SarahA33

http://www.disabilitysecrets.com/question16.html This excerpt is from Disability Secrets, written by: Melissa Linebaugh Postural Orthostatic Tachycardia Syndrome (POTS) and Social Security Disability Postural orthostatic Tachycardia Syndrome, or POTS, is a form of dysautonomia. It causes a rapid increase in heart rate when changing positions, most often when moving from a vertical to an upright position, but it can occur even when sedentary or when making less pronounced changes in position. Severely decreased blood flow to the brain is often seen in patients with POTS, and the condition can vary significantly in severity level from one patient to the next. Though some are able to continue working or otherwise leading an active life, POTS is often debilitating and can be completely incapacitating in the most severe cases. The list of symptoms that can result from POTS is extensive and a well documented case file for Social Security Disability (SSD) benefits will include as much detail of those symptoms as possible, including how they affect you on a daily basis. Medical records are an important part of any SSD application, and can make it possible to clearly match a Social Security Administration’s (SSA’s) listing for POTS or to qualify for benefits under a “medical vocational allowance” following an evaluation of your residual functional capacity (RFC). SSA Listings for POTS The SSA maintains a manual, known as the Blue Book, of potentially disabling conditions. There is no distinctive listing for POTS in the Blue Book, and therefore you cannot “meet” predefined criteria for SSD qualification with POTS. There are however, several listings in the Blue Book that your POTS application for disability benefits may “match”. When the SSA reviews your application to see if it matches a listing, your medical records and all your other documentation are evaluated to see if your condition is equally as severe as a listing that does appear in the Blue Book. Based on the kinds of symptoms you experience, the listings which may apply to your POTS application include, among others: Section 4.00 – Cardiovascular Section 5.00 – Digestive System Section 11.00 – Neurological Residual Functional Capacity and POTS If your POTS doesn’t match a listing in the SSA’s Blue Book, you may still qualify for SSD benefits under a medical vocational allowance, which simply means that while you don’t suffer from a listed condition, you are still severely disabled, unable to maintain gainful employment, and therefore eligible for disability benefits. To qualify for SSD under a medical vocational allowance, your residual functional capacity (RFC) will be evaluated by the SSA. Your medical records play a big part in determining your RFC and the more detailed those records, the easier it is to substantiate your claim. In addition to your medical records, the SSA must also look at your employment history, including your acquired job skills. Your education level and your overall employment qualifications are also evaluated. Your RFC results must show that your POTS so severely limits you that you’re unable to find and maintain gainful employment in any field of work for which you would otherwise be qualified. Medical Documentation and your SSD Application for POTS Medical evidence is a crucial aspect of the SSA finding you eligible for disability benefits, regardless of whether it’s your RFC that qualifies you or the fact that your application matches a listed condition in the Blue Book. Your records should include: Records of the formal diagnosis of the condition Diagnostic test results that show there is an organic cause of your POTS Treatment records, including all treatments attempted and their affect on your symptoms and overall condition Results of mental or psychological evaluations, if applicable Documentation of the frequency, duration and severity of syncope episodes (loss, or near loss of consciousness) Statements from your treating physician(s) documenting diagnosis, prognosis and your functional capacity Seeking Assistance with your POTS SSD Application Because there is no single, dedicated listing for POTS in the SSA’s Blue Book, and because proving disability can be challenging, particularly if your symptoms are not consistently present, you may wish to consider getting assistance from a Social Security advocate or disability attorney when filing your claim.

Hi, goodr189, This is taken from our "What to Avoid" page from the main site. "Holding the arms up in the air can cause problems for some individuals. Holding the arms up requires the heart to work harder to counteract the effects of gravity. This is especially difficult for the heart if there is already excessive venous pooling in the lower limbs. The heart may not be able to effectively pump blood up into raised arms and tachycardia will result from its effort." http://www.dinet.org/index.php/information-resources/pots-place/pots-what-to-avoid

Oh one thing I forgot.. I just had a test done (non invasive) sonogram that measures how much your bladder is emptying. It took just a few minutes. A cause of UTI's can be your bladder not emptying completely. Hope she finds relief w/ the macrobid!

