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Everything posted by ~elizabeth~

  1. I've exhausted pain management specialists, my local one (in Oxford Uk) won't have anything to do with me as they say I'm too complex, I'm being seen by various people at the main specialist neurological hospital in London, but the latest one has just dumped me because he refuses to deal with patients using opioids on ethical grounds, the one I'm seeing tomorrow has failed to organise the ketamine infusion that I was meant to be having a year ago (a whole year with no word about it, even though I was supposed to be on the emergency list for it). I'm not sure that they would count IVIG as being a pain treatment, they were very keen to play down its use when I was admitted there last year (side effects outweigh benefits etc). If I have a ganglionopathy, it is definitely a sensory one, so I'm not sure if the detection of G-AchR antibodies is relevant to that (although something must be causing the dry mouth attacks that seem to accompany flares of the pain condition). I'm not sure whether G-AchR antibodies is something they test for in the UK anyway (they wouldn't tell me exactly what they tested me for, it included all known parasites/infections that cause neuropathy, the only one I have antibodies against was historical Epstein Barr. I can trace the beginning of my problems back to a severe bout of it many years ago, I have a feeling this problem has been lurking since then). From what I understood from the articles I found, if you have non length-dependent neuropathy, that is now considered diagnostic of an autoimmune neuropathy, as 50% of people with this kind of neuropathy have an existing AI disease (like Sjogrens or lupus), and I think opinion is growing that the other 50% may represent unknown autoimmune disease of the nerves. I've only ever had low doses of prednisone (10-30 mg daily), which causes worse facial flaring, but then these doses might be too low to do any good anyway.
  2. This is the only other article I could find at all, anywhere, on non length-dependent neuropathy, it seems that a preexisting immune disorder is found in half of cases (which to me suggests that the other half may have non-diagnosed autoimmune causes). The part about 'refractory to treatment' is depressing, although exactly what I have found in terms of response to all painkillers. However, I guess none of these patients had been tried on IVIG at all, and certainly not soon after the problems began, so this study does not necessarily mean that IVIG is guaranteed not to work.
  3. This is the article that suggests that evaluating whether neuropathy is length-dependent is significant to the diagnosis of sensory ganglionopathies I think at the very least I want to suggest that they perform punch biopsies at my foot and my thigh. I wanted them to do a skin biopsy last year, they said no as it was so obvious that I was suffering from very severe sensory neuropathy.
  4. This is the first article I found that first raised my suspicions: I've had my doctors rubbish some articles I've shown them in the past, I doubt they can argue with a professor of neurology and neuroscience, a peripheral neuropathy expert as well.
  5. Can anyone give any advice on how to go about checking for these types of disorders? I can't go through all my story here, it's too long, but 4 years ago I was stricken suddenly with severe facial flushing/pain (erythromelalgia) which has continued to spread (now all over face, scalp, chin and down on to neck, chest and shoulders). A year ago the same reddening and pain started in my feet and hands, and the burning, tingling pain has now spread all the way up my legs. I spent weeks in hospital last year where they diagnosed idiopathic (possibly hereditary) neuropathy, put my on lidocaine for 10 days which was a complete disaster. Having spent a whole year arguing for some sanity on opioid prescription, my current pain doctor has dumped me. In the last couple of weeks, I've had significant trophic skin changes all over the previously tingling areas on my neck/shoulders, and clear flushing of the skin in tandem with my erythromelalgic ear flushing, normally it starts in the very longest nerves which are those of the feet, and gradually spreads up the body. When it appears in other places, or randomly, it's termed non length-dependent neuropathy (which is very rare I think). The very first hints that anything might be wrong were 5 years ago. My father had died 2 weeks before; suddenly I developed non-infective mouth sores, then a couple of weeks later suddenly lost my salivary gland function completely. This remained the case for several months, over which time I developed burning pain and numbness in my tongue. The facial erythromelalgia appeared a year later, and has progressed so that my legs, lower arms/hands, neck/chest and possible urethra area are now affected. After talking to someone about possible IVIG treatment, I did some research and found some interesting things. IVIG is being used increasingly for 'idiopathic' neuropathy on the assumetion that certain cases may be autoimmune ganglionopathies. One of the criteria for case selection is apparently where it does not follow the traditional foot-up pathway, but is multi-focal or non length-dependant: In fact, this article goes on to say that establishing that non length dependence can be diagnostic of an autoimmune sensory ganglionopathy (possibly avoiding the need for a sural nerve biopsy, something I was advised against due to the risk of nerve damage. They did say to me when I was in hospital that is was possible that it might be something in this area, but that the risks of the latter biopsy or IVIG outweighed possible benefit. That's all nonsense now, as this thing has simply got too bad to live with, I can't icepack my whole body overnight if it spreads to the trunk, which is the only way I've been coping with it in my face so far. I really need to find more good evidence that the involvement of my glands and the non length-dependence thing is significant enough to fund IVIG treatment.
