Unfavourable Left-Right Asymmetries of the Brain and Autism: A Question of Methodology

1982 ◽  
Vol 140 (3) ◽  
pp. 312-319 ◽  
Author(s):  
Luke Tsai ◽  
Charles G. Jacoby ◽  
Mark A. Stewart ◽  
Jean M. Beisler
Keyword(s):  
Language Development ◽  
Neurological Disorders ◽  
Ct Scanning ◽  
Infantile Autism ◽  
Ct Scans ◽  
Autistic Children ◽  
Delayed Language Development ◽  
The Brain ◽  
Methodological Difficulties

SummaryThirty-six patients with infantile autism and various neurological disorders underwent computerized tomographic (CT) scanning of the brain. All CT scans were assessed blindly and independently by a diagnostic radiologist. Two techniques modified from two previous studies were used for measuring parieto-occipital asymmetry. The frequency of reversed asymmetry in autistic patients was the same as that in patients with various neurological disorders, and there was no significant association between reversed asymmetry and delayed language development. The study does not support the concept that unfavourable morphological asymmetries of the brain near the posterior language zone may contribute to the difficulties autistic children experience in acquiring language. Methodological difficulties and the design of new studies are discussed.

scholarly journals Cerebral Cavernous Hemangioma in a Dog

2019 ◽  
Vol 47 ◽  
Author(s):  
Viviane Motta dos Santos Moretto ◽  
Luciana Maria Curtio Soares ◽  
Esthefanie Nunes ◽  
Uiara Hanna Araújo Barreto ◽  
Valéria Régia Franco Sousa ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Endothelial Cells ◽  
Cavernous Hemangioma ◽  
Clinical Signs ◽  
Ct Scanning ◽  
Ct Scans ◽  
Elastic Fibers ◽  
Post Contrast ◽  
The Right ◽  
The Brain

Background: Cerebral cavernous hemangioma is a rare neoplasm of vascular origin in the brain, characterized by abnormally dilated vascular channels surrounded by endothelium without muscle or elastic fibers. Presumptive diagnosis is performed by magnetic resonance or computed tomography (CT) scanning and can be confirmed by histopathology. The prognosis of intracranial cavernous hemangioma is poor, with progression of clinical signs culminating in spontaneous death or euthanasia. The purpose of this paper is to report a case of cerebral cavernous hemangioma in a dog, presenting the clinical findings, tomographic changes, and pathological findings.Case: This case involved a 2-year-old medium sized mixed breed female dog presenting with apathy, hyporexia, ataxia, bradycardia, dyspnea, and seizure episodes for three days. Hemogram and serum biochemistry of renal and hepatic function and urinalysis did not reveal any visible changes. CT scanning was also performed. The scans revealed a hyperdense nodule of 15.9 x 14 mm, with well defined borders, and a hypodense halo without post-contrast enhancement and mass effect in the right parietal lobe was observed in both transverse and coronal sections. Based on the image presented in the CT scans, the nodule was defined as a hemorrhagic brain lesion. The animal died after a seizure. The right telencephalon was subjected to necropsy, which revealed a reddish-black wel-defined nodule 1.7 cm in diameter extending from the height of the piriform lobe to the olfactory trine at the groove level and extending towards the lateral ventricle, with slight compression and deformation of the thalamus but no other macroscopic alterations in the other organs. The histopathology indicated that this nodular area in the encephalus contained moderate, well-delimited but unencapsulated cellularity, composed of large vascular spaces paved with endothelial cells filled with erythrocytes, some containing eosinophilic fibrillar material (fibrin) and others with organized thrombus containing occasional neutrophil aggregates. The endothelial cells had cytoplasm with indistinct borders, elongated nuclei, scanty crust-like chromatin, and cellular pleomorphism ranging from discrete to moderate, without mitotic figures.Discussion: The histological findings characterized the morphological changes in the brain as cavernous hemangioma, and the growth and compression of this neoplasm were considered the cause of the clinical signs of this dog. The main complaint was seizures, although ataxia and lethargy were also noted. These clinical signs are often related to changes in the anterior brain and brainstem. The literature does not list computed tomography as a complementary diagnostic method in cases of cerebral cavernous hemangioma in dogs, but CT scanning was useful in confirming cerebral hemorrhage. The main differential diagnosis for cerebral cavernous hemangioma would be a hamartoma, but what differentiates them histologically is the presence of normal interstices between the blood vessels, since no intervening neural tissue occurs in the case of cerebral hemangioma. Therefore, even in the absence of immunohistochemistry to more confidently confirm a cavernous hemangioma, the clinical signs, CT scans and especially the pathological findings were consistent with a case of cerebral cavernous hemangioma, a benign neoplasm with a poor prognosis due to the severe neurological changes it causes and its difficult treatment.

