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Cholinergic Component of Autism Spectrum Disorder. Elizabeta B. Oxytocin and Autism. Pharmacological Treatment of Autism. Back Matter Pages About this book Introduction The recent perceived rise in autism worldwide has spurned a dramatic increase in autism research, but few studies have focused on determining the neurochemical basis of the disorder. About the Editor Dr.

GABA autism cerebellum dopamine etiologies limbic system neurochemical mechanisms neuropathology neurotransmitter systems therapy. Editors and affiliations. The range of possible scores is 0 no distress to The questionnaire data for each subject are given in Supplementary Tables S1—S3. During imaging, subjects were stimulated with s segments of broadband continuous noise delivered binaurally at 50, 70, and 80 dB SPL. The periods of stimulation were separated by or s periods of no stimulation. Noise level was the same for all stimulation periods of a given run and was varied pseudorandomly across runs.

The noise was low-pass filtered kHz cut-off and spectrally shaped to account for the frequency response of the insert earphones used for delivery of the sound stimulus Sensimetrics, Malden, MA. The noise spectrum measured on an artificial ear was flat to within 5 dB. In the scanner room, before imaging, detection threshold for the noise stimulus was measured separately for each ear to establish stimulus levels in dB SL. The scanner coolant pump was turned off for these measurements and during the functional imaging described below. Also, in the scanner room before imaging, subjects were presented with each stimulus level for the full s duration to be used during imaging.

Based on this exposure longer than during the LDL test and in a different environment , eight subjects declined to be imaged with the 80 dB SPL stimulus. Subjects were instructed to watch a black cross in their field of view that briefly turned red at random intervals throughout each run throughout both stimulation and no stimulation periods.

They were further instructed to press a button whenever the color changed. Subjects were imaged in a 3-T scanner using a channel head coil Siemens Trio with Matrix head coil. In each imaging session, the following occurred. Ten parallel slices covered the brain stem, thalamus, and temporal lobe. The second posterior-most slice was positioned to intersect the inferior colliculi and cochlear nuclei. Typically, three runs were collected at each stimulus level, yielding images per level.

Functional image acquisition was synchronized to the subject's first pulse measured using a pulse oximeter following a minimum interimage interval of 7. Image signal in the functional data were 1 corrected for slight movements of the head using SPM2, 2 corrected for drifts in amplitude over time, and 3 normalized such that the time-average signal had the same arbitrary value for all runs Harms and Melcher The time series of images corresponding to functional runs at the same stimulus level were concatenated to form a single data set from which activation maps were derived by comparing image signal between sound on and off periods using an unpaired t -test see Fig.

A hemodynamic delay of 4 s was assumed in the assignment of images to the on and off periods. For subjects in whom two, rather than three, runs were obtained 1 or 2 stimulus levels in 3 subjects or where four runs were obtained, the P value result of the t -test was adjusted to what it would have been if the number of runs had been three. This adjustment was to multiply the t -score by the square root of the following: the number of images in three runs divided by the actual number of images collected.

A : subcortical regions of interest ROIs. Location of the inferior colliculus IC and medial geniculate body MGB is shown by the images from 1 subject The IC and MGB are shown in enlargements of the rectangular area red outline in near-coronal images of the whole head.

Sound-evoked activation color is localized to the inferior colliculi top and medial geniculate bodies bottom. The activation is superimposed on anatomical images obtained in the same imaging session grayscale. B : cortical ROIs. The location of each analyzed region is indicated on a reconstructed superior temporal lobe.

Activation was quantified within regions of interest ROIs defined relative to gross anatomical landmarks. They also included the following cortical ROIs Fig. Results of a previous cytoarchitectonic study of human superior temporal lobe guided the choice of cortical ROIs and their detailed definition. The study, by Fullerton and Pandya , concluded that auditory cortex in humans has the same organizational plan as that of monkeys: a central core surrounded by medial and lateral belts.

Neurodevelopmental Hypothesis about the Etiology of Autism Spectrum Disorders

These relationships were used to define AMA and PT to approximate the medial and lateral belt, respectively. Quantification of activation for each ROI was as follows. Third, activation was quantified by averaging percent signal change across the remaining voxels. Note that the voxels included in this average were the same for all stimulus levels.

