Do you have fever as a part of PEM?

Is personal temperature sensing based on direct signals from sensors (ie. skin nerves send x pulses per second depending on temperature) or a comparison between signals from the brain or core? Since I often feel feverish when my core temperature is low, that makes me wonder about it being a comparison.
This paper might be of interest:

TLDR: a cluster of hypothalamic neurons gets input both from peripheral thermosensitive neurons, and can also directly detect temperature in the brain as well (the latter has been observed to override input from the former).

The actual fever response is driven by prostaglandin-mediated signaling to other hypothalamic neurons which result in an increased body temperature via changes in systemic metabolism. So an actual fever would also stimulate those heat-sensing neurons via peripheral sensing and make you feel hot when your body actually is getting hot, but it's also possible to just stimulate those heat sensing neurons without that prostaglandin signal that actually creates fever.

Interesting, H2O2 (mainly formed as a byproduct of mitochondrial respiration) is known to strongly sensitize the heat-sensing hypothalamic neurons.
 
Is personal temperature sensing based on direct signals from sensors

Sensors tell us whether the world around us is hot or cold. Sense of our own temperature is based on an inference made by the hypothalamus as to whether or not our core temperature is appropriate for the circumstances. So we feel shivery if the hypothalamus decides we need to be hotter. That is either because we are in a very cold environment and our blood is being cooled a lot by a cold wind or because the hypothalamus is directing a rise in temperature (fever) in response to infection of toxins. When the hypothalamus decides there is no longer a need to raise body temperature we will feel too hot - so feeling hot occurs when a fever is fading.
 
Sensors tell us whether the world around us is hot or cold. Sense of our own temperature is based on an inference made by the hypothalamus as to whether or not our core temperature is appropriate for the circumstances. So we feel shivery if the hypothalamus decides we need to be hotter. That is either because we are in a very cold environment and our blood is being cooled a lot by a cold wind or because the hypothalamus is directing a rise in temperature (fever) in response to infection of toxins. When the hypothalamus decides there is no longer a need to raise body temperature we will feel too hot - so feeling hot occurs when a fever is fading.
It’s really interesting how it detects temperature conductivity as much as temperature.

Touch a piece of wood at 18 degrees and it feels normal temp, touch a piece of metal at 18 degrees and it feels cold. Because the metal conducts temperature to you faster.

Same thing. Touch a 40 degree rock and itll feel almost burning, but a 40 degree piece of cardboard feels pleasantly warm.
 
It’s really interesting how it detects temperature conductivity as much as temperature.
I think it's not detecting temperature conductivity. The conductivity influences the rate of heat transfer to your body.

The amount of heat materials can store also varies and this plays a role as well.
 
@Jonathan Edwards - where do autonomic hot flushes or surges fit into this?

As I’ve got worse I’m experiencing intense hot flushes part way through eating for example and you can visibly see increased blood flow to skin across my chest sometimes palms which go bright red along with my ears often only one. It’s thought to be erythromelalgia/red ear syndrome as once triggered they can remain burning hot to touch for some time after.

I assume it’s aberrant peripheral nerve signalling to brain from temperature changes when eating hot foods or drink. But exertion can also do the same. Could this signalling result in neuropeptide release causing vasodilation?
 
The paper on the hypothalmic heat sensor seems to be about temperature regulation, but not about perception of temperature, which might be different. I'm guessing there are other neurons involved in perceiving skin temperature and internal temperature. In short, we don't understand how it actually works, and how it might give false impressions.
 
The paper on the hypothalmic heat sensor seems to be about temperature regulation, but not about perception of temperature, which might be different. I'm guessing there are other neurons involved in perceiving skin temperature and internal temperature. In short, we don't understand how it actually works, and how it might give false impressions.
The study is about the sensory neurons that provide input to the parts of the POA that we already knew regulate body temperature.

They are the same sensory neuron channels, along with TRPV1, that have been pretty conclusively implicated in ambient temperature sensing and temperature-dependent behavior changes. We know that these neurons are present underneath the skin, along the spine, and around organs—ambient temperature sensing happens through internal temperature sensing of these peripheral neurons, so the processes are one in the same. Their input gets integrated in the POA, and we know that this is the region governing temperature perception because it is the one that gets activated by thermal stimulus.

There are still unknowns about temperature regulation, such as how the POA integrates disparate temperature sensations from various parts of the body. But we now know a lot about how sensing works and which neural circuits are involved, as well as the main agents that create “false impressions” (reactive oxygen species). Work from the Julius, Siemens, and Jan labs might be of interest. The field has covered a lot of ground pretty rapidly
 
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