scholarly journals Oxidative Stress, Folate Receptor Autoimmunity, and CSF Findings in Severe Infantile Autism

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Vincent T. Ramaekers ◽  
Jeffrey M. Sequeira ◽  
Beat Thöny ◽  
Edward V. Quadros
Keyword(s):  
Oxidative Stress ◽  
Folate Receptor ◽  
Regulation Of Gene Expression ◽  
Reactive Oxygen ◽  
Infantile Autism ◽  
Serum Folate ◽  
Controlled Study ◽  
Autistic Children ◽  
Serotonin Turnover ◽  
The Brain

Background. Biomarkers such as oxidative stress, folate receptor alpha (FRα) autoimmunity, and abnormal brain serotonin turnover are common in autism. Methods. Oxidative stress biomarkers with pro- and antioxidants were measured in the severe form of infantile autism (n = 38) and controls (n = 24). Children and parents had repeated testing for serum FR autoantibodies, spinal fluid dopamine and serotonin metabolites, pterins, and N5-methyltetrahydrofolate (MTHF). Statistical analysis assessed correlations between variables. Genetic analysis included the SLC6A4 and SLC29A4 genes encoding synaptic serotonin reuptake proteins. Results. Compared to controls, the autism group showed a significant increase in oxidative DNA damage in lymphocytes, plasma ceruloplasmin and copper levels with a high copper/zinc ratio, thiol proteins, and superoxide dismutase (SOD) activity. Vitamin C levels were significantly diminished. In most autistic patients, the vitamin A (64%) and D (70%) levels were low. Serum FR autoantibodies fluctuating over 5–7 week periods presented in 68% of all autistic children, 41% of parents vs. 3.3% of control children and their parents. CSF showed lowered serotonin 5-hydroxyindole acetic acid (5HIAA) metabolites in 13 (34%), a low 5HIAA to HVA (dopamine metabolite) ratio in 5 (13%), low 5HIAA and MTHF in 2 (5%), and low MTHF in 8 patients (21%). A known SLC6A4 mutation was identified only in 1 autistic child with low CSF 5HIAA and a novel SLC29A4 mutation was identified in identical twins. Low CSF MTHF levels among only 26% of subjects can be explained by the fluctuating FR antibody titers. Two or more aberrant pro-oxidant and/or antioxidant factors predisposed to low CSF serotonin metabolites. Three autistic children having low CSF 5HIAA and elevated oxidative stress received antioxidative supplements followed by CSF 5HIAA normalisation. Conclusion. In autism, we found diverse combinations for FR autoimmunity and/or oxidative stress, both amenable to treatment. Parental and postnatal FR autoantibodies tend to block folate passage to the brain affecting folate-dependent pathways restored by folinic acid treatment, while an abnormal redox status tends to induce reduced serotonin turnover, corrected by antioxidant therapy. Trial Registration. The case-controlled study was approved in 2008 by the IRB at Liège University (Belgian Number: B70720083916). Lay Summary. Children with severe infantile autism frequently have serum folate receptor autoantibodies that block the transport of the essential vitamin folate across the blood-brain barrier to the brain. Parents are often asymptomatic carriers of these serum folate receptor autoantibodies, which in mothers can block folate passage across the placenta to their unborn child. This folate deficiency during the child’s intrauterine development may predispose to neural tube defects and autism. Oxidative stress represents a condition with the presence of elevated toxic oxygen derivatives attributed to an imbalance between the formation and protection against these toxic reactive oxygen derivatives. Oxidative stress was found to be present in autistic children where these reactive oxygen derivatives can cause damage to DNA, which changes DNA function and regulation of gene expression. In addition, excessive amounts of these toxic oxygen derivatives are likely to damage the enzyme producing the neuromessenger serotonin in the brain, diminished in about 1/3 of the autistic children. Testing children with autism for oxidative stress and its origin, as well as testing for serum folate receptor autoantibodies, could open new approaches towards more effective treatments.

