Loss of education seen as a crisis for non-disabled kids but NOT for disabled kids.

So true.

If an NT kid was "not in school for two months, [the school district] would be coming after [the parents]. A non-disabled "child who has missed about 18 school days... [is considered] a crisis that triggers a range of emergency interventions."

But a disabled kid not coming to school seems to be a relief the school district, there is no urgency to bring them back. A disabled kid not being able to attend school is never a crisis.

 
They can be left without services, and at the drop of a hat [for staff shortages and a thousand other excuses by the school] and the child is literally asked not to come to school and stay at home instead. Education it seems, is the responsibility of parents and not the school district when it comes to disabled children.

 

https://www.npr.org/2024/05/15/1247795768/children-disabilities-special-education-teacher-shortage 

New ED for DREDF

DREDF gets a new captain. 

Two press releases 

Announcing Nicole's hiring  at DREDF 

https://dredf.org/2024/05/08/bohn-new-dredf-executive-director/

Nicole's departure from the San Francisco Mayor's Office on Disability:

https://www.sf.gov/news/press-release-nicole-bohn-depart-mayors-office-disability

Refocusing the Autism Conversation: Beyond Terminology

Refocusing the Autism Conversation: Beyond Terminology

In his insightful book The Brain Inside Out, György Buzsáki highlights a significant challenge in scientific discourse: the tendency to create new terminology in an attempt to explain complex phenomena. He shares his frustration, echoed by his mentors, that these "filler terms" often obscure the true nature of the mysteries they aim to unravel. This practice can mislead readers into believing that a mechanism has been identified, when in reality, it remains elusive.

This phenomenon is particularly relevant in the field of autism, where debates over terminology often overshadow the more pressing goal of finding solutions. The discussion around whether to use "person with autism" or "autistic person" is a prime example. While language is undoubtedly important, the energy spent on these debates could be better directed towards understanding and addressing the needs of autistic individuals.

The focus should shift towards practical outcomes and real-world solutions. Instead of getting caught up in linguistic nuances, we should prioritize research that improves the quality of life for autistic people. This includes exploring interventions that address sensory processing differences, finding biomedical solutions to pressing health concerns, developing educational strategies that support diverse learning styles, lowering cost of support care, and creating inclusive environments that accommodate a wide range of abilities.

Buzsáki’s critique of explanatory terms serves as a reminder to the autism community: let’s not lose sight of our primary objective. By moving beyond terminology debates and concentrating on tangible solutions, we can make meaningful progress in enhancing the lives of those on the autism spectrum.

LTP and LTD and their Role in Autism

The Neuroscience of Autism 
Long Term Potentiation (LTP),  Long Term Depression (LTD) and their role in Autism.

LTP and LTD are critical forms of long term synaptic plasticity that underlie learning and memory. These processes are governed by Hebbian plasticity, a principle summarized as "cells that fire together, wire together." This means that the synaptic strength between two neurons increases when they are frequently active together (LTP), and decreases when they are less synchronized (LTD).

Spike-Timing Dependent Plasticity (STDP), a form of Hebbian plasticity, emphasizes the precise timing of neuronal spikes:

• LTP: Induced when a presynaptic neuron fires just before a postsynaptic neuron, typically within 20 milliseconds. This leads to a significant influx of calcium (Ca2+) through NMDA receptors and voltage-gated calcium channels (VGCCs), strengthening the synapse.
• LTD: Occurs when the postsynaptic neuron fires before the presynaptic neuron, usually within 20-100 milliseconds. This results in a weaker Ca2+ signal, leading to synaptic weakening.

Research has revealed substantial alterations in LTP, LTD, and Hebbian plasticity in autism, providing insights into the neural mechanisms that contribute to autism’s cognitive and behavioral characteristics

1. Hippocampal Dysfunction:

   • Studies on animal models, such as the BTBR mouse model of autism, show impaired hippocampal LTP. This impairment correlates with the learning and memory deficits commonly observed in autism (Rubenstein & Merzenich, 2003; Bourgeron, 2015)​ (Frontiers)​​ (Nature)​.

