delphicdragon

I was able to get the article. This is a long post as I've copied and pasted the article here as I have no idea how to link to it, especially since it's behind a firewall. I also don't have the graphs here. If you want a copy please PM me. Sara Orthostatic and non-orthostatic headache in postural tachycardia syndrome Ramesh K Khurana and Lindsay Eisenberg Introduction Post?lumbar puncture headache that develops in the upright position and improves when the patient is recumbent is a familiar entity (1). Orthostatic headaches brought on by other causes, such as tumors of the central nervous system, are considered rare (2,3). Recently, spontaneous intracranial hypotension, with or without cerebrospinal fluid (CSF) leak, has been increasingly recognized as a cause of orthostatic headache. (1). The headache occurs or worsens within 15 minutes after sitting or standing. In some patients this lag period may extend to several hours. The headache then disappears or improves within 15 to 30 minutes after lying down. Orthostatic headache also occurs as a manifestation of autonomic dysfunction (4). Orthostatic headache in patients with orthostatic hypotension affects occipital, nape of neck and shoulder regions, coinciding with the fall in blood pressure (4). Orthostatic headache is a known clinical manifestation of autonomic dysreflexia. A spinal lesion at or above the T5 level disconnects the caudal spinal region from supraspinal control. Over the ensuing weeks or months, the visceral or somatic, noxious or innocuous stimulation below the lesion produces pulsating headache, flushing, hypertension and hyperhidrosis (5). In 2003, Mokri and Low reported four patients with orthostatic headache who failed to show a CSF leak. Three had been treated with a lumbar epidural blood patch without relief. Rather than low CSF pressure, a standard battery of autonomic function tests revealed postural orthostatic tachycardia syndrome (POTS). The authors noted that orthostatic headache may occasionally be a presenting manifestation of POTS (6). However, the relationship between POTS and orthostatic headache has not been fully investigated. POTS affects an estimated 500,000 Americans between the ages of 14 and 45 years, with a 5 : 1 ratio of females to males. It can be a disabling disorder (7?9). This autonomic disorder is characterized by orthostatic dizziness and other symptoms mimicking panic disorder including palpitations, presyncope, breathing difficulty, fatigue, chest pain and tremulousness.An orthostatic heart rate (HR) increase exceeding 30 beats per minute (bpm) over the supine baseline or over 120 bpm without orthostatic hypotension is a diagnostic criterion for this disorder. Patients may demonstrate an orthostatic rise in blood pressure and exaggerated increase in norepinephrine levels. It is commonly associated with orthostatic purplish acral discoloration. A retrospective review of 50 POTS patients revealed a history of orthostatic headache during daily activities in 22% and during head-up tilt (HUT) in 18% (10). The objectives of the current study were to prospectively study the spectrum of headache in POTS patients and to examine the relationship of orthostatic headache to several cardiovascular variables that could contribute to orthostatic headache. Patients and methods Institutional review board approval was obtained. Twenty-four consecutive patients with orthostatic symptoms of dizziness, palpitations, nausea, excessive or reduced sweating and difficulty breathing were prospectively studied. All 24 patients referred to the senior author (RKK) had a detailed clinical evaluation, including elaboration of the chief complaint and various somatic neurologic symptoms affecting cranial nerves, the motor system, the sensory system, as well as cerebellar and higher cortical functions. A detailed questionnaire was used to assess autonomic symptoms in several domains. Informed consent was obtained. A standard battery of autonomic tests was done to document the diagnosis of POTS (11). Patients were monitored for HR by a beat-to-beat HR monitor and for blood pressure by a plethysmographic device fastned around the left middle finger (Finapres, Ohmeda 2300). The HR response to deep breathing (HRDB) and Valsalva ratio (VR) were used to assess cardiovagal function. Blood pressure responses to the Valsalva maneuver and head-up tilt HUT were used to evaluate sympathetic adrenergic function. Thermoregulatory sweat test was employed to assess sympathetic cholinergic function. The patients were off all medications for five days. They were studied in headache-free phase. They were instructed to avoid alcohol, caffeine and nicotine overnight and to arrive at the laboratory after a light breakfast. Procedures Heart rate response to deep breathing All patients were verbally instructed to breathe evenly and deeply at a rate of six breaths per minute, five seconds in and five seconds out. The difference between the maximum and minimum HR during each respiratory cycle was determined. The mean of differences during six consecutive breathing cycles provided HRDB. The normal value in our laboratory is 25.632.3 standard error (SE) (age 