Jun 17, 2013
ways to access the brain own plasticity and has demonstrated over and over seemingly miraculous transformations. She says, “When the brain gets information it needs it will organize that information . . . [and it] starts forming new connection at a ridiculously fast pace.”
<17:36 they move and you’re there when they move
17:50 in order to form patterns … open the conversation, get new information
All kids want to be successful. But some don’t know better options.
Hit the table. Hit it harder. They learn the difference.
The brain learns how to learn.
Keywords: Anat Baniel, Anat Baniel Method
Getting Emotions ‘Switched On’ After Decades Of Asperger’s
March 22, 2016
I had constructed this fantasy in my mind about disability and I had thought to myself, because I can’t read unspoken cues from other people, that I am missing all of these messages of beauty and sweetness and light, and if only I could see those things, my life would be immeasurably better. But when the ability to see into people came on …
TMS actually changed how I saw my memories as a child. I now remember times when people were laughing, but now thanks to TMS, I realize they were laughing at me.
The forgotten history of autism
TED2015 (Mar 2015)
Wong, C., Odom, S. L., Hume, K. et al. (2014). Evidence-based practices for children, youth, and young adults with Autism Spectrum Disorder.
Chapel Hill: The University of North Carolina, Frank Porter Graham Child Development Institute, Autism Evidence-Based Practice Review Group.
ASD is identified by two primary diagnostic markers: difficulties in social communication and restricted or repetitive behaviors and interests.
Examples of difficulties in social communication include challenges in social reciprocity, nonverbal social behaviors, and establishment of social relationships. Restrictive and repetitive behaviors include stereotypic behavior or speech, excessive adherence to routines, and highly fixated interests.
ASD is diagnosed about three times more frequently in boys than in girls.
Intellectual disability was once thought to be a condition that typically accompanied ASD; however, current estimates are that 35% of individuals with ASD score above the IQ cutoff (i.e., around 70 depending on the test) for intellectual disability (Dykens & Lense, 2011).
the Cochrane Collaboration to host reviews of the literature about scientifically supported practices in medicine (http://www.cochrane.org).
The subsequent adoption of the evidence-based conceptual approach in the social sciences is exemplified in the work of the Campbell Collaboration (http://www.campbellcollaboration.org ) and currently the What Works Clearinghouse (http://ies.ed.gov/ncee/wwc )
Identification of risk loci with shared effects on five major psychiatric disorders: a genome-wide analysis.
Lancet. 2013 Apr 20;381(9875):1371-9.
Cross-Disorder Group of the Psychiatric Genomics Consortium.
Erratum in: Lancet. 2013 Apr 20;381(9875):1360.
Findings from family and twin studies suggest that genetic contributions to psychiatric disorders do not in all cases map to present diagnostic categories.
We aimed to identify specific variants underlying genetic effects shared between the five disorders in the Psychiatric Genomics Consortium: autism spectrum disorder, attention deficit-hyperactivity disorder, bipolar disorder, major depressive disorder, and schizophrenia.
We analyzed genome-wide single-nucleotide polymorphism (SNP) data for the five disorders
SNPs at four loci surpassed the cutoff for genome-wide significance (p<5×10(-8)) in the primary analysis: regions on chromosomes 3p21 and 10q24, and SNPs within two L-type voltage-gated calcium channel subunits, CACNA1C and CACNB2.
Model selection analysis supported effects of these loci for several disorders.
Loci previously associated with bipolar disorder or schizophrenia had variable diagnostic specificity.
Pathway analysis supported a role for calcium channel signalling genes for all five disorders.
Our findings show that specific SNPs are associated with a range of psychiatric disorders of childhood onset or adult onset. In particular, variation in calcium-channel activity genes seems to have pleiotropic effects on psychopathology.
These results provide evidence relevant to the goal of moving beyond descriptive syndromes in psychiatry, and towards a nosology informed by disease cause.
Genes and the Human Condition (From Behavior to Biotechnology)
Oxytocin enhances brain function in children with autism
PNAS. December 24, 2013. 110(52)
This article presents our discovery that intranasal administration of oxytocin enhances activity in the brain for socially meaningful stimuli and attenuates its response to nonsocially meaningful stimuli in children with autism spectrum disorder (ASD) as measured via functional MRI. We also identified a relationship between changes in salivary oxytocin following administration and enhancements in brain function.
