~elizabeth~

I had these effects with the propranolol before weaning off clonidine, that's largely what decided me to try to come off as I feel I might be having a somewhat unusual reaction to it. It has symptom relief in that somehow it is reducing the postural aspect of my flushing, since starting it I can sit down long enough to watch a film whereas the painful flushing would start after about half an hour after sitting down; that was the case on just clonidine alone, although combining with nortriptyline made it much worse. No one understands why this is happening, this postural flushing problem doesn't seem to have any correlation with BP or pulse rate. My GP just says 'it's all above my pay grade' when I tell her about these things, and none of the other specialists I've seen say they have the slightest clue about what's going on either, no one has ever seen anything like it before. I feel if we can get to the bottom of why these odd things are happening it might throw some light on things. My current theory is that my alpha 2 receptors are unusually sensitive, so somehow the clonidine is having a greater stimulant effect on peripheral receptors than central ones. Apparently, clonidine can increase the number of peripheral alpha 2 receptors, leading to supersensitivity issues, which is one of the reasons withdrawal effects can be so severe until receptor populations adjust (i'm not sure whether this just applied to alpha receptors on platelets, or blood vessels as well). It also makes them more sensitive to small temperature changes, and I've noticed a significant worsening of these problems last Sept/Oct as temperatures dropped. This is only a theory though, whether I can get anyone to take it seriously I don't know.

Something I'd forgotten, Clonidine used to be used as a diagnostic test for pheochromocytoma, so how you respond to the drug might be indicative. "One diagnostic test used in the past for a pheochromocytoma is to administer clonidine, a centrally-acting alpha-2 agonist used to treat high blood pressure. Clonidine mimics catecholamines in the brain, causing it to reduce the activity of the sympathetic nerves controlling the adrenal medulla. A healthy adrenal medulla will respond to the clonidine suppression test by reducing catecholamine production; the lack of a response is evidence of pheochromocytoma." http://en.wikipedia.org/wiki/Pheochromocytoma Another drug that has consequences in pheochromocytoma is Metoclopramide, it's contraindicated because it has a strong pressor effect in people with the latter. I don't know whether this is something peculiar to pheochromocytoma or hyperadrenergic states in general. What I do know is that I react really badly to it. I was admitted to hospital for a drip after I got really dehydrated last year (due to pregabalin withdrawal), they gave me Metoclopramide intravenously, my pulse rate went through the roof and I nearly passed out, and felt really agitated for hours afterwards. I was taking a large dose of clonidine at the time, and it still had this effect on me.

Kris, taking clonidine did help with my flushing when I started it, when it started it was constant and worsened greatly by things like eating meals (even cold ones), hot drinks or other tiny changes in temperature, like changing the settings of the aircon in the car. The clonidine did reduce the reactivity and general flushing. I'm sure at that stage it was being caused by high norepinephrine levels, as I was also having cold sweats, agitation, tachycardia, diarrhoea etc. The side effects do wear off with time, and in many ways I did feel a lot better on it, I completely lost that wired, shaky feeling I'd had most of my life. I found I needed to take it 4x, as I've always found the effects wear off really quickly for me. The worse side effects for me were dryness issues, but I had sicca beforehand, and these side effects did wear off with time too. I did find the fatigue, brain fog and general symptoms of cerebral hypoperfusion very difficult to deal with, plus I started to get weird symptoms when taking other drugs with it. Also, it has never helped with the middle of the night flushing episodes I get, even after taking extra at night, I still found myself waking up with my face red, painful and swollen and having to get up and trudge around for 40 mins+. I'm wondering now if this nocturnal problem is due some additional neurological issue. I know I suffer from sleep paralysis, and also have nocturnal dystonias. I seriously grind my teeth, when I wake up my whole face is twisted into odd grimaces. I used to think this was a reaction to the pain, but now realise it's due to muscle rigidity, which I have all over my body (according to EMG test results). I think there is some connection with catecholemines, this happens at exactly the time in the early morning when levels and body temperature begins to rise and has been made worse by drugs that elevate norepinephrine, as the current bad phase started when I tried nortripytline last year, but it can't be the whole story as I still have these terrible nocturnal flushing episodes after taking clonidine doses which must be working to some extent, as they significantly reduced BP, HR and body temperature.

