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Rexie

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  1. Dry mouth and eyes seem to go hand-in-hand and are found in many people with POTS and other autonomic diseases and conditions. Both my mouth and eyes are often uncomfortably dry. Increasing the amount of Omega-3 polyunsaturated fatty acids in my diet has helped and there is scientific evidence that this works. Hemp seeds are high in plant-based Omega 3 fatty acid as are walnuts. I use a hemp seed drink in my morning smoothie and try to eat a few walnuts as part of my regular diet. I also take a capsule or two of Slippery Elm herb which helps increase internal moisture, particularly in the digestive system, not so much for dry mouth and only a slight help for dry eyes. Slippery Elm does lessen the overall sensations of feeling dehydrated. I recently started using TheraTears 1200mg Omega 3 Supplement for Eye Nutrition, a product often recommended by ophthalmologists and other doctors – so far, so good (I space the three recommended capsules out over the day and take them with meals or a smoothie). TheraTears capsules contains all forms of Omega 3 fatty acids in the correct recommended daily requirement amount. Omega 3's are also good anti-inflammatories and have other health benefits. My dentist recommends Biotene which is of some help for dry mouth but I am not a big fan. I try to sleep on my side to help prevent open mouth breathing during sleep which is very dehydrating. Dry Eye Syndrome and Sicca Complex are Commonly Found in Patients with Postural Orthostatic Tachycardia Syndrome, Dave S Ho, Okeanis E Vaou, and Anna D Hohler, Clin Ophthalmol., Vol. 14, pp. 4015-4021; 2020 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7685370/ The Role of Nutrition and Nutritional Supplements in Ocular Surface Diseases, Marco Pellegrini et al, Nutrients, Vol. 12(4), pp. 952; 2020 https://www.mdpi.com/2072-6643/12/4/952/htm The Effect of a Unique Omega-3 Supplement on Dry Mouth and Dry Eye in Sjögren’s Patients, A. Papas; M. Singh; M. Singh, ARVO Annual Meeting Abstract, May 2007 https://iovs.arvojournals.org/article.aspx?articleid=2382584
  2. Elizaangelica, just covering over-sensitivity to light (I’m over-stimulated by many things and this all manifests like chronic regional pain syndrome for which I meet the definition), I’ll mention some eye stuff for you I found interesting in my research of this topic. Think circulation. From what I understand, Transient visual loss (TVL) is an ophthalmological symptom referring to mild blurring of vision to complete blackness; it can be monocular (one eye, TMVL) or binocular (both eyes). TVL may alternate from eye to eye and it is hard to tell sometimes whether or not one or two eyes are involved. Many conditions, from serious to not-so-serious, can cause TVL. Precipitating factors for transient monocular visual loss (TMVL) include posture, light, eating, exercise, hypotension, arrhythmia, and heat. For those of us with dysautonomia involving changes with blood pressure, etc., hypoperfusion (reduced amount of blood flow) of the optic disc or retina, either directly or indirectly, may be common, from what I understand. Visual loss is usually of short duration (2 to 4 minutes), and may be postural, may recur many times a day, and may be associated with photopsia (eye floaters or flashes). There may be associated features like headaches, jaw claudication (pain and tiredness of face and jaws after chewing), scalp tenderness, fever, polymyalgia rheumatic (an inflammatory disorder causing muscle pain and stiffness around the shoulders and hips), etc. Some common causes for hypoperfusion include but are not limited to low blood pressure (hypotension), loss of blood volume, retinal vasospasm, reduced cardiac output, low oxygen levels in the blood, low hemoglobin levels in the blood (oxygen is carried by hemoglobin), dry eye disease, hyperviscosity states, and migraine/retinal migraine. TVL can also be light induced apparently. People like me with light-induced TVL suffer from poor to blurry vision or prolonged after image when exposed to bright lights or sunshine. In theory, when the retina is exposed to light, there is an increase in retinal metabolic demand that is unmet by ocular circulation. This can be common in those with choroidal vascular insufficiency from significant carotid stenosis (narrowing of the large arteries on either side of the neck) as in atherosclerosis/high cholesterol. The mechanism behind the more serious hypoperfusion retinopathy results from an overall ischemic cascade and starts with comorbid cardiovascular conditions, such as hypertension, hypercholesterolemia, diabetes, heart disease, and history of smoking. Or for me, less serious ocular ischemic syndrome triggered by low blood pressure causes me visual issues, especially when coupled with light sensitivity. Or maybe it’s vasospasms or all three plus a neuro glitch. I've read that retinal vasospasm with decreased arterial perfusion can be precipitated by emotional stress, cold, or exercising. Vasospasm can occur in the cervical portion of the left internal carotid artery, which diminishes blood flow to the ophthalmic artery. Once an episode of delayed central retinal artery circulation ends, all abnormalities resolve. Ocular ischemic syndrome is the term used when TMVL lasts longer than a few minutes (30 minutes plus). Apparently it is often precipitated by orthostasis (postural hypotension/orthostatic hypotension), general hypotension, postprandial hypotension (drop in blood pressure after a meal), abnormal vasomotor control, hyperviscosity, exercise, sexual