Hi there, How exhausting, that poor thing! Have they done a culture to see what the bacteria is? Like - e-coli, etc.? They have been starting to test mine, then they are able to see what the bacteria is antibiotic resistant and respondent to, instead of just throwing random antibiotics at what's "usually" successful at treating UTI's. For example, this last urinary tract infection I had, would only respond to Cipro and Macrobid, but had gone to my kidney and my doctor said that Cipro is more effective for treating UTI's that are "upper" and "lower" in the urinary tract. Have they done a cystoscopy yet? I cant remember, sorry. This seems next on the agenda for me if I get another infection. Also, a prophylactic antibiotic that I am starting seems like it could provide some good results. http://emedicine.medscape.com/article/2040239-overview#a3 My temp does the same thing and I feel awful.

Hi Draven, When I was anemic, I had this symptom pretty frequently. It went away once I started receiving IV iron infusions. They also checked thyroid labs when I told them about having a metallic taste, too. You mentioned its not medication related, but do you take any supplements? certain supplements can cause it. Also, if you have sinus infections, upper resp. lingering colds, etc. those can cause that symptom also. Hope you get it figured out soon!

Hi Ancy, Will be thinking of you this weekend and Tuesday. As you can see, lots of people here pulling for you to get better! How long will you be in the hospital for? Your a really strong young lady, so you just hold tight. I have hope like Corina does that this will help you, also.

Hi Sara! Like your dr. mentioned, mido can cause supine hypertension, so I'm not so sure why your having low BP with it. In another post you had talked about going off the florinef and switching to mido, my only thoughts are maybe your body is adjusting to that? Since Florinef makes your body hold onto Salt, do you think you maybe you have to play around with the amount of sodium intake throughout the day? That always makes a huge difference in how I'm feeling. Sorry you aren't feeling well -- gotta be hard to teach dancing feeling so dizzy and w/ low #'s! Hang in there!

you might find this list helpful http://forums.dinet.org/index.php?/topic/1954-frequently-asked-questions-help-yourself-to-answers/

hi dancer, after all you've gone through, I'm so happy to have read that you found a great doctor. It's so nice that he seemed very willing to listen to you and he and his staff are so helpful! its a bonus when these doctor visits result in quality time with our spouses or friends, how nice for you both! I hope the medication changes will be helpful for you! Sarah

sorry I was recommending that the pcp call the pharmacy-- that way she could verify the atenolol until the cardio opened back up Monday. regarding the questions, I have the medical assistants ask me those at my primary's too. its a really unsettling and terrible feeling to have an "off" appointment. Not every doctor is for every patient, that's for sure and you just know it will never work. that sounds like a good plan to me with regard to your pcp in the future!

hi-- sorry you are feeling upset. I would ask the secretaries to not schedule with this particular Dr. Anymore and continue with your regular pcp. I'd express my thoughts to your physician when they get back. why can't she call your pharmacy? They will surely have a record of all your medications. Can you go through the secretary?

Hi DB, propranolol has helped, also so has Ativan because it lessons adrenaline. However, for me, anything that alters my serotonin (which is another neurotransmitter) also causes intense flushing. https://en.wikipedia.org/wiki/Serotonin

Ancy, have you checked our physicians list for anyone in your area? One of our medical advisors, Dr. Blitsheyn does Skype or phone consults, she specializes in autonomic disorders. Brady must be terrible. I suppose I'll take tachy if I have to pick. Ugh! http://circ.ahajournals.org/content/111/7/839.full This article is by Dr. Goldstein from the NIH. Neurocirculatory Abnormalities in Chronic Orthostatic Intolorance http://www.dinet.org/index.php/information-resources/ncs/ncs-links Here's our site's NCS info, not sure if you've seen it. I'll keep looking for you. Feel Better Sarah