This averaging was deemed appropriate because systematic differences in percent change between the left and right hemispheres were not seen for any structure or for any subject group. In instances where percent change could only be determined for the ROI on one side because of poor signal-to-noise ratio on the other side , the activation from that one ROI was used instead of the average. ROIs that failed to show activation at any sound level were handled in one of two ways depending on the most likely reason for the lack of activation, either ratio low percent signal change or poor signal-to-noise ratio SNR , where SNR was defined as the mean signal over time divided by the SE.

If at least two thirds of the voxels comprising an ROI had a high enough SNR at a particular level to detect signal changes of 0. All other ROIs failing to activate were excluded from analysis because they could not be reasonably assigned a percent signal change value of zero. Because fewer than one half the CNs produced usable data and firm conclusions could not be drawn from the remaining data, the CN will not be considered further in this report. Subjects reported numerical loudness ratings that increased with increasing stimulus level: from 1 very soft to 7 uncomfortably loud or from 1 to 6 loud, but okay in nine subjects for whom even the highest intensity stimulus possible with our equipment was not uncomfortable.

These data provided one of the two measures of SLT used in this study: LDL the sound level assigned a 7 or a lower bound on LDL in subjects whose highest numerical rating of loudness was 6. The second measure was SLTQ score. Classification of subjects by SLT. Each symbol corresponds to a subject. The division between normal and abnormal SLT regions was defined such that subjects unable to tolerate the 80 dB SPL stimulus during scanning symbols with horizontal line below would lie in the abnormal SLT region.

The dark solid line in each panel is a linear fit to the data, whereas the lighter dotted lines each show what the fit would be if one of the data points were absent. The fact that this trend is apparent in all of the dotted line fits to the data indicates that it is not reliant on any one data point. Stimulus level: 70 dB SPL. Each symbol in each panel corresponds to an individual tinnitus filled symbol or non-tinnitus unfilled subject.

The solid line is a linear fit to all of the data. Spearman's coefficient and associated P value are given in the bottom left of each plot. Each dotted line is the result of a linear fit to all but 1 data point; a different data point was omitted for each line. The dependence of percent signal change in the IC and MGB on SLT was confirmed by a complementary analysis that involved classifying tinnitus and non-tinnitus subjects into two SLT groups normal and abnormal. Average percent change was greater for the two groups with abnormal SLT Fig.

Auditory activation in subject groups defined by SLT and tinnitus. PAC also showed a significant effect of tinnitus. Each subject contributed a single value to the mean. For MGB in the non-tinnitus, abnormal SLT group, circles indicate individual subject data because only 2 subjects contributed to the mean. At 70 dB, the two groups with normal SLT, one with tinnitus and one without, showed comparable percent signal change in both the IC and MGB, suggesting that there was little or no effect of tinnitus on the sound-evoked activation levels of these structures.

In the IC, average activation showed a distribution across the four subject groups defined by tinnitus and SLT that was qualitatively similar to the distribution for 70 dB Fig. Mean activation at 80 dB Table 2 was similar for these two groups in both the IC 1. Thus the 80 dB data supported the data at lower levels in indicating no effect of tinnitus on sound-evoked activation levels in the IC and MGB. Table 2. Percent signal change for each subject group, structure, and stimulus level.

Eileen Nicole Simon (Author of Language, Brain, and Iatrogenic Peril)

To address whether the activation might depend on some variable correlated with SLT rather than depending on SLT per se, the following analyses were performed. The IC and MGB activation data at 50 and 70 dB were cross-correlated with each of the following: age, threshold for the continuous noise stimulus, score on the anxiety inventory, and score on the depression inventory. Cross-correlation with these variables was performed separately for each of the two structures and each stimulus level.

Note that P value results of the correlations have not been corrected for multiple comparisons. A three-way ANOVA was also performed on the activation data for each structure and stimulus level but replacing age with threshold, anxiety score, or depression score.

The only exception was an effect of anxiety in the IC data. The results of the analysis suggest that age and anxiety may have played some role in determining the magnitude of IC activation, but indicate that, among the factors tested, the dominant factor in the IC, and indeed the only apparent factor in the MGB, was SLT. Note that SLT would have emerged as even more dominant if the P value results of the analyses had been corrected for multiple comparisons and hence increased , especially because the correction is only applicable to those variables not hypothesized, a priori, to be related to activation i.