intercourse (I do remember seeing stars from time-to-time), and exposure to bright light. Phosphenes and impaired dark adaptation are common. (Phosphenes are the luminous floating stars, zigzags, swirls, spirals, and squiggles that occur when the cells of the retina are stimulated). By definition, people with transient visual loss (TVL) almost always present at the doctors’ offices after episodes have resolved and neurologic and ophthalmologic examinations are usually normal. Nothing was ever picked up during routine eye exams for me. The pupillometry portion of my autonomic function testing at UTSW-Dallas did reveal “large baseline pupils and impaired constriction responses to standard light stimulus.” Maybe I’ll learn some new things with my first interventional cardiologist, I go back soon for stress testing with exercise myocardial perfusion imaging and also an echocardiogram. My vision is off with eyes seeming out-of-sync when my blood pressure is low or I’ve skipped a meal or had a long day or flare of my deal. I wear transition lenses (photochromic lenses) in my glasses when out which is helpful since they change according to light levels, even in stores. At home, I like my LED light bulbs best, followed by halogen lights or the old fashioned bulbs as opposed to fluorescents. After a stimulating outing or day I like low light levels and quieter activities. After calming herbs to help balance the sympathetic/parasympathetic nervous system, when I can read again, I love to read. If I must read or insist on reading when the novel gets good and my vision gets bad, I’ll close one eye to continue. Often I’ll just listen to news or a TV show instead of actually watching it if my eyes hurt or are not focusing right. I find that improved nutrition which gives my body the raw material to make the neurotransmitter it needs helps me a lot. My latest addition is powdered collagen in my morning smoothie. Regular exercise as tolerated is also helpful. When over-stimulated I’ll pause and not move for 20 minutes to an hour while playing simple phone games so I can regroup and let everything come back into homeostasis, eyes included. Sometimes a short 5-20 minute nap helps. I hate the down time, but such is my life which is better than no life. Elizaangelica, learning new things is always nice and it’s perfectly normal to want to know how things work, as well as being often useful. I think we should all be proactive in our health care, going as far as we want and can with education. It amazes me that I never knew much about my body and all its systems much less how it works before my own health downturns. It has given me a new appreciation for life. We are indeed “fearfully and wonderfully made”.
  3. Hi Pietrol, sorry you're experiencing yet more misery. Dyspnea – inability to take a deep breath; breathlessness I get this a lot and have for many years and I’m still here. Yesterday morning was bad as I was trying to get it together to go to the ER to see why I was having continuous chest (heart) pain. I also get this during or before other stressful adventures, when the weather is extreme (too hot/too cold), when my blood pressure is low, or I’ve had a busy day, or for no obvious reason. My best quick fix or help is an extra calming herb (ashwagandha) coupled with a touch-my-toes posture which I hold for awhile while breathing better (coming up slowly afterwards). Also useful is a about half a cc (mL) of pure lavender oil massaged into my abdomen right below the sternum at the diaphragm. I then inhale with cupped hands the residual lavender oil which is very calming. If seated, a bend forward at a 40-45 angle also helps better breathing for me, as while reading or eating or texting. Throughout the day I watch breathing to make sure I am not shortchanging efforts or breathing too shallowly. Earlier this year I went to minimal shoes and love the change which makes better posture easier, lessening episodes of dyspnea. I also try to walk more when I can, not pushing length of walk on bad days. Some days it may take all day to really get a first deep, good breath, then the rest are easier. There are many reasons for dyspnea and it is associated with many neurological conditions and dysautonomia. There are also many suggested solutions or helps. Here is a very easy to read journal article related to POTS: Breathlessness and dysfunctional breathing in patients with postural orthostatic tachycardia syndrome (POTS): The impact of a physiotherapy intervention, Charles C. Reillya et al; Autonomic Neuroscience: Basic and Clinical, 223, 102601; 2020 https://www.autonomicneuroscience.com/article/S1566-0702(19)30099-2/fulltext I tripped out the other day in a bit of a silent, mental PTSD rage after talking to my PCP. When I mentioned that I seem to have a credibility issue with many doctors who seem not to believe anything I say, her response was that I need more documentation of my dysfunctional self. As if autonomic testing and other tests I’ve had are not enough to prove I have issues that someone, somewhere should help me address. One of my professional neuro buds did defend his fellow professionals by saying it is as frustrating for them as it is for us when they have to deal with and manage patients like me who present with a variety of troubling symptoms. Days later, I am still not sure I am totally mollified, but I have soften my heart with regard to him. I still care for and about my PCP who is doing her best and is good for me. If you find professionals who seem the least bit interested in helping you, keep them, don’t push them away, and move forward as best you can.