Before my POTS diagnosis, I was seeing a dermatologist who started me on clonidine, and then tried adding other drugs to try to control my painful flushing. He tried 2 betablockers (atenolol and labetolol) but they both made things much worse, and I stopped them immediately. Recently my GP suggested trying propranolol (inaddition to clonidine) to try to control the problems. This time I monitored things a little more closely. I'd already begun to suspect I might have Raynaud's in my face, I'd had a bad bout of facial pain after trying nortripytline (by pain I mean pins and needles/numbness sensations). The nortripytline raised my BP a lot, presumably because it acts as an NRI, which negated some of the effects of the clonidine on lowering BP. After starting the propranolol, I noticed that it was having some of the same effects as the nortripytline. My blood pressure had been low on clonidine alone (80/50 ish) but went up to 115/90 ish, and the facial dysaesthesias were also bad. I found some references to reports of clonidine and propranolol paradoxically causes a rise in BP, also that propranolol, can actually cause catecholemines/BP to rise when given to control severe hypertension during clonidine withdrawal. Given that it seemed to have the same effect on me as nortripytline, my hunch is that propranolol somehow actually raises norepinephrine levels. On the propranolol wikipedia page it says: "Research has also shown that propranolol has inhibitory effects on the norepinephrine transporterand/or stimulates norepinephrine release (present experiments have shown that the concentration of norepinephrine is increased in the synapse but do not have the ability to discern which effect is taking place).[27] Since propranolol blocks β-adrenoceptors, the increase in synaptic norepinephrine only results in α-adrenergic activation, with the α1-adrenoceptor being particularly important for effects observed in animal models. Therefore, some have suggested that it be looked upon as an indirect α1 agonist as well as a β antagonist." http://en.wikipedia.org/wiki/Propranolol

I had a very bad reaction to nortripytline, it definitely raises norepinephrine worsening tachycardia, Raynaud's type symptoms, triggered a very bad episode of jaw clenching that broke a tooth and raised my BP a lot. I couldn't sit down for 6 hours after taking otherwise I'd flush immediately. I don't know why, other than it must have been something to do with increasing my blood pressure/cardiac output. It actually made my face pain worse, and triggered burning pain inside my mouth and nose, and flushing in new areas of my face. My GP made me stick it for a month saying it takes a long time to start working, but nothing altered in that time. I think the pain I was experiencing was Raynaud's type vasospasm, there are reports of tricyclics triggering this, so there was no way it was actually going to help my facial erythromelalgia however long i stuck it.

Yes, I've been having terrible problems recently, blepharospasm and oromandibular dystonia. I've shattered two molars, my jaw also keeps clamping shut, and the muscles around my lips close so tightly sometimes I can't open my mouth probably. I don't know what to make of it either, these problems are common in EDS (which I have) however I'm sure they are also exacerbated by sympathetic overactivity, they get worse with stress, drugs like nortripytiline, so I'm sure they are related to POTS. Mine are so bad I'm asking to be referred for Botox treatment. The underlying cause in EDS is supposed to be poor proprioception feedback which mean inappropriately strong messages are sent to muscles. However, my spasms seemed to appear and worsen over exactly the same time time frame as the POTS and other weird autonomic symptoms, so I think it's more likely in my case to be either related to the drugs I've taken for the POTS (clonidine, pregabalin) or have the same underlying neural pathology as the POTS (some deficits of cholinergic innervation of muscles perhaps?) The EMG tests I had the same day as the autonomic ones apparently showed I have widespread muscle rigidity.

