I’ve started tracking the skin temperature on my toes nightly to try to identify my triggers and document how often I am flaring. Apparently the normal resting temperature of the tips and undersides of my toes is in the upper 60s to low 70s (F). When I have a flare, the temperature rises to 95 to 96 F, though it feels like my toes are burning up (hot, RED, and some swelling-based discomfort, but not what I would call pain). My fingers can also be similarly cold at times, though they are often more in the 80’s range.
Do other people experience cold toes when you are not flaring? I’ve never had what I would call classic Raynaud’s symptoms and in fact didn’t realize until now that my “normal” toe temperature is not normal for most people.
I’m at the beginning of the diagnosis process, and would also appreciate any advice on tests that are worth doing to rule out any underlying cause. I’ve already had a normal ABI (ankle brachial index), echocardiogram, blood clot test, and neurological exam. My podiatrist is not interested in this (if it’s Reynauds- just keep your feet warm!), so I’ve been looking into vascular specialists. All of my blood work (including autoimmune screening) is normal. My former GP who just moved away unexpectedly actually had another patient with EM and thinks that the diagnosis is probably correct, but now that she’s gone, I’m shopping for a new doctor again.
I haven’t recorded my skin temperatures personally, but I think this happens to me too – that when I am not flaring actively, the skin can feel “too cold”. I don’t have raynaud’s (I think …) , but perhaps tendencies.
I’ve read this is normal for EM people – "They often seek medical advice after experiencing an acute period of `hot,
burning feet’, but on examination in our vascular laboratory their limb temperatures are
often abnormally low. "
I guess they think it’s particularly weird since the sympathetic fibers (underneath the skin) are reduced in EM folk (these would otherwise cause some basal constriction). There seems to be a theory that “denervation hypersensitivity” could occur, where we become overly sensitive to the same constricting agents in circulation (not released by the sympathetic fibers underneath the skin). Though I’m not sure if I’m getting that quite right, and have no idea how valid that is
I am not sure on bloodwork - I had my PCP run basic bloodwork; my derm who ran autoimmune screening, clotting factors, homocysteine, b12, folate; my neurologist who did a basic neurology panel, neurodiagnostic testing like tilt table / sweat test, punch biopsy for SFN.
I hope you find a doctor who can thoroughly look into your case, or at least agree to trial different meds in the meantime (if you feel you need it more under control …). While I was doing the referral after referral game, that I know too many of us go through, I regret not actively asking for meds to trial in the meantime.
a side anecdote – My neurologist made the remark the other day that Raynaud’s is often misdiagnosed as EM. He then asked me if I was triggered by cold or triggered by heat. I said heat, and he promptly moved on like like he could now thoroughly rule out raynaud’s … but I was thinking if he thought it was often misdiagnosed, shouldn’t he be asking me more questions??!
Thanks so much for the information. My toes have been really cold and kind of purple at my last two Dr. appts, so my new PCP is certain that I have Raynaud’s even if I’ve never had the classic blanched fingers. It would be great if there were some test that could be definitely used to diagnose either Raynauds or EM, though it sounds like they often coexist. (So YES with the asking more questions! :)) My new Dr. does however seem interested in trying to track down any underlying cause for the Raynauds/EM, which is great, and she is wiling to try meds now if I want. For the moment, though, I’m focusing on trying to identify any triggers (dehydration, for instance, seems to make things worse for me, which seems to fit in with some theories about EM stemming from the body’s overreaction to an inability to cool via normal sweating).
I’ve been doing lots of reading of the medical literature since my original post and also found some references to cold toes, but it sounds like there are no good reference values for what constitutes a normal toe temperature, so the authors were unable to say if the cold toes they observed were significant.
I’ve had a lot of the same bloodwork done now, but am having trouble finding a neurologist to do any testing. I did have some basic testing done, but that neurologist also saw my toes turn purple and said that this is ‘definitely vascular, not neurological’. That does not seem to be the consensus in the literature, but given his overall demeanor, I think I need to try again with someone else.
Ya no diagnostic testing for Raynaud’s vs EM I think unfortunately (i guess except for the genetic testing for pathogenic mutation) … and on top of that most cases of each seem to be idiopathic. I get bloodwork done routinely just to make sure a root cause doesn’t pop up, and also since I’m trialling a lot of different meds all the time.
Honestly I’m not sure if a particular diagnosis would be helpful either way, since it seems like they both might be symptom complexes as opposed to a disease state (well, I know this is true for EM … just speculating this is also true for Raynauds), as long as you find a doctor willing to advocate for you and any treatments that might help you, and is willing to think beyond these labels and more about the complexities of your case. (If disability is an issue then diagnosis would be more important.) That is just my opinion though I’m sure others might disagree.
I tried to read about the differences between EM and raynaud’s, and asked a couple derms, and I still don’t really know lol. My sense is that vasospasm is what is underlying Raynaud’s (at least this is the traditional view), while AV shunting is the underlying final common pathway in EM but I don’t know if these are necessarily distinct.
The sympathetic fiber dysfunction (and denervation hypersensitivity) I referred to above, can occur in both EM and Raynauds (I think).