  4. I haven’t hit the floor due to low blood pressure since starting ashwagandha 4 years ago; among its many virtues is that it is an adaptogen (helping one function better at the extremes while increasing endurance). About the same time and more rigorously after autonomic testing revealed an orthostatic component to my dysfunction, I started pausing throughout the day or as part of my walking exercise, to touch my toes and hold the downward position for 20-30 seconds or more before coming very, very slowly back up. (I get better deep breaths while in the downward position, too). I do this standing near a railing out back or near furniture or a free wall inside where I can have a hand on support. Doing this exercise does give a major head rush and often greying of vision – a whoosh. It also gives me controlled training in sailing right through a big dip and out the other side in a few minutes. Helpful, for example, if you reach down to get something while at home, or, get up from an activity on the floor, or for example, while out shopping and getting something from a bottom shelve. The training keeps me on my feet, although I must pause for a moment, while giving my body and mind (yes, it is freaky and disconcerting and enraging and sad all at once) a chance to regain homeostasis. A brief pause while out in public is acceptable (lots of people seem to pause for reasons unknown) and a pause is far better than the embarrassment that stems from dramatically crashing into a display of store goods. Hope this is a little clearer than mud – it’s training in getting use to being functional while being dysfunctional. Kind of like establishing muscle memory – your body will remember it does not have to collapse during blood pressure drops even if you are not actively conscious and “present” at these times. A service dog might be useful if one thought one would never get a handle on these blood pressure crashes. My first German shepherd was highly trained and we were quite bonded. When I got Lyme disease he took to herding me to a chair or other place to sit down when I went through a phase of petit mal (absence) seizures – he’d know one was coming before they happened. Some service dogs can detect orthostatic hypotension. (My present shepherd is self-centered and uncaring, but she is sweet in her own way). Service Dog for POTS – How They Help & How To Qualify: https://usserviceanimals.org/blog/service-dog-for-pots/
  5. cmep37 I've been selective with my music since encephalitis 9 years ago and now even more so with dysautonomia. Sometimes I just have to jump up and turn off music and sound that makes me feel icky. While I love old rock sometimes, I much prefer modern electronic progessive tonal music now - pure sounds that gently engage the mind with simple, repetitive musical themes that move me forward. They are generally geared to heart rate and activate specific brain waves (like brain entrainment strives to do). A few weeks ago I recorded a 70 minute tune set of Ben Bohmer's works and liked it so much I recorded another 90 minute set. His works are energizing but mellow and seem to have the right balance for me. I have pleasantly flowed right along all morning and into the afternoon listening to Ben Bohmer while doing chores, paperwork, taking photos, interacting with clients, etc. My cats, kittens, and even the dog who can be picky about music like Ben Bohmer and get happily energized. I've shared Ben's works with others of all ages and all like his music, too. If you explore you might find musical offerings that do it for you. Happy listening! (I can't sing right to save my life and my animals look at me like I'm crazy if I do break out into song)
  6. @ pistol & cmep37 Consistent with an increased activity of the sympathetic nervous system, a decreased activity of the parasympathetic nervous system can occur during the course of chronic inflammatory systemic diseases such as IBD. The sympathetic nervous system and the parasympathetic nervous system are often working in opposite directions. In chronic inflammatory systemic diseases, the sympathetic nervous system is switched on at the expense of the parasympathetic nervous system, which is linked to reduced gastrointestinal activity, decreased nutrient uptake, diminished glucose uptake into the liver, and a more proinflammatory situation due to the loss of the cholinergic anti-inflammatory influence. Ch. 5 - Origin of Typical Disease Sequelae, Rainer H. Straub, In: The Origin of Chronic Inflammatory Systemic Diseases and their Sequelae, pp. 173-235, 2015 In POTS patients, Pyridostigmine has been shown to reduce tachycardia (a higher than usual heart rate) and produce short-term improvement in symptoms. Cholinergic side effects are common (severe cramps, diarrhea, nausea, vomiting, increased salivation, and miosis) and may be dose-limiting. Unfortunately, these significant gastrointestinal side effects limit the efficacy of this medication in about 20% of POTS patients (Toal et al). Serotonin and its big influence on digestive health is often overlooked. Enterochromaffin cells in the intestines and colon synthesize 95% of the body’s serotonin and release serotonin in response to mechanical or chemical stimulation where it effects of gut motility, secretion, and visceral sensation. Abnormal