on qEEG and brain network connectivity. Methods: Analysis of qEEG spectral and functional connectivity was performed, to identify associations with the presence or absence of retained primitive reflexes (RPRs), before and after an intervention based on TENS unilateral stimulation. Results: The results point to abnormal lateralization in ASD, including long-range underconnectivity, a greater left-over-right qEEG functional connectivity ratio, and short-range overconnectivity in ASD. Conclusion:. Clinical improvement and the absence of RPRs may be linked to variations in qEEG frequency bands and more optimized brain networks, resulting in more developmentally appropriate long-range connectivity links, primarily in the right hemisphere.

The paper discusses and provides support for diverse processes of brain plasticity in visual function after damage in infancy and childhood in comparison with injury that occurs in the adult brain. We provide support and description of neuroplastic mechanisms in childhood that do not seemingly exist in the same way in the adult brain. Examples include the ability to foster the development of thalamocortical connectivities that can circumvent the lesion and reach their cortical destination in the occipital cortex as the developing brain is more efficient in building new connections. Supporting this claim is the fact that in those with central visual field defects we can note that the extrastriatal visual connectivities are greater when a lesion occurs earlier in life as opposed to in the neurologically mature adult. The result is a significantly more optimized system of visual and spatial exploration within the ‘blind’ field of view. The discussion is provided within the context of “blindsight” and the “Sprague Effect”.

Several authors have reported finding retained primitive reflexes (RPRs) in individuals with autism spectrum disorders (ASD). This case report describes the reduction of RPRs and changes in cognitive function after transcutaneous electrical nerve stimulation (TENS) of muscle. Three individuals were examined in a study at the Institute for Neurology and Neurosurgery in Havana, Cuba. Two child neurologists, not involved in the study, conducted clinical examinations on each participant and diagnosed each with ASD based on DSM-V criteria and the Autism Diagnostic Interview-Revised (an autism evaluation tool). Each child with ASD possessed a triad of impairments in three domains: social interaction, communication, and repetitive behaviour. Individuals were evaluated by quantitative electroencephalographic measures and tested by standardised cognitive function tests before and after 12 weeks of intervention. These interventions were associated with reduced ASD symptoms in the three domains, significant changes in qEEG network connectivity and significantly improved performance on standardised cognitive tests.

Confirmation from structural, functional, and behavioral studies agree and suggest a configuration of atypical lateralization in individuals with autistic spectrum disorders (ASD). It is suggested that patterns of cortical and behavioral atypicality are evident in individuals with ASDs with atypical lateralization being common in individuals with ASDs. The paper endeavors to better understand the relationship between alterations in typical cortical asymmetries and functional lateralization in ASD in evolutionary terms. We have proposed that both early genetic and/or environmental influences can alter the developmental process of cortical lateralization. There invariably is a “chicken or egg” issue that arises whether atypical cortical anatomy associated with abnormal function, or alternatively whether functional atypicality generates abnormal structure.

We, in these proposed projects, have endeavored to understand better the importance of ‘retained’ primitive reflexes (RPRs) and examine the effect of RPRs in children, adolescents, and adults, as well as examine treatment alternatives based on the findings of the studies included in this dissertation.Melillo and colleaguesstudied a series of 2,175 children between and 3.2 and 22.04 years, applying a 12-week interventional program. Initial pre-intervention assessments were comprised of the functional assessment of sensory-motor and reflex function and on a separate day, academiccognitive examination. The reduction of primitive reflexes was found to be highly associated with increased performance in mathematical problem-solving and listening comprehension as measured by the components of the Wechsler Individual Achievement Test. Numerous studies have been performed over the past 30 years demonstrating the effects of RPRs on behavior and learning. Research has additionally demonstrated that individuals significantly reduce symptoms and effect change in diagnosis when participating in a protocol that focuses on specific reflexes.In previous work, we have argued that many aspects of these disorders are related to the presence of a functional disconnection syndrome. We have also demonstrated that this functional disconnection relates to a cortical maturational imbalance between networks. A delay in cortical maturation in certain networks we think may result in an increase in cortical maturation and development in other networks leading to a developmental asynchrony and an unevenness of functional skills and symptoms.In ADHD for instance, the underdevelopment of networks such as the dorsal attention network in the right hemisphere leads to an “attention deficit”. Overactivity and development in frontocortico-striatal networks in the left hemisphere can lead to hyperactivity and impulsivity.There has been reported an over-connectivity of short-range more immature connections and an under-connectivity of long-range more mature connectivities. We think that one of the best indicators for the existence of a maturational delay in the brain and nervous system are RPRs. With central nervous system maturation, primitive-reflex activity is suppressed during the second six months of life. A relationship between delayed suppression of primitive reflexes and delayed development of motor skills has been identified. When these retained primitive reflexes are also asymmetrically present, there is good evidence for us to hypothesize that this directly relates to maturational delays as opposed to maldevelopment in the relationship between-hemisphere network communication in what we term a functional disconnection syndrome.We realize of course that there exist numerous theories attempting to validly explain possible etiologies of ASD. It is beyond the scope of this proposal and at this point in the dissertation to delve into each in depth, especially considering that our focus is on the nature of network connectivities. Succinctly reviewing alternative theories, we can indicate and will expand upon them later but now note that they collectively they consist of: a) The signaling imbalance theory of autism arises from a hyper-excitable brain.

Both the prevalence and incidence of autism have been confirmed to have increased dramatically over the past two decades. In considering what environmental factors are driving this increase, the researchers must first understand what is actually happening in the autistic brain. They have previously stated and shown that the primary problem is a functional disconnection which is precipitated by a developmental delay of the right hemisphere. Environmental factors along with genetic and epigenetic factors essentially result in either mutating, damaging, deleting or silencing genes that are primarily responsible for the development of functional connections and the growth and maturity of neurons. There have been a number of environmental factors already identified as playing a role in the possible causation of autism including various chemicals, drugs and maternal infection. When looking at the candidate environmental factors that may play a significant role we believe that maternal stress resulting in an elevation of glucocorticoids and inflammation may be the single most significant factor.