23?49 years) (11). Valsalva maneuver The patient, in a semi-recumbent position, started forced expiration from the normal inspiratory position and maintained expiratory pressure of 40mmHg for 10 seconds. A mouthpiece attached by connective tubing to a mercury manometer quantified expiratory pressure. Care was taken to ensure that pressure rose sharply at the onset and fell abruptly at the termination of expiratory strain. The VR, an index of cardiovagal baroreflex activity, was calculated from the ratio of maximal to minimal HR. The test was repeated three times, and the highest VR was selected. The normal value in our laboratory is 1.750.03 (12). Head-up tilt test The patient was strapped across the knees, thighs and chest. Baseline blood pressure and HR were recorded for five minutes. The patient was tilted to 90 for 10 minutes. The patient was asked to enumerate symptoms as they occurred. Blood pressure and HR were recorded continuously during 10 minutes of tilt and for three minutes after the table was returned to the horizontal position. The normal value for HR increase under these conditions in our laboratory is 18.82.3 bpm (13). Thermoregulatory sweat test The patient, in supine position and unclothed, was exposed to a heated environment (45?50C) at 35%?40% humidity in a sweat chamber. Iodine and starch combination was employed as a color indicator. The test was continued until generalized sweating occurred or a rise in oral temperature of >1C above baseline was observed (11). Autonomic laboratory data obtained from each patient was compared with historic controls from our laboratory. If patients met the defined criteria of POTS, laboratory tests were performed to evaluate its possible etiology. All patients were asked about orthostatic and nonorthostatic headache. The headache-related questions were based on the classification criteria of the International Headache Society (14). Questions were asked about frequency, duration, severity, location, character, aggravating factors, relieving factors and associated symptoms. The patients were asked whether headache began before or after the onset of POTS symptoms. Occurrence of orthostatic headache prompted questions about the duration of upright position needed to precipitate headache, the influence on daily activities and the effect of recumbency. The patients were specifically asked about the occurrence of headache at one, three, five, seven and 10 minutes during HUT. If the patient developed headache during the HUT test, details of headache symptoms were recorded during and after tilt, including severity, character, location and accompanying symptoms. The patients were asked if their headache was relieved when the table was returned to the horizontal position. At the follow-up visit, the patients were asked to supplement information about orthostatic and non-orthostatic headache, if necessary. Autonomic and headache data were tabulated and analyzed by descriptive statistics. An unpaired twotailed t-test was used to compare patients with HUT-induced headache (HUTHA?) to those without HUT-induced headache (HUTHA) for average age and several cardiovascular variables, including baseline HR, changes in HR, pulse pressure, baseline systolic blood pressure, baseline diastolic blood pressure, maximum diastolic blood pressure during HUT, HRDB and VR. The number of HUTHA? patients under and above the age of 30 years were compared using the Chi-square test. Results The patients included 19 women and 5 men, age range 17?47 (33.42.08 meanSE) years. Their presenting complaints in decreasing order of frequency were orthostatic dizziness, fatigue, palpitations, headache, nausea, abnormal sweating, shortness of breath and blurred vision. The duration of symptoms varied from three months to 29 years, with an average of 7.9 years, exceeding six months in all but one patient. All 24 patients had a normal somatic neurologic examination. The data on MRI were available on 16 patients; 15 were normal, and one had a small non-secreting pituitary adenoma. Laboratory tests including complete blood count, sedimentation rate, antinuclear antibody, serum electrolytes, blood glucose, rapid plasma reagin, urine porphyrin and tests of thyroid and adrenal gland function revealed no significant abnormalities. Serum protein immunoelectrophoresis, heavy metal screen and paraneoplastic profile, including ganglionic acetylcholine receptor antibodies, were also normal. The results of various autonomic function tests confirmed the diagnosis of POTS (Table 1). The HUT test was abnormal in all patients, as expected. All 24 patients had orthostatic HR increase exceeding 30 bpm above the supine baseline or over 120 bpm along with symptoms of orthostatic intolerance. HRDB and VR, both indices of cardiovagal activity, did not show evidence of vagal neuropathy. Systolic blood pressure overshoot during the fourth phase of the Valsalva maneuver was exaggerated, indicating sympathetic overactivity. The thermoregulatory test was performed in 21 patients. Six patients demonstrated distal anhidrosis suggesting neuropathic pattern. One patient had hyperhidrosis (8). Three patients had orthostatic headache