regulation of serotonin occurs in gastrointestinal disorders such as inflammatory bowel disease (IBD), irritable bowel syndrome (IBS), diarrhea associated with bacterial toxin induced enterocolitis, and has possible associations with celiac disease, diverticular disease and colorectal cancer where serotonin may represent a key player in the pathogenesis of intestinal inflammation due to abnormal serotonin signaling. Upregulation of mucosal serotonin has been hypothesized to underlie the development of postinfectious bowel disorders where inflammation-induced upregulation of serontin signaling persists after inflammation has decreased. In these cases, microbe to enterochromaffin cell signaling may result in persistent symptoms of bowel dysfunction in humans, such as in post infectious irritable bowel syndrome (IBS). Serotonin is not directly connected to CNS activity since it cannot cross the blood brain barrier. However, serotonin released from enterochromaffin cells can potentially participate in brain-gut communication by modulating vagal afferent activity and inflammatory responses in the gut. Mechanosensory Signaling in Enterochromaffin Cells and 5-HT Release: Potential Implications for Gut Inflammation, Andromeda Linan-Rico et al, Front. Neurosci., 2016 https://www.frontiersin.org/articles/10.3389/fnins.2016.00564/full The Microbiome, Michela Bistoletti et al, In: Progress in Molecular Biology and Translational Science, 2020 https://www.sciencedirect.com/topics/neuroscience/enterochromaffin-cell
  7. For Mike: Activation of the sympathetic nervous system (“fight or flight“) increases the neurotransmitters epinephrine (adrenaline) and norepinephrine (noradrenaline), and the hormone cortisol. Epinephrine increases heart rate and metabolism. Norepinephrine constricts blood vessels, increasing blood pressure. Cortisol increases glucose in the blood and suppresses the digestive system. In general, the sympathetic nervous system inhibits salivation and the activities of the stomach, intestines, and gallbladder, plus it relaxes the bladder. The sympathetic nervous system is also an important regulator of the circulation. Its activity is increased in hypertension and heart failure. Dysregulation of the cardiovascular system by the autonomic nervous system with enhanced activity of the sympathetic nervous system and reduced parasympathetic nervous system tone is among the characteristic symptoms of hypertension and cardiac failure. The parasympathetic nervous system (“rest and digest” and “feed and breed”) stimulates salivation, and the activities of the stomach, intestines, and gallbladder, and contracts the bladder and thus has important positive influences on digestion and defecation. When the parasympathetic nervous system is activated, it slows our heart and breathing rates, lowers blood pressure, promotes digestion, contracts smooth muscles, dilates blood vessels, and increases bodily secretions. Acetylcholine is the principal neurotransmitter of the parasympathetic nervous system. The balance between sympathetic and parasympathetic activity determines heart rate. Sympathetic control to the heart is via T1–T4 nerve roots, while parasympathetic control is via the vagal nerve. Sympathetic activity increases and parasympathetic activity decreases heart rate. Without input from either source, in normal people the heart will beat at approximately 70–80 beats per minute. This is due to the intrinsic firing rate of the sinoatrial node in the heart. Pyridostigmine is a medication used to improve muscle strength in people with myasthenia gravis by indirectly increasing the concentration of acetylcholine at the neuromuscular junction and promoting increased cholinergic nicotinic receptor activation. This results in increased cardiovagal tone, helping to reduce heart rate. One common side effect of using Pyridostigmine is diarrhea. In patients with orthostatic hypotension, pyridostigmine has improved orthostatic tolerance and blood pressure. The mechanism of action is believed to be the augmentation of autonomic ganglionic transmission. Theoretically, pyridostigmine has a lower risk of supine hypertension than sympathomimetic or volume-expanding agents by potentiating ganglionic transmission selectively during orthostatic stress. Pyridostigmine has no unwanted CNS effects; its quaternary ammonium molecular structure prevents it from readily crossing the blood brain barrier, relegating its effects on acetylcholinesterase to outside the central nervous system. Amlodipine (a dihydropyridine) acts by blocking the influx of calcium ions into vascular smooth muscle and cardiac muscle cells during membrane depolarization. This action causes relaxation of vascular and arterial smooth muscle cells, resulting in arterial vasodilation and a decrease in cardiac work and oxygen consumption. Thus, its action does not involve the CNS in most cases. Some mention has been made that calcium channel blockers may cause constipation. There have been some reports that in people with hypertension treated with long-acting dihydropyridines and presumably little activation of the arterial baroreflex, sympathetic activity (as assessed by plasma norepinephrine) was reduced. However, other studies reported increases in CNS activity (as assessed by plasma