Could you explain the above bit about parasympathetic withdrawal? About the only thing I know about my autonomic test results is that I have an imbalance of sympathetic/parasympathetic activity. Could that cause hyperP symptoms, and what are the implications for medication? I've just come off clonidine, I've been on it for 2 years and any positive effects seem to have worn off with time. Adding propranolol actually caused my BP to rise. Also the effects of clonidine seem to wear off too quickly, they last for about 4 hours then I seem to get symptoms of NE surge or vasoconstriction, perhaps because the peripheral agonist effects last longer than the central sympatholytic ones. I'd been wondering about asking about methyldopa, as clonidine has such an inconsistent effect. However, I've had really bad reactions to drugs like metoclopramide that inhibit dopamine, so I guess this means methyldopa might be a bad idea too.

I have problems in the early hours of the morning, I get very hot and suffer painful facial flushing. Since it's become clear that NE surges cause these symptoms, I did a bit of research and found that there is a spike in NE levels early in the morning when you begin to come out of deep sleep, and again on actually rising. This matches the pattern of my worst problems. Apparently this phenomenon is quite well know, as it's the commonest time of the day to experience angina or heart attacks, for this reason. Stands to reason it will make POTS type symptoms worse.

I'm confused about this stuff as well, I just seem to keep getting paradoxical results from whatever drug I try. My problems started off 2 year ago with what now seem like classic hyperadrenergic symptoms - sweating, severe flushing, prolongued diarrhoea episode, tachycardia, agitation. Clonidine did help with most of these symptoms, but not the painful flushing which has got worse. Last year my GP suggested trying nortripytline. This made my BP rise hugely, and made the postural aspect of my flushing much worse, I was unable to sit down for hours after taking otherwise I'd flush painfully within seconds (it also started up in new areas, including the insides of my mouth and nose). I also tried duloxetine, which was an immediate disaster, flushing much worse and onset of severe Raynaud's symptoms/pain in feet. Same thing with Citalopram, worsening of flushing even in tiny doses. My first thought was I was experiencing problems with clonidine interacting oddly with other drugs. Then I wondered if Clonidine just not a strong enough drug to completely suppress hyperadrenergic symptoms completely, or whether the central effects were wearing off too soon for me (relief from flushing seems to only last about 4 hours, major pain in middle of night). Another possibility is that some of the facial flushing is actually the hyperemic phase of a Raynaud's reaction. Clonidine can apparently increase supersensitivity to catecholemines by increasing the number of alpha 2 receptors in peripheries (not sure if it's on just on platelets or blood vessels as well), and also increase their reactivity to cold. I guess this might explain why I have high BP despite blood pooling/peripheral denervation? I've now come off clonidine to see what happens, as I think it was somehow causing confusion. I'm still in the withdrawal phase, which as been terrible. Not sure when it will be clear what is withdrawal and what is underlying hyperadrenergic state. Although I've had autonomic testing, and had POTS confirmed (secondary to denervation/EDS) no one has measured my norepinephrine, so it's still only speculation that the worst of my symptoms are due to hyperadrenergic state.

I originally had a dx of UCTD (based on positive ANAs and polyclonal gammopathy) but that was because the the rheum missed the Ehlers Danlos completely. I think you can get those markers with autonimmune thyroid disease without them being particularly significant. I was originally taking hydroxychloroquine when all of this started, we also added mepacrine (which apparently usually works well to get rid of lupus rashes) but it didn't alter a thing. The specialist who originally diagnosed the POTS (the leading autonomic specialist in the UK) didn't think it was Mast Cell issue, he wrote that it was 'some variant of erythromelalgia, possibly related to sudomotor issues'; I think he also thought I might have hyperpots as he suggested I double my dose of Clonidine from 200mcg a day to 400mcg. This didn't help, I find if I increase the dose it seems to wear off after about 4 hours and have a severe rebound/hyperemia episode. I've since read that suppressing NE can actually worsen supersensitivity issues by increasing the number of peripheral alpha2 receptors, platelet aggregation and increases their sensitivity to temperature. I tried duloxetine (SNRI) for a few days, it really made things much worse for me, and had terrible rebound Raynaud's symptoms when I stopped that took weeks to wear off. I'd be wary of coming off as I think withdrawal from SNRIs can be very difficult. I'd hoped betablockers would work better than the clonidine (particularly as they come in slow release form) but other than stopping the tachycardia from going through the roof, they aren't helping with the NE excess symptoms. My BP is still high, I feel wired and hot, my face is painful. I found an article on Clonidine withdrawal in which betablockers didn't help alleviate symptoms, they actually raised BP and NE levels for some patients. I really need help with these issues, but I've a feeling even the specialists won't know what's going on. My gut feeling is that what I have is denervation supersensitivity to neurotransmitters inc. NE, which is why I'm reacting badly to even fairly subtle spikes of NE due to the short-acting nature of the clonidine. My problems are all worse in the early hours of the morning and get worse on rising, I think that's the worst time of the day for suffering increases in NE levels.