2. Cerebellar Abnormalities:

   • Atypical LTD has been noted in the cerebellum, a region critical for motor control and coordination. This could underlie the motor deficits observed in autism (Fatemi et al., 2012)​ (Nature)​.

3. Genetic Factors:

   • Mutations in synaptic genes such as SHANK3, NRXN1, and NLGN3, which are vital for maintaining synaptic plasticity, have been linked to autism. These mutations can disrupt the balance of LTP and LTD, leading to synaptic dysfunctions associated with autism (Durand et al., 2007; Südhof, 2008)​ (Frontiers)​​ (Nature)​.

4. Neuromodulators:

   • Dopamine (DA) is a key neuromodulator that can modulate the direction and extent of synaptic changes. It acts through D1/D5 receptors to enhance LTP or through D2 receptors to promote LTD. This modulation is essential for adaptive learning and behavior in autism (Yagishita et al., 2014)​ (Frontiers)​.

2 versions of this post

PlainSpeak. Plain Language for the Lay Reader

For the Academic/Scientific Audience

References:

• Rubenstein, J. L., & Merzenich, M. M. (2003). Model of autism: increased ratio of excitation/inhibition in key neural systems. Genes, Brain and Behavior, 2(5), 255-267.
• Bourgeron, T. (2015). From the genetic architecture to synaptic plasticity in autism spectrum disorder. Nature Reviews Neuroscience, 16(9), 551-563.
• Fatemi, S. H., Aldinger, K. A., Ashwood, P., Bauman, M. L., Blaha, C. D., Blatt, G. J., ... & Welsh, J. P. (2012). Consensus paper: Pathological role of the cerebellum in autism. The Cerebellum, 11(3), 777-807.
• Durand, C. M., Betancur, C., Boeckers, T. M., Bockmann, J., Chaste, P., Fauchereau, F., ... & Bourgeron, T. (2007). Mutations in the gene encoding the synaptic scaffolding protein SHANK3 are associated with autism spectrum disorders. Nature Genetics, 39(1), 25-27.
• Südhof, T. C. (2008). Neuroligins and neurexins link synaptic function to cognitive disease. Nature, 455(7215), 903-911.
• Yagishita, S., Hayashi-Takagi, A., Ellis-Davies, G. C., Urakubo, H., Ishii, S., & Kasai, H. (2014). A critical time window for dopamine actions on the structural plasticity of dendritic spines. Science, 345(6204), 1616-1620.

The Social Responsiveness Scale SRS

What is it? 

The Social Responsiveness Scale (SRS) is a tool primarily used for quantitative measurement of autism symptoms in the general population, including individuals who do not have a clinical autism diagnosis. 

It measures the severity of autism spectrum symptoms as they occur in natural social settings [1]. Although it is not a diagnostic tool for autism, it provides a clear picture of functioning in areas that could be impacted in autism.

There is both a child version filled out by caregivers and an adult self-report measure. 

Five Subscales

1. Social Awareness: Recognition of social cues 
2. Social Cognition: Interpretation of social cues 
3. Social Communication: Conveyance of appropriate responses to social cues 
4. Social Motivation: The extent to which a respondent is generally motivated to engage in social-interpersonal behavior. 
5. Autistic Mannerisms: Stereotypical behaviors and highly restricted interests characteristic of autism [2].

Scoring and Interpretation

The SRS is a 65-item rating scale, with responses ranging from "not true" to "almost always true." Scores are computed for each subscale as well as a total score that measures severity along the autism spectrum.

• Scores of 76 or higher: severe
• Scores of 60-75: mild-moderate, indicates presence of some autism symptoms
• Scores below 59: considered within typical limits, indicating no significant issues with social responsiveness [2]

History

The SRS was first developed by John N. Constantino and Christian P. Gruber, who published it in 2005. It was designed to be a quantitative measure of autism traits in the general population, including individuals who do not necessarily have an ASD diagnosis [3]. The child version was filled out by caregivers. The SRS for adults was designed to extend the applicability of the SRS to adults, addressing the need for a quantitative measure of autistic traits across the lifespan [3].