  6. What medications are you on? A number of POTS meds (betablockers, midodrine, clonidine etc) can all cause peripheral numbness. I was on clonidine and/or propranolol for a long time, and assumed it was due to the drugs, but it finally turns out its due to small fibre neuropathy, which appears to have now become very aggressive. Tingling or electric shock sensations (dysaesthesias) are characteristic of small fibre neuropathy, which can affect both sensory and autonomic nerves.
  7. You are so lucky to have found something that helps Kris, I'm truly happy for you. I hope it continues to work. What I haven't isn't 'flushing' though, it's facial erythromelalgia, which is extremely painful and has now spread to my feet as well. I feel I have no option but to pursue the autoimmune route, as I've exhausted all forms pain relief with zero success, nearly all have made it significantly worse, which leaves no where else to go. Since coming out of hospital I'm bedridden, I can't walk due to the pain in my feet, and have to keep my face permanently on an icepack plus the mouth and throat pain is making it increasingly difficult to eat. It's horrific, to be honest I don't know how much longer I can go on like this. Whatever the problem is caused by, it's progressed very rapidly over the last few months. I was diagnosed with UCTD a few years back (I have positive ANAs 1:160 and polyclonal gammopathy, I think they diagnose UCTD in people with vague signs of AI disease and then keep an eye on them to see if a differentiated form of CTD arises), but the rheumatologist changed her mind about this when she got letters about the EDS and autonomic stuff, said it was all nothing to do with her and dumped me.
  8. Hi, I'm wondering about all of this too. I had EBV in 1985, and have suffered with CFS type symptoms ever since. At the time, I had a bout of facial swelling with dyseasthesias, and was left with throat pain for years after. It probably triggered autoimmune thyroid disease, although there was a delay of some 10 years before I could get the condition diagnosed properly (GPs tested only TSH, rather than thyroid antibodies). About 3-4 years ago, symptoms of autonomic dysfunction started to increase rapidly. First I had a loss of salivary function; a few months later, my eyes became red, painful and very swollen. A few months later, the POTS and facial erythromelalgia (EM) started quite abruptly. Since then, signs of autonomic dysfunction and pain have gradually got worse, the EM has now affected my feet badklyand now purple discolouration and pain is spreading gradually up my arms and legs. Last year I had a work up for MCAS, and the immunologist found high IgG, polyclonal gammopathy and raise ANAs 1:160, with historical IgG against EBV. I'm increasingly of the mind that the historical infection and the neurological issues have to be connected. The small fibre specialist I saw kept on saying 'we have to find the cause of this' but the other neuros don't seem keen. I did raise trying IVIG with them, but they said it wasn't clear that risks would outweigh benefits. I'm in the UK too, being seen at Queen Square. I am being taken seriously as they realise I'm in a desperate degree of pain from the EM and am refractory to all symptomatic relief. Just wondering who you saw about EBV and CFS, and whether this line of approach might yield anything if I can't persuade my neuros that this is an inflammatory condition.
  9. I have high IgG, plus polyclonal gammopathy and positive ANAs 1:160. I feel that this is significant to my dysautonomia, but my doctors disagree. I have IgG against Epstein Barr, but I'm told this is historical. However, something is causing my severe autonomic neuropathy which is progressing very rapidly. I don't really know where to go from here, or what further tests to ask for. They said they don't want to do a sural nerve biopsy (to look for chronic inflammatory polyneuropathy) due to the risk of nerve damage.