as the chief presenting complaint. One of them, a chef, could not perform her professional activities. Of the 24 patients, 14 (58.3%) reported orthostatic headache during daily activities (Figure 1). Orthostatic headache occurred usually within the initial 10 minutes of being upright, although two patients reported headache occurrence after being upright for up to two hours. Headache was mostly frontal or holocranial in location, pressure or throbbing in character and moderate to severe in intensity. Frequent accompaniments were photophobia, phonophobia and nausea. In 10 patients, headache subsided within 2 to 15 minutes of being recumbent. In four patients, relief from headache did not occur until 24 hours after onset. Clinical features were consistent with migraine without aura in four patients. Shorter duration, absence of accompanying symptoms or both excluded other ten patients from current IHS criteria for migraine. Orthostatic headache induced by HUT in the laboratory was reported by 15 (62.5%) of the 24 patients (Figure 1). Orthostatic dizziness was reported by 75% of patients, followed by paresthesias (50%), palpitations (37.5%) and difficulty breathing (33.3%). Twelve of the 15 patients were younger than 30 years of age. Three of three patients younger than 20 years and eight of nine patients aged 20 to 29 years developed headache during HUT. Only four of 12 patients age30 years had HUT headache (Figure 2). Headache was mostly frontal or fronto-temporal in location and pressure type in character. Photophobia accompanied headache in five patients, and three complained of nausea. Eight had no accompanying symptoms. Five patients had mild headache, and 10 patients had moderate to severe headache. Only two patients developed headache within two minutes of HUT, but the number of patients developing headache increased gradually to 15 of 24 as the tilt duration increased (Figure 3). The duration of tilt was limited to 10 minutes per the protocol. Upon return to the horizontal position, four patients reported headache improvement within 10 to 15 minutes, nine improved in one to four hours, and two patients took up to two days to improve. There was no correlation between severity and duration of headache. Based on current IHS criteria, only two of 15 patients developed migraine without aura. Nine patients developed migrainous symptoms but did not fit the criteria for migraine or probable migraine due either to shorter duration or absence of accompanying symptoms. Four patients reported mild frontal or occipital headache lasting a few minutes. None of the 24 patients developed aura in response to orthostatic challenge. HUT failed to precipitate headache in two patients who complained of orthostatic headache, and a few patients with HUT-induced headache did not complain of orthostatic headache during daily activities. Of 24 patients, 23 (95.8%) had non-orthostatic headache (Figure 1). Headache preceded the onset of POTS in 10 patients, and only four had been diagnosed with migraine. Imitrex improved headache in one patient, had no benefit in two patients and worsened headache in one patient. Seven patients developed headache concomitantly with onset of POTS. In six patients, headache began after the onset of POTS. Precipitating factors of headache included change in barometric pressure, fatigue, odors, sounds and menstruation. One patient reported visual aura. The headache was of variable frequency and of moderate to severe intensity. Unilateral and retro-orbital locations were common but temporal, occipital and holocranial locations were also reported. Nausea (65%) and photophobia (60%) were frequent accompaniments, followed by sonophobia and vomiting. Headache was aggravated by standing in 56% of patients. For example, six of 10 patients in whom headache preceded POTS reported aggravation of headache upon standing and marked improvement when supine. One had migraine with aura, 19 had migraine without aura and three had probable migraine (14,15). One patient did not have a history of nonorthostatic headache. Statistical analysis (Table 2) revealed no significant differences between HUTHA- and HUTHA? patients in baseline HR, change in HR, pulse pressure, baseline systolic blood pressure, baseline diastolic blood pressure, maximum diastolic blood pressure, VR and HRDB. The average age of the HUTHA group was 37.0 ?/ 2.5 years (mean ?/ SE), significantly higher than in the HUTHA? group (26.4 ?