I'm really at my wit's end and wondered if anyone can help me work out what's going on? My problems started 2 years ago. The first signs were a prickling, numb pain around the eyes which no one could get to the bottom of, plus numbness in the mouth and white, prickling tongue. Then a few months later I had what I thought was an extended bout of flu, shivering/sweating/diarrhoea and tachycardia, followed by uncontrollable flushing, which has not ceased for 2 years (not MCAD before anyone suggests it). A feature of the flushing from the start is that it's always been worse sitting or supine. Eventually I saw a dermatologist who put me on clonidine, which helped a bit. However, I was still having He later added atenolol, which seemed to make things go downhill again, so I stopped. He tried labetalol instead, which didn't help either. At this point I worked out my pulse was increasing on standing and that I probably had POTS, and sought help for that instead. The first suggestion I had from the POTS specialist was to increase clonidine. I have a feeling he thought I might have hyperadrenergic POTS, but increasing the clonidine didn't help at all. A year later I'm still waiting for tests and to see him again. In the meantime, the initial improvement I saw with clonidine has seemed to ebb away. Last October, my face discomfort and flushing took a sudden, serious turn for the worse. My ears started flushing as well, and I developed a painful sore that stubbornly refuses to heal. My GP suggested trying nortripytline for the burning face pain. This actually made the facial flushing worse, esp while sitting, and extended the burning pain to my nose, brow and inside mouth and nose, as well as raising my BP a lot. I It was clear that this drug was raising my norepinephrine levels, in turn causing vasoconstriction, and both these things were making the face pain worse.It dawned on me then that the sore on my ear might be a Raynaud's ulcer, given that the worsening of these symptoms started with colder weather. I assumed that the problem was an interaction between the clonidine and the nortripytline, came off the latter and tried starting propranolol to see if this helped. The problem was repeated again, a worsening of the face prickling sensations and a rise in blood pressure, plus an increase in waking up with burning, swollen face in the middle of the night. I had to come off BP meds a few weeks back for a cardiac stress test. At that point I decided to come off the clonidine completely to see what happened. I've gradually been reducing it over the last month, and have been off it completely for about a week. I've had terrible problems with withdrawal, my BP shot up to 146/100, I've been bathed in sweat, shaking, flushing with high body temperature, very similar to the symptoms that occurred when the problems started 2 years ago. Taking 80mcg of Propranolol didn't really seem to help lower the BP very much, and what I now think is probably facial Raynaud's has been pretty bad too. I think the withdrawal symptoms are finally decreasing, BP has been 100-114 systolic for the last 2-3 days, but body temperature is still raised and the Raynaud's symptoms still very bad. What I want to know is at what point can I be sure that the clonidine withdrawal symptoms have stopped, and assess whether I'm still having 'hyperadrenergic' symptoms. Also, what can be done if I am, as clearly the clonidine wasn't helping this much, and appears to have been making the Raynaud's type symptoms worse over time (certainly I've become a lot more sensitive to cold since I started taking it). I feel I should really be getting some help with this from the medical fraternity, but my GP has no clue and apart from having tests I haven't really seen anyone yet. I've been told that the tests done so far show I definitely have POTS, that I have an imbalance of sympathetic/parasympathetic (whatever that means) but I still have no idea when I will actually see a neurologist about what's going on. No measurement has actually been made of plasma norepinephrine levels (another reason why I felt I needed to come off clonidine as I'm sure it would screw up the result even if they do suggest testing this).

