I recently saw a social media post with arguments over "neurodiverse" v "neurodivergent."
Seriously!
Are we now going to start another decades-long, never-ending conversation, parallel to the disproportionate airtime spent on arguing "with autism" vs "autistic,"
Can we focus on ACTUAL SOLUTIONS FOR AUTISM - benefits our Quality of Life on the ground
(There seems to be no similar passion or urgency in seeking solutions)
A mere 13% of the world is primarily english-speaking, but autistics exist all over the globe.
A majority of us desperately need SOLUTIONS, and care much less about re-arrangements of letters or grammar.
Understanding Short-Term Brain Changes and Autism
PlainSpeak Plain Language Version for the Lay Reader
Our brains constantly change how neurons (nerve cells) communicate to help us learn and remember things. Some of these changes happen very quickly and are known as short-term synaptic plasticity. This is when the connection strength between two neurons changes for a few seconds to a few minutes. Two important types of these changes are paired pulse facilitation (PPF) and paired pulse depression (PPD).
Paired Pulse Facilitation (PPF) happens when two signals arrive close together at a neuron connection, and the second signal is stronger than the first. This is because the first signal leaves behind some calcium, which helps release more chemical messengers for the second signal, making it stronger.
Paired Pulse Depression (PPD) is the opposite. When two signals come close together, the second signal is weaker. This happens because the first signal uses up most of the available chemical messengers, leaving fewer for the second signal.
These short-term changes are important for how our brains process information. In autism, scientists have found that these changes can be different. For example, certain gene mutations linked to autism can affect how well these short-term changes work. Some of these genes, like SYN1 and SYN2, help control the availability of chemical messengers at neuron connections. Mutations in these genes can lead to an imbalance in brain activity, making some signals too strong and others too weak (Frontiers, 2015) (Frontiers).
Other studies have shown that mutations in another gene, neuroligin-3, which is also linked to autism, can change how neurons communicate in different parts of the brain. These mutations can increase the strength of certain signals and disrupt the balance of brain activity (Molecular Psychiatry, 2015) (Nature). This imbalance can contribute to some of the behaviors seen in autism.
Understanding these short-term brain changes helps scientists learn more about how autism affects the brain and can lead to new ways to help people with autism.
2 versions of this post
For the Academic/Scientific Audience
PlainSpeak in plain language for the lay reader
Disclose or not to disclose your dx.
Sometimes I have to wonder about how inclusive the term neurodiverse itself is.
For example there is an assumption that "to disclose or not to disclose" is a problem for every ND person in higher ed or employment.
For many of us with visible disabilities, (my autism is very very very apparent), we DON'T have the luxury of choice; to disclose or not to disclose our disability.
Not having that choice puts us at a huge disadvantage; as many doors of opportunities are shut in your face (you are deemed unworthy off the bat), you don't even get to cross the threshold of many such doors before you even coming to the issues like deciding to disclose or not disclose.
So how inclusive is ND movement if makes such sweeping generalizations around who is considered ND.
Diagnostic Overshadowing
Autism Lexicon: Diagnostic Overshadowing
Diagnostic overshadowing in autism occurs when the symptoms and behaviors associated with autism obscure or overshadow the presence of other mental or physical health conditions. This can lead to misdiagnosis, underdiagnosis, or delayed diagnosis of other conditions, ultimately impacting the individual's overall care and treatment outcomes.
PlainSpeak: Diagnostic overshadowing in autism is when doctors focus too much on autism and miss other health problems because they think it must be all because of autism.
Read in more detail...
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.
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.
New ED for DREDF
DREDF gets a new captain.
Two press releases
Announcing Nicole's hiring at DREDF
Nicole's departure from the San Francisco Mayor's Office on 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.
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
Hippocampal Dysfunction:
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).
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).
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
- Social Awareness: Recognition of social cues
- Social Cognition: Interpretation of social cues
- Social Communication: Conveyance of appropriate responses to social cues
- Social Motivation: The extent to which a respondent is generally motivated to engage in social-interpersonal behavior.
- 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].
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 PDActive 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:
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.
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