/ 2.5 years, p?.01). Of the HUTHA? patients, 73% were under 30 years of age, compared with 11% of HUTHA patients (p?.003). Discussion Orthostatic headache was reported by two-thirds of the 24 patients in the current study, and three patients had it as a presenting complaint. Younger age (under 30 years) and increasing duration of upright posture were predictive of increased incidence of orthostatic headache. Orthostatic headache had a ??migrainous?? character, but duration was usually short. In 1999, Jacob and colleagues observed orthostatic headache in 45% of POTS patients (16). Our findings indicate that orthostatic headache is frequently associated with POTS and that recording of HR and blood pressure in the supine and standing positions may help avoid unnecessary invasive studies to exclude low CSF pressure headache. Awareness of association of orthostatic headache with duration of upright posture may reduce morbidity by limiting the duration of orthostatic stress. Non-orthostatic headache, migraine without aura, occurred in almost all patients. Migraine prevalence in the U.S. population is 17.6% for women and 6% for men (17,18). A cross-sectional population based survey of 21,177 Norwegians showed lifetime prevalence of migraine of 18.5% in men and 34.1% in women (19). The present data show that incidence of migraine in POTS patients far exceeds that found in the general population and is higher than the 27.6% incidence reported previously in POTS patients (20). POTS and migraine are strongly associated. Both occur predominantly in women, with higher incidence during the productive years of life (9,21). Migraine patients display frequent autonomic manifestations including nausea, vomiting and flushing during an attack (22). Cyclical vomiting, a variant of migraine, may be accompanied by postural tachycardia syndrome (23). These findings suggest that migraine is co-morbid with POTS, and like other conditions that are comorbid with POTS, such as chronic fatigue syndrome, it adds to the disability (24,25). However, this co-morbidity, if appreciated, also provides a therapeutic opportunity in that drugs such as beta-blockers may benefit both disorders. Can orthostatic headache be differentiated from migraine aggravated by physical activity? Aggravation of migraine by physical activity, a specific diagnostic criterion of the International Headache Society classification, may occur in 90% of patients (26) and incidence may decline with advancing age (21). POTS patients also report aggravation of non-orthostatic headache with physical activity, but they may be free from headache when supine and develop headache with orthostatic challenge. The current finding of increased likelihood of orthostatic headache with longer upright posture suggests that orthostatic stimulus must reach a threshold to precipitate headache. In contrast, in migraine patients, any physical activity, including upright posture, immediately worsens the headache. The cause of orthostatic headache in POTS is not known. Impaired cerebrovascular autoregulation may explain orthostatic headache and orthostatic intolerance. However, the data on cerebral hypoperfusion in POTS are conflicting (27,28). In the present study, orthostatic headache was never preceded by aura even in a patient who had migraine with aura and orthostatic headache did not correlate with various cardiovascular variables. Migraine and POTS co-exist in a majority of patients. POTS is a heterogeneous disorder with several possible pathophysiological mechanisms, including hyperadrenergic state and beta-receptor supersensitivity (8,27). The perturbations in the dorsal raphae nucleus and locus coeruleus initiate events that generate migraine without aura through the trigeminovascular system along with altered monoaminergic modulation of pain (28). Allodynia, cephalic and extracephalic, is now a recognized manifestation of migraine with clinical and neurophysiological correlates (29,30). Intracranial hypersensitivity from migraine may predispose POTS patients to orthostatic headache. There are extensive interconnections between the nociceptive and visceral inputs at all levels of the neuraxis for the modulation of pain and autonomic output. The nucleus tractus solitarius, the locus coeruleus and the periaqueductal gray regions have been shown to be important both in pain processing and cardiovascular control. The lateral periaqueductal gray region, which receives cutaneous nociceptive inputs from the spinal and trigeminal dorsal horn, initiates ??fight or flight?? responses characterized by sympathetic activation with hypertension and tachycardia (31). Additionally, vagus nerve stimulation in awake rats has been shown to significantly reduce formalin-induced trigeminal nociception (32). It can be postulated that migraine induces central somatic and visceral sensitization in POTS patients. Convergence of inputs from the nucleus tractus solitarius, altered central monoaminergic balance and withdrawal of vagal tone with reduction of antinociceptive effect upon orthostatic challenge activates the trigeminovascular system to produce orthostatic headache. In our study, the incidence of orthostatic headache was substantially higher than previously reported (16), due possibly to specific inquiry about the symptom. The current data were collected from a small subspecialty referral sample, a fact that may have resulted in overestimation of incidence of headache in POTS. However, evidence for co-morbidity of orthostatic headache and migraine with POTS was clearly observed. In conclusion, orthostatic headache affected two thirds of POTS patients, especially those under age 30. Patients with orthostatic headache should be clinically assessed for POTS and informed of this association to reduce short-term morbidity. Migraine afflicted almost all POTS patients. This co-morbidity should be considered in management of POTS.