  10. My GP took me off plaquenil when my face problems started as she thought it might be due to that. However, it didn't go away when I stopped and has got progressively worse. I'm actually considering going back on it again as I'm beginning to think my neurological problems must be autonimmune in some way. I'm really worried now, as the purple discolouration, skin changes and pain is now working it's way up my legs and arms. I can't tolerate any neuropathic painkillers as they make the facial problem worse. I really want to press my doctors to consider IVIG or PE. I feel I don't really have any choice as we've exhausted all ways of trying to control pain. I've just been in hospital for ages, they had me on lidocaine for a week which just made everything a lot worse.
  11. Thanks. DGW, the article you link to suggests that serum catecholamines are low in AAG, if that's true it seems unlikely in my case as my serum norepinephrine is high, both supine and standing. I'm wondering if what I have may be some other kind autoimmune dysautonomia, triggered originally by the Epstein Barr virus. I don't know how to convince my doctors of this though. From my point of view, I am completely refractory to any symptomatic relief (either of pain or dysautonomia) due to the facial erythromelalgia, so the only way forward is to look for a treatable underlying cause. However, I can't convince them that my positive, mildly raised ANAs are significant; although polyclonal gammopathy is found in in conditions like CIDP, it's not clear whether its cause or effect of the condition (it is also a finding in non-immune neurological damage, e.g. stroke). The lead specialist has said he thinks its irrelevant, but then he also confidently predicted it was a sodium channelopathy, which seems to have been undermined by the failure of lidocaine to help at all. I just think it's unusual to have such serious neuropathy mostly affecting both aspects of the autonomic system. I even think the pain is primarily autonomic, as it does not respond to any of the usual neuropathic painkillers, and is made worse by any drug that mimics or stops reuptake of catecholamines. Apparently sympathetic terminals can regrow around sensory nerves, sensitising them to norepinephrine, plus they can invade the dorsal horn of the spine, causing neuropathic problems. I think the fact that lidocaine infusion was so catastrophic for me suggests that the primary problem can't be sensory. I really don't know what to do, they are now suggesting even more invasive pain treatments without really having diagnosed what's going on properly in my view.
  12. Thanks so much, that's very helpful. No, I don't think the do test for AAG here. It's annoying when they don't actually give you a proper breakdown of results on paper, so that you know what they've tested for, but I've never heard of anyone else in the UK being tested or diagnosed with it. I'm sure the EDS vasomotor instability plays a part, I have very high standing norepinephrine (which they don't ever seem to refer to as hyperPOTS here) so I'm sure hugely fluctuating catecholamine levels with changes of posture don't help. However, I've had low BP and floppy veins all my life, and the onset of these symptoms was very sudden and acute, so I'm sure there's an additional factor at play somewhere. I can't tolerate any POTS drugs, as they all seem to destabilise the pain in some way or other, I guess because the process of small fibre disease may have caused 'sympathetic pain', either due to sensitisation of adrenergic receptors on sensory nerves, or regrowth of sympathetic nerves entangling with sensory ones. I can't really test the 'floppy vein' vasomotor scenario because I can't tolerate drugs like midodrine, or anything else that mimics norepinephrine or affects catecholamine levels. Propranolol helped a lot with the POTS symptoms, but I had to come off it because I have histamine intolerance as it lowers your diamine oxidase levels, and I'm limited enough in what I can eat as it is. The more widespread your neurological deficits, the more difficult it become to treat any part of them without affecting something else adversely. Yes, I'm having a 'holiday' for now, at least until the hospital gets back in touch. They are trying to all meet up with the pain team to discuss multiple sensory nerve blocks. I'm not sure about this, as I can't find much evidence they are effective for erythromelalgia (which undoubtedly has an autonomic element of some kind, which why be the reason it is usually refractory to all the usual sensory neuropathy drugs), plus when your face, ears, eyes, mouth, throat, feet and hands are affected, it's impossible to block the pain in all those areas. I'm looking into botox injections, which I feel might be more effective as it can block sympathetic vasodilator nerves, which personally I think may be the main culprit in erythromelalgia pain. I'll get back in touch with my private autonomic specialist and ask him if he can have a word in the right ear about AAG, as I'm sure he keeps up to date with latest developments in the US.