Ancy, you poor thing. I am so sorry. This is a perfect reason why the forum exists - to support and encourage each other! Especially when we are down and out (no pun!). I've read in the past that your fam sounds pretty awesome, but at times, try as they may, just can't grasp the emotional and physical toll this can take. You just hang in there, it seems like your doing a good job of that! When you pass out, how long are you out for, and are they always when you are standing? (as opposed to sitting, reclined, etc) , and do your eyes ever remain open when you pass out? I ask because there are many types of seizures, and non epileptic seizures can occur with "floor drops" and happen multiple times a day. I was curious about the eyes thing because usually when you've blacked out, your eyes are closed. And in a seizure, I believe they are open. During these events, Bradycardia or Tachycardia can occur. Have they ever had you wear a holter monitor to record one of these events? Ancy here is an article by Dr. Grubb that discusses POTS and overlapping NCS. - I pasted it from dynakids, so it may look kind of funny. Neurocardiogenic Syncope Coexisting with Postural Orthostatic Tachycardia Syndrome in Patients Suffering from Orthostatic Intolerance: A Combined form of Autonomic Dysfunction KHALIL KANJWAL, M.D.,* MUJEEB SHEIKH, M.D.,† BEVERLY KARABIN, PH.D.,* YOUSUF KANJWAL, M.D.,* and BLAIR P. GRUBB, M.D.* From the *Section of Electrophysiology, Division of Cardiology, Department of Medicine, The University of Toledo Medical Center, Toledo, Ohio; and †Division of Internal Medicine, Department of Medicine, The University of Toledo Medical Center, Toledo, Ohio Introduction: There is anecdotal evidence that one or more forms of orthostatic intolerance (OI) subgroups may coexist in the same patients. However, there is a paucity of published data on the clinical featuresandmanagementofpatientswhosufferfromcoexistingfeaturesofposturaltachycardiasyndrome (POTS) and neurocardiogenic syncope (NCS). We herein present our experience of 18 patients who we found displayed evidence of coexisting NCS and POTS. Methods: We reviewed charts of 300 POTS patients seen at the University of Toledo Syncope and Autonomic Disorders Center from 2003 to 2010 and found 18 patients eligible for inclusion in this study. Patients were included in this study if they reported clinical symptoms consistent with bothPOTS and NCS and then demonstrated atypical lPOTS pattern(arise in heart rate without change in blood pressure[BP]) on head up tilt table(HUTT)within the first 10minutes off upright posture followed by a neurocardiogenic pattern (a sudden fall in heart rate and/or fall in blood pressure) reproducing symptoms that were similar to the patients spontaneous episodes. Results: We found 18 patients, mean age (30 ± 12), with 15 (84%) women and three (16%) men, who met the inclusion criterion for this study. Each of these 18 patients demonstrated a typical POTS pattern within the rst 10 minutes on initial physical exam and on a HUTT. Continued tilting beyond 10 minutes resulted in a sudden decline in heart rate (which in some patients manifested as an asystole that lasted anywhere between 10 and 32 seconds [mean of 18 seconds]) and/or a fall in BP in each of these patients demonstrating a pattern consistent with neurocardiogenic subtype of OI.The meantime to the NCS pattern of a fall in BP and heart was 15 minutes with a range of 13–20 minutes. This group of patients was highly symptomatic and reported frequent clinical symptoms that were suggestive of OI. Recurrent presyncope, syncope,orthostatic palpitations,exercise intolerance, and fatigue were the principal symptoms reported. Conclusion: NCS may coexist with POTS in a subgroup of patients suffering from OI. (PACE 2010; 1–6) orthostatic intolerance, postural tachycardia syndrome, neurocardiogenic syncope Introduction Orthostatic intolerance (OI) syndromes refer to a heterogeneous group of disorders of hemodynamic regulation that are characterized by excessive pooling of blood in the dependent areas of the body during upright posture, thereby resulting in insufcient cerebral perfusion during upright posture causing a variety of symptoms Address for reprints: Blair P. Grubb M.D., F.A.C.C., Division of Cardiology, Department of Medicine, The University of Toledo Medical Center, Mail Stop 1118, 3000 Arlington avenue, Toledo, OH 43614. Fax: 419-383-3041; e-mail: blair.grubb@utoledo.edu Received September 12, 2010; revised October 13, 2010; accepted October 31, 2010. doi: 10.1111/j.1540-8159.2010.02994.x that are relieved by recumbency. Symptoms may include syncope, near syncope, fatigue, palpitations, exercise intolerance, lightheadedness, diminished concentration, and headache.1–4 Based on clinical presentation and head up tilt table response (HUTT), OI can be broadly divided into subgroups that include neurocardiogenic syncope (NCS), postural tachycardia syndrome (POTS), and dysautonomic (autonomic failure) syndromes. There is anecdotal evidence that one or more forms of these subgroups may coexist in the same patients. However, there is paucity of published data on the clinical features