Effexor For Pots---posting For A Friend

[Maxine]

Hi,

Posting for a friend here. Has anyone been prescribed effexor for POTS symptoms.

She is currently on Celexa, and now her neurologist wants to change her POTS med to Effexor. He said to stop the Celexa one day, and the next start the Effexor.

Any thoughts?

Maxine :0)

[summer]

Hi Maxine,

We are all so individual in our responses to meds, that I hesitate to post about a bad experience, because it may work very well for your friend. I believe lots of others here have had success with effexor. For me, it made my symptoms much worse. Actually, I only took one dose which they told me was a pediatric dose (37.5mg). I had an increase in all my symptoms, and terrible anxiety which I do not usually have. I have not tried any other SSRI or SNRI since.

In the Winter 2009 dinet newsletter, there is a question answered by one of the doctors (I don't remember which one) that talks about this (on page 7). As I said, I know some others have not had problems, but it seems that SNRI's are not so great for some of us with POTS. Hope your friend has a better experience.

Summer

[vemee]

I can't say if going from celexa to effexor in one day is a good idea but I would recommend she have her serum norepinephrine levels checked before going on effexor. There is no use increasing those levels if they are already high in fact it could be detrimental if they are increased too high.

[Angelika_23]

As Summer said, I hesitate to dwell on negatives, but I too had a horrible reaction to Effexor. It actually landed me in the hospital. It totally exacerbated every symptom I had, and invented a few new ones. I don't tolerate meds well, so maybe that was my crazy body, and the meds might work well for your friend. If she's on something similar, maybe it would work.

Good luck to your friend,

Angela

[Maxine]

Thanks for your replies.

I e-mailed them to my friend, plus I did a search of previous posts on effexor.

Thankfully, she hasn't started the effexor yet.

I've known her since we had our local support group. I live close to Dr. Grubb's office---actually about 1/2 mile.

We had a local support group for about 3 years, but I also took flyers to Dr. Grubb's office until 2006 with information where they can get support on line, including listing this web site. I also listed my phone number, and what I usually did was connect POTs patients with other local pots patients in their area so they could have local support, and a friend who totally understands because they have been through it. Networking---- .

When she first called me she was a train wreck, and weighed only 95 pounds from being so sick with this stuff. since then Dr. Grubb has stabilized her a great deal, but she still suffers with severe migraine type headaches, and spasms in her neck. Her local neurologist has two POTS patients, and thought changing her from taking celexa for her POTs symptoms to effexor would help the headaches. However, one of the major side affects of effexor is headaches!

Maxine :0)

[valliali]

I posted this topic on another forum, after I had a horrible reaction to Effexor, and no one responded so I thought I was the only one. But you guys sound like you had the EXACT same thing. I pretty much had a seven hour panic attack, and that was my first small starting dose. It was horrible, and I too, will never ever use SNRI or SSRI again.

I will say though that knowing what I know now about Effexor and its withdrawal, I sure am glad it didn't work out for me!

If your friend does decide on Effexor, please, please encourage her to read some of the stories about the withdrawal. Many people agree that although the drug helped ease all their symptoms, the withdrawal alone made them wish they never took it.

[pat57]

I have been told that Pristiq is very similar to Effexor but less is needed and so less side effects. The Pristiq is working great for me.

I was given it for depression and anxiety. Please note I have NCS and OH I do not have POTS. It is definitely helping me with

my OH and NCS. I am taking one 50mg every other day. I was nauseous taking it once a day. It does make me sweat but I have extreme dry skin so that's a good thing.

Also, I am told, it is non addicting.

good luck

[ramakentesh]

Norepinephrine reuptake inhibators are not great for some POTS patients because this very mechanism is implicated as a causal factor for POTS in some patients.

That is, acquired or inherited deficiencies in norepinephrine transporter protein which leads to reduced norepinephrine reuptake, increased peripheral resistance and fluctuating blood pressure and blood flow to the brain.

In others Ive heard that they can reduce symptoms so its hard to say.

[ramakentesh]

A severe and sustained reaction to an SNRI could be indicative of where your problem lies.

[summer]

A severe and sustained reaction to an SNRI could be indicative of where your problem lies.

Do you mean that a severe reaction to an SNRI could indicate deficiencies in norepinephrine transporter protein?

Summer

[ramakentesh]

Possibly. If it worsened your POTS symptoms then its might suggest that yes.