norepinephrine or microneurography). Still other studies that looked at muscle sympathetic nerve activity (MSA) by microneurography found that Amlodipine does not change MSA. The best review and advice about taking Amlodipine in spite of a possible marginal increases/decreases in CNS activity is found in the first reference (Toal et al) below. All of the above is very simplistic in explanation. In reality, all our systems experience many other influencing factors, both internal and external, as well as enjoying cross-linkage with one another. Side effects of medications may also come into play and in your case may be balancing one another out (Amlodipine-Pyridostigmine) or not. Finding things that work for you and your case is as you are experiencing – a try and see approach, as pistol has reminded us. You can increase acetylcholine through diet and herbs but most folks prefer to just take a pill. A simple way to stimulate parasympathetic activation (known as the relaxation response) is to do some slow, deep breathing (10 or 20 deep sighs a day). This stimulates the vagus nerve, and the vagus nerve is one of the main stimulators of this relaxation response. Alternately, try to exercise – in normal people regular physical activity is followed by post-exercise parasympathetic activation, which, if achieved, will become more robust and efficient as time passes, improving autonomic tone. I have trouble relaxing after exercise or stimulating activities due to dysautonomia, so exercise, for me right now is a mixed bag – part good but with a lot of physical stir and often lots of pain. For greater parasympathetic activity I rely on my favorite herbs to bring me down. Another easy way to trigger the relaxation response (parasympathetic activation) is to listen to music (or play music or sing) and arouse a sympathetic response which is followed by an increase in parasympathetic activity after the music stops. Stress and pharmaceutical-induced sympathetic excitation do not count – they do not lead to substantial increases in parasympathetic activity after sympathetic arousal. I feel for you, Mike, as I struggle to understand my own unrelated dysautonomia deal. Chin up! Long-acting dihydropyridine calcium-channel blockers and sympathetic nervous system activity in hypertension: A literature review comparing amlodipine and nifedipine GITS, Corey B. Toal, Peter A. Meredith & Henry L. Elliott, Blood Pressure, Vol. 21, Issue sup1, pp. 3-10; 2012 https://www.tandfonline.com/doi/full/10.3109/08037051.2012.690615 Sinus Tachycardias: Inappropriate Sinus Tachycardia and Postural Tachycardia Syndrome, B.H. Shaw et al, In: Encyclopedia of Cardiovascular Research and Medicine, Ramachandran S. Vasan and Douglas B. Sawyer (Editors); Elsevier Inc.; 2018 Difference Between Sympathetic And Parasympathetic, BYJU’S internet, 2021 https://byjus.com/biology/difference-between-sympathetic-and-parasympathetic/ Dysregulation of the Renin-Angiotensin System and the Vasopressinergic System Interactions in Cardiovascular Disorders, Ewa Szczepanska-Sadowska, Katarzyna Czarzasta & Agnieszka Cudnoch-Jedrzejewska, Current Hypertension Reports, Vol. 20, Article number:19; 2018 https://link.springer.com/article/10.1007/s11906-018-0823-9 Pyridostigmine, Tim Anderson, Carey N. Pope, In: Reference Module in Biomedical Sciences, Elsevier; 2017 Cardiovascular fitness training, Lisa Harvey B, AppSc, GradDipAppSc(ExSpSc), MAppSc, PhD, In: Management of Spinal Cord Injuries, 2008 Calcium channel blockers, Mayo Clinic: https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/in-depth/calcium-channel-blockers/art-20047605 Effects of Chronic Calcium Channel Blockade on Sympathetic Nerve Activity in Hypertension, Christian Binggeli, Roberto Corti, Isabella Sudano, Thomas F. Luscher, and Georg Noll, Hypertension, Vol. 39, No. 4, pp. 892–896; 2002 https://www.ahajournals.org/doi/full/10.1161/01.HYP.0000013264.41234.24 Mechanisms of Music Impact: Autonomic Tone and the Physical Activity Roadmap to Advancing Understanding and Evidence-Based Policy, J. Matt McCrary, and Eckart Altenmüller, Frontiers in Psychology, Vol. 12; 2021 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8429896/ David Rakel, M.D., University of Wisconsin, December 23, 2008, ABC News: https://abcnews.go.com/Health/AlternativeMedicine/relaxation-response-ease-stress/story?id=9411762
  8. CallieAndToby22 wrote: "It seems quite torturous to travel to UAB just for the small fiber testing, can't somebody locally do it?" It seems torturous sometimes to me just to go grocery shopping (which I absolutely must do today), much less travel to Dallas for further testing at UTSW, so I know where you're coming from. I have an upcoming PCP appointment in 10 days during which I will ask about getting a skin biopsy done in my town. I have a medical coordinator contact at one of our local hospitals who might be able to help. How hard could this be? Results could be sent to the neurologists. I had Lyme disease for 16 1/2 years and it almost killed me. There is a condition called post-treatment Lyme disease syndrome (PTLDS)* that is defined by fatigue, cognitive complaints and widespread pain following the treatment of Lyme disease. It is associated with small fiber neuropathy (SFN) manifesting as autonomic and sensory dysfunction. I’d