My three hour test was even stranger. Start --74 1 hour - 60 2 hour -84 3 hour -80 I was feeling like crap throughout the whole test. Granted it was years ago. I was told it was reactive hypoglycemia and that I would get diabetes, but I never went high. I've had readings of as low as 12 for blood glucose-- most of my low readings are in the 30s. I carry food with me at all times and eat throughout the day. I usually can't go 90 or more mins without eating / getting mean and can drop up to 4 pounds a day if I don't eat. Thoughts? Sara

Crow- the message boards are notoriously picky. Half the time I'm banned from them as well or I can't post or something strange like that. I don't think it has anything to do with you! Sometimes if you don't pay your dues on time, they block access to the boards - which I think is really dumb. I would rather get a notice in the mail saying I need to pay than have my access to the community cut off. I'll mention this to a couple people at the conference and see what we can do about that - it's awfully alienating for them to do it without warning... Maxine et al, I am on facebook too. Search for sara strecker in CT and you should find me. Sara

Thanks Sugartwin for letting me know that the ring splint people are going to be there. I seriously need to be fitted in my thumbs and first fingers (and ring fingers)!! :-) They should do toe splints too- sick and tired of my middle left toe dislocating.... Maxine- You have no idea how scared I am that I might not be able to do all that they want of me. It's one thing to plan out everything on a computer with my feet up - it's quite another to be actually up and doing things. Hopefully the kids will be nice to me. I am bringing my friend Matt with me. He's done teen programing before and doesn't have either EDS or POTS so hopefully he'll be able to take care of me AND the kids if I crash -- which I really hope doesn't happen. I'm presenting form 4 to 5 on Friday to the adults, and I definitely plan to discuss POTS in my presentation. I've made them get me a chair for my presentation in case I need it and plan to be pushing fluids, salt and Sudafed (which works for me but makes most uber tachy) to hopefully get me through the two days. I wanna try to aquatics classes offered, but think I might only try it on Saturday evening- that way all I'll need to do is get on a bus and GO HOME! Sara

I'm going as well, and speaking there too. Come see me Friday 4-5pm (Unique Perspectives in Ehlers-Danlos) I'll be staying at the same hotel too, and will be running the kids/teens program. Can't wait to see/ meet all of you!! Sara

Hey Everyone- I'm heading to the EDNF conference in July in Baltimore - and am presenting (I know, it scares me too). Wanted to know who else is going... it would be great to finally meet some of you (as there is such of an overlap with EDS and POTS). I plan to speak a little bit on POTS as well as on EDS. Look for Unique Perspectives in Ehlers-Danlos: Both a Patient and a Scientist Sara PM me if you want more info.

Get your liver function checked! Tea colored sinking pee is sometimes due to high bilirubin, which is indicative of liver problems. The drugs you're on could be causing issues with your liver. No amount of water is going to change the color of your urine if it's due to bilirubin. Sara

I yawn at the wrong time too. I'm especially bad during lectures where I really want to pay attention; I start yawning uncontrollably. I also yawn a lot if I'm concentrating hard. It's obnoxious!!! Wish I had a solution. Sometimes chewing gum helps, but not substantially. Sara

So wait, you're not supposed to have spots upon standing? I always do, esp if I get up too fast. I'll take the spots as opposed to the blackouts, but I get those most of the time too. Sara

Thanks everybody! Still feeling crappy but getting tested so hopefully I will feel better soon :-) Been off the Asthma meds and Sudafed for a while now. Only take them when my asthma acts up (aka someone around me smokes) or if I get sick. The sudafed is only if I need a LARGE energy boost as I've built up a tolerance for it. I do have low potassium (3.5). Getting it tested again today to see if it is low enough for IV supplementation. Eating potassium rich foods does NOTHING. Heart rate was 114 today, which is better but still not perfect. I also got 10 hours of sleep which helped with the muscle pain. For all the other questions, I have been tested for pheo and am completely caffeine free as caffeine tends to put me to sleep. I think I might ask the doc for some Xanax, though that isn't ideal. Got a script for a beta blocker too. I think most of this is b/c of low potassium and too much exertion. I drank a ton of water this week, went from peeing 3-5 times a day to peeing every hour. (Was told liver enzymes were elevated due to dehydration, so I tried to fix it ) I'm thinking that probably flushed out my potassium and sodium. Still thinking POTS is kidney related as much as it is cardiac and nervous system related. Sara

