SarahA33

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
 

On ‎3‎/‎3‎/‎2016 at 8:10 AM, Lily said:

Strattera makes me feel like I have access to the full power of my intellect.

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!!

I thought the theory of higher NE level's associated w/ brainfog was interesting for a few reasons. Mine have been really high, so I wonder if that contributes to my fog. I have to start paying attention to a correlation between adrenaline spikes and increased fogginess. "Since high levels of norepinephrine in the brain can disrupt cognitive function, it has been proposed that this mechanism could contribute to cognitive dysfunction in POTS patients with elevated norepinephrine levels (hyperadrenergic)"

There are many POTS patients who have elevated norepinephrine levels, so I do wonder if in the future they will find link. "Postural changes in serum norepinephrine levels are much more pronounced in POTS patients" - Dr. Grubb POTS Eval & Management

Anyway, I just started Provigil 4 days ago. I am taking 100 mg. I was able to get it covered through my insurance ,so I am very pleased. They denied it initially so my doctor had to do a prior authorization.. 30 pills are $699! No side effects to report as of yet, and I am noticing improvements!

Hi juls! Welcome Here's the link to our physicians list: http://dinet.org/index.php/physician-list

Nick Tullo is in NJ, he treats general dysautonomia and syncope. His contact info is in the list above.

The following doctors are from the American Autonomic Society's Website. DINET doesn't have any affiliation with these physician's, and I'd suggest calling their offices to see if they treat your specific condition, how many patients they've treated with it, etc. Best of luck on your search. Let us know if we can help further! -Sarah

Pennsylvania -

Wishwa Kapoor, M.D.
Suite 933 MUH, 200 Lothrop Street
Pittsburgh, PA 15213
USA
Phone: 412-692-4821
Fax: 412-692-4825
E-mail: wnk@med.pitt.edu
Orthostatic Intolerance (POTS, mitral valve prolapse)
Syncope, Neurally Mediated Syncope

Richard Malamut, M.D.
Crozer-Chester Medical Center
Ambulatory Care Pavillion
Suite 533
Chester, PA 19013
USA
Phone: 610-874-1184
Fax: 610-874-4258
Diabetic neuropathy
Neuropathic Pain

New York -


Dr. Felicia B. Axelrod
New York University Medical Center
530 First Avenue, suite 9Q
New York, NY 10016
USA
Phone: 212-263-7225
Fax: 212-263-7041
E-mail: Felicia.Axelrod@popmail.med.nyu.edu
Familial dysautonomia (FD)
Hereditary sensory and autonomic neuropathy
Other pediatric patients with congenital autonomic disorders

Ludmilla Bronfin, M.D.
650 First Avenue, 7th Floor
New York, NY 10016
USA
Phone: 212-532-6298
Fax: 212-545-8530
e-mail: lumsig@aol.com
Postural Tachycardia Syndrome (POTS)
Autonomic Neuropathy
Orthostatic Intolerance
Hyperhidrosis

Horacio Kaufmann, M.D.
Dpt. of Neurology,NYU School of Medicine
530 First Avenue, Suite 9Q
New York, New York 10016, USA
horacio.kaufmann@med.nyu.edu
Multiple System Atrophy (Shy-Drager Syndrome)
Autonomic Failure (PAF, secondary autonomic failures)
Orthostatic Intolerance (POTS, mitral valve prolapse)
Other autonomic disorders

Lindsey Lee Lair, M.D.
35 East 35 St, Suite 202
New York, NY 10016
USA
Phone: 212-683-4640
Fax: 212-671-1466
E-mail: contact@autonomicmd.com
Multiple System Atrophy
Pure Autonomic Failure
Orthostatic Intolerance, POTS
Neurally Mediated Syncope
Hyperhidrosis

Frank Mazzola, M.D., F.A.C.C.
Clinical Assistant Professor
State University of New York at Stony Brook
North Suffolk Cardiology Associates
2500-1 Nesconset Highway
Stony Brook, NY 11790
USA
Phone: 516-689-7700
Fax: 516-689-7720
E-mail: fmazz@compuserve.com
Multiple System Atrophy (Shy-Drager Syndrome)
Autonomic Failure, (PAF, secondary autonomic failures)
Orthostatic Intolerance (POTS, mitral valve prolapse)
Neurocardiogenic Syncope
Developmental Dysautonomia
Chronic Fatigue Syndrome

Emilio Oribe, M.D., F.A.C.P.
162 East 78th Street
New York, NY 10075
USA
Phone: 212-794-2281
Fax: 212-517-5991
E-mail: exoribe@nyp.org
Website: www.nynapc.com
Syncope/Fainting
Orthostatic Intolerance/POTS
Multiple System Atrophy
Parkinson’s Disease
Autonomic Failure

Mark S. Pecker, M.D.
Hypertension Division
New York Presbyterian Hospital-Cornell Campus
525 East 68th Street
New York, NY 10021
USA
Phone: 212-746-2210/2124
Fax: 212-746-8451
E-mail: mpecker@mail.med.cornell.edu
Multiple System Atrophy (Shy-Drager Syndrome)
Autonomic Faliure (PAF, secondary autonomic failures)
Orthostatic Intolerance (POTS, mitral valve prolapse)
Other autonomic disorders (Circulatory)

Rohan G. Perera, M.D.
Division of Cardiology
St. Luke's -Roosevelt Hospital
1111 Amsterdam Avenue
New York, NY 10025
USA
Phone: 212-523-4007
Fax: 212-523-3915
E-mail: pererarohan@hotmail.com
Multiple System Atrophy (Shy-Drager Syndrome)
Autonomic Failure (PAF, secondary autonomic failures)
Orthostatic Intolerance (POTS, mitral valve prolapse)
Other autonomic disorders