See Fig. Data for one region showing dependencies on both variables, PAC, can be seen in Fig. For the 50 dB stimulus, the dependence of PAC activation on tinnitus was even more apparent than at 70 dB, and one other cortical region, HGal, also showed significant effects of tinnitus. These analyses indicate that tinnitus, more than any other variable considered, influenced PAC and HGal activation levels at 50 dB. Importantly, the correlations were shown in subjects with clinically normal hearing thresholds using the same physical stimulus levels in all subjects.

Furthermore, the correlations could not be attributed to other factors potentially affecting the magnitude of fMRI activation, including stimulus threshold, depression, anxiety, and age.

Similar authors to follow

Thus the results provide strong evidence for a relationship between the magnitude of sound-evoked fMRI activation in the auditory pathway and SLT. The nature of the relationship was as follows: activation from sound increased with decreasing SLT. These results are, to our knowledge, the first to directly show a physiological correlate of abnormal SLT, that is, hyperacusis.

Our results pertain specifically to people with mild hyperacusis, because hyperacusis was never the primary complaint among the tinnitus patients recruited for this study and was self-recognized by only a few of the subjects who ultimately showed abnormal SLT under the controlled conditions of our testing. Interestingly, we had difficulty finding subjects with tinnitus and completely normal SLT as defined by our behavioral tests.

Although anecdotal, this observation nevertheless suggests the possibility that abnormal SLT, by which we mean hyperacusis ranging from mild to severe, may be more directly related to tinnitus than generally appreciated. This result suggests that previous demonstrations of elevated sound-evoked fMRI activation in the IC of tinnitus subjects were likely related to abnormal perception of the sound stimulus rather than the phantom perception of sound, that is, tinnitus Lanting et al.

We suspect that a sizable fraction of the tinnitus subjects in these previous studies had abnormal SLT, which would account for the previous findings of elevated activation in the subject groups with tinnitus. Thus the activation enhancements seen subcortically at 50 dB were not simply reflected verbatim in cortex. In particular, at both 50 and 70 dB, activation in the subject groups with tinnitus was elevated regardless of whether SLT was normal or abnormal.

We can only speculate as to why this was the case, but one possibility is suggested by neuroimaging data showing that sound produces increased activation in auditory cortex during selective attention to the auditory domain Degerman et al. In other words, the elevations in sound-evoked cortical activation that occurred with tinnitus irrespective of SLT might not reflect the tinnitus percept per se but rather reflect attention drawn to the auditory domain by the presence of tinnitus.

The absence of tinnitus-related effects in subcortical centers in our data is consistent with this attention-based hypothesis for the tinnitus-related effects in PAC because attentional state has a far subtler effect on subcortical compared with cortical auditory fMRI activation Rinne et al. However, undue attention drawn to the auditory domain by the tinnitus percept is just one possible explanation for the tinnitus-related elevations in PAC activation.

Others include the possibility that cause and effect are reversed such that the tinnitus percept results because PAC activity is enhanced by overattention to the auditory domain e. Also, enhancement of PAC activity and tinnitus perception might build on one another. For instance, aberrant auditory activity that is not consciously perceived as sound might become perceptible because it is assigned behavioral significance through what amounts to implicit aversive conditioning. The emergent percept reinforces the aversive response, enhancing the aberrant activity and hence the percept, and so on.

Thus any cortical dependencies on SLT and tinnitus seemed limited to the core of auditory cortex. The elevations in activation to sound seen in this study are highly suggestive of abnormal gain within the auditory pathway. Perhaps the most directly relevant animal work is that showing abnormally elevated responses to sound in the inferior colliculus of acoustically traumatized animals, a finding potentially relevant to this study of subjects with normal audiograms, because it was seen for sound frequencies at which threshold was normal i.

The elevated responses in animals have been postulated to arise as a result of reduced GABA-mediated inhibition, a possible mechanism by which the elevations in fMRI activation seen here might arise. Two previous studies showing increased activation of auditory cortex with increased sound loudness—as distinct from physical sound level—warrant consideration in light of these results. One study found that the amount of activation produced by a variety of pure and complex tone stimuli was better correlated with the calculated loudness of the sound stimuli than to their level Hall et al.

The other showed that activation increased similarly with loudness, but not level, for two subject groups: normal hearing listeners and hearing impaired listeners in whom loudness grew abnormally with stimulus level because of recruitment Langers et al. Both studies indicated that the degree to which auditory cortex activates is directly related to the perceived loudness of a sound stimulus. Although these results are somewhat different in that they show a correlation between activation and the upper limit of comfortable loudness, they can be seen to be consistent with a dependence of activation on loudness by noting the following.