Development of Neural Structure and Function in Autism Spectrum Disorder: Potential Implications for Learning Language

2020 ◽  
Vol 29 (4) ◽  
pp. 1783-1797
Author(s):  
Kelly L. Coburn ◽  
Diane L. Williams
Keyword(s):  
Autism Spectrum Disorder ◽  
Language Development ◽  
Diffusion Tensor ◽  
Autism Spectrum ◽  
Language Intervention ◽  
Spectrum Disorder ◽  
Autistic Children ◽  
Neural Structure ◽  
Complex Information ◽  
And Function

Purpose Neurodevelopmental processes that begin during gestation and continue throughout childhood typically support language development. Understanding these processes can help us to understand the disruptions to language that occur in neurodevelopmental conditions, such as autism spectrum disorder (ASD). Method For this tutorial, we conducted a focused literature review on typical postnatal brain development and structural and functional magnetic resonance imaging, diffusion tensor imaging, magnetoencephalography, and electroencephalography studies of the neurodevelopmental differences that occur in ASD. We then integrated this knowledge with the literature on evidence-based speech-language intervention practices for autistic children. Results In ASD, structural differences include altered patterns of cortical growth and myelination. Functional differences occur at all brain levels, from lateralization of cortical functions to the rhythmic activations of single neurons. Neuronal oscillations, in particular, could help explain disrupted language development by elucidating the timing differences that contribute to altered functional connectivity, complex information processing, and speech parsing. Findings related to implicit statistical learning, explicit task learning, multisensory integration, and reinforcement in ASD are also discussed. Conclusions Consideration of the neural differences in autistic children provides additional scientific support for current recommended language intervention practices. Recommendations consistent with these neurological findings include the use of short, simple utterances; repetition of syntactic structures using varied vocabulary; pause time; visual supports; and individualized sensory modifications.

Moving past the vaccine/autism controversy - to examine potential vaccine neurological harms

2020 ◽  
pp. 1-15
Author(s):  
Peter R. Breggin
Keyword(s):  
Neurological Disorders ◽  
Developmental Disorder ◽  
Physical Symptoms ◽  
Psychosocial Disorders ◽  
The Us ◽  
Potential Vaccine ◽  
Research And Education ◽  
The Brain ◽  
New Vaccines