I had something similar, because it started with some reflux problems my GP and I initially assumed it was a hiatus hernia, but endoscopy didn't find a problem or any evidence of long-standing reflux. Since then I've developed lots of problems with involuntary muscle spasms, so my guess is that it was some sort of oesophagal muscle spasm related to the more widespread dystonias / lots of general nerve damage. I also have intermittent hoarseness, which is consistent with laryngeal dystonia. I'm not sure what you mean by neck vessel pressure. Do you mean the veins in your neck appear distended, that your blood pressure is high, or just that there is a sensation of pressure in your neck?

I don't think there were any problems with large fibres, that's what the neurologist said at the time anyway. From what it says about Dystonia on wikipedia, spasm and weakness go together, as some portions of muscle groups over-respond (causing spasm) and others fail to respond at all (weakness). I guess I'll have to wait for the full report to find out exactly what they found. There is a specialist unit for neuromuscular disorders at King's College Hospital (where I'm being seen for POTS/autonomic), I guess I'll get passed on to them.

It doesn't but virtually everyone with EDS (3) has the same issues with muscle spasms. I'll mention it when I see a neuro, I was going to ask them about antibodies against ACh anyway, as not that many people with EDS have the additional sicca/anhidrosis.

I was tested for rheumatological/inflammatory markers for years without anything showing up until I was finally diagnosed with Ehlers Danlos last year. I think the spasms are almost certainly down to EDS, so many other people with the condition also have them although no one seems to get any sort of explanation of their cause other than muscle weakness. I guess I will know more if and when I ever see a neurologist, but so far there is still no sign of an appointment to see anyone about this or my other autonomic problems.

Recently I went to my dentist because of toothache pain, and he discovered that I had completely shattered two large molars from grinding. I've been aware for some time that my jaw is in spasm, even during waking hours I'm constantly suffering involuntary spasms where my jaw clamps shut, as well as lots of fasciculations around my eyes and jaw muscle. On Friday, I had a cardio stress test, and the girl doing it looked through my notes and said the my EMG test showed muscle rigidity caused by nerve damage (I should add that I have EDS). The autonomic tests showed that I there was some unspecified problem with parasympathetic responses, which didn't surprise me as all my problems seem to be in this area (vision, gastroparesis, sicca, urinary retention, and now increasing muscle weakeness/spasm, and as I understand it muscle innervation is cholinergic). Other members of the family have Adie's pupil, which again I believe is due to a problem with parasympathetic nerves in the iris. If what I am suffering turns out to be a problem with parasympathetic/cholinergic system, would mestinon be any help in damping down this pathelogical spasming? I've been told the forces I'm using to clench my jaw mean a bite guard won't necessarily help that much in protecting my teeth or preventing pain). I've tried diazepam but even at small doses it makes my facial erythromelalgia worse. My EDS physio has suggested exercises but they seem to aggravate the problem, as does any light physical activity. Whenever I've tried any sympathomimetic drug, this also makes the spasm problem and the erythromelalgia worse, so I don't think the answer to any my problems lies with classes of drug that upregulate or mimic norepinephrine or cause even slight rises in supine BP.