I thought that maybe one difference between them is that EM is usually associated with small fiber neuropathy, but I then I found a paper by Mark Davis (EM guru at mayo) finding Raynaud’s and small fiber neuropathy might be linked as well. So both Raynaud’s and EM could be neuropathies in which the neural control of blood vessels gets messed up (?)
I don’t think this idea is thoroughly explored in the context of Raynaud’s, at least it seems to be investigated a little more in EM.
Article I was referring to
I get the feeling that there is a tendency for people to maybe look down “raynaud’s” – like maybe it doesn’t accurately capture their pain or something. But I don’t think there should be this stigma . Most good derms/docs I think realize it can be very painful.
Those are just some of my thoughts at least GOod luck on your treatment/doctor path!
Best
PS - one quote I thought was interesting in the Davis paper above I thought - “To which facet of primary RP – pallor, cyanosis, or rubor – should symptomatic treatment be directed? The answer is not apparent …” which makes it seem like the basic idea of throwing a vasodilator at Raynaud’s is too narrow.
I think it’s pretty typical. I was at dinner tonight, it was 90 some degrees out, the restaurant was comfortable but warm, and my knees (my primary EM site) were ice cold. Because I was wearing crew socks and sneakers my feet were slightly warm, but my knees above them were anything but.
Interesting. A vasodilator is the first thing my PCP wants to try, but I’m holding off on meds for now so I can start tracking my symptoms and see what I can manage with lifestyle changes. That raises a good point, though. Since my pain/discomfort is tolerable at this stage, I’m not sure I want to treat the EM just for the sake of treating it. I’m more focused on trying to identify or rule out any underlying causes, and like your idea of repeating bloodwork periodically since it sounds like the cause to which EM is secondary often doesn’t become a significant issue until years after the EM diagnosis.
One question that makes me second guess this approach, though, is the possibility that allowing the flares to continue will cause the EM to worsen to the point where the flaring is extremely painful. I’ve not found much about this in the literature. There was one paper where they had a class of patients with all the EM symptoms except for pain, and they alternatingly referred to them as having either a milder form of the disease/symptoms or as being pre-EM. Have you seen any other research on whether flares (hot, red, swollen toes) causes irreversible damage that in turn causes the EM to progress?
No I haven’t seen anything on that. If you learn more, I’d be very interested so def. please update!
My hunch however is that there’s a good chance you’ll never need medications.
My sense is medications (in idiopathic cases) just provide symptomatic relief (eg lyrica lessens pain sensation from SFN … doesn’t reverse it) so unless an underlying cause can be identified, I’m not sure these symptomatic meds would slow down the progression of the disease. Vasoactive meds can be helpful to lessen the heat or redistribute heat but I am similarly doubtful they would be addressing the underlying anomaly(ies). If AV shunting is indeed the final common pathway in EM for example, then it seems like the ideal treatment would be to push blood flow into the starving capillaries in a way that would NOT contribute to more blood going into the thermoregulatory shunts … but there’s no vasoactive med that docs can point to and say, yes, this will definitely help with that and not make it worse (whether immediately or down the line). And who knows what is driving the AV shunting in the first place.
By the way, I misread something you wrote in your second post on here (I thought you were asking a question when you weren’t! … I blame my meds ) hence my random rambly prior post haha.
In the months after my symptoms began, I urgently sought treatment based on the presumption there was a finite window of opportunity to halt or reverse symptoms. Approximately 6 months after symptom onset I found effective treatment. In the 3 years since, I’ve seen no discernible progression. The drugs prevent me from flaring and I function normally with only negligible lifestyle modifications. It’s anecdotal for sure, but I’ve been well served by my approach.
I’m saying we don’t know. It’s a possibility. Absent proof to the contrary, I think you have to presume it may. To assume it does not exposes one to great risk.
Feet may be cold from some kind of mix of conditions. With Raynalds you may have cold feet. Some have cold feet and numbness as nerves start to all die off as in Small fiber Neuropathy from Diabetic foot conditions. They will experience EM flares mixed with cold periods of a frozen foot or cold foot.
If you’re condition has mixed conditions you may be cold and not have pain for part of the day. That’s actually a good thing.
I believe at least some forms of EM like my mom are a kind of pure EM where only flares exist. My mom’s feet almost never are cold. They are never cold normally unless its from a drug reaction like a mixture of a muscle relaxant with Cymbalta. Otherwise her feet can only be cold if they are environmentally chilled.
So to me, personally this is a pure EM or only burning variety. I actually think people who have cold and hot EM are fortunate. But any kind of neuropathy may include other things like numb feet with electrical spikes of pain, which is not fun either.
" In the asymptomatic state, skin temperatures at the toes varied from 20.4°C to 28.4°C (mean, 23.5°C). During symptoms, skin temperatures at the toes varied from 29.6°C to 33.7°C (mean, 31.3°C), for a statistically significant mean increase in temperature of 7.8°C ( P <.001, Wilcoxon signed rank test)."
(I just bought a temp sensor thing, was interested to see how cold/hot I get, and remembered this thread…)
) hence my random rambly prior post haha.