Understanding Sensory Sensitivities

What I learned in the last 12 years that you should know

Hi All: Most of this is posted as a comment at ADHDWeasel. I was not allowed to post the entire comment, so here it is. ADHD Weasel did a great job. I will have to say, my response is not as nicely brief. But, hopefully, helpful.

I would like to add to ADHDWeasel’s post my deep dive into understanding and finding treatment strategies for what I call "sensory amplification syndrome" (SAS). I spent more than 10 years gathering data and interviewing hundreds of clients to determine if they fit the criteria for what we currently call ADHD/ASD. Within the first two years, I added in evaluations for working memory and Sensory Sensitivities. I wanted to figure out the roles of working memory and sensory sensitivities in the lives of those who did, or did not, fit the criteria for the diagnosis of ADHD or ASD or a combo of the same. I wrote about much of this in My 2013 Book, in which I coined the term "sensory amplification syndrome."

This response contains much of my recent review of the literature from 2013 to 2025. It confirms and expands on what I communicated in 2013.

I learned from both the literature (see below for some of it) and my comprehensive evaluations of more than 400 clients that the best way to describe the sensory processing challenge is sensory "amplification," not sensory "responsiveness." Reason? It is not the response that is the key to what takes place, it is the amplification of sensory signals that can range from just a little too much, to way too much. In a very real sense, SAS is a huge challenge in our "new age" of sensory overload. However, in the old days, the persons in the tribe who had such a capability were most likely drafted as the tribe's "radar." Especially, nocturnal guards, but also water tasters, food tasters, and movement, sound, touch, and smell sensors. Other things too, but, I am going to try to keep this fairly short. My book about my current understanding of SAS would be called "All Amped Up, But No Place to Go."

One of the very clear conclusions in the literature is that sensory sensitivities should be assessed in any evaluation, whether suspected ADHD, ASD or not. Many folks who do not fit the criteria for ADHD/ASD are affected by SAS and just never got asked the right questions, or figured that everyone had the same sensitivities, so no point in asking about it. Or, when they did describe their sensory scenario, they got laughed at or shamed or treated with disdain, instead of curiosity and deeper understanding. SAS is not a respecter of any particular brain set and can be found as a "standalone" challenge for those who do not necessarily fit any particular "disorder" diagnosis.

One thing that has become clear to me is that SAS can set up anyone for sensory overload, whether or not they have some other diagnosis. Such SAS can lead to what might look like forgetfulness, disorder, distractions, confusion, overwhelm (burn-out, anxiety, OCD, agoraphobia, escapism, and such) which could lead to a misdiagnosis of ADHD/ASD. Such a misdiagnosis can then lead to mistreatment of various kinds, including dopamine enhancers which can make things worse. It can set folks up for even worse sleep disorders and sensory issues due to the dopamine enhancers they do not actually need. What they needed was to understand their SAS and figure out how to deal with it. For SASers who also fit the criteria for ADHD/ASD, it is absolutely important to know the kinds and levels of SAS that they experience to fully understand what they are dealing with. The literature is pretty clear on it. The first article cited below is a great shorter published argument for subtypes of, or co-occurring challenges, called sensory processing challenges (not disorders).

One other very straightforward way to picture the SAS situation is to refer to what used to be called "amplifiers." Kind of mostly associated with the music industry. If you don't know what an amplifier is, then think in terms of the volume (loudness) control on other electronics. From my extensive reading and my own evaluations of hundreds of clients which included assessments of SAS (including self-report plus third-party reports), I can say this.

The literature clearly indicates that an area of the CNS called the locus coeruleus ("LC" - blue spot) has a huge influence on all sensory signals in terms of amping them up or keeping them baseline. By amping up sensory signals, you can imagine what would happen. It would be like turning your radar up so high that even little objects look big, sounds are louder, etc. Not an easy world to concentrate in with most or all signals dominating the thought waves, making it harder to choose what to notice and what not to notice or stay focused rather than changing focus when you want to. SAS might have been a great plug-in for someone who was a tribal scout (guard) in the old days, but not so great for apartment living, etc.

I was fortunate enough to be able to stay caught up with a decade of findings about the LC and its huge impact on sensory processing. I can't go into all that detail right now. That will be for a deeper, longer discussion which I will be posting as I revise that section of my new book. For now, though, here are the further important findings and conclusions I have arrived at.

1. Poor working memory (WM) at baseline (non-threat) is the key to understanding almost all of the upsides and downsides of the so called ADHD brain. Think of WM as RAM in a computer. More RAM, more capability to hold data temporarily to work with it before it has to go to the hard drive. Those of us who experienced the era of 6 kb to 64 kb RAM can tell you what an ADHD computer would be like (4 kb in the first Apple).

