Auditory Processing in Autism and Ultrasound-altered Hearing

Auditory Processing in Autism and Ultrasound-altered Hearing

I thought this correlation was concerning. While the ultrasound hearing study dismisses that ultrasound can cause damage to hearing as though it were nothing big, perhaps the improved hearing in infants is a red flag that ultrasound could be promoting auditory hypersensitivity.

This would not have to be a big thing — ASD is a gradient, right? So, children who were near threshhold would be tipped over, while it may possibly help infants with worse hearing. There’s two sides to every coin, and every tool can harm or heal.

http://www.sciencedirect.com/science/article/pii/S0149763411002065
Abstract
For individuals with autism spectrum disorder or β€˜ASD’ the ability to accurately process and interpret auditory information is often difficult. Here we review behavioural, neurophysiological and imaging literature pertaining to this field with the aim of providing a comprehensive account of auditory processing in ASD, and thus an effective tool to aid further research. Literature was sourced from peer-reviewed journals published over the last two decades which best represent research conducted in these areas. Findings show substantial evidence for atypical processing of auditory information in ASD at behavioural and neural levels. Abnormalities are diverse, ranging from atypical perception of various low-level perceptual features (i.e. pitch, loudness) to processing of more complex auditory information such as prosody. Trends across studies suggest auditory processing impairments in ASD are most likely to present during processing of complex auditory information and are more severe for speech than for non-speech stimuli. The interpretation of these findings with respect to various cognitive accounts of ASD is discussed and suggestions offered for further research.

http://www.ncbi.nlm.nih.gov/pubmed/23663515
OBJECTIVE:
Prenatal ultrasound exams have become increasingly frequent. Although no serious adverse effects are known, the public health implications would be enormous should adverse effects on auditory development be shown. This study looks to establish a possible correlation between hearing loss and increased prenatal ultrasound exposure.
CONCLUSIONS:
Our results show that there is no correlation between a higher level of prenatal ultrasound exposure and hearing loss. Indeed, infants who had more prenatal ultrasounds in the third trimester were more likely to pass their screening hearing exams. The finding that children receiving more prenatal ultrasounds have a higher likelihood of passing newborn hearing screens serves as an excellent reminder of the classic statistics rule that correlation does not imply causation.

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8 thoughts on “Auditory Processing in Autism and Ultrasound-altered Hearing

  1. I’ve done some work on US in relation to ASD. The second study is intriguing and certainly calls for more in depth (non-correlative) research. But, as an aside, I find it very bizarre that this study, for such a design, had quite a small total number of samples (100), and yet they didn’t perform what is called a Power Analysis to determine whether they have large enough samples to perform the statistical analyses intended. I.e., if you only have a sample of 2, and 1 sample exhibits Outcome A, and the other Outcome B, and you run stats on this, then of course you’ll have a statistically significant outcome. Heck, 50% of your sample displayed Outcome B! MOST surprisingly, the researchers of the ultrasound study didn’t appear to have performed a Power Analysis and even admitted it: “Additionally, our study had a relatively small n and may not have the power to detect a difference if present.” As a researcher, I’m actually quite appalled the study got published without that being done. It doesn’t mean that the results are false, but a Power Analysis is an assurance that the study has enough samples to adequately measure what the researchers are attempting to measure. Still, it raises some potentially interesting questions if the study, in spite of the missing analysis, does indeed have enough power.

    • Ha, excellent retort Emily. On that note, isn’t it ironic that the author in the conclusion so smugly notes that ‘correlation is not causation’ given that weakness in the study?

      This study definitely needs to be verified.

      On the note of sensitization, I have read papers that suggest ultrasound is able to trigger neuron firing. (http://www.ncbi.nlm.nih.gov/pubmed/19163650)

      Given Ang, 2006’s findings that ultrasound can cause improper localization of neurites and this combined, I could envision a plausible mechanism for sensory sensitization if it were indeed true.

      Here’s hoping it’s not –

      • Yes it’s sadly ironic. And yes, you’re right about ultrasound being used transcranially. It’s most likely to do with the fact that ultrasound can create temporary pores within cells, which subsequently allow an inward rush of excitatory ions like sodium and calcium; in the case of neurons this would promote firing. Ang et al.’s study is highly interesting and we’re hoping to study other more neurodevelopmental aspects in a similar study (if only we can convince NIH for funding such a topic!), but Ang’s study also doesn’t address whether the effects seen are due to the cavitational threshold being crossed or are instead from other noncavitational mechanical effects, which occur at subthresholds of cavitation (the formation and bursting of microscopic bubbles, in case you’re not familiar). Which is important to know so as to better understand how the migrational abnormalities occurred in the first place. I for one find their hypothesis that the neurons were “shaken” off the radial glial scaffolding during migration rather simplistic. But hey, none of the authors were ultrasound physicists, so we can cut them some theoretical slack. πŸ˜‰

      • Hah, well… I do not think that cavitation is likely to happen given the parameters in the Ang study. I do not believe that there was significant gas body in the fetal rat brains to elicit cavitation with the dose they used. They recorded an Ispta of 1.5 mW/cm^2, which is very low.

        Indeed, however, ultrasound’s impact on neuronal migration needs extensive research – there are many plausible mechanisms… what I envision to be more consistent with these results have to do with cell to cell signaling.