  13. Thanks Arizona Girl, that's useful to know (I'm in the UK by the way). The person who told me that was part of the headache team (treating me for my facial erythromelalgia), it's possible they aren't completely up to date with stuff on the edge of their main specialism. I saw the small fibre guy for only a few minutes, but he kept on repeating 'we must find what is causing this'. He didn't seem particularly keen on taking me on though, he was only seeing me to give a second opinion. I had a fairly full workup from the immunologist they work with last year. Apart from the ANAs and polyclonal gammopathy, he found elevated IgG4 with historical evidence of IgG antibodies against Epstein Barr, which was no longer active. I've always thought that my thyroiditis was triggered by the EBV infection I had 27 years ago, as that's when a lot of the odd symptoms started, but something seems to have activated again in the last few years. Thyroid antibody activity was zero, as evidently all thyroid tissue has now been destroyed, so it seems unlikely that any inflammatory activity can still be related to this. ANAs, IgG and the gammopathy did all decrease while I was on the hydroxychloroquine, so it must have been interfering with some active inflammatory process. I'm inclined to ask my GP about trying a course of prednisone, at least while I'm waiting to hear back from the neurological hospital again. They do perform IVIG and plasma exchange there, but only for a very limited range of conditions (Guillain Barré, demyelinating polyneuropathy, MG, I'm guessing they are only licensed for these conditions). I'm not sure they recognise AAG there. It doesn't help that the autonomic department is at odds with everyone else there, they are maintaining I don't have small fibre neuropathy and everything can be explained by vasomotor instability due to my hypermobility. I'm glad to say that none of the other neuros agree with any of this, one of the others said that was 'nonsense' but I it should be the autonomic unit that is looking into conditions like AAG for patients with signs of autonomic neuropathy with an inflammatory component. I did have quite a positive response to pyridostigmine in terms of increased muscle strength, which has been declining gradually for years. To me that sounds like something interfering with nicotinic receptors, if it was just EDS-related weakness, it wouldn't have had any effect. It hasn't helped my lack of sweating though, in fact I'm limited in how much I can take as it just seems to trigger worse thermoregulatory flushing/cholinergic urticaria in response to heat, I can only tolerate about 60mg a day, half of what I was told to take to help the POTS symptoms I was put on it by the previous head of the autonomic team there, I get the impression he's more open minded on this stuff (sadly now retired). Maybe I should see him again and ask him about his thoughts on AAG, he probably still has a fair amount of influence there.
  14. At one point my rheumatologist in Swindon did diagnose me with undifferentiated connective tissue disease, but when she got the letters about the hypermobility and autonomic problems, she just said it was all beyond her expertise and dumped me, so I don't have a rheumatologist any more. When they thought it was UCTD, I was on hydroxychloroqine for a couple of years, I did feel better on it and eventually stepped it right down, which is when the problems suddenly got worse. That may have been a co-incidence though, upping it back to full dose certainly didn't help with the neurological problems once they'd started. However, hydroxychloroquine isn't an immunomodulatory drug they ever seem to use for these autoimmune ganglionopathies; they seem to use either prednisone and/or IVIG/plasma exchange. I got the impression I'd have be at death's door before they'd consider trying the latter though. I don't know if they can test for AAG antibodies there, I didn't get the feeling that they do.
  15. I've just spent 2 weeks in a specialist neurological hospital, trying to get to the bottom of what is going on. They seem to be sure that I have substantial small fibre neuropathy affecting both sensory, sudomotor and autonomic nerves affecting large areas, not just the peripheries. The small fibre expert there is into looking for underlying causes of these conditions, but they said that there a lots of things they know exist but can't test for. I'm guessing they mean autoimmune diseases against autonomic receptors. I asked about IVIG and plasma exchange, but they said they don't like using them, because of the risks of contracting something from blood products. I really don't know what to think now. They are doing genetic testing to look for mutations that cause small fibre degeneration, as there is family history of problems, and also another rare autonomic problem (hereditary Holmes Adies). However, in other family members the problems are very mild, limited to mild sudomotor/parasympathetic involvement, without the degree of sympathetic/sensory involvement. I also have positive ANAs (last titre 1:160) and polyclonal gammopathy, plus longstanding autoimmune thyroid disease. The sensory nerve pain/erythromelalgia I have is completely refractory to treatment, I spent 7 days receiving lidocaine infusion in hospital, which just seems to have made things worse. I don't know whether I should be insisting on trying immunosuppressive approaches to this, given that we are running out of options rapidly. They are looking at nerve blocks now, but given the burning pain is spreading across my whole body, including throat and thorax, even if particular blocks worked it wouldn't improve the overall pain situation much. I'm not really sure the neuros have come to any particular conclusion about what's wrong, they seem to keep changing their minds, as I'm such an untypical and complex case.