and management of patients who suffer from coexisting features of POTS and NCS. We herein present our experience of 18 patients who we found displayed evidence of coexisting NCS and POTS. C 2010, The Authors. Journal compilation C 2010 Wiley Periodicals, Inc. PACE 2010 1 KANJWAL, ET AL. Methods This was a retrospective study approved by our Institutional Review Board (IRB) at the University of Toledo. We reviewed charts of 300 POTS patients seen at our autonomic center at the UniversityofToledofrom2003to2010andfound 18 patients eligible for inclusion in this study. Criterion for Diagnosis of OI As mentioned earlier, OI consists of a heterogeneous group of disorders of hemodynamic regulation characterized by excessive pooling of blood in the dependent areas of the body during upright posture resulting in insufcient cerebral perfusion causing symptoms during upright posture relieved by recumbency. POTS POTS was dened as ongoing symptoms o fOI (of greater than 6 months duration) accompanied by a heart rate increase of at least 30 beats/min (or a rate that exceeds 120 beats/min) observed during the rst 10 minutes of upright posture or HUTT occurring in the absence of other chronic debilitating disorders.1,2 Symptoms may include fatigue, orthostatic palpitations, exercise intolerance, lightheadedness, diminished concentration, headache, near syncope, and syncope. In a retrospective chart review, we collected data, including demographic information, presenting symptoms,laboratory data,tilt-tableresponse,and treatment outcomes. Neurocardiogenic syncope NCS was dened as episodic syncope (transient loss of consciousness) with spontaneous recovery. Criterion for diagnosis of NCS included a HUTT response consistent with NCS (a sudden decrease in heart rate and/or decrease in blood pressure) that reproduced a patient’s spontaneous symptoms of recurrent transient loss of consciousness with spontaneous recovery. Protocol for HUTT The protocol used for tilt table testing has been described elsewhere,1–8 but basically consisted of a 70-degree baseline upright tilt for a periodof30minutes,duringwhichtimeheartrate and blood pressure were monitored continually.If no symptoms occurred,the patient was lowered to the supine position and an intravenous infusion of isoproterenol started with a dose sufcient to raise the heart rate to 20%–25% above the resting value. Upright tilt was then repeated for a period of 15 minutes. Criterion for Diagnosis of Combined OI Patients where included in this study if they reported clinical symptoms consistent with both POTS and NCS and then demonstrated a typical POTS pattern (a rise in heart rate without change in blood pressure) on assuming upright posture or HUTT within the rst 10 minutes followed by a neurocardiogenic pattern on continued HUTT (a sudden fall in heart rate and/or fall in blood pressure)reproducingsymptomsthatweresimilar to the patients spontaneous episodes. Treatment Protocol The treatment protocol semiployed were based on our previous experiences with orthostatic disorders and are described in detail elsewhere.1–8 Briey, a sequence of therapies was employed that included physical counter maneuvers and aerobic and resistance training as well as increased dietary uids and sodium. If these were ineffective, pharmacotherapy was initiated in a sequence generally consisting of β-blockers, central sympatholytics, udrocortisone, midodrine, and selective serotonin reuptake inhibitors, either alone or in combination. If patients failed to respond to these medications, second- and third-line medications such as octreotide, erythropoietin, and pyridostigmine were employed. As this was a retrospective chart review, a formal questionnaire to assess the response to treatment or assessment of response to treatment by HUTT testing was not employed. The information about the subjective symptoms and sense ofwellbeingfromeachpatientwascollectedfrom thepatientcharts,physiciancommunications,and directpatientinquiry.Atreatmentwasconsidered successful if the patient reported that it provided symptomatic relief. Statistics This is an observational study. The statistical analysis was done by using SPSS 17 version (SPSS Inc., Chicago, IL, USA). Continuous data are presented as mean ± standard deviation and categorical data as percentages. A t-test was used for comparisons of means, and a statistical signicance was reached at a P value of <0.05. Results A total of 300 charts of patients followed at the University of Toledo Syncope and Autonomic Disorders center were screened. These patients had been seen over a period of 7 years. We found 18 patients, mean age (30 ± 12), with 15 (84%) women and three (16%) men, who met the inclusion criterion for this study. Table I summarizes 2 2010 PACE COEXISTING POTS AND NCS Table I. Baseline Clinical Characteristics of the Study Patients (N=18) Age (years) 30±12 Sex (females) 15 (84%) Symptoms of orthostatic intolerance Orthostatic palpitations 17 (95%) Dizziness 16 (89%) Inability to concentrate 16 (89%) Syncope 18 (100%) Presyncope 18 (100%) Fatigue 17 (95%) Chest pain 11 (61%) Medications β-blockers 9 (50%) Selective serotonin reuptake 8 (45) inhibitors (SSRI) Norepinephrine reuptake inhibitors/SSRI 11 (61%) Midodrine 9 (50%) Modanil 3 (16%) Fludrocortisone 4 (22%) Pyridostigmine 17 (94%) Octreotide 1 (6%) Erythropoietin 4 (22%) Comorbid conditions Hypermobility 4 (22%) Hypertension 4 (22) Diabetes Mellitus 1 (6%) Migraine 9 (50%) Precipitating factor None 10 (83.3%) Infectious mononucleosis 2 (16.6%) the clinical features, comorbid conditions, and medications used in these patients. This group of patients was highly symptomatic with frequent clinical symptoms that were suggestive of OI. Recurrent presyncope, syncope, orthostatic palpitations, exercise intolerance, and fatigue were the dominant symptoms reported. Each of these patients carried a diagnosis of POTS initially, but due to the nature of their symptoms each patient was further evaluated by a HUTT. HUTT Response All the patients reported here had clinical features and a physical exam consistent with the diagnosis of POTS. In view of their refractory symptoms and frequent syncope, they were referred to our center for further evaluation. A detailed physical examination was performed in each of these patients .All of these patients demon Table II. Hemodynamic Parameters as Assessed in an Outpatient Ofce. Most of These Patients Demonstrated This Pattern of Increase in Heart Rate Without Signicant Change in Blood Pressure (POTS Pattern) within 5 Minutes of Standing trated a typical POTS pattern with minimal change in blood pressure and an increase in heart rate in an ofce-based physical examination, conrming their diagnosis of postural orthostatic tachycardia (Table II). Each of these patients was further evaluated by a standard HUTT. The HUTT conrmed the diagnosis of POTS, but in addition, continuing the tilt beyond 10 minutes demonstrated a response consistent with NCS. Thus, a dual response was noted on a HUTT with initial POTS followed by neurocardiogenic decompensation pattern (see Table III and Fig. 1). Continued tilting beyond 10 minutes resulted in a sudden decline in heart rate (which in some patients manifested as an asystole that lasted anywhere between 10 and 32 seconds, mean of 18 seconds). The mean time to the NCS pattern of a fall in bloodandheartwas15minuteswitharangeof13– 20 minutes. Thirteen patients demonstrated NCS without a provocative isoproterenol infusion and three patients demonstrated NCS response after isoproterenol infusion. Table III. Heart Rate and Blood Pressure Response in Patients with Combined Orthostatic Intolerance on a HUTT. Note a Dual Response with Initial Pattern Consistent with POTS (Increase in Heart and Minimal Change in Blood Pressure); Prolonged Tilting at 20 Minutes Demonstrated a Typical Neurocardiogenic Pattern with Fall in Heart Rate Associated with Fall in Blood Pressure 0 minutes 10 minutes 20 minutes Heart rate (beats 73±10 123±15 43±15 per minute) Blood pressure 126±15 118±14 75±12 (mmHg) PACE 2010 3 KANJWAL, ET AL. Figure 1. Line diagram demonstrating a dual response with initial pattern consistent with POTS (increase in heart and minimal change in blood pressure);prolonged tilting at 20 minutes demonstrated a typical neurocardiogenic pattern with fall in heart rate associated with fall in blood pressure. Response to Medications All of these patients failed rst-line medications. Second-line medications including pyridostigmine was tried in 17 of 18 patients. Of these 17 patients, improvement in symptoms of OI was observed in ve patients only. None of these patients had complete elimination of their syncope. However, a subjective improvement in the severity and frequency of symptoms of OI intolerance was reported by ve (30%) of the patients treated with pyridostigmine. One patient is being treated with octreotide and another four with erythropoietin, as pyridostigmine failed to improve heart rate and blood pressure in these patients. Pacemaker Implantation Nine patients were further evaluated by implantable loop recorder (ILR). Five patients demonstrated prolonged periods of complete heart block and asystole on the tracings that were downloaded following episodes of abrupt onset of convulsive syncope. Each of these ve patients received dual chamber closed loop cardiac pacemaker with near complete elimination of their episodic loss of consciousness. Discussion The exact pathophysiology of postural tachycardia syndrome remains elusive. Our understanding of the disorder now called POTS has substantially increased in the last two decades. The early descriptions of the disorder focused on a group of patients who had been previously healthy until a sudden febrile illness (presumably viral) brought on an abrupt onset of symptoms.9 Later investigations revealed that POTS is better un derstood as a physiological state most commonly due to inability of the peripheral vasculature to maintain adequate resistance in the face of orthostatic stress,allowing for excessivepoolingof bloodinthemoredependentareasofthebody.10,11 The resultant functional decline in circulatory volume elicited a compensatory increase in heart rate and myocardial contractility. While compensatory in mild cases, this mechanism is unable to fully compensate in more