2. Think of a low RAM computer with increasing environmental sensory data loads every year due to all the usual suspects -- population density (people everywhere), construction, vehicles, tools, planes, poor housing insulation, etc.)

3. Think of what SAS would do to almost all sensory data – louder, stronger – Meaning, even if the frequency of the data might be the same, the amplification of the data carries a bigger "noise" level that produces a bigger data processing burden.

4. Thus, for even the high WM brainset, SAS could make it look like you fit the criteria for ADHD/ASD, even if you have high working memory. Working memory in humans is dynamic due to a number of factors that require too much to describe here. However, it does have a limit. Unlike RAM in a computer, humans cannot yet plug in some extra RAM above a certain limit. Those with suboptimal dopamine for good working memory, however, can plug in the correct dopamine enhancer for them at the correct dose to increase working memory to optimal, while it lasts. Too much dopamine enhancer makes things worse. And, yes, unfortunately, tons of folks are being prescribed the wrong enhancer or too much of the right one.

5. In the ADHD/ASD types, if they look like they fit the criteria, but do not have low working memory, any dopamine enhancer could make them worse. Not all ADHD/ASD diagnosed folks have been tested for working memory. Thus, you can look like it, but you may not be helped at all by a dopamine enhancer.

6. I tested all my evaluation clients (more than 400) with a reliable working memory test tool called "reverse digit span." There is clear literature on its credibility and reliability. One of the key elements I used was for tracking the results of a dopamine enhancer was tracking how working memory changed over time or not, in addition to changes in behavior and thinking processes that should take place if the real issue is low working memory.

7. From what I learned during those 10 years of reading, writing, and clinical practice is that quite often good working memory folks ended up getting diagnosed as ADHD, even by me a few times, who did not and would not respond positively to a dopamine enhancer. BTW, "stimulants" is a very misleading term. They will over-amp those who don't really "need" it, and can be used for so-called "wakeful state," "buzz," or other euphoria-like effects, but those are all side-effects of too much dopamine. If you don't need it to optimize working memory, you can use it for its side-effect ("stimulation"). By doing that, you might actually be able to stay up all night (on a "super-caffeine"), but it will not actually improve working memory. Or, for that matter, allow what goes into working memory to be retained for the long term. So, great for "cramming" but not for learning. And not so great for your brain to over-dopamize.

8. If a person who fits the criteria for ADHD and also the criteria for low working memory utilizes the correct dopamine enhancer at the correct dosage, it should *not* have a "stimulant" side effect, unless, UNLESS, they also fit the criteria for SAS. Almost always, as I learned from consistently evaluating for SAS, dopamine enhancers made the SAS worse (meaning, it produced a lot of side effects). There were a number of clients who fit the criteria for ADHD/ASD and had low baseline working memory who did not benefit from any of the dopamine enhancers. It took me a couple of years to figure out what was going on. I felt like a detective on the search. Turns out that the literature and my clinical experience pointed to the culprit. Any dopamine enhancer even if the correct one at the correct dose in someone who fits that criteria for Low Working Memory, ADHD/ASD, and SAS will experience worse SAS (worse sleep, more sensitive, more easily overwhelmed, shaky, more anxious, etc). Why? See next.

9. It turns out that anytime a dopamine enhancer (most if not all typical ADHD meds) is used in a scenario where it would be correct but for the SAS, it makes the SAS worse. So, I learned that. What took a little longer was figuring out what the "problem" was. Any dopamine enhancer at about any dose is going to have ripple effects on the presence of norepinephrine (NE). Why? By increasing the presence of dopamine for working memory improvement, that extra dopamine presence means extra NE presence. That is due to a number of things, the most important being that dopamine outside of the nerve cell is broken down quickly to NE. Now, enzymes work at a certain speed to process the dopamine to NE, so it’s not like all the dopamine enhancement gets destroyed, but the NE increases. Why does that matter in SAS?

10. From the literature and my experience with clients, I learned that SAS is produced primarily by amplification of sensory data by a mechanism that is NE dependent. Why does that matter? Well, NE receptors and manufacturers of NE are used by the locus coeruleus to control how much those signals are amplified. It's a much longer story to detail that whole mechanism at this point. I will do that in the near future. However, here's a short version: If an SAS person uses a small dose of what is called an alpha-2 adrenergic receptor agonist (clonidine or guanfacine) it turns down the amplification of sensory signals by turning down tonic and synaptic NE. The locus coeruleus is well known to be the physical site of the production and use of NE to amplify sensory signals sent to the cortex for interpretation.

11. My conclusion based on all this is that those who are dealing with SAS, no matter who they are, are dealing with a locus coeruleus that contains a higher NE tonic and phasic presence, and, thus a higher baseline amplification which when stimulated further by extra NE, produces even further amplification. If you can turn down the stimulation of the receptors, you can turn down the amplification.