Having normal thresholds for detecting sound, as in this study, but reaching uncomfortable loudness at a lower-than-normal sound level, implies the perception of greater-than-normal loudness for at least some sound levels below those deemed uncomfortable. Given the relationship between loudness and auditory midbrain activation described in the introduction, the elevated inferior colliculus activation seen for 50 and 70 dB SPL in subjects with abnormal SLT may also reflect abnormal that is, heightened loudness perception.

These results provide an entrance to understanding and quantifying physiological effects of candidate treatments for tinnitus and hyperacusis, perhaps most particularly sound therapies designed to promote a reduction in central auditory gain Davis et al. Such therapies, which involve the delivery of controlled sounds in a prescribed manner, along with counseling, have been shown to ameliorate hyperacusis and reduce tinnitus severity as assessed from behavioral tests and questionnaire evaluations.

Based on these results, we hypothesize that such improvements coincide with reductions in sound-evoked fMRI activation in the auditory pathway. This hypothesis could be tested by comparing measurements of sound-evoked fMRI activation, like those of this study, before and after administration of sound therapy. A variety of clinical conditions are characterized by disordered perceptions that, like tinnitus and hyperacusis, have been hypothesized to arise from abnormal elevations in neural activity in the CNS.

They also include conditions analogous to hyperacusis: the heightened sensitivity to light occurring with migraine and the lowered thresholds for stimulated pain e. In some of these cases of disordered perception, there is evidence indicating underlying elevations in neural activity Ambrosini and Schoenen ; Cook et al. These previous data combined with these results reinforce proposals that the neurophysiology behind tinnitus and hyperacusis may not be entirely unique to the auditory system but may rather have strong commonalities with the disordered perceptions characterizing other clinical conditions involving the visual and somatosensory domains.

Table of contents

No conflicts of interest, financial or otherwise, are declared by the authors. We thank R. Tyler for very helpful discussions concerning behavioral measurements and questionnaires. We also thank B. Norris for assistance with data collection and figure making, D. Langers for assistance with data collection and comments on an earlier version of this manuscript, E.


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Volume Issue 6. Volume Issue 5. Volume Issue 4. Volume Issue 3. I am pretty sure his issues are genetic, possibly linked to his genetic heart disorder. Except, now it is. Anyway, there is one definite known reason cause of autism: congenital rubella syndrome. As for same sex relationships, preferences, etc. What happened off duty? Which would impact unit efficacy. Not happening on our watch.

That belongs to my wife. The same was true for females adventuring into who could perform the duties required. As in shooting people, putting a knife into someone, kill someone on a bad day. But then, it was indeed a war environment. After, I went into IT, where I got to meet a part of the spectrum. Initially, it felt like trying to lead a flight of gnats. Eventually, I learned the distraction points, boredom points, etc and learned to lead, outdistracting, out outbordomeing, etc. In short, learning inside of the curve. The team is far too valuable and creative, when guided properly.

The team members, just as my military team members, are very special resources, when properly guided. My 34 yr old son is another adult on the spectrum [and he received many fewer vaccines than his younger brother, not on the spectrum]. I assume that this is meant as some misguided anti-fraud provision as well as a means, however flawed, to pare down eligibility for impossibly scare resources. Another issue is the increasing move away from clinical dx following ADI [even by clinicians renowned in the field for many yrs, as the one who diagnosed my son at WUMS-StL] per se and to bureaucratically stubborn insistence on a formalized ADOS process, thus requiring dx before age 21 to have been established by an instrument that did not yet even exist.

In reading and re-reading these comments, I found myself wishing I had been clearer in my own references to vaccines. Does he addresses the more recent developments in autism science,that show autism can be a presenting feature of either mitochondrial disease,or of an inherited autoimmune encephalopathy in children born to mothers with autoimmune disease? These are the two of main types of regressive autism,that mothers like those that post at Age of Autism are most likely to have kids with. These are very serious diseases,that have both autism,and complex medical issues.

Except they are congenital in nature,and not caused by vaccines. Unfortunately I can no longer find this video on the web. But the thing is,once these underlying causes are found,and treated,the autism,seizures,and other brain related problems improve dramatically. The person may even become neurotypical,if they stay on treatment long enough. This was the case with me. The diagnosis was so severe that I would have ended up in an institution had my mother not intervened. I was rediagnosed as an adult,and it was pretty much the same story.