[valliali]

Rama

I became interested in the norepinephrine transport deficiency as a result of my reaction to Effexor. It was earlier on in my "POTS" diagnosis (which I say loosely as my current docs and myself don't really agree with the diagnosis) when I was given the Effexor and after my reaction, I was like no way was that normal!!! I found some info about NET and was certain that was my problem. I have also tested very low for normetanephrines, the metabolite of norepinephrine, and was diagnosed with a dysautonomia because, although my TTT was completely normal, at the end of the test, after the isuprel infusion, I developed a heart arrythmia which my doctor considered a result of norepinephrine. So I felt sure, and still feel fairly sure, that there is an issue with norepinephrine going on. However, my NE tests have always been normal, both urine and plasma.

Also, a norepinephrine problem (whether NET or a defunct in the COMT enzyme, the enzyme that metabolizes NE) doesn't explain some of my symptoms, like the arthritis that came out of nowhere.

Rama, do you know of other norepinephrine problems that would make a person continue to have normal NE levels? Is it possible for just the receptors to develop a sensitivity to the NE, though the NE is actually acting normally? How can I find more about this? The NIH researcher I spoke to, who has published a great deal of info about POTS and other dysautonomias and their relationship to catecholamines, told me that there is only one study linking NET deficiency to POTS and that he himself isn't quite convinced. How can a person get this tested?

[valliali]

Rama

I became interested in the norepinephrine transport deficiency as a result of my reaction to Effexor. It was earlier on in my "POTS" diagnosis (which I say loosely as my current docs and myself don't really agree with the diagnosis) when I was given the Effexor and after my reaction, I was like no way was that normal!!! I found some info about NET and was certain that was my problem. I have also tested very low for normetanephrines, the metabolite of norepinephrine, and was diagnosed with a dysautonomia because, although my TTT was completely normal, at the end of the test, after the isuprel infusion, I developed a heart arrythmia which my doctor considered a result of norepinephrine. So I felt sure, and still feel fairly sure, that there is an issue with norepinephrine going on. However, my NE tests have always been normal, both urine and plasma.

Also, a norepinephrine problem (whether NET or a defunct in the COMT enzyme, the enzyme that metabolizes NE) doesn't explain some of my symptoms, like the arthritis that came out of nowhere.

Rama, do you know of other norepinephrine problems that would make a person continue to have normal NE levels? Is it possible for just the receptors to develop a sensitivity to the NE, though the NE is actually acting normally? How can I find more about this? The NIH researcher I spoke to, who has published a great deal of info about POTS and other dysautonomias and their relationship to catecholamines, told me that there is only one study linking NET deficiency to POTS and that he himself isn't quite convinced. How can a person get this tested?

[valliali]

One more thing I wonder, that maybe you can help clarify:

From what I understand, SNRIs act to inhibit the NET. If a person has a NET deficiency, then wouldn't that make it so that their bodies were just acting as if they were on an SNRI? Likewise, if a SNRI is working to prevent the NET deficiency from working to the fullest, why don't people who take SNRIs all develop the same symptoms that are linked between POTS and NET deficiency?

[Carolyn Morris]

I would just like to add that I have been trying to come off Effexor for a year now. It helped with my anxiety when I was initially diagnosed with POTS.

After my initial "crash", I started to gradually improve and then after two years decided to stop taking Effexor. I have been slowly weaning for this past year

and it is an absolutely excruciating experience. The addictive quality of that drug and its withdrawal symptoms are immense! I have read that its withdrawal compares

to trying to come off heroine.

Think very, very carefully before taking Effexor because if you ever decide to go off it, that will be quite a challenge.

b'shert

[Lizzegrl]

Speaking from my own experience, Dr. Grubb wants me off Effexor. Your friend might want to check with him to see how he feels about her going on it, if it is another dr. prescribing. Just a thought!

[ramakentesh]

Rama, do you know of other norepinephrine problems that would make a person continue to have normal NE levels? Is it possible for just the receptors to develop a sensitivity to the NE, though the NE is actually acting normally? How can I find more about this? The NIH researcher I spoke to, who has published a great deal of info about POTS and other dysautonomias and their relationship to catecholamines, told me that there is only one study linking NET deficiency to POTS and that he himself isn't quite convinced. How can a person get this tested?

