Dysautonomia And Concussion

[Katybug]

Woot woot....now you might actually be able to do a happy dance!!

[Guest ANCY]

Yes lol! My dr already did a whoop and happy dance for me, I think he's as excited as I am! I have not passed out at all in the last 24 hours, have not had a syncope free day for two and a half years, it's amazing! 

So the nurse from the pacemaker clinic came by this morning said everything looks great, explained a little more about the rate response. So this particular pacemaker they can set to sense if blood pressure is to low and speed up the pacing to compensate. Said it predicts, at current settings, that it will last about 10 years. Pacing 100% Atrial and Ventricle is set to sense.

So excited cardiologist fully expects me to get back to a normal life, without a wheelchair! Said I'm to young and have to much living left to do to be stuck in a wheelchair the rest of my life. Sending me home and told me to get moving lol!

I'm so amazed! Thank you all for being so supportive!

[corina]

Glad to hear you're feeling better Ancy! Now onwards and upwards! (after resting up and recuperating from all this of course!)

[Guest ANCY]

Yes upwards is a nice change! Just finished PT and first time in years I didn't pass out once through the entire session! Approaching 48 hours without passing out, yeah!

 

[Amalia01]

How's it going Ancy?

[Guest ANCY]

Thanks for checking on me, Still going strong! Have not passed out and it's astounding the amount I'm able to do now. My activity level has increased by about 3 times what it was before which is awesome. Took it easy today because all the activity has caught up with me and was really exhausted. Looking forward to being able to go to church tomorrow and stay conscious through the whole service.?

Have seen on my heart monitor a couple times where it has ramped my heart rate up in coralate to my bp drops. Working really well, have a in home device check on the 5th of May and in clinic on July 5th, will be interesting to see what it says in the report.

[Katybug]

I'm so very excited for you!

[Amalia01]

Awesome!  That's funny because I thought that might happen. We can all certainly relate to overdoing it when we have better days.  I hope the church service/sermon went well.  Were you too tired to stay awake? Just kidding.  So glad that you are functioning better.

[Guest ANCY]

Lol! Overdid it again but church was really nice and didn't pass out. ?resting today for PT tommorow, should be walking. 

[corina]

Happy for you Ancy!

[Guest ANCY]

Just wanted to post an update. It has now been 5 weeks since I have passed out! I can walk about 500 yards or so a day, that's changed from not walking at all except occasionally with PT. I only require 1 person assist now as well. Making so much quick progress it's amazing! Back in the kitchen cooking all sorts of things for my family. Can stand at the sink and do dishes for about 5 minutes at a time. Neurology even wants to start cutting down on some of my meds!

Thank you everyone for being so supportive. I hope you all are doing as well as can be!

[Katybug]

That is such fantastic news! I'm so happy for you! 

[dancer65]

Amazing ? Enjoy you deserve it so pleased to hear you are making such progress

[corina]

That's awesome news, happy for you!!!

[Psalm 23]

What a wonderful update ANCY ! I am so very happy for you ! I hope you're still continuing to improve and having fun in the kitchen today.

[Lburnham]

On 3/18/2016 at 2:08 PM, SarahA33 said:

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
 

 

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."

- That's ME!  But I don't understand if I have POTS and NCS or just NCS.

[Pistol]

@Lburnham 

7 hours ago, Lburnham said:

That's ME!  But I don't understand if I have POTS and NCS or just NCS.

I have both, POTS and NCS. When I faint from NCS the HR speeds up and then both HR and BP suddenly drop, causing a faint. The HPOTS causes a compensatory reaction of the sympathetic ANS to increase the BP and HR - this causes a dump of adrenaline which in turn causes the vessels to constrict, BP rises but there is no circulation to the brain - in my case this has caused seizures. 

The best way to clarify NCS vs POTS is a tilt table test