BACKGROUND: The vaccine/autism controversy has caused vast scientific and public confusion, and it has set back research and education into genuine vaccine-induced neurological disorders. The great strawman of autism has been so emphasized by the vaccine industry that it, and it alone, often appears in authoritative discussions of adverse effects of the MMR and other vaccines. By dismissing the chimerical vaccine/autism controversy, vaccine defenders often dismiss all genuinely neurological aftereffects of the MMR (measles, mumps, and rubella) and other vaccines, including well-documented events, such as relatively rare cases of encephalopathy and encephalitis. OBJECTIVE: This report explains that autism is not a physical or neurological disorder. It is not caused by injury or disease of the brain. It is a developmental disorder that has no physical origins and no physical symptoms. It is extremely unlikely that vaccines are causing autism; but it is extremely likely that they are causing more neurological damage than currently appreciated, some of it resulting in psychosocial disabilities that can be confused with autism and other psychosocial disorders. This confusion between a developmental, psychosocial disorder and a physical neurological disease has played into the hands of interest groups who want to deny that vaccines have any neurological and associated neuropsychiatric effects. METHODS: A review of the scientific literature, textbooks, and related media commentary is integrated with basic clinical knowledge. RESULTS: This report shows how scientific sources have used the vaccine/autism controversy to avoid dealing with genuine neurological risks associated with vaccines and summarizes evidence that vaccines, including the MMR, can cause serious neurological disorders. Manufacturers have been allowed by the US Food and Drug Administration (FDA) to gain vaccine approval without placebo-controlled clinical trials. CONCLUSIONS: The misleading vaccine autism controversy must be set aside in favor of examining actual neurological harms associated with vaccines, including building on existing research that has been ignored. Manufacturers of vaccines must be required to conduct placebo-controlled clinical studies for existing vaccines and for government approval of new vaccines. Many probable or confirmed neurological adverse events occur within a few days or weeks after immunization and could be detected if the trials were sufficiently large. Contrary to current opinion, large, long-term placebo-controlled trials of existing and new vaccines would be relatively easy and safe to conduct.

Lipidomics and cognitive dysfunction – A Narrative review

2020 ◽  
Vol 45 (2) ◽  
Author(s):  
Arpita Chakraborty ◽  
Samir Kumar Praharaj ◽  
R. V. Krishnananda Prabhu ◽  
M. Mukhyaprana Prabhu
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Vascular Dementia ◽  
Cognitive Dysfunction ◽  
Neurological Disorders ◽  
Brain Lipids ◽  
Complex Lipids ◽  
Functional Components ◽  
The Brain

AbstractBackgroundMore than half portion of the brain is formed by lipids. They play critical roles in maintaining the brain's structural and functional components. Any dysregulation in these brain lipids can lead to cognitive dysfunction which are associated with neurological disorders such as Alzheimer's disease, Parkinson's disease, schizophrenia, vascular dementia etc. Studies have linked lipids with cognitive impairment. But not much has been studied about the complex brain lipids which might play a pivotal role in cognitive impairment. This review aims to highlight the lipidomic profiles in patients with cognitive dysfunction.ResultsForty-five articles were reviewed. These studies show alterations in complex lipids such as sphingolipids, phospholipids, glycolipids and sterols in brain in various neurological disorders such as vascular dementia, Parkinson's and Alzheimer's disease. However, the classes of fatty acids in these lipids involved are different across studies.ConclusionsThere is a need for targeted lipidomics analysis, specifically including sphingolipids in patients with neurodegenerative disorders so as to improve diagnostics as well as management of these disorders.

scholarly journals Maternal toxoplasmosis and the risk of childhood autism: serological and molecular small-scale studies

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jamila S. Al Malki ◽  
Nahed Ahmed Hussien ◽  
Fuad Al Malki
Keyword(s):  
Neurodevelopmental Disorders ◽  
Repetitive Behavior ◽  
Saudi Arabian ◽  
Childhood Autism ◽  
Small Scale ◽  
Autistic Children ◽  
High Prevalence ◽  
Life Threatening ◽  
The Relationship ◽  
Delayed Language Development

Abstract Background Toxoplasmosis resulting from infection with the Toxoplasma parasite has become an endemic disease worldwide. Recently, a few studies have reported a high prevalence of Toxoplasmosis infections among Saudi Arabian women. This disease could become life threatening for pregnant women and for immunodeficient people. There is evidence that infections during pregnancy, especially in the early stages, are associated with neurodevelopmental disorders. Autism disorder represents one of the most common neurodevelopmental disorders worldwide; it is associated with delayed language development, weak communication interaction, and repetitive behavior. The relationship between prenatal toxoplasmosis and autism in childhood remains unclear. The present study aims to report a link between maternal toxoplasmosis and autistic offspring among Saudi Arabian women. Method Blood samples (36 maternal, 36 from their non-autistic children, and 36 from their autistic children) were collected for serological and molecular evaluation. Results A toxoplasmosis infection was reported for 33.34% of participants using an ELISA assay (5.56% IgG+/IgM+, 11.11% IgG−/IgM+, and 16.67% IgG+/IgM-); however, a nested PCR assay targeting B1 toxoplasmosis specific genes recorded positive tests for 80.56% of the samples. In addition, the present study detected several points of mutation of mtDNA including NADH dehydrogenase (ND1, ND4) and Cyt B genes and the nDNA pyruvate kinase (PK) gene for autistic children infected with toxoplasmosis. Conclusion Considering previous assumptions, we suggest that a maternal toxoplasmosis infection could have a role in the development of childhood autism linked to mtDNA and nDNA impairment.