Psychometrics

The SRS demonstrates good psychometric properties. It has high internal consistency (Cronbach's alpha = .97) and test-retest reliability (Intraclass correlation = .88) [4]. The inter-rater reliability is also good, ranging from .76 to .95 [5].

For related posts on other measures

References: 

[1] Constantino, J.N., & Gruber, C.P. (2012). Social Responsiveness Scale, Second Edition (SRS-2). Torrance, CA: Western Psychological Services.
[2] Constantino, J.N., & Gruber, C.P. (2012). Social Responsiveness Scale (SRS). Torrance, CA: Western Psychological Services.
[3] Constantino, J.N., & Gruber, C.P. (2005). The Social Responsiveness Scale. Los Angeles: Western Psychological Services.
[4] Constantino, J. N., Davis, S. A., Todd, R. D., Schindler, M. K., Gross, M. M., Brophy, S. L., et al. (2003). Validation of a brief quantitative measure of autistic traits: Comparison of the social responsiveness scale with the autism diagnostic interview-revised. Journal of Autism and Developmental Disorders, 33, 427–433.
[5] Bölte, S., Poustka, F., & Constantino, J. N. (2008). Assessing autistic traits: cross-cultural validation of the social responsiveness scale (SRS). Autism Research, 1(6), 354-363.ckles, A., Kreiger, A., Buja, A.,

The nuts and bolts of PD

The nuts and bolts of Parkinson's Disease.

Parkinson's disease (PD) typically manifests in individuals over the age of 50, with about 5% prevalence in those over 85 years old. Most cases are sporadic with rare inherited variants, suggesting that environmental or toxin-related triggers are likely contributors. PD is characterized by symptoms such as rhythmic tremors in the hands and feet, especially at rest, bradykinesia (slow movement), and akinesia (difficulty initiating movement). These symptoms result from damage and cell death in the brain regions such as the substantia nigra in the brain stem and the locus coeruleus, leading to decreased levels of norepinephrine and dopamine (DA). The substantia nigra projects to the striatum, where DA is the principal neurotransmitter involved in relaying movement messages to the cortex. Neuromelanin, a byproduct formed from the oxidation of DA to quinones and semiquinones and subsequent metal ion binding, is evident in PD due to its black pigmentation. The disease also features Lewy bodies in the substantia nigra and other brain areas, which are composed primarily of the protein alpha-synuclein, abundant in presynaptic neuron terminals. The major treatment for PD is L-DOPA, but excessive DA can lead to the formation of hydrogen peroxide and reactive oxygen species when released into the cytoplasm. This oxidative stress contributes significantly to the neurodegeneration observed in PD 

Active Sensing and Autism

Neuroscience Concepts: 

Active Sensing

Active sensing refers to the process by which organisms actively control their sensory organs to acquire and process sensory information more effectively. In the context of multisensory integration, active sensing involves the coordination and adjustment of different sensory inputs based on motor actions to enhance the perception of the environment. For instance, moving the head or eyes to better see or hear a source of interest, or manipulating an object to better gauge its properties. This form of sensing is crucial because it allows an organism to integrate sensory information from various sources in a way that is aligned with current behavioral goals, thereby enhancing decision-making and interaction with the environment.

In autistics, active sensing and multisensory integration can manifest differently compared to NTs. Research suggests that autistics may experience variations in how sensory information is integrated, leading to differences in perceiving and responding to the environment. For example:

• Hypo- and Hypersensitivities: Autistic individuals often exhibit sensory sensitivities that can affect their active sensing behaviors. Hypersensitivities (over-responsiveness) might lead to avoidance of certain sensory inputs, while hyposensitivities (under-responsiveness) might lead to seeking out more intense sensory experiences. This can affect how they use active sensing in daily interactions.
• Attention and Filtering: Differences in attentional mechanisms in autism can influence active sensing. Autistic individuals might have difficulty filtering out irrelevant sensory stimuli, leading to challenges in focusing on specific sensory inputs necessary for effective multisensory integration.
• Motor Coordination and Planning: Difficulties with motor coordination and planning, commonly observed in autism, can also impact active sensing. If motor actions are less precise or more effortful, it may affect the ability to actively manipulate sensory inputs effectively.
• Neural Processing Differences: Studies have shown differences in neural processing pathways involved in sensory perception in autism. Research has noted that autistic individuals might process sensory inputs in a more localized manner, potentially affecting the global integration of multisensory information (Marco et al., 2011)
• Predictive Coding: Some theories, such as those involving predictive coding, suggest that autistics might have a different approach to anticipating sensory inputs, which impacts how sensory information is integrated and processed. This can lead to differences in how expected and unexpected stimuli are managed, further influencing active sensing behaviors.

These differences highlight the need for a nuanced understanding of how multisensory integration and active sensing operate in autism. They also underscore the importance of creating environments and interventions that are sensitive to the unique sensory processing characteristics of autistic individuals, thereby supporting better integration of sensory information and more effective interaction with the world.

Yearning for Human Connections

  https://time.com/6551520/loneliness-autism-essay/

Victor Pineda the new head of CIL

Excellent news about Victor Pineda getting to be the new head of Center for Independent Living. 

https://thecil.org/press-release/center-for-independent-living-welcomes-dr-victor-santiago-pineda-as-new-executive-director-amid-crucial-times-for-disability-rights/ 

Great pick for CIL. I remember former CIL head James Stuart referring to Victor as a "Super Crip".

In an old blog post, I had written  "I’ve come to deeply admire Dr. Pineda and I have a lot to learn from him on deconstructing the seemingly impossible into a possible." 

Other blog posts on Victor

• https://uniquelyhari.blogspot.com/2019/04/dr-victor-pineda.html
• https://uniquelyhari.blogspot.com/2019/02/role-of-disability-in-society.html
• https://uniquelyhari.blogspot.com/2019/02/lives-worth-living_2.html 
• https://uniquelyhari.blogspot.com/2019/09/word-enabled-summer-internship.html
• https://uniquelyhari.blogspot.com/2020/04/a-chilling-waiting-game-disability-and.html

The Cocktail Party Effect

The cocktail party effect refers to the brain's ability to focus on a specific auditory stimulus, such as a single conversation, in a noisy environment. In autism, difficulties with this selective auditory attention may contribute to sensory overload and challenges in social communication.

PlainSpeak:  The cocktail party effect is the ability to tune into one conversation in a noisy room. Many autistic individuals may find this difficult, leading to sensory overload and making social situations challenging.

Read more on the Cocktail Party Effect: 

Academic/Scientific Audience 

PlainSpeak for Lay Reader

OCD

https://www.dailycal.org/2018/04/12/compulsion-complexity

 

Impact of language choices in scientific publication on representation of autistic researchers.

The impact manifests in several key ways.

1. Inclusivity and Accessibility. Language that is clear, direct, and jargon-free is more accessible to a wider audience. Which means a wider spectrum of autistics can engage more fully with scientific content, whether they are authors, reviewers, or readers.
2. Bias and stigma. 
3. Representation. Who is getting left out and who is getting included. 
4. Authorship and collaboration. Autistics may face barriers in scientific publishing due to implicit biases in what is considered rigorous or appropriate academic language. This can discourage participation or lead to under representation in authorship and peer review processes.
5. Ethical considerations. Engaging the autistic community ensures that scientific discourse does not inadvertently marginalize or misrepresent groups.
6. Policy and guidelines. Journals and publishers can influence language norms through their style guides and editorial policies. By adopting guidelines that favor inclusive and respectful language, publishers can lead the shift towards more equitable representation in scientific literature.

Even after being told to stop

Quote from my chapter in the Anthology Below.

"Survival of the Kindest - Truths from a Zoom Reality"

Book available at https://www.peasepress.com/product-page/essential-truths-the-bay-area-in-color