be interested in learning the state of my small fibers. Like you, I need some answers to help better manage my current situation. I have had autonomic testing done at UTSW-Dallas which showed abnormalities. For me there is also postherpes simplex type 1 neuralgia – feels like all my nerves have been gone over with a cheese-grater every time I have a breakthrough fever blister (like now). Also some neurologists have suggested a possible diagnosis of Myasthenia gravis (MG) but AChR antibody tests have been negative. However, none have ordered an anti-MuSK antibody test, the other version of MG which is more consistent with my symptoms and history, especially since I have lab test confirmed striational antibodies. I want this test ordered, or can have it done myself. MY endocrinologist wants me to see a cardiologist but the last time I went that way nothing was done except to suggest I drink more fluids and stay with increased dietary salt (heart was apparently fine then, as per echo and other tests). So, I know how frustrating and scary life must be for you. Maybe we can both learn some things to share. *Association of small fiber neuropathy and post treatment Lyme disease syndrome, Peter Novak, Donna Felsenstein, Charlotte Mao, Nadlyne R Octavien, Nevena Zubcevik, PLoS One, Vol. 14; 2019 https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0212222
  9. @MikeO Not going there, Mike. I have trouble keeping all this up, down, and all around straight in my head for my own case. I have a touch of faulty proprioception, which seems to extend into the mental realm sometimes. Thank goodness we are getting cooler now in Texas; I rejoice to have lived through another summer. Happy Halloween everybody!
  10. CallieAndToby22 - sorry you’re still miserably suffering. Has anyone tested you for Small Fiber Neuropathy (SFN)? It can be cause by cancer and the neurotoxic effects of some cancer medications. It can cause all these symptoms you are having. Skin biopsies for assessment of epidermal nerve fiber density (ENFD), sweat gland nerve fiber density (SGNFD) and functional autonomic testing (deep breathing, Valsalva maneuver and tilt test) can assess SFN, as well as the severity of the associated dysautonomia and cerebral blood flow abnormalities. Heart rate, end tidal CO2, blood pressure, and cerebral blood flow velocity (CBFv) from middle cerebral artery using transcranial Doppler can also be tested. If SFN is what you have, treatment options are good and bring good results. You should follow through with the upcoming appt. at UAB even if you are half dead and ask about SFN. You could write your questions out beforehand and hand them over if you are in a bad way during your appt. It is often useful if docs get to see you at your worst. Then again, sometimes not. Tinnitus, for me, was horrible the first year after HSV-1 encephalitis back in 2012 and added to my feelings of craziness. It has lessened but is still there - I just don’t pay attention to it now. It, at least, won’t kill you and seems to crop up here and there with lots of ailments and health conditions. Pistol – so sorry you are back in the hospital. Hope they fix you up soon! Both you gals hang in there! Let us know how you are doing.
  11. Pistol wrote: “So sad that IV fluids are still not a known go-to fix for acute flares. A port is not needed unless they are given weekly or daily, so everyone should just be able to walk into a clinic or ER, mention POTS and get a bag.” From what I understand, there are a number of hemodynamic parameters that should be considered in the treatment of POTS patients, blood viscosity being just one of them. Within the POTS crowd, everyone is still unique and the handling of their cases needs to reflect this, IMO. It’s good that IV fluids work for you now but they may not be the right or complete treatment for others at this time in their lives and might explain why you can’t just present with POTS at a clinic or ER and ask for a saline IV. From what I know, one of the goals of keeping the circulatory system in equilibrium is to prevent ischemia and the resultant reduction of oxygen supply to tissues. This is important to all of us whether we have POTS or not. Learning some of the basics about hemodynamic stability helps me make sure I am not inadvertently harming myself with my personal coping tricks but instead doing all I can to self-nurture correctly. This often cite article helps explain some of the basics of hemodynamic stability with charts and graphs (you can skip the tech parts and still get a good grasp of the interplay between different parameters, to which these finding about barometric pressure can be added): Blood viscosity and blood pressure: role of temperature and hyperglycemia, Yildirim Çinar, A. Mete Şenyol, Kamber Duman, American Journal of Hypertension, Vol. 14, Issue 5, pp. 433–438, 2001 https://academic.oup.com/ajh/article/14/5/433/205476 Pistol, this post is not a criticism – just an observation. I love your spirit of meeting your challenges head-on and your attitude helps me keep trying with my own challenges. Your post makes me feel a little better about the failure of my vigorous declaration “I am not a human barometer!” to have any effect on worsening symptoms during weather changes before resorting to my bag of tricks.