  16. Just found this article, which is very interesting. A recent study found sodium channel SCN9A mutations in a significant percentage of people with idiopathic small fibre dysfunction with severe autonomic involvement. http://brain.oxfordjournals.org/content/135/9/2613.long
  17. Apart from paresthesias in throat and mouth, I didn't have a lot of side effect on 60mg a day, but since raising it to 120mg I've been feeling awful. My vertigo has been really disabling, plus my muscles appear to be getting weaker and worsening the EDS. Given that anticholinergic drugs are used to suppress vestibular problems, I'm not surprised it's worsened the vertigo, but I was sure it was actually helping my muscles at the start. I think in myasthenia gravis, too high a dose can actually worsen the neuromuscular problems, I don't know whether taking too high a dose can cause problems in people without MG. It has helped the hyperadrenergic symptoms a lot though, which was the worst aspect of POTS for me, so I'm reluctant to stop it altogether.
  18. Nothing very helpful Kris. He thought that only 5 days of continuous lidocaine infusion, followed up by oral mexiletine would actually be much help, which I can't afford as I don't have private insurance (this is rather similar to the regime they now use for CRPS). He said he'd come to this conclusion about lidocaine after treating someone else with a very similar presentation of extreme facial flushing and burning, and found this protocol helped after every other option had failed miserably (as it has done for me). He left me with a prescriptions for the sodium channel blocker lamotrigine, though clearly with little faith that it would help much.Because of that, he thinks it's pretty likely to be due to a sodium channel problem, as other forms of EM do tend to respond at least partially to tricyclics, duloxetine or pregabalin, albeit usually at high doses. I actually felt much better when I came off clonidine, although stopping it did corresponded with when the weather warmed up a bit. The rebound effects were awful, very high BPs and at it's worst it triggered EM symptoms in my ear canals, nose, throat in addition to my face, ears and lips (that was with careful tapering). From that, I think being hyperadrenergic must be a factor in irritating sensory nerves (they finally confirmed high plasma NE during upright TTT in September). It can be due to immune-mediated connective tissue diseases as well, usually scleroderma. For this type they seem to favour medications that alter endothelial/platelet function like iloprost, if you've got a dx of arthritis, then you might have this variation, rather than the purely neurological kind.
  19. My blood pooling/POTS appeared almost overnight in my legs quite soon after the erythromelalgia started, they'd been a reasonably normal colour before then, something suddenly caused a widespread dysfunction in small C fibres and autonomic nerves. I'd had dysaesthesia sensations in my face/eyes for about 8 years before that, which is exactly the same time frame during which I'd noticed my muscles were weakening and that I'd become hypermobile (I certainly wasn't as a child, I remember being pilloried by a teacher for not being able to get my hands much below my knees, let alone touch my toes). Personally I think EDS III will turn out to be due to a number of different syndromes, rather than a single disease entity/mutation.
  20. This article doesn't seem to rule out other mutations might exist, I think there are thought to be 10 separate mutations on the SNC9A gene causing differing variability of pain, so I guess it's possible to have a variation where the sensory pain is not that severe but the autonomic dysfunction is. EM doesn't just affect the feet, it can spread from the extreme peripheries towards the core of the body. I only noticed signs of blood pooling in my legs (purple discolouration on calves and knees) and pronounced tachycardia at the same time as the facial problems started. What I really want to know is if the intense vasodilation in EM is caused by the hyperactive sensory nerves churning out neuroirritants, or by the lack of constriction due to the hypoactive sympathetic nerves. My hunch is that it's due to the former, as blood pooling by itself isn't usually painful. My reason for wanting to know is that I'm considering Botox injections, as my pain is refractory to other treatment. If the paroxysmal flushing is due to neuroinflammation, then there's a chance botox will help, as it there's increasing evidence that it blocks these substances in trials for neuropathic pain. If, however, it's due to blood pooling, then lowering sympathetic tone further will make things worse. My neurologist is willing to try botox, but on the understanding he has absolutely no way of predicting what will happen as it's never been used before for primary EM. As I understand it, sensory C fibres detect noxious changes in blood chemistry, as well as heat/cold/mechanical stimulus in the skin, so I feel the fact that I have high plasma norepinephrine levels which rise significantly on standing, might be one of the triggers for the sensory nerve misfiring (I think I'm right in saying that C fibres have alpha receptors, which is why norepinephrine has an important relation ship with pain; midodrine also made the pain much worse, so clearly it's not a simple issue of lack of constriction). Equally the sensory nerves might be reacting to hypoxia due to blood stagnation from pooling. I did actually find the flushing improved a lot when I started pyridostigmine, and all the hyperadrenergic symptoms (tachycardia, anxiety, sweating, shivering, flushing on posture change) more or less went away, but the onset of cold weather and starting lamotrigine seem to have sent it back into the pain stratosphere again.