Except not long after that second diagnosis,I found another doctor willing to run some real medical tests on me. I have serious inborn metabolic and mitochondrial disorders that were the cause of my autism. The many medical issues I have have been much slower to respond to treatment than the autism,learning disabilities,etc have been. Going from moderate to severe autism to basically neurotypical in a few years is incredible. The best thing that ever happened to me.

Of course not. Or someone born deaf,who was able to get a cochlear implant and hear. I am a pioneer in this area,especially for an adult. But I believe as the science advances,this will become more and more common in the autism community. It will be something you will have to come to grips with eventually. There will be debates much like there have been in the deaf and blind communities.

The closure of the foramen ovale and ductus arteriosus largely are to bring the lungs fully online. What is any of lupinssupin talking about when it is at home? How is any of this helpful to autisic people? It does not help disrespected under estimated non speaking autistic people. Does not help older autistic people. It is useless speculation! We ought to be giving non speaking autistic people all kinds of communication devices and not tormenting them with behaviourlism and other nonsense that gets in the way.

Bull Crap. That in itself is a mild disability, akin to my hearing loss, which can make communication problematic. Or should we just give up? But then, I was trained to leave no person behind. Idevices and tablets for all autistic people. But you know folks will be like why should we give all of them these?

Because it is helpful, dang it. Behavioralism is a sacred cow that needs to be slaughtered. Autistic people need to learn how to cope with their differing neurology in a hostile world and non autistic people need to get used to the existence of autistic people and to respect their needs. Spending hours on forced normality is a waste of time and energy just like blaming vaccines. That sounds like behavioralsim. I do agree, neurotypicals need to be educated to the needs of those with different neurological capabilities.

Educating the general populace on how to work with disabled and non-neurotypical people is necessary to provide a far better life experience for all. Wrong, it teaches the non-neurotypical to interface with the neurotypical in daily life. It teaches islands of stability in an otherwise disorderly life experience with neurotypicals, who are phenomenally disorderly by nature.

Not being trained to deal with that would result in incessant meltdowns, which would have otherwise been prevented. Just as neurotypicals need training in dealing with others with different capabilities. Our operation would be incapable of operating without his work. When he asked for a snack, I had completely forgotten he was incapable of feeding himself. Quite embarrassing all around. With his formidable knowledge and capabilities, forgotten was his disability. I admit I have not read this book I have looked at the AoA website. It is a trap where one can easily blame and become jealous of those who adhere to acceptance and Neurodivercity.

When I think about it even in preschool for developmentally delayed my 3 year old was not included. They sent him out everyday with his aide who walked him in a stroller At lunch time all the kids got to watch a movie but him.

They told me he was disruptive I called and said to let him at least watch the movie. The teacher said there was no room for him. I took him to Head Start where they were very sweet to him and included him in every way. Every child is entitled to a meaningful education. Those were his wild days filled with shaking wires and hyperactivity.

We moved and he went to a better school that included some ABA for a little while so he could sit still enough to understand the spoken word. You are commenting using your WordPress. You are commenting using your Google account. You are commenting using your Twitter account. You are commenting using your Facebook account.

Notify me of new comments via email. Notify me of new posts via email. This site uses Akismet to reduce spam. Learn how your comment data is processed. E or CADE for short. So they stuck in my mind and I decided recently to check into them again. The name […]. A few years back the Age of Autism converted from a business to a nonprofit.

That means we get some information on their financial status. As a nonprofit, their tax forms become public. The most recent informaiton we can get is for […]. When Donald Trump was running for president has he ever stopped running for president and started governing? They were excited because here was a candidate who publicly accepted and promoted the fake and damaging idea that vaccines cause autism. Before running, Trump supported the idea that vaccines […]. You had hopes and dreams.

And that the dream lives on—having […]. Autism Science, News and Opinions since Left Brain Right Brain. Home About Books and Movies. Go to the next article in the google search and one finds The coverage below is very convincing. Which it is.

So well, in fact, that I will copy that paragraph here: Silberman believes that our conversation about autism could be made a great deal clearer and more humane if we viewed the condition as a disability. Like this: Like Loading Here is one Reply. How many politicians care at all about issues 2 years down the road, much less 10? I do not and will not lend my name to the Age of Autism website.