So I've been feeling a lot more human over the past year with the addition of Folic Acid, B12 and D. However lately I'm experiencing a lot more pain in my muscles (got a fibromyalgia diagnosis out of it) and more palpitations. All of this started after my last period (2 weeks ago). Went to the cardiologist for my 3 month followup and my heart rate is 130 laying down. Needless to say, he wasn't too pleased, so now I have a holter monitor and an echo. Grumble. Need some support here. I thought I was mostly over the POTS crises, but they seem to keep coming - especially after stress. I need to hold out for 5 more weeks before I can give in to this disease again - if I can't hold out, I lose my job. Wish me luck! Sara

Also D and B12 deficient. Been taking 5000IU of D3 per day and 1000mcg of B12 per day. Didn't notice any difference until I added Folic Acid (400mcgs a day); then I finally started noticing a difference. At this point my D and B12 are both normal and I would have to say I feel a lot better energy-wise. Not sure if it's the D or not, but the last two colds I had did not progress to bronchitis or pneumonia. :-) That's a plus. (Keeping my fingers crossed) Sara

I'm not married, but I'm going to comment on this thread anyway. I've been dating a guy for about a year - he knows about my limitations. I try my best to push through them and not complain. He knows I go to get IV saline once a week and can see how sick I get if I push myself too far. I like to go to the gym with him, but if I jog too much and start to get chest pain I get incredibly pale and more than once he has offered to take me to the hospital instead of home just because I look that bad. He understands (I think) but I try not to complain. He's seen me with multiple joints out of place and with an asthma attack. I think my attitude helps him deal with it - most of the pain I try to laugh about and I only complain if it's really bad. I know that he really cares about me and loves me but he's always known me "sick". On the other hand, my mother is the exact opposite. If I tell her I'm having a POTS attack or that I need to lie down or that I popped a joint she gets mad at me. I think the fact that I do have so many issues upsets her because she doesn't want to see her daughter in pain or not well. I think your husband may fall into that category - he loves you a lot and doesn't want to see you hurt. Mom saw me before I got bad (though I have had POTS all my life) so she's got a different perspective and it's hard for her to admit that I'm not going to go back to the way I used to be. Sara

I've had the tests come back as low morning cortisol as well (also in the 4s). Yet, it stimulates fine with ACTH. I've actually asked to be given ACTH, but sadly no doctor will prescribe that, especially as an energy booster. My last set of cortisols came back low when they were first scanned, then normal when they repeated the scan for the ACTH test. Wondering if the low cortisol is an intermittent thing. (I've had two lows and 3 normals in the past 5 years - similar trend with aldosterone) I sometimes wonder if my hormones are cycling on the wrong clock - like every week it goes back to a normal pattern, then the pattern gets off throughout the week until finally it resets itself. That would explain a lot. Sara Feel better Maxine!

I love Seltzer. And Juice. And seltzer mixed with juice. Sara

Well, Easter was just so beautiful I had to sit outside and enjoy the nice weather with my family. Sadly, the mosquitoes were enjoying the nice weather, and plethora of puddles from the recent rain. Said mosquitoes also enjoyed me, and I got 10 bites on my legs (who knew they bit through nylons...) My question is this... do you guys swell up a TON from mosquito bites? I was getting quarter to half-dollar sized welts. Happy Easter to everyone. Sara

I'd have to agree with Reen. I would love for my dysautonomia to be "fixed" by a diet change or a lifestyle change, but that isn't going to happen. All my disorders are explainable by my Ehlers-Danlos Syndrome. This is a collagen disorder - my collagen doesn't hold my joints or veins or heart or intestines OR CELLS together like it should. Therefore my blood pools in my legs when I stand up and I go into hypovolemic shock. No amount of diet/ exercise is going to change that - the veins are broken. I can rebuild collagen just fine, except the mechanism which tells it where to go and how to line up isn't there. Nature and evolution are in no way near perfect. I'm saying this as a biologist. Evolution ultimately sorts out SOME of the genetic disorders. Genetic disorders that don't affect fertility stay around because there is no mechanism to sort them out. In the old days - before civilization, I would have been sorted from the population b/c I would not be as likely to survive. This is no longer the case. My genetic disorder has a 50-50 shot of being given to my kids. My dad gave it to me. He wasn't diagnosed until I was. We need more research. The body has not been mapped out. We're still trying to figure a lot of it out. As I said before, I'm a biologist - a researcher. We are only scratching the surface of what we know. The answers are out there, but I doubt they are as simple as avoid wheat, dairy and aspartame. If it was that simple, I'd be cured. Sara