  12. While most of us might need antibiotics at some time in our lives, some antibiotics are known to cause reversible neurological issues in some people. Those of us with dysautonomia and central nervous system diseases may have a greater risk factor for encephalopathy (primarily fatigue, cognitive complaints, and brain fog, as documented for cephalosporins and penicillin) and other neurological side effects. Most often if people are going to react to antibiotics only the non-neurological, antibiotics-related complications occur (nausea, diarrhea, gastrointestinal bleeding, fever, anemia, allergic reactions and embolism). Dysautonomia is not likely to be caused by the toxic effects of antibiotics, but antibiotic use can make us feel worse during treatment. Here are two articles that address antibiotic side effects. Life is full of compromises; sometimes knowing symptoms are reversible after an antibiotic course is complete makes these experiences easier to tolerate. Neurotoxic effects associated with antibiotic use: management considerations, Marie F.Grill, Rama K. Maganti, British Journal of Clinical Pharmacology, Vol. 72, Issue 3, pp. 381-393; 2011 https://bpspubs.onlinelibrary.wiley.com/doi/10.1111/j.1365-2125.2011.03991.x Antibiotic-associated encephalopathy, Shamik Bhattacharyya, R. Ryan Darby, Pooja Raibagkar, L. Nicolas Gonzalez Castro, Aaron L. Berkowitz, Neurology, Vol. 86 (10), pp. 963-971; 2016 https://n.neurology.org/content/86/10/963.full Full text: http://prd-medweb-cdn.s3.amazonaws.com/documents/darbylab/files/Neurology-2016-Bhattacharyya-Darby_antibiotic_encephalopathy.pdf
  13. Here's an interesting article on autonomic dysfunction and concurrent cutaneous (dermatological) manifestations from folks at UTHealth McGovern Medical School at Houston, Texas. It mentions orthostatic intolerance (OI), POTS, NCS, Ehlers-Danlos syndrome (EDS), mast cell activation disorders, rheumatologic disorders, multiple system atrophy, Parkinson's disease, pure autonomic failure, multiple sclerosis, etc. Cutaneous manifestations of dysautonomia include, but are not limited to, cutaneous flushing, hypo- and hyperhidrosis (too little/too much sweating), Raynaud's phenomenon, livedo reticularis, evanescent hyperemia, pallor, urticaria, and erythromelalgia. Cutaneous manifestations of orthostatic intolerance syndromes, Caroline T. Starling, BSA, Quoc-Bao D. Nguyen, MD, Ian J. Butler, MB.BS, Mohammed T. Numan, MD, and Adelaide A. Hebert, MD, Int J Womens Dermatol., Vol. 7(4), pp. 471–477; 2021 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8484984/
  14. jillmae wrote: "I'm losing my mind. How do you go weeks on end without sleeping well?" I like sleep and have found things that help me sleep, most of which everyone could do or take safely regardless of their issues and current meds. My body errs on the side of cold most of the time now (I don't sweat much anymore) although lately things have gotten better. For sleeping I like comfortable light cotton sweat pants, a cotton T-shirt, a chamois or other cotton flannel overshirt, and a simple cotton blanket (cotton fabric is breathable and transmits moisture away from the body while being absorbent enough to remove prickly sweat from the skin without feeling damp itself). I adjust the house thermostat until I am comfortable, keeping it within a 74-77F (23-25C) range. If I get too warm it is easy to remove the overshirt, toss back the blanket, and adjust the thermostat (fans, wind, wind noise, and things touching or pressing against my body are totally irritating except for a purring kitty tucked under my neck, close to my heart). A light snack with a short glass of milk is most often a must and can be sweet/high carb, salty, or high protein/low sugar or a combination. For some of you, a snack before night resting may not work. Depending on one's issues, it might be necessary to experiment with eating (and what you're eating) vs. not eating before sleeping. Fasting suppresses the sympathetic nervous system, and this conserves calories by diminishing metabolism and heat production. Eating stimulates the sympathetic nervous system - norepinephrine and epinephrine are selectively influenced in response to eating. During eating, stimulation of sympathetic activity expends calories by accelerating metabolism and producing heat. Ingestion of glucose or fat only minimally increases the metabolic rate. However, protein stimulates oxidative metabolism, typically increasing the metabolic rate approximately 20%. Eating and increased sympathetic activity may account for the increased incidences of uncomfortable sweating, hypertension, coronary syndromes, and arrhythmias in some people. For me, running cold and tending toward hypotension, fasting at night with its withdrawal of