Indu Taneja, MBBS, Ph.D.
19 Bradhurst, Suite 3050 North
Hawthorne, NY 10532
USA
Phone: 914-593-8885
Fax: 914-593-8890
E-mail: indu_taneja@hotmail.com
Orthostatic Intolerance
Neurally Mediated Syncope

Louis H. Weimer, M.D.
Neurological Institute of New York
710 W. 168th Street
New York, NY 10032
USA
Phone: 212-305-1330
Fax: 212-305-5396
E-mail: lhw1@columbia.edu
Multiple System Atrophy
Pure Autonomic Failure
Orthostatic Intolerance
Autonomic Neuropathy
Other Autonomic Disorders

Hello, Draven. Welcome to the forum.

I see that Katie has given you the link to dysautonomia specialists, hopefully someone is in your area. Reading through your list of symptoms, it sounds like you would really benefit from a facility that has access to dysautonomia testing. I had a really complicated case, and my local doctor's had tried everything they could and eventually sent me to the Cleveland Clinic and I had a full autonomic workup. The following test's are from the cc's website:

"The Cardiovascular Autonomic Test with Tilt assesses how well a patient’s autonomic nervous system controls blood pressure and heart rate during different maneuvers: deep breathing, the Valsalva maneuver and head-up tilt. These tests are particularly helpful in assessing patients with fainting or syncope.
The Quantitative Sudomotor Axon Reflex Test (QSART) measures the autonomic nerves that control sweating. This test utilizes a method to stimulate sweat glands and measure the volume of sweat that is produced. The QSART is useful in assessing many autonomic disorders, especially autonomic and small fiber neuropathies as well as some types of pain disorders. The QSART also is helpful in localizing the site of the autonomic disorder to the peripheral or central autonomic nervous system.
The Quantitative Sensory Test (QST) measures a patient’s ability to feel vibration and temperature sensation. This test is useful in the assessment of patients with polyneuropathy, especially small fiber neuropathy.
The Thermoregulatory Sweat Test (TST) is a measure of a patient’s ability to sweat when stimulated by a warm and humid environment. This test assesses both the central and peripheral autonomic nervous system’s control of sweating and body temperature regulation (thermoregulation). The pattern of sweating abnormality detected by this test can be helpful in diagnosing a variety of neurological and autonomic disorders that may cause reduced sweating (anhidrosis) or excessive sweating (hyperhidrosis). These disorders include small fiber and autonomic neuropathies, radiculopathies, and central autonomic disorders including multiple system atrophy, Parkinson’s disease with autonomic dysfunction, and pure autonomic failure."


I have night sweats also, it's better now, but I had a really hard time for years. I would wake up with tremors, drenched in sweat, heart racing, headache (if I didn't have a migraine already). Medications have improved it -- propranolol, clonidine, Ativan, Ivabradine. I have POTS with a hyperadrenergic state and Inappropriate Sinus Tachycardia, Raynaud's phenomenon, chronic migraine, and generalized epilepsy.

I'm just wondering if any of your doctors have mentioned Small fiber neuropathy to you?
"Small fiber neuropathy is a condition characterized by severe pain attacks that typically begin in the feet or hands. As a person ages, the pain attacks can affect other regions. Some people initially experience a more generalized, whole-body pain. The attacks usually consist of pain described as stabbing or burning, or abnormal skin sensations such as tingling or itchiness. In some individuals, the pain is more severe during times of rest or at night. The signs and symptoms of small fiber neuropathy usually begin in adolescence to mid-adulthood.

Individuals with small fiber neuropathy cannot feel pain that is concentrated in a very small area, such as the prick of a pin. However, they have an increased sensitivity to pain in general (hyperalgesia) and experience pain from stimulation that typically does not cause pain (hypoesthesia). People affected with this condition may also have a reduced ability to differentiate between hot and cold. However, in some individuals, the pain attacks are provoked by cold or warm triggers.

Some affected individuals have urinary or bowel problems, episodes of rapid heartbeat (palpitations), dry eyes or mouth, or abnormal sweating. They can also experience a sharp drop in blood pressure upon standing (orthostatic hypotension), which can cause dizziness, blurred vision, or fainting." https://ghr.nlm.nih.gov/condition/small-fiber-neuropathy

Hi, Emma--

Do you have migraines?

I was told I have something called Prinzmetal's Angina. (squeezing in my chest, difficulty breathing, tachycardia, and even in some occasions eye pain, I've had capillaries in both eyes break and it was attributed to a spasm) The chest pain is better now that I'm on Ivabradine and Clonidine. I'm not sure why the combination has helped, maybe the clonidine has helped control the norepinephrine spikes - adrenaline, which is a vasoconstrictor. But, I have migraine's and Rayaud's, too, which actually led to the Prinzmetal's Angina diagnosis.

I've had an a really thorough cardiac workup recently at the Cleveland Clinic, so I know it's basically a combo of my POTS and possibly this angina that's causing the chest pain for me. I know many people find relief for chest pain with Calcium Channel Blockers, but there's an interaction with Ivabradine, and I see your taking that. Also, Nitro, or even Aspirin, has been helpful for many. Have you considered talking to your dr. about those? I mostly get my Chest pain when I'm relaxing and laying flat. It rarely happens when I'm out and about, running errands, etc.

I'm sorry that you are feeling a bit sad about this, I know it can be frustrating and scary. I know what you are going through, I wish you relief for your symptoms and some answers.. Sarah