My initial reaction was that the sensory issues didn't get worse, but I'm tired and can't cope around them. There is a lot you have to do as you have more responsibilities, my "autism flareup" happened after moving out, but it was 3 years after. I think I gradually took pver more responsibilities, I sometimes have to help my parents as well.
Certainly plausible. Added stress in your life can leave you mentally exhausted. It certainly is a precursor and contributor to the autistic burnout, that, in turn, can lower the threshold for autistic shutdowns and meltdowns. If you're just in that "coping" mode, then, at least in my experience, those background sensory issues can and do come to the forefront.
But I don't know any more, wouldn't it show somehow if it was like it is now?
I suppose it would if you were monitoring things like hormone levels, cerebral perfusion pressures, blood pressure, ECGs, and PET scans. Obviously, that's not something one would do unless you were involved in a study.
But would it work long term as well? Stress gives a "hightened sensory experience", in exteme cases, it feels like slow motion moments in films if the situation is a real danger or you perceive it as such and get a panic attack. I rememeber you(?) mentioned that antipsychotics can influence the way neural connections are formed and deleted in such a way that they decrease sensory issues over the years? Can it work the opposite way long term with activating substances such as catecholamines (in this case released by the body in response to cortisol)?
So, yes, there is evidence that prolonged use of certain antipsychotics can influence neuroplasticity and density. A 2011 study in rats, and a 2012, 2018, and 2020 study in humans did find evidence of that.
Now, within the context of autism, a condition where the stress response is often dysregulated, with a heightened cortisol baseline and exaggerated response to stressors, it appears to be a set up for sensory modulation. Several studies performed in human autistic subjects show evidence of sensory amplification via mechanisms leading to elevated cortisol. Amongst many other things in this regard, in a 2019 study, it was found that cortisol impairs the inhibitory GABA function, reducing the brain's ability to filter sensory input. In ASD, where GABA deficits are already common, this could contribute to amplification of the sensory experience. As it pertains to the amygdala, often hyperactive in ASD and stress, an area that integrates sensory and emotional data, elevated cortisol enhanced the amygdala-to-sensory cortex activity, thereby enhancing sensory sensitivities.
Catacholamines can also amplify auditory and visual cortex sensitivity. Dopamine, another catecholamine, is often dysregulated in ASD. Prolonged stress increases dopamine release in the sensory-related areas like the thalamus, potentially making routine inputs, like a humming refrigerator, feel overwhelming. It can cause an "over-attention" to irrelevant stimuli.
In summary, there are only a handful of studies relating to this topic, so all one can say is that all of this is "plausible" given what evidence we do have.