I can't drink either. One glass of wine will get me giddily drunk. I had one shot, once - the immediate illness I felt was NOT worth it. I'm about 4 years post college. I'm in grad school. Everyone here drinks too - often to excess and pretty much everyone drank in college - except me. Over the years I've learned a couple things. 1) If you can drive, you are always the designated driver. Most people are perfectly willing to accept that and won't put pressure on you to drink, especially if you drive them home at the end of the night. 2) Order a virgin drink if you are at a bar, but tell people it isn't a virgin drink. ie - order a coke, but call it a rum and coke, or orange juice and call it a screwdriver. 3) Have a table/ couch where you can sit down if you need to. I've played drinking games with coke. It works out well. Say beer is gross and play the game with your "drink". There are plenty of things you can do if you don't drink so you can still associate with the drinking crowd. I played the game throughout college and am playing it in graduate school. Those who know me, know that I don't drink. Most don't know why but are happy to have a consistent DD around. GO out. Go to Karaoke or trivia night. Don't let POTS and the inability to drink cramp your social life unless you have to. Sara

They are called Petechia. I get them too especially when there has been too much pressure on a certain area. (ie - tight jeans give me them across my thighs or a too heavy bag gives them to me on my shoulders. http://en.wikipedia.org/wiki/Petechia Sara

I've taken it without problems. I usually don't do the double dose on the first day because otherwise it comes back. Always, and I can't stress this enough - eat yogurt with it or take probiotics, because it does tend to cause diarrhea/ uncomfortable feelings in the gut. Sara

I have asthma and can't take albuterol because of the tachycardia (heart rate jumped up to 180 and stayed there last time I took it) Instead I take something called Xopenex which is "albuterol lite". It tends to cause much less tachycardia than the Albuterol - but, most hospitals don't stock it, so be aware of that because they will give you albuterol anyway. I love my Xopenex. I also take Maxair, which may or may not be off the market right now. That opens me up without making me too tachy, though it doesn't last as long as the Xopenex. http://www.xopenex.com/ http://www.maxair.com/ Sara

For me, consistently high blood pressure, and still feeling cruddy, was due to my BCP. I was on NuvaRing and getting readings of 135/85, which I was really not happy with, but most doctors were not worried about. My normal before was 110/60. I'm off the Ring now and though it took about 3-4 weeks, my BP went back down to 110/60. Though it is lower, and does drop to 80/50 around my period, I feel better off the BCP. Not sure if it applies for you, but it's a thought. Sara

I've ridden horses since I was about 12 even through college with a POTS diagnosis. It's inordinately expensive around here, which is the only mitigating factor in my not continuing. It helped strengthen my leg muscles and my balance which was great. I ride English. Even with the Ehlers-Danlos, riding was wonderful for me, though I do need a wider saddle to compensate for my sub-luxing hips. I can't wait for when I have a real job, so I can get back to it and have my own horse someday. For me, it's been a godsend. It helps me both mentally and physically, though I do need someone to help me put a saddle on a taller horse. Sara

To answer your questions - The folic acid doesn't make me nauseous, but I take it with my biggest meal of the day, so there's plenty of food in the stomach to soften the blow. I tried other Vitamin B products (B complexes) and they made me very headachy and fluish, so I figured I'd just try one at a time. I didn't notice a huge effect of the B12 by itself. My bruising started to go away, which was good, but there was almost no change with my energy levels. I needed the folic acid to feel better energy-wise. I don't know if we need a lot of the vitamins or not. I personally think I have too fast gastric emptying (I eat almost constantly), hence the need to supplement with large doses of vitamins, but this hasn't been proven (and I'm too chicken to undergo the studies). Sara

Hey Everyone- I posted here a while ago about a diagnosed B12 deficiency. Since then I've been taking 1000mcg B12 daily. I didn't notice much but recently decided, on a whim, to add Folic Acid 400mg. I talked with a friend of mine who is B12 deficient and she was also told she was folate deficient, so I figured it couldn't hurt to supplement. It's been about a month of doing both and I'm noticing that my energy is coming back (knock on wood) and a lot of the bruising I had is going away. I actually was on time for work for 4 out of 5 days this week - usually I'm late 4 of the 5 days. No side effects thus far, but I notice if I miss it for 2 days. Thought this little bit of good news might help some people out there - probably a good idea to supplement both if you are deficient in one. Sara