toddm1960

I think the exhaustion level varries depending on your underlyng cause of your dysautonomia. Mine happens to be mitochondrial disease, I'm not sure if any studies have been done to compare subgroups. For me nothing helps, I'm awake about 12 hours a day and I'm sitting, reclining or laying down 11 of those hours. The heavy arms and legs and feeling like I'm walking through water never leaves.

The salt loading issue has been a discussion point on a few post lately looking at the long term cardiac risks of it. The idea behind even people with orthostatic hypertension salt loading is because they can have thoracic hypovolemia, their blood just pools in the splanchnic region. The bottom line is, there is a blood volume shortage in the heart/chest area, and also to the brain just like people who are orthostatic hypotensive. One symptom both groups share seems to be we're all hypovolemic.

OK so I've looked back through this post and the score still seems to be people cured by exercise........ZERO. If I missed someone please stand up and let us know you're cured, because that is his statement at the end of the study. That's all I have a problem with. Anyone one of us with dysautonomia would do ANYTHING to get better, to have a doctor tell us we're not getting because we're not trying is just too much.

Firewatcher that might be a very good call on pheochromocytoma......you're one smart egg. Hey you want to take my case over

In my past life I was a personal trainer, I worked out 6 days a week when this hit me. So I'd say that exercising didn't keep it away, and I continued to try and push myself after I first was getting sick, only to feel worse and worse. I love exercising so much for the past 6 years I keep trying, holding out hope I can find my old self again. The hardest part of it all is that 6 years later I'm still at square one, i can't build on my workouts. On day one I can do 5 minutes on my schwinn Airdyne, on day two I can only do 2 and half minutes but I'm trying twice as hard. On day three I'm a car wreck and can't even get on the bike, and more of the same for day 4. I can't get back on until day 6, so I start over......you get the picture 6 years later I'm still here at square one. I'm very happy for those this helps, I just have a huge problem with studies that say they have CURED pots all you need to do is try. And if you're not cured you didn't try hard enough. I kept looking for the study to say CBT was also needed for the cure. So by his study I should be cured Not so much, but I still dream about the day I'll be able to workout and feel that rush of lifting weights till you dropped.......oh what a feeling.

I'm not so sure hypertension is rare in POTS, there's just way less research done on us with orthostatic hypertension. I think you'll find it's about 50/50 hypotension to hypertension. Many on this forum also fit into multiple categories, they have POTS along with PAF

Hi Elfie, Bone-crushing fatigue is my favorate medical term, I use it all the time..... I'm really sorry you're feeling so bad, but if you're concered your cardio is leaving you with an untreated heart problem.......call and ask him if he's now ruled out CHF. I can tell you dysautonomia can have some ups and some major downs, I hope it doesn't last long and that you feel better soon.

For starters wearing support tights will have an affect on the test results, you should also be off all drugs that slow or speed up your HR. Naomi is correct if your HR increases by 30 bpm or goes over 120 in the course of your test......it's POTS. Then it's a matter of trying to find his underlying cause. In some cases if you can find this and treat it you'll have some symptom relief, it doesn't cure it but it can sure make life a little easier. One thing in his favor is the age he came down with it, alot of research points to this age group of as having a good recovery rate. Good luck and I hope you can find somethings to make him feel better.

In the long run I do think that your underlying cause of POTS will determine which treatments work or not for you. Until a single causative thing thing is found to trigger dysautonomia (maybe XMRV) there will never be ONE treatment that works for all of us. That's why I really like Julian Stewart's research, it's the direction we need to follow. He's looking at ALL types of POTS, though I wish at times he would study older patients.

Claims like this drive me crazy........27 patients and he claims to have cured pots with exercise. We need to put his brain to work on curing cancer now.

I hope your trip goes well and you find the answers you're looking for. Keep us updated on how you're doing.

I agree 100% that this needs to be placed right along side beta blockers, helps some, makes others worse and in no way should be looked at as a cure. This is my only point.

Sorry but if this was for real do you think there would be anyone left with POTS?

Not sure what drugs you take, if any, but were you talking anything that would slow your HR before you took your TTT? Many drugs affect TTT results. I love these doctors.....if you can't stand up for 10 minutes you're very sick, if you can make it for 12 minutes nothings wrong with you?

Good inforation as long as you're orthostatic HYPOTENSIVE. You sure don't see much research on the orthostatic hypertensive group. Just as an aside, when I was first pushing to get a TTT my neuro told me you don't have POTS because you don't pass out..... I wonder if this is even being taught in medical schools yet?

I was hoping for more also, but it's a start.............