12. So, in fact, even if that is not the true mechanism, using the correct alpha-2 agonist is, and, I am not exaggerating, highly successful. The protocols I developed were impressively successful at changing SAS to AAS (average amplification syndrome). That means fragmented sleep (gone) due to sensory amplification of sound, touch, light, temperature. Most, if not all, SAS folks I met said their ideal sleeping place was or would be in a totally air-controlled walk-in closet. No light, soundproofed, air controlled, no interior noises, with preferred bedding.

13. Such appropriate use of NE modifiers to turn down sensory “loudness” without producing drowsiness or changing tones created less distractibility, less overwhelm, better sleep, etc. at work. One of my clients who had serious SAS was on the verge of being fired from his office job, where he had a cubicle which he had modified with boxes to tone down noise and light. With the correct NE modifier, he was able to remove the boxes, sleep properly at night, etc. He impressed his boss so much, that the boss eventually gave him his own office.

14. Finally, so, in fact, those clients who clearly fit the criteria for ADHD/ASD and poor working memory and in which the dopamine enhancer they used clearly optimized working memory but caused worse SAS, adding in the correct alpha-2 NE agonist was powerfully helpful at not only knocking down the side-effects but also changing the baseline SAS. It was also clear that some folks with only SAS but good working memory who may have been previously diagnosed with ADHD/ADD became "less" ADHD/ADD with just SAS mitigation with an alpha-2 NE agonist. With no need for a dopamine enhancer. I will be writing further about the data I gathered and the research literature I read. Also, I will be detailing the protocols that I used and fine-tuned that made huge changes in SAS, with no significant side effects.

I had several colleagues use my protocols for assessing and treating SAS with much success. A few of those I have heard about even after my retirement.

I think I have covered this with the right amount of text but, as noted, there is more to the story. If you wish to explore the research literature, some of it is cited below. Other recent reports have looked at clonidine and guanfacine as useful in ASD. I identified the SAS scenario and wrote about it in My 2013 Book. Then, I followed the literature and have updated and fact-checked my earlier knowledge base and conclusions. I can say this for sure: I was on the correct path in 2013 and 12 years later, it is still standing. If you hang around here enough, you will get updates on what has been learned and reported since 2013. Otherwise, my book on SAS should be fully completed by mid-2016.

Feel free to ask questions!

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Lane SJ, Reynolds S. Sensory Over-Responsivity as an Added Dimension in ADHD. Front Integr Neurosci. 2019 Sep 6;13:40. doi: 10.3389/fnint.2019.00040. PMID: 31555103; PMCID: PMC6742721.

Lane SJ, Reynolds S, Thacker L. Sensory Over-Responsivity and ADHD: Differentiating Using Electrodermal Responses, Cortisol, and Anxiety. Front Integr Neurosci. 2010 Mar 29;4:8. doi: 10.3389/fnint.2010.00008. PMID: 20556242; PMCID: PMC2885866.

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Kamath MS, Dahm CR, Tucker JR, Huang-Pollock CL, Etter NM, Neely KA. Sensory profiles in adults with and without ADHD. Res Dev Disabil. 2020 Sep;104:103696. doi: 10.1016/j.ridd.2020.103696. Epub 2020 Jun 8. PMID: 32526674; PMCID: PMC7786815.

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Scheerer NE, Pourtousi A, Yang C, Ding Z, Stojanoski B, Anagnostou E, Nicolson R, Kelley E, Georgiades S, Crosbie J, Schachar R, Ayub M, Stevenson RA. Transdiagnostic Patterns of Sensory Processing in Autism and ADHD. J Autism Dev Disord. 2024 Jan;54(1):280-292. doi: 10.1007/s10803-022-05798-3. Epub 2022 Oct 28. PMID: 36306002.

Itahashi T, Aoki R, Nakamura M, Ohta H, Hashimoto RI. Sensory seeking and its influence on sustained attention performance in adult males with Autism Spectrum Condition. Sci Rep. 2025 Feb 3;15(1):4047. doi: 10.1038/s41598-025-88733-7. PMID: 39901051; PMCID: PMC11790954.

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Disclaimer: As is necessary these days, I must remind you that this article and other articles and my comments at Substack are not intended to be used as a substitute for direct medical care from the appropriate professional. Please, always do your best to get diagnosis and treatment recommendations from in-person evaluations. It would be unprofessional for me to provide such services by way of non-in-person visits. In addition, I am retired and no longer provide direct medical care of any kind. Learn what you can from me, fact-check what I say, and, possibly, use what I have written to help other folks get up to date, including your health care providers.