sympathetic activity to the kidney and in general, increases my risk for hypotension. Not eating for long hours also makes my body work harder to supply glucose sufficient for the requirements of the brain and nervous system which use glucose as a major source of fuel. Fasting tends to flip my body to gluconeogenesis and protein catabolism in muscle, something that isn't good for my body. I like to take ashwagandha (660 mg pressed root herb powder) with slippery elm herb (400 mg, for digestive health) before time to sleep, sometimes with chamomile tea (it’s almost as good as a Xanax). If daytime activities have really overdone me, I'll take a passion flower (passiflora incanata, 350 mg) herb capsule, too. If spasticity is an issue as it often is for me, I'll add a touch of cannabinoids (THC/CBD). Mental preparation before retiring is extremely helpful (objective review of the day, gratitude list, prayers, meditation, dispensing with unjustified self-condemnation or undue fault-finding, reading, whatever) and to this routine I make sure to brush my teeth and wash up before lying down since 'arctic fresh' toothpaste and brushing can wake me right up with their sensory stimulation. This personal program has added several hours of nice sleep time to my nights with no side effects (it seems like a lot all written out, but is really not in life practice). If I get up to pee or get awakened, I can go right back to sleep which wasn’t always the case before these GABA-enhancing, calming herbs. I always keep a book novel handy for those times when my mind is too fretful - reading is a great, quiet distraction and sanity-saver. My eyes are usually peacefully closing before I've read too many pages... Sleep well!
  15. Psychological stress can contribute to the development or exacerbation of low-grade fevers in some people through activation of the sympathetic nervous system which is known to increase core body temperature by increasing thermogenesis. Plasma levels of noradrenaline and adrenaline increase during times of stress. Heat loss decreases due to peripheral vasoconstriction. This thorough study (below) of a woman with CFS demonstrated that her low grade fevers were stress induced: Psychological stress contributed to the development of low-grade fever in a patient with chronic fatigue syndrome: a case report, Takakazu Oka, Yoshio Kanemitsu, Nobuyuki Sudo, Haruo Hayashi & Kae Oka, BioPsychoSocial Medicine, Vol. 7, Article number: 7; 2013 https://bpsmedicine.biomedcentral.com/articles/10.1186/1751-0759-7-7 This head-busting article demonstrates just how complicated the subject of fevers can be: Central mediators involved in the febrile response: effects of antipyretic drugs, Aleksander R Zampronio,Denis M Soares, and Glória E P Souza, Temperature (Austin), Vol. 2(4), pp.506–521: 2015 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4843933/ And just so we all know – humans have changed over the 150 years since the average normal body temperature of 98.6° F (37° C) was established. Recent studies indicate that 98.2° F (36.8°C) is a more accurate average, and in older individuals it may be about 1° F lower. One small study even suggested that in healthy older patients, body temperature ranged from 94° F to 99.6° F, with an average of 97.7° F. “When is body temperature too low?”, Harvard Health Publishing, January 29, 2020 https://www.health.harvard.edu/staying-healthy/when-is-body-temperature-too-low When I was younger, I always seemed to run a low-grade, unexplained fever and then later, too, with Lyme disease. My youth was filled with tons of stress and Lyme disease was awful. After encephalitis in 2012, I stopped sweating entirely for about two years and now sweat some. Before beginning ashwagandha herb in 2017 body temp ran about 99.7° F post-encephalitis, but now stays around 97.5-98.6° F whether I feel “normal” or cold. I did recently lower the dose of ashwagandha (I lost weight) and have stopped feeling freezing all the time. In the summer I did get occasional increased body temperature if outside too long in the heat due to my anhidrosis. I rarely ever take my temperature anymore and don’t worry about it. Autonomic dysfunctions, including autonomic neuropathies and ganglionopathies, can impair thermoregulatory pathways and added stresses can compound the problem. I always feel better if I keep personal stress at low levels whenever possible, but sometimes negative experiences linger in mind or pop back up when you least expect the memories, or, darn it, a totally new, stressful issue crops up. You have been greatly stressed by Covid and then the issue with legs, so hopefully your entire system will settle down as you get further past these unpleasant experiences.
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