I think last time I replied I gave you a link to a study where five out of six POTs patients had nearly no peripheral NET expression yet all had only slightly or normal elevation of NE levels on tilt. Infact one of two studies on NET inhibition and its relation to orthostatic intolerance found that despite an increase in MSNA activity, NE levels didnt rise which seems paradoxical.

Perhaps the peripheral NET inhibition is a reflex mechanism as a result of faulty NE release or some other receptor abnormality? Its still not 100% clear and certainly it hasnt been proven 100% to be a causal mechanism in POTS. There are definately however patients that appear to overconstrict from excessive sympathetic activity - which would suggest increased transduction and a primary hyperadrenergic problem.

Dr Blair Grubb, the Baker Institute in Melb and Vandy all believe or have proposed the NET deficiency as a likely culprit in this situation. Ofcourse, it could be a cause or a consequence, but the study I posted to you last time found it as a definate abnormal expression in 5 of 6 POTS patients tested.

Its also important to realise that some NET deficient patients may exhibit paradoxical symptoms - some suggesting NE excess such as increased peripheral resistance and postural hypertension, some suggesting low NE levels from depleted NE levels from overstimulation of release due to increased transduction. Dizziness and lightheadedness would appear paradoxical in elevated NE states, but is also a common feature. Cerebral vasospams have been speculated as a possible mechanism for this.

There are two studies suggesting NET deficiency as the primary cause of POTS in some patients, as well as unpublished findings at Toledo, Vandy and elsewhere that also suggest that NET deficiency is implicated in some forms of POTS. Dr Grubb's recent Clinical Update, and work by Dr Stewart also note it as a likely mechanism, so its fairly commonly accepted, but not definitively proven as a cause of POTS.

Again, I think last time I also talked about parasympathetic withdrawal in POTS and dysautonomia. There is much work coming out on this side of things in the near future. Normal sympathetic activity unopposed by faulty parasympathetic activity. Would result in normal NE levels.

[ramakentesh]

From what I understand, SNRIs act to inhibit the NET. If a person has a NET deficiency, then wouldn't that make it so that their bodies were just acting as if they were on an SNRI? Likewise, if a SNRI is working to prevent the NET deficiency from working to the fullest, why don't people who take SNRIs all develop the same symptoms that are linked between POTS and NET deficiency?

I think most patients that are speculated to have orthostatic intolerance from NEt deficiency have reduced NET expression but probably not a complete loss of NET expression. So SNRI would likely worsen a deficiency, but if there was none to begin with then this result seems unusual.

There is a study of rob. something which is a selective NE reuptake inhibator that demonstrated POTS-like symptoms in patients which was part of the reason NET was investigated in the first place in POTS.

[Maxine]

Thanks again for all your replies! My friend thought it was very interesting, but at that time she only read a couple responces.

I'm sure she will find the rest of the responces this very interesting and helpful. I had kind of a bad feeling for her on taking effexor, as I know how terribly sick she was in the beginning, and she got very overstimulated. Just certain smells would send her ANS spiraling out of control.

She has been trying to get through to Dr. Grubb, but she still hasn't received a call back. I know how busy is office is, and I'm not surprised. She just decided to check with a neurologist that has some knowledge on dysautonomia, and he has two POTs patients. He doesn't have nearly the experience of Dr. Grubb. Dr. Grubb knows her case, and he would be the best person to talk with about this. I told her to keep trying, and hopefully she'll get through.

Maxine :0)

[pat57]

ramakentesh,

I'm not understanding your points. (not your fault) But since I saw you mention vasospasms, and I get vasospasms (in my hands)

I have a question.

Do you suppose an SNRI would reduce the occurrence?

thanks,

Pat

[valliali]

Rama, do you know what some realistic tests are to test the NETs function? Tests one can have done without hving to enroll in a study or travel to Vandy or the Mayo? Have you had yours tested? I am not really sure I understand what the MSNA is and what it can tell you?

Also, how can one tell if they have parasympathetic withrdawal?

And lastly, is a NET deficiency/dysfunciton considered a genetic problem, or can it also result from something else (virus, lyme, etc)?

Thanks so much for sharing your wealth of knowledge. I have a lot to learn!

[ramakentesh]

Vasospasms in general - like in Raynauds are thought to occur from an overactive sympathetic response. In theory, SNRIs would result in a worsening of raynauds and a worsening of anything where an overactive sympathetic nervous system is implicated.