Let's see if this works: 1. Introduction In 1996, following a multi-specialty Consensus Conference sponsored by the American Academy of Neurology and the American Autonomic Society, a brief definition of orthostatic hypotension was published. This definition has been widely used and has withstood the test of time. Fifteen years later, advances in the understanding of orthostatic hypotension and disorders of orthostatic tolerance have made it necessary to clarify and expand the earlier definition. In this updated consensus statement, endorsed by the American Autonomic Society, the European Federation of Autonomic Societies, the Autonomic Research Group of the World Federation of Neurology and the Autonomic Disorders section of the American Academy of Neurology, we refine and update the definition, pathophysiology and clinical features of orthostatic hypotension. We also add the definitions of two highly prevalent disorders of orthostatic tolerance, neurally mediated (reflex) syncope and the postural tachycardia syndrome. This update is the product of a group of experts in the field but is not an evidence based clinical guideline. 2. Orthostatic hypotension 2.1. Definition Orthostatic hypotension is a sustained reduction of systolic blood pressure of at least 20 mm Hg or diastolic blood pressure of 10 mm Hg within 3 min of standing or head-up tilt to at least 60° on a tilt table. Orthostatic hypotension is a clinical sign and may be symptomatic or asymptomatic. In patients with supine hypertension, a reduction in systolic blood pressure of 30 mm Hg may be a more appropriate criterion for orthostatic hypotension because the magnitude of the orthostatic blood pressure fall is dependent on the baseline blood pressure. 2.2. Pathophysiology Immediately after standing, there is gravitationally mediated redistribution of the blood volume, and a pooling of 300 to 800 ml of blood in the lower extremities and splanchnic venous capacitance system. As a consequence, venous return to the heart falls and cardiac filling pressure is reduced. This results in diminished stroke volume and cardiac output. In response, sympathetic outflow to the heart and blood vessels increases and cardiac vagal nerve activity decreases. These autonomic adjustments increase vascular tone, heart rate and cardiac contractility, and stabilize arterial pressure. During standing, contraction of the lower body skeletal muscle prevents excessive pooling and augments venous return to the heart. Orthostatic hypotension is caused by an excessive fall of cardiac output or by defective or inadequate vasoconstrictor mechanisms. The focus of this consensus statement is neurogenic orthostatic hypotension, i.e., orthostatic hypotension due to inadequate release of norepinephrine from sympathetic vasomotor neurons leading to vasoconstrictor failure. 2.3. Epidemiology Orthostatic hypotension occurs in patients with neurodegenerative disorders such as multiple system atrophy, Parkinson's disease and pure autonomic failure and in individuals with peripheral neuropathies and ganglionopathies that affect the autonomic nerves. The prevalence of orthostatic hypotension increases with age. Orthostatic hypotension is more common in institutionalized (up to 70%) than community dwelling elderly (~ 6%). 2.4. Clinical features Characteristic symptoms include lightheadedness, dizziness, pre-syncope and syncope. Loss of consciousness is usually of gradual onset but may occur suddenly. Some patients present with more general complaints such as weakness, fatigue, cognitive slowing, leg buckling, visual blurring, headache, neck pain, orthostatic dyspnea or chest pain. 2.5. Confounding variables Several confounding variables may influence the extent of the orthostatic blood pressure fall. 2.5.1. Supine hypertension Many patients with neurogenic orthostatic hypotension have supine hypertension even before treatment of hypotension is initiated. Some of these patients have blood pressure falls on standing that fulfill criteria for orthostatic hypotension although blood pressure remains at or above normal range. The clinical significance of this phenomenon is not known. 2.5.2. Diurnal variability Orthostatic hypotension is more common and more severe in the morning. This phenomenon is most likely due to high supine nocturnal blood pressure which causes a pressure diuresis and results in intravascular volume depletion over night. Redistribution of intravascular volume also may contribute to diurnal variability. 2.5.3. Food ingestion Patients with autonomic failure and the elderly are susceptible to significant falls in blood pressure associated with meals. This is exacerbated by large meals, meals high in carbohydrate, and alcohol intake. 2.5.4. Age The orthostatic blood pressure fall increases with age in many elderly individuals. This is due to several factors including supine hypertension, age associated changes in baroreflex function, inadequate vasoconstrictor responses, reduced cardiac and vascular compliance, decreased blood volume and lesser efficiency of the skeletal muscle pump. 2.5.5. Medications Diuretics, sympatholytic agents and other vasodilators may increase the postural blood pressure fall. Such medications include blood pressure lowering medications, antidepressants (particularly tricyclic agents) and certain anti-Parkinsonian agents. 2.5.6. Other variables The orthostatic blood pressure fall is also influenced by hydration, cardiac and vascular stiffness, ambient temperature, gender, prolonged recumbency and deconditioning. 2.6. Variants 2.6.1. Initial orthostatic hypotension An exaggerated transient fall in blood pressure may occur shortly upon standing accompanied by symptoms of hypoperfusion. Initial orthostatic hypotension is defined as a transient blood pressure decrease (> 40 mm Hg systolic blood pressure and/or > 20 mm Hg diastolic blood pressure) within 15 s of standing. This blood pressure fall, which occurs in both old and young subjects, is observed with continuous beat-to-beat blood pressure monitoring. It may occur during active standing and to a lesser degree with passive tilting. This may be a common unrecognized cause of syncope. The underlying pathophysiology is thought to be a transient mismatch between cardiac output and peripheral vascular resistance that occurs with rapid postural change. 2.6.2. Delayed orthostatic hypotension Some patients present with symptomatic orthostatic hypotension that occurs beyond three minutes of standing. The clinical significance of delayed orthostatic hypotension is unknown. These delayed falls in blood pressure may be a mild or early form of sympathetic adrenergic failure. This disorder may be revealed in patients with suspected orthostatic hypotension by extending the period of orthostatic stress (head-up tilt or stand) beyond 3 min. 3. Neurally mediated (reflex) syncope 3.1. Definitions 3.1.1. Syncope and transient loss of consciousness There are several different mechanisms that result in transient loss of consciousness. Causes may be traumatic or nontraumatic; the latter include syncope, epileptic seizures, metabolic disorders, and very rarely a transient ischemic attack in the posterior circulation. The term syncope indicates a specific pathophysiology and should only be used to describe a transient loss of consciousness and postural tone resulting from global cerebral hypoperfusion with spontaneous and complete recovery and no neurological sequelae. When the cause of unconsciousness is not clear the episode should not be called syncope. 