If I were me too, I would, but 2 years on I am still waiting to no avail. I keep getting passed on from one person without clue to another, and despite autonomic testing and a dx of POTS, I have not yet seen a neurologist or received any treatment of any of my autonomic issues. I have been discharged by my pain consultant, who says that the autonomic involvement means that painkillers do no behave predictably and I need to see the main autonomic specialist in the UK (1 year on from referral and still waiting...) In the absence of any informed help, my GP and I have to keep trying different things and praying eventually something works. We finally worked out what was happening with the nortriptyline. Nortriptyline interacts with clonidine to produce quite a powerful vasoconstrictor effect, which was what was raising my BP from 90 to around 120. However, in the portions of my face that aren't pathelogically vasodilated/pooled with blood, the effect is too strong, the capillaries constrict too much and trigger reactive hyperemia, resulting in more painful flushing due to the sensory nerves being starved of oxygen. The effect was also being made worse by cold weather. Sitting/lying resulted in a relative increase of the BP in my head, increasing the hyperemic response and the burning pain. I don't know why the nortriptyline didn't help the neuropathic pain, but it's possible that clonidine somehow interferes with the central mechanism, as apparently this is also true for betablockers and tricyclics.

There is no difference between EDS III and BJHS. There is a difference between people who have a couple of hypermobile joints (which includes my husband who scores about 4/9 but has no other symptoms or family history) and EDS, but no difference between the other two. Prof Grahame believes they are the same. The Beighton scale tests give a good initial indication of whether you are likely to be a good candidate, but full diagnosis requires a full examination by someone well-enough qualified to tell the difference and establish the full context. Prof G spent a whole hour testing all my joints (not just the Beighton ones) but all the others as well, taking a full family health history, testing proprioception, skin flexibility/transparency and load of other things I forget now. I already had a diagnosis of POTS, sicca and a family history of orthostatic hypotension, peripheral neuropathy and connective tissue ills, so we didn't really go into that side of things. I don't think the EDS label is being over-used, rather that historically the condition has been seriously underdiagnosed (being as I am the first in my not-terribly-well family to have been picked up with the condition, as it isn't of the kind that causes dislocations etc) From what I have read, it's probably unlikely that there will be a genetic test for EDS III, as whenever samples have been taken, there are never any common genes, suggesting that it is highly heterogenous, genetically. When ever we go to an EDS gathering, most people have type III, but the individual familial variations are very wide. In my own family, the hypermobility aspect is relatively low but the neurological involvement quite high (small fibre as well as autonomic) whereas in other families there are severe dislocations but no POTS etc. Which is why it is important to a wide range of diagnostic criteria into account when making a diagnosis.

Chronic fatigue and autonomic problems (which includes POTS) are also very common with Ehlers Danlos/Joint hypermobility syndrome, which is probably the most common cause of POTS here in the UK (I barely know of anyone with POTS here who hasn't been diagnosed as having hypermobile joints) and is a genetic condition where you body produces too much of the wrong sort of collagen. I had no idea I might have this condition until my autonomic problems started, although since I've started having a lot of arthritis problems. Not every family member with EDS necessarily shows the full range of symptoms although conditions like flat feet, varicose veins, hiatus hernia and GERD that suggest weak connective tissue maybe more prevalent than the average, and affect males as well as females in equal proportions. Google Beighton Scale, and see how you score to get an idea if this may be a problem for you, or your relatives. It's important to know, as people with EDS do not respond as well to surgery or other invasive medical procedures as people with normal collagen, so it's as well to know if you have it.

I decided to try nortriptyline again as my facial erythromelalgia pain suddenly got a lot worse with the cold. I previously gave up on it as it was causing severe tachycardia/worsening of POTS symptoms. This time the tachy hasn't been too bad (probably because clonidine is helping reduce it). However, since starting it I've had terrible burning pain in areas of my face where I previously didn't have it - my forehead/eyelids/eyes and inside nose and mouth. The pain gets worse on sitting or lying down, as does the EM, but the effect is now almost instantaneous. Apart from this I'm actually feeling a lot brighter and less faint, probably because my BP is a lot higher. However, the increase in neuropathic pain is unbearable, and it's now a lot more unpredictable whereas previously it was at least partially controlled by the clonidine. My GP says I have to stick it out for at least a month, preferably 6 weeks but personally I think that the nature of the drug, either the inhibited re-uptake of serotonin or of norepinephrine is causing the worsening of the neuropathic pain (I've read that either can worsen pain from nerve damage). I really don't know what to do, I'm not currently under any neurologist or other specialists for either the autonomic problems or the pain, my GP has said all of these issues are way beyond any of her experience and I don't know where to turn for advice. I'm only trying nortriptyline again because I've tried every other kind of pain relief without success.

