I see that there is an overlap of symptoms from other conditions, but the lack of sweat when the body heats up (through exercise, stress etc.) coupled with the burning, itching or fiberglass sensation is called Anhidrosis. I specifically have Acquired Generalized Anhidrosis which is a form of sudomotor failure (sweat gland failure). There are a lot of potential causes, from bacterial infection (Staphylococcus epidermidis, which can cause lesions on the sweat gland tubes that go from the dermis to the epidermis), to neuropathy or autoimmune conditions.

I have had Anhidrosis since 2019 (I am almost 24 now), and for a period of roughly a year in between 2021 and 2022 where I did not have it. I could not treat it with conventional medicine, as they either did not manage the symptoms or caused other problems. So, I managed it with homeopathic medicine (I know the general consensus on homeopathy, but I can make a case for it as it worked for a while and only stopped working because I was attempting to treat a different issue that predated my anhidrosis).

As far as my understanding goes, the medicines worked on the Muscarinic receptors in the sympathetic nervous system (responsible for the fight or flight response and eccrine sweat glands). The itching, needles, burning or fiberglass sensation which I call "heat flash" is a response of the Cholinergic fibers which are in the peripheral nervous system.

For anyone that is curious about the nerve structure, the Peripheral nervous system operates the Motor Nerve Fibers, which send impulses from the Central Nervous System through the Peripheral Nervous System. These impulses go to the Autonomic and Somatic system, with the former controlling the visceral (involuntary) responses such as gland function, cardiac function etc. The Autonomic system itself is responsible for the Sympathetic (fight or flight) and Parasympathetic (housekeeping, non-active functions during rest) systems. So, the medicines I took worked on the Muscarinic Acetylcholine receptors on the Cholinergic Fibers. My hypothesis is that the peripheral nervous system was unable to send the correct impulses, which eventually caused sudomotor failure. The specific receptors that need to receive the impulse are the M1. M3, M5 muscarinic acetylcholine receptors. These are Gq protein coupled ganglionic receptors on the cholinergic fibers. The MI, M3 and M5 being Gq coupled receptors is important, as sweat glands function by contracting and contraction requires calcium. It might be worth checking your Calcium levels and also if your Thyroid gland is functional, it may help to know in some of your cases.

If you have other conditions or symptoms that you think are unrelated, they may not be entirely unrelated. It is rare for such isolated systems to have dysfunction by themselves. You may have pre-existing problems that also fall under the sympathetic, autonomic, peripheral nervous systems and other postganglionic fibers. Or other problems that impede the M1, M3, M5 receptors, cholinergic fibers or acetylcholine production. For instance, the M3 receptor is also important for the function of eyes, lungs, gut systems or even blood vessel and muscle contraction. This of course extends to all gland functions, or any sort of secretion within the body (as this uses contraction of blood vessels and glands themselves).

On the Muscarinic receptors themselves, there are 5 of them and the odd numbers act on the Gq coupled proteins. The numbering system is based on the importance of their roles in our overall ability to function. So the primary functions are: M1 is neural, M2 is cardiac, M3 is glandular or smooth muscle etc. The M1, M3 and M5 are key for full function of the eccrine sweat glands. Last thing to add, there are other agonists for these receptors (like acetylcholine, agonists bind to the receptor to illicit a biological response). Pilocarpine is an example that works especially well with the M3 receptor and causes glandular secretion, but I suggest conducting your own research on the function, response and administration. This is because there is chance that they won't just make you sweat, but also salivate abundantly and experience other secretions. In some cases you can use an opioid or other indirect-M3 agonist which works by way of inhibiting Acetylcholinesterase (inhibiting it prevents the Acetylcholinesterase enzyme from hydrolyzing or breaking down Acetylcholine, thus improving neurotransmission). Certain medicines are also Muscarinic ANTAGONISTS, not to be confused with AGONISTS. Antagonists will inhibit the function of the M3 receptor and could be a cause of the problem, or will make it worse.

If nothing else, I hope the breakdown of the problem helps.

Feel free to reach out if you have any questions.