severe cases, resulting in a reduction in effective circulation and varying degrees of cerebral hypoperfusion. Later investigations revealed that POTS is not a singlecondition,butratheraheterogeneousgroup of disorders resulting in similar physiological state.9–13 Recentresearchhasshownthatthissyndrome may have multiple etiologies and we now know that POTS can have multiple variants such as partial dysautonomia,9 centrally mediated hyperadrenergic stimulation,12,13 norepinephrine transporterdysfunction,14 andanautoimmuneantibody against acetylycholinesterase receptors,15 POTS associated with deconditioning,15 and hypovolumia.16 In a recently published study, it was reported that POTS may be a manifestation of autonomic cardiac neuropathy.17 More recently, interest has grown in the assessment of parasympathetic function in patients sufferingfromPOTS.RajreportedagroupofPOTS patients in whom vagal function was preserved as assessed by normal sinus arrhythmia ratio on deep breathing.18 Alshekhlee et al. describe a series of four POTS patients who had a surge of parasympathetic activity resulting in marked cardioinhibition and vasodepression.19 They postulated that either a compensatory parasympathetic surge or a central aberration altering both sympathetic as well as parasympathetic output in a balanced fashion may account for increased parasympathetic activity in this group of patients. We postulate that an initial compensatory increase in sympathetic outow that increases the inotropy as well as chronotropy of the heart may fatigue or norepinephrine stores may become exhausted,resultinginastateofrelativesympathetic withdrawal causing a state of bradycardia and hypotension in this group of patients. Assessing bothsympatheticaswellparasympatheticnervous system function at various stages of the HUTT may answer many of the questions, which our report could not address. Ojha et al. have reported that as many as 38% of patients suffering from POTSexperiencesyncopeduringHUTT,andthey suggest that the low-pressure baroreceptors that have been implicated as contributing to some forms of POTS may confer upon these patients an increased riskofsyncope.20 Inarecentstudyfrom 4 2010 PACE COEXISTING POTS AND NCS Fuetal.,21 itwasobservedthatpatientswithPOTS haveasmallerheartincomparisontothecontrols. Also they observed that the autonomic function was intact in their group of patients. In this report, exercise training improved or even cured symptoms of POTS. With continued research in the area of OI, we hope to learn more about the pathophysiology of the POTS and its related syndromes. There were some interesting observations from our study. Syncope (which, as mentioned previously, occurs in 10%–38% of historical controls of POTS patients in general) occurred in all patients in this group. This observation could be explained by a late-phase surge in parasympathetic tone or sympathetic withdrawal leading to both cardio inhibition as well as vasodepression. Almost all patients in this study had difculty treating OI with each patient failing rst- and second-line medications. Response to third-line medication, including Pyridostigmine, was also modest. Recently, Ivarbidine, a selective inhibitorofacardiacpacemakercurrentinhibitor, has been reported to be effective in patients with inappropriate sinus tachycardia,22 tachycardia with POTS,23 and tachycardia associated with autonomic dysfunction.24 In one report,23 Ivarbidine was reported to improve symptoms of POTS in a patient who had failed multiple other medications. The patient described in the report had history of intermittent bradycardia and heart block for which he had received a pacemaker. Since these results were recently published, none of our patients had received Ivarbidine so far. But Ivarbidine therapy may be benecial in patients sufferingfromPOTS.Inthefuture,weexpectmore studies will be published on the use of Ivarbidine in postural tachycardia that will dene the role of this therapy in POTS patients a better way. In our study, the patients who were found to have prolonged episodes of asystole or complete heart block on ILR subsequently beneted from dual-chamber pacemaker placement. Thus, POTS patients who present with unusually frequent and severe episodes of syncope should be considered for evaluation by an ILR to assess whether baradycardia and/or asystole occurs during clinical events. Limitations There were several important limitations in the current study. The study was retrospective and included small number of patients. None of the patients underwent additional autonomic function assessment besides HUTT. Response to therapy was subjective and not objectively assessed by a formal questionnaire or a response to a repeat HUTT. Conclusion NCS may coexist with POTS in a subgroup of patients suffering from OI. This group of patients with mixed-form OI may be difcult to treat and may have syncope as a dominant symptom. Also, POTS patients presenting with unusually frequent and severe episodes of syncope may benet from further evaluation by ILR, as some of these patients, having NCS as well, may be candidates for cardiac pacing. Anyway, all my best! Sarah