I don't really see the point of doing sudormotor testing for the EM, I'm sure it is down to widespread autonomic denervation in my face. It's not as if testing would necessarily result in any sort of tailored and effective treatment. The only hope of any means to manage the pain is to control the vascular symptoms by trying to restore normal vasoconstriction. Serotonin antagonists (of which octreotide is one) have been used to treat EM, so it seems logical to me to treat the POTS and the EM as different manifestations of the same condition.

I don't actually have a doctor. I had autonomic tests a while back but have to wait months before I see anyone about it, I haven't seen anyone yet, apart from 9 months ago when I had a preliminary dx with someone else. I was originally hoping it would help my erythromelalgia by constricting my face, but then I heard that it can worsen flushing, as you say it's probably exacerbating existing tendencies. I desperately need to find something that helps my face, I simply can't go on with this problem, I've only survived this long with it in the hope that taking POTS medications might help, which is looking more and more unlikely.

Any ideas anyone? This is a really important issue for me, I desperately need to know there is hope that my autonomic conditions can be treated, I'm in a very bad place at the moment.

I don't know if what I'm suffering from is presyncope, but most of the time I feel terribly lightheaded, depersonalised, vision is highly disturbed (blurry, inability to judge distance, paving patterns jump out like 3d pictures). This feeling has become pretty much constant over the last couple of months. I'm not getting tachycardia due to the high dose of clonidine I take; I'm currently feeling terrible, so just took my standing pulse and it was only 71. The purple colour in my legs used only to be around my knees, now it's spread down to my calves, possible up to my abdomen too, so I guess that means it must be progressing somehow. I can't wear compression stockings as they worsen the paresthesias in my feet. Does this sound like I might be suffering presyncopal symptoms ?

I would try Midodrine if only I could find anyone to prescribe it. I've been waiting nearly a year to see anyone about my autonomic problems, since my original session with Prof Mathias. I had autonomic testing performed a month ago but still no word about when I'll see a doctor about it. My local hospital keep saying it's all well beyond their paygrade. I suspect I won't be able to tolerate Midodrine, or most of the other POTS treatments because anything that simulates the effect of norepinephrine will probably make the erythromelalgia worse (things like pseudoephedrine or phenylephrine trigger bad flares). Does anyone find that it improves cognitive function? At the moment I just feel like I'm walking underwater; everything is hard work, slowed down and distorted. I'm just terrified that the cognitive and vision issues maybe the start of sort of dysautonomic dementia or something. I'm gradually reducing my pregabalin as that affected my cognitive function, memory and vision greatly when I started taking a very high dose recommended by a pain specialist for the erythromelalgia, but my problems have just been steadily increasing over the 5-6 months that I've been stepping it down. I did as a pharmacist about it, she thought that taking the very high dose might have sensitised me to the drug and made any existing EDS neurological and muscle weakness problems worse. That said I'd put up with any medication that stopped the erythromelalgia as it is completely and unbearably life-limiting (no heating on in doors, have to stay in one room under 2 fans, can't go anywhere or visit anyone who has heating on, can't even tolerate my husband's breath on my cheek. Pain is like a hot water scald, this can actually break the skin like a real burn, I have an sore from it on my ear that just won't heal. It is gradually destroying my appearance. I can't wear make up as my skin peels constantly due to the anhidrosis/small fibre neuropathy, it's more like a diabetic's foot than a face). No pain medication has made any difference to it apart from the Clonidine, I've tried them all now apart from carbamazepine and lidocaine/ketamine infusion.