3.1.2. Neurally mediated syncope Neurally mediated (reflex) syncope, e.g., vasovagal, situational (cough, swallowing, micturition) or carotid sinus syncope refers to a heterogeneous group of conditions in which there is a relatively sudden change in autonomic nervous system activity leading to a fall in blood pressure, heart rate and cerebral perfusion. Neurally mediated syncope is best understood as a reflex with afferent, central and efferent pathways. The term ‘neurocardiogenic syncope’ is frequently used to describe reflex syncope but it should be abandoned because the origin of the reflex is rarely in the heart. 3.2. Clinical features Neurally mediated syncope is typically preceded by prodromal symptoms and signs that may occur up to 60 s prior to loss of consciousness. Prodromal features include pallor, diaphoresis, nausea, abdominal discomfort, yawning, sighing, and hyperventilation. These are followed by the features of cerebral and retinal hypoperfusion such as visual and auditory disturbances, concentration difficulties and cognitive slowing. 3.3. Pathophysiology During neurally mediated syncope, efferent sympathetic vasoconstrictor nerve activity decreases leading to a loss of vasoconstrictor tone and parasympathetic (vagal) outflow increases causing heart rate slowing. The range of bradycardia varies widely in reflex syncope, from a small reduction in peak heart rate to several seconds of asystole. The trigger for reflex syncope can be central (e.g., emotions, pain, blood phobia) or peripheral (e.g., prolonged orthostasis, increased trigeminal or carotid sinus afferent activity), but the precise afferent nerve pathways and central nervous system mechanisms involved in reflex syncope are largely unknown. In addition to reflex-mediated neural changes, other environmental or physical factors frequently contribute to lower blood pressure and diminish cerebral blood flow during reflex syncope. For example, heat exposure leading to peripheral vasodilatation may contribute to hemodynamic stress; straining with a closed glottis reduces venous return and increases intracranial pressure; and hyperventilation-induced hypocapnia reduces cerebral blood flow and induces vasodilatation in skeletal muscle. In some instances, these factors may be the main reason for the loss of consciousness. As reflex syncope requires a reversal of the normal autonomic outflow, it usually occurs in people with a functional autonomic nervous system. Reflex syncope should be distinguished from syncope due to neurogenic orthostatic hypotension in patients with chronic autonomic failure. 3.4. Epidemiology The prevalence of syncope in the general population is high. The vast majority of syncope is caused by reflex syncope. The frequency of reflex syncope increases during adolescence and in those over 55 years. Many adults with reflex syncope have had similar episodes in their youth. In the young, orthostatic and emotional vasovagal faints accompanied by characteristic prodromal symptoms are common, while in the elderly, typical prodromal symptoms are less frequent. Carotid sinus hypersensitivity, cough and defecation syncope occur almost exclusively in the elderly. 4. Postural tachycardia syndrome 4.1. Definition The postural tachycardia syndrome (POTS) is characterized by a sustained heart rate increment of ≥ 30 beats/min within 10 min of standing or head-up tilt in the absence of orthostatic hypotension. The standing heart rate for all subjects is often ≥ 120 beats/min. These criteria may not be applicable for individuals with low resting heart rates. For individuals aged 12–19 years the required increment is at least 40 beats/min. The orthostatic tachycardia may be accompanied by symptoms of cerebral hypoperfusion and autonomic overactivity that are relieved by recumbency. 4.2. Pathophysiology The etiology and pathophysiology of POTS are unknown but are likely to be heterogeneous. The syndrome is associated with deconditioning, recent viral illness, chronic fatigue syndrome and a limited or restricted autonomic neuropathy. The differential diagnosis includes conditions that cause tachycardia, such as thyrotoxicosis, inappropriate sinus tachycardia and other cardiac rhythm abnormalities, pheochromocytoma, hypoadrenalism, anxiety, dehydration, and medications (e.g., vasodilators, diuretics, and ß-agonists). 4.3. Epidemiology and clinical features The prevalence of POTS is not known. The syndrome is more common in women. The orthostatic symptoms consist of lightheadedness, visual blurring or tunnel vision, palpitations, tremulousness, and weakness (especially of the legs). Other symptoms include fatigue, exercise intolerance, hyperventilation, shortness of breath, anxiety, chest pain, nausea, acral coldness or pain, concentration difficulties and headaches. On clinical examination, in addition to the heart rate increment, pulse pressure may be reduced and acral coldness may be present. Continued standing may lead to venous prominence, cyanosis and foot swelling. A hyperadrenergic state is present in some patients who have a resting tachycardia, sweating, and tremulousness. Corresponding author at: Autonomic and Peripheral Nerve Laboratory, Department of Neurology, Beth Israel Deaconess Medical Center, 1 Deaconess Road, Boston, MA 02215, U.S.A. Tel./fax: + 1 617 632 8454. Note to users: The section "Articles in Press" contains peer reviewed accepted articles to be published in this journal. When the final article is assigned to an issue of the journal, the "Article in Press" version will be removed from this section and will appear in the associated published journal issue. The date it was first made available online will be carried over. Please be aware that although "Articles in Press" do not have all bibliographic details available yet, they can already be cited using the year of online publication and the DOI as follows: Author(s), Article Title, Journal (Year), DOI. Please consult the journal's reference style for the exact appearance of these elements, abbreviation of journal names and the use of punctuation. There are three types of "Articles in Press": Accepted manuscripts: these are articles that have been peer reviewed and accepted for publication by the Editorial Board. The articles have not yet been copy edited and/or formatted in the journal house style. Uncorrected proofs: these are copy edited and formatted articles that are not yet finalized and that will be corrected by the authors. Therefore the text could change before final publication. Corrected proofs: these are articles containing the authors' corrections and may, or may not yet have specific issue and page numbers assigned. -------------------------------------------------------------------------------- Autonomic Neuroscience Article in Press, Corrected Proof - Note to users