  21. Very interesting, particularly the bit about sodium channels in muscle. I also have severe muscle spasms, along with what looks like central vertigo and severe tinnitus, which are other conditions which appear to have a sodium channel pathology. A lot of people with Ehlers Danlos have the same range of problems, along with the autonomic dysfunction, hyperalgesia and widespread insensitivity to lidocaine, which to me suggests some sort of sodium channel defect. My guess it that you may get a cluster of related sodium channel mutations, as although erythromelalgia is not common among the POTS/EDS community, these related disorders are.
  22. The truth is, no one knows what the mechanism is. All I was told is that it's due to 'bendy veins' which frankly I don't really buy as a solution as it doesn't explain why I've had so many odd neurological symptoms and tachycardia present at the same time as the erythromelalgia started, despite having bendy veins and very low BP for all of my life. The last neurologist I saw diagnosed the facial flushing (previously misdiagnosed as MCAS) as facial erythromelalgia, and thinks the cause is likely to be a mutation in a particular sodium channel. Having spent the last few days researching this, I now find there are links between NaV 1.7 sodium channel polymorphisms and dysfunction of the sympathetic ganglia. It's known that people with EDS are often insensitive to lidocaine, and also have accompanying tendency to experience hyperalgesia in response to painful stimuli, which are both signs of defective sodium channel function. My guess is that this will eventually prove to be a large part of why sympathetic system is dysfunctional in people with EDS, along with lots of other neurological deficits that have a sodium channel pathology (vertigo, tinnitus etc). My head pain neurologist wants to get funding to do a study on me, which will involve genetic testing so I guess if there is a connection then it will eventually be brought to light. He also thinks that facial erythromelalgia is probably underdiagnosed (not surprising given how everyone on these boards makes an automatic assumption that ALL facial flushing/burning is MCAS). I do find it quite worrying that I had to see a headache neurologist to get this problem correctly diagnosed, having been assured by the autonomic department that it wasn't a channelopathy. If they missed it in me, then they may be missing it in other people too. http://forums.dinet.org/index.php?/topic/24785-nav-17-mutations-and-sympathetic-dysfunction/
  23. Just before christmas, I saw another neurologist who specialises in head pain, as my main reason for pursuing diagnosis for my autonomic dysfunction is to try and stop the horrendous flushing and burning in my face. He diagnosed my problem as facial erythromelalgia (which is what we always thought it was, he thought that previous diagnoses of rosacea and MCAS were 'nonsense') and thinks it's very likely the cause a NaV 1.7 sodium channel polymorphism, especially given that all other forms of pain relief are completely ineffective. Researching today I came across the following research that links hyperactivity of the NaV 1.7 sodium channel with underactivity of the sympathetic ganglion neurons ( "These data provide an explanation of why primary erythromelalgia presents with pain due to hyperexcitability of nociceptors together with sympathetic dysfunction (flushing/erythema) that is at least in large part due to hypoexcitability of sympathetic ganglion neurons") I've never come across this as a potential cause of autonomic dysfunction before but the neurologist said that he thinks it's probably greatly underdiagnosed. Disturbingly, none of the neurologist in the autonomic department seem to know of any connection between NaV 1.7 and autonomic dysfunction, and almost dismissed the possibility of the facial flushing problem being a channelopathy. I think it's important, as some people with this disorder may be mistakenly being diagnosed with MCAS.
  24. Small nerve fibres do grow back, but they don't necessarily return to normal. A lot of the problems with autonomic dysfunction are due to increased autonomic receptor sensitivity to neurotransmitters, or sometimes an increase in density after damage to nerves (denervation supersensitivity) in the various systems of the body.
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