So I would think that in theory SNRIs would worsen vasospasms.

it has been suggested that the dizziness in 'hyperadrenergic' POTS (which itself is still somewhat a theory rather than a fact) is a result of a cerebral vasospasm from excessive norepinephrine and sympathetic activity. (too much NE results in whole body vasoconstriction to a degree - more specifically to the arms, legs, catorids and head). Other theories are that excessive NET results in eventual depletion of NE and impaired vaso/veno constriction and compensatory epinephrine and peripheral activation. (Not enough NE, so not enough vasoconstriction, epinephrine shoots off to increase blood flow to heart, hands and feet vasoconstrict to compensate).

Dr Stewarts work on low flow POTS also results in a type of sympathetic excess according to his recent work where reduced NO results in potentiation of NE activity with normal NE levels.

You can test NE reuptake by getting or requesting an MIBG scan of the heart with radiotagged Norepinephrine. This can measure reuptake quite easily. You can also get someone to take a vein biospy but that isnt so easy.

As for the suggested cause of NET deficiency:

http://jop.sagepub.com/cgi/content/abstract/20/4_suppl/60

Acquired hypermethylation - an epigenetic mechanism that results in a loss of function of the gene that regulates the expression of NET protein is implicated but not yet definitively demonstrated.

Abherant hypermethylation of gene promoters is the same mechanism that is implicated in many types of cancers (scary) and why this occurs is unknown - but exposure to chemicals and certain viruses have been implicated in the hypermethylation of promoters in other diseases for other genes (cancers, lung, breast and prostate as well as that one ive forgotten where a virus was implicated).

Again it could be that the functional loss of peripheral NET serves some other purpose or is the result of faultly release of norepinephrine.

parasympathetic withdrawal is still a fairly new area so i dont know enough to comment. Id suggest that it would result in a lower increase in heart rate, but similar symptoms to hyper types of POTS. (peripheral vasoconstriction, etc).

MSNA is the nerve firing rate that is used as a measure of sympathetic nervous system function. In POTS it is generally elevated - particularly on tilt and this increase does not always correlate with NE levels. why this is still unclear, but the nitric oxide thing earlier might explain it to some degree.

[ramakentesh]

To be honest possibly one of the only ways to tell would be through treatment. parasympathetic withdrawal may respond very well to mestinon; sympathetic excess would in theory respond well to some sort of alpha/beta blockade or alpha 2 agonists (clonidine, methyldopa)

[ramakentesh]

I dont get the arthritis connection - wish I did because I came down with Ank Spond as well as what was originally described as hyperadrenergic POTS out of the blue at the same time.

[valliali]

Hi Rama,

The other unusual thing in my case is that my NE and epi levels were actually on the lower end of normal. From what I am understanding, a person with NET deficiency but still "normal" NE levels would be on the high end of normal. However, I also did not have my NE levels tested during the TTT. I have only had urine tests and one plasma test in which they were drawn sitting then standing.

Also, I don't really have postural changes. Some days I do, but it's definitely not one of my most defining symptoms. Nor do I have much dizziness. Again, I go through periods with these symptoms, but when I describe my most troubling symptoms, they are not at the top of the list. Which seems to make me an unlikely fit for NET issues in that sense, though I have clear signs that I am overly sensitive to adrenaline. I am also GREATLY helped by beta blockers, especially non-selective ones. The amount that a small dose of propranolol has helped me is quite dramatic. So I know that there is something going on with my NE and epi, but I don't know if it's necessarily the way in which they are processes or the way in which my beta receptors respond to them.

I'm also troubled by some of the other symptoms that I have that don't match a profile for a solely NE issue. The bout of arthritis I experienced was just weird, as it sounds like your issues with ank spond are. You are fairly sure that they are related? The arthritis I had came several months after I started noticing changes, affected me pretty severely in the fingers, then went away. I also have enormous pressure in my head and neck, which I actually suppose could be related to NE if it is causing major vasoconstriction because it does feel as though my blood is unable to circulate and is just pounding through my arteries/veins. But beta blockers don't relieve that symptom at all. I also have not seen this symptom described when reading about NET, and it's probably my most severe one.

I am not really sure what kind of doctor I need to see to investigate this further. I have mentioned it to several, and they don't know what I'm talking about. Nor am I totally sure it's worth it to travel somewhere for some more tests. What can they do about it?

What do your doctors think about your ank spond and its relationship to your dysautonomia? What do they think triggered your problems? Have you ever tried an SNRI and had a similar response?