Wow, Lily! What a great feeling that must be. I miss that feeling so much. I'm grateful for the doctors and researcher's who give us the chance to have that feeling once again. It's really just a terrible feeling, how it feels to lose little pieces of yourself cognitively. I have some doctors who don't really understand the decline because they've only known me after I got sick. And it's not like this all the time, but if I'm at a party for example, I'll be standing upright and sometimes can't remember what the conversation was about. Things like that. For the first time since I've started Provigil, I haven't had to re-count change in line 2 or 3 times, the fatigue has improved greatly, too. Coffee helps me as well, only one cup and just like you describe - a boost. That's pretty interesting that you mention Dopamine actually, mine have been all over the place, high, normal, but have actually not measured detectable twice. Is dopamine serum accurate though.. I mean, is it produced in the gut? I get the same effect on Clonidine. It's a great medication for me, not only for BP control. I'm sure it's added to the fatigue which is a bummer, but not enough that it's stopped me from taking it throughout the day. I have a lot of adrenaline, so I'm sure it's doing it's job in that arena.. Clonidine has helped my anxiety as well, and it does give me a "flat" feeling. Out of all the meds that I've tried for POTS and related ailments, clonidine by far has been one of the top 3 most successful. Oh - and it's also regulated my sleeping schedule, too. Do you use compression? That helps me a lot, too I've always wondered about Methyldopa. Clonidine was just a better choice for me because my doctor's used it in the beginning as a PRN for hypertensive episode's. Thanks to all who've shared in this topic! Sarah