Sandy you're 12 years shy of a medical degree, but you're much smarter than most of the doctors out there. It's just crazy how doctors treat us when there isn't a test and a pill and don't take more than your 12 minutes in my office.

This was a hot item 3 or 4 years ago for treating CFS and fibro, I jumped right on giving it a shot. Didn't help me at all, but I know a small group of people on another forum saw some good symptom relief. Of course back then I didn't have my POTS diagnosis, but that doesn't mean that some POTS can be helped with it. I'm glad you're feeling better using it, keep us updated on how things continue for you.

Issie my BP monitor does the same thing, when my pulse pressure is too narrow it gives me an error.

Just had an ah-ha moment........all of my back pain, starting at my neck and traps, to my mid back (lower lats) and my lower back (lumbar region) really kicks in when I'm standing, muscle relaxers or massage don't seem to work all. Laying down seems to be the only thing to lessen the pain. The pain is always there just much less when I'm laying or reclined. I never connected the increased BP & HR together with the increased neck and back pain.

Diagnosed at 48, currently 50

The only research on this that I've seen is from Julian Stewart, here's the link: http://www.nymc.edu/fhp/centers/syncope/splanchnic%20pooling.htm It seems for us we have a blunting of the splanchnic vasoconstrictors when standing and even worse with the valsalva maneuver. It's good to see Vandy start to reproduce some of Dr Stewart's findings, but I still haven't seen them do the sub grouping he has. This research isn't new either, it's been out there awhile.

There was a poll awhile back on this orthostatic hyper or hypotensive, and I was surprised it was 50/50 on the forum. You hear more about and see more research on the hypotensive (or passout) group, but there are plenty of us just like you. When we stand up our BP starts going up, the longer we stand the higher it goes.....along with our HR. One thing to look for also is a narrowing pulse pressure, this is a sign of hypovolemia. In my case once I stand my pulse pressure narrows to 10-15, then my BP rises while my belly fills up. It continues this all the time I'm standing. Good with yours and I hope you feel better......

I have this exact pain, though mine can be on either side (never at the same time) After years of x-rays, MRI's seeing a cardio, a pulmonologist, and a rheumatologist, blood work and visits to the ED no one has found any problems. So if you do find some answers let us know what you find out.