These discoveries are particularly important given the urgent need for treatments that target the core social dysfunction in ASD. The functional neural attunement we demonstrated might facilitate social learning, thus potentially bringing about long-term change in neural systems and subsequent behavioral improvements.
Our results illustrate the power of a translational neuroscience approach to facilitate the development of pharmacological interventions for neurodevelopmental disorders like ASD.
Promoting social behavior with oxytocin …
PNAS February 16, 2010
Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism
The FASEB Journal. June 2014. 28(6): 2398-2413
Rhonda P. Patrick and Bruce N. Ames
Serotonin and vitamin D have been proposed to play a role in autism; however, no causal mechanism has been established.
Here, we present evidence that vitamin D hormone (calcitriol) activates the transcription of the serotonin-synthesizing gene tryptophan hydroxylase 2 (TPH2) in the brain at a vitamin D response element (VDRE) and represses the transcription of TPH1 in tissues outside the blood-brain barrier at a distinct VDRE.
The proposed mechanism explains 4 major characteristics associated with autism:
Two peptide hormones, oxytocin and vasopressin, are also associated with autism and genes encoding the oxytocin-neurophysin I preproprotein, the oxytocin receptor, and the arginine vasopressin receptor contain VDREs for activation.
Supplementation with vitamin D and tryptophan is a practical and affordable solution to help prevent autism and possibly ameliorate some symptoms of the disorder.
Patches of Disorganization in the Neocortex of Children with Autism
N Engl J Med 2014; 370:1209-1219March 27, 2014
Autism involves early brain overgrowth and dysfunction, which is most strongly evident in the prefrontal cortex.
As assessed on pathological analysis, an excess of neurons in the prefrontal cortex among children with autism signals a disturbance in prenatal development and may be concomitant with abnormal cell type and laminar development.
To systematically examine neocortical architecture during the early years after the onset of autism, we used RNA in situ hybridization with a panel of layer- and cell-type–specific molecular markers to phenotype cortical microstructure. We assayed markers for neurons and glia, along with genes that have been implicated in the risk of autism, in prefrontal, temporal, and occipital neocortical tissue from postmortem samples obtained from children with autism and unaffected children between the ages of 2 and 15 years.
We observed focal patches of abnormal laminar cytoarchitecture and cortical disorganization of neurons, but not glia, in prefrontal and temporal cortical tissue from 10 of 11 children with autism and from 1 of 11 unaffected children.
We observed heterogeneity between cases with respect to cell types that were most abnormal in the patches and the layers that were most affected by the pathological features.
No cortical layer was uniformly spared, with the clearest signs of abnormal expression in layers 4 and 5. Three-dimensional reconstruction of layer markers confirmed the focal geometry and size of patches.
In this small, explorative study, we found focal disruption of cortical laminar architecture in the cortexes of a majority of young children with autism. Our data support a probable dysregulation of layer formation and layer-specific neuronal differentiation at prenatal developmental stages.
Dissociations of cerebral cortex, subcortical and cerebral white matter volumes in autistic boys
Brain (2003) 126 (5): 1182-1192.
M. R. Herbert
Emotional contagion for pain is intact in autism spectrum disorders
Translational Psychiatry (2014) 4, e343
N Hadjikhani, et al.
Individuals with autism spectrum disorders (ASD) have impaired social understanding, and seemingly reduced reactions to others’ emotions, which may be interpreted as lack of empathetic concern.
Empathy can be defined as ‘the ability to form an embodied representation of another’s emotional state, while at the same time being aware of the causal mechanism that induced the emotional state in the other’.
Empathy is a multicomponent process, consisting mainly of experience sharing and mental state attribution.
The evolutionary precursor of empathy is emotional contagion, a phylogenetically old phenomenon, even observable in distressed mice.
Emotional contagion is a precursor of emotional empathy, whereby embodiment entails the forming of a representation of the other person’s feelings, and thereby sharing of their experience.
In the observer, this ‘perception-action’ coupling mechanism elicits the activation of the same neural networks as in the person experiencing the emotional state.