scholarly journals Genetic Approaches Using Zebrafish to Study the Microbiota–Gut–Brain Axis in Neurological Disorders

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 566
Author(s):  
Jae-Geun Lee ◽  
Hyun-Ju Cho ◽  
Yun-Mi Jeong ◽  
Jeong-Soo Lee
Keyword(s):  
Neurological Disorders ◽  
Genetic Model ◽  
Molecular Genetic ◽  
Autism Spectrum ◽  
Behavioral Abnormalities ◽  
Bidirectional Signaling ◽  
Intestinal Dysbiosis ◽  
The Central Nervous System ◽  
The Brain

The microbiota–gut–brain axis (MGBA) is a bidirectional signaling pathway mediating the interaction of the microbiota, the intestine, and the central nervous system. While the MGBA plays a pivotal role in normal development and physiology of the nervous and gastrointestinal system of the host, its dysfunction has been strongly implicated in neurological disorders, where intestinal dysbiosis and derived metabolites cause barrier permeability defects and elicit local inflammation of the gastrointestinal tract, concomitant with increased pro-inflammatory cytokines, mobilization and infiltration of immune cells into the brain, and the dysregulated activation of the vagus nerve, culminating in neuroinflammation and neuronal dysfunction of the brain and behavioral abnormalities. In this topical review, we summarize recent findings in human and animal models regarding the roles of the MGBA in physiological and neuropathological conditions, and discuss the molecular, genetic, and neurobehavioral characteristics of zebrafish as an animal model to study the MGBA. The exploitation of zebrafish as an amenable genetic model combined with in vivo imaging capabilities and gnotobiotic approaches at the whole organism level may reveal novel mechanistic insights into microbiota–gut–brain interactions, especially in the context of neurological disorders such as autism spectrum disorder and Alzheimer’s disease.

scholarly journals Brain stimulation used as biofeedback in neuronal activation of the temporal lobe area in autistic children

2016 ◽  
Vol 74 (8) ◽  
pp. 632-637 ◽  
Author(s):  
Vernon Furtado da Silva ◽  
Mauricio Rocha Calomeni ◽  
Rodolfo Alkmim Moreira Nunes ◽  
Carlos Elias Pimentel ◽  
Gabriela Paes Martins ◽  
...  
Keyword(s):  
Data Collection ◽  
Brain Stimulation ◽  
Mirror Neurons ◽  
Brain Area ◽  
Control Group ◽  
Autistic Children ◽  
Emotional Stimuli ◽  
The One ◽  
The Brain ◽  
Data Collection Procedure

ABSTRACT This study focused upon the functional capacity of mirror neurons in autistic children. 30 individuals, 10 carriers of the autistic syndrome (GCA), 10 with intellectual impairments (GDI), and 10 non-autistics (GCN) had registered eletroencephalogram from the brain area theoretically related to mirror neurons. Data collection procedure occurred prior to brain stimulation and after the stimulation session. During the second session, participants had to alternately process figures evoking neutral, happy, and/or sorrowful feelings. Results proved that, for all groups, the stimulation process in fact produced additional activation in the neural area under study. The level of activation was related to the format of emotional stimuli and the likelihood of boosting such stimuli. Since the increase of activation occurred in a model similar to the one observed for the control group, we may suggest that the difficulty people with autism have at expressing emotions is not due to nonexistence of mirror neurons.

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