        Ultrasound could alter cell adhesivity, thus leading to the observed effect in the Ang study. To justify, here is a study that describes cell adhesiveness as critical to neurons migrating to appropriate cortical layers. In the absence of SPARC-1, a protein critical for cell adhesivity, the neurons fail to acquire proper cortical positions. http://www.ncbi.nlm.nih.gov/pubmed/14715135

        Since ultrasound is used in industry for cleaning and such (jewelry cleaning, weapons, metals etc) — one could imagine, through symmetry, such an effect happening in a biological system as well.

        Thoughts?

      • Cavitation occurs in biological tissues. All tissues house microscopic bubbles, although many forms of medicine and research use injectable bubbles to enhance effects. The reason I suspect Ang’s results were due to cavitation was due to the threshold effects seen with absolute time of exposure. Only longer times of exposure produced the effects seen. Noncavitational mechanical effects I suspect would produce a more gradual effect curve as opposed to the sigmoidal one seen with cavitation. The longer exposure times also match with known effects of cavitation: the longer a tissue is exposed to ultrasound, the lower the threshold for detrimental cavitation because microscopic bubbles gradually grow with each expansion half cycle. Cavitation risks are comparably more severe at 30 minutes than 10 minutes at the same intensity/frequency, greater at 120 minutes than 30, and so on.

        Regarding cell adhesion, I do agree that ultrasound may affect cell adhesion, but were it to do so it would more likely be a biochemical result rather than a mechanical “shaking from the branch” as Ang et al. had suggested.

      • Ah, so — let me dust off my glasses and see if we can get on the same page, here… bare with me –

        In reading back over the article, I do see this..

        At the frequencies and intensities we have used (see Material and Methods; see also Supporting Text, Tables 2–5, and Figs. 8–14 which are published as supporting information on the PNAS website), it is unlikely that cavitation or temperature changes play a role in the effects noted (36).

        I believe that the author claims the cavitation risk is exceptionally low in this case because of two factors… First, his waveform –

        For ultrasound exposure, we used an Ultramark 4 Plus (ATL, Bothell, WA) ultrasound system and an Access 10 transducer … Unanesthetized pregnant mice were exposed to B-mode, 6.7-MHz, pulsed USW with a pulse duration of 0.2 ms … Dosimetry testing of the ultrasound system showed spatial peak pulse average intensities (Isppa) of 330 W/cm^2, and spatial peak time average intensity (Ispta) of 1.5 mW/cm^2 when measured in water. The estimated Isppa at the fetal locations was on the order of 1 W/cm^2.

        The spatial-peak time-average intensity (Ispta) is typically associated with temperature measurements, but overall it is a good guestimation of how much ultrasound power is being delivered over time.. 1.5 mW/cm^2 is very low, much lower than the 720 mW/cm^2 maximum Ispta used today in fetal scanning. So, at a first glance their overall energy input is very low relative to studies that have detected significant cavitation in biological tissues… do you have any studies on mind that have detected cavitation at lower powers, by chance?

        **EDIT: As well, the estimated 1W/cm^2 Isppa at the fetal loci near no significant gas bodies is far below the cavitational threshhold that I am aware of. But, if you can offer a study to sway me elsewise, I relent gladly -**

        I have more questions for you, but let’s focus on one at a time instead of just dropping all the bricks in at once. It’s easier for me to keep track of conversation that way. πŸ™‚

      • Sadly, I don’t have any studies primarily because they haven’t been performed. While there’s plenty that have tested thresholds for cavitation in various media dependent upon intensity and frequency, there are few to none who have concentrated on duration of exposure, whose threshold will subsequently reduce with continued exposure. As I said before, the reason I suspect the effects from the Ang et al study were in fact due to cavitation is due to the sudden appearance of an effect with the longer duration exposures. And that’s one aspect of ultrasound studies we’re interested in looking further into. I’d personally love to quote the studies for you, but they’re not there. Ultrasound research in terms of its effects on biological tissue is currently incomplete.

  2. I see. I think I understand your logic. Maybe I can tell you about how I look at this, and we can work together on meeting halfway.

    As I understand cavitation, the threshold for bubble growth is based on several key environmental conditions. Elasticity of a material, temperature, internal vs. external pressures, composition (including presence or non-presence of gas bodies and nuclei) and some electrical properties. There have been studies evidencing cavitation in vivo, but in vivo there is lots of circulatory action that cools down areas and helps disperse localized energy input. So, cavitation is harder to achieve in vivo than it is in vitro.

    I currently have a 20 mW/cm^2 unit operating at 1MHz sitting in a closed cup with a thermocouple hooked into it, ..I can detect no change in temperature over a period of two hours – it just cools down too fast for any heat input to be kept inside. I think that a rat’s circulatory system would disperse energy pretty quickly. So, what parameters would be lowering the threshold down to the point where 1.5 mW/cm^2 would allow cavitation? It would not be temperature, unlikely vapor pressure, . . .

    Further, cavitation at >6 MHz – as used in the Ang study – would require quite a lot more energy to form than at lower frequencies, which is common in therapeutics and studies which have detected cavitation in vivo..

    so, being in vivo, the very low energy input, combined with the fairly high frequency do seem to make cavitation unlikely in these particular parameters. Not saying impossible, but improbable as far as I am aware.

    Even if it did – all things considered – how would you justify that cavitation would alter neurite path? If you speak of inertial cavitation, would not shear forces disrupt a neurite and lead to dye leakage?

    Now — that is not to say microstreaming does not occur. Ultrasonic pressure waves do likely bump neurites around — that is the basis of the cell adhesion argument..

    My apologies if I rambled a little… very happy to have an intellectual discussion on this topic. πŸ™‚ Thank you for the good debate.

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