hi artluvr and all members, yes, indeed our forum has a new updated look with some new features! We recently performed an upgrade to better enhance the forum experience! We hope that you all enjoy it. Feel free to ask any questions. thank you! the moderating team Katherine, Corina , Sarah

Welcome to DINET. I've also had great success with Ivabradine. After failed trials of Beta beta bockers, alpha/beta,calcium channel blockers, Central Agonists, Ivabradine was the only agent that lowered my HR by at least 1/2. Congratulations to you for hanging in there until you found something so helpful. It's not easy. I get the luminous Phenomena -- mine includes brief moments of sudden brightness usually due to an increase of light in my surroundings. I've heard from some doctors that they're patients describe it as a halo affect or kaleidoscope. What's interesting is it's supposed to dissipate within the first 2-3 months of treatment. I'm going on a year this May, mine has definitely improved. So, just goes to show - we're all different. Best of luck. Sorry you had to dx Ancy! bummer

Ancy -- so glad your on the road to recovery! Fingers crossed so that your HR behaves itself and stays above 60 bpm so that you can restart our favorite med "corlanor/Ivabradine". Were you symptomatic with the low potassium? Take care!! Sarah

Ancy, I wish I had something helpful to offer, just wanted to tell you to hang in there. SO sorry this happened. Wishing you all the best. Sarah

There is a flashing lights portion during an EEG that I just had done. It's awful. Why the hesitation when bringing it up to the girls' neurologist? Are you worried he may dismiss it because it was your idea and not his? I come armed with research articles when I approach my doctors with new ideas. He should be open to hearing you out. I know you've mentioned in the past that they have a good primary care doctor who addresses all of your concerns, maybe you could start with him. Then, when talking to the neuro, lead with the foot, "The Primary doc and I spoke about this.." etc. etc.

Yay Sarah, I'm glad you've got this appointment coming up with a dysautonomia specialist! Good luck and let us know how it goes. We're rooting for you! A lot of members here know what you are going through. It's a frustrating situation to be in, so don't feel guilty for how you feel. Your entitled to your feelings! Keep hanging in there! Sarah

So interesting! I just had 2 rounds of IV antibiotics for a bad kidney infection today. I felt like I immediately noticed clarity. Like a fog was lifted or something. It could be a coincidence, as I did start Provigil last week, but the timing is uncanny. I remembered this post written. (look at the last post written by chaos) http://forums.dinet.org/index.php?/topic/23873-new-to-dinet/page-2 Best of luck to you Sue, I hope you are onto something here. Also, I hope you continue to recover well from your surgery. Sending positive thoughts your way! Sarah

Thanks everybody! The Provigil seems to be working quite well. I've noticed I can't take it after 10 am though or I have more difficultly falling asleep -- And, as I've dealt with insomnia on and off for years, this is something that could be a potential issue. My POTS specialist was concerned about tachycardia, however, that's not occurred, hooray! I am able to focus on tasks for longer periods of time, can absorb information faster while having conversations and fatigue has improved. Draven and Lily, I'm happy that you've had success as well with your medications. What symptom improvement have you noticed? Thanks - Sarah

Hmm.. There are various Aura's that can be associated with Epilepsy. One of them is a visual Aura. Flashes/bright lights, zig zags, seeing spots, disorientations of the size, shape or distance of things. Auditory Aura's, like Ringing/buzzing, or muffling in the Ears does also occur, as well as Autonomic Phenomena, my epilepsy specialist said Heart Rate, Increased Sweating, Goosebumps, and Nausea all can be an aura. A lot of these auras are migraine related too, but I know what you mean about basically exploring all avenue's. Have they ever had an EEG? Just throwing it out there, the difficult part with a "scheduled" EEG is basically if they aren't symptomatic at that particular moment, it may not necessarily be positive. There are portable EEG's that can be worn for up to 7 days. Take care, Sarah

Welcome everyone!!