so very tired and it isn't getting better

[robertmarilyn]

Conclusion
Desvenlafaxine is an effective treatment for menopausal HFs.[/i]
____________
Curious about those side effects, I went down to the liberry to read that article and see how many patients discontinued desvenalfaxine. It was 28.5%, which struck me as a lot, especially if you're in a study. 93% of patients had adverse events, mostly nausea and dizziness. And that dosage is up there.
Muffy

In the last few months I have been experiencing my first major case of hot flashes. They started between the 7 weeks where my thyroid test showed 6.75 for TSH and when my TSH reading went down to .0somethingorother. I went from hypo to hyper. Went I started feeling them I thought I must not be so hypo anymore...I was right.

I started the Pristiq after that. Would I have even more hot flashes without it? or what? I'm hoping the hot flashes will become fewer or stop once my TSH is back up to a 'normal' (about 2?) level. I have been making sure my room is cool and I have the ceiling fan going and I wear very scant PJs so I don't notice them bothering me at night so much.

mar

[Muse-Inc]

....CrazyDrug boards...Desvenlafaxine for the treatment of vasomotor symptoms associated with menopause: a double-blind, randomized, placebo-controlled trial of efficacy and safety

Make ya wonder IF women will ever realize that big pharma wants you on one of their designer drugs for life when perfectly functional topical progesterone which is identical to what your body produced (21-23 mgms every day) before you stopped ovulating work so well and helps resolve sleep issues (falling and staying asleep). After menopause, women like men rely on the 2-4 mgms our adrenal glands produce. For most women, this is just not sufficient and we get unpleasant symptoms of too little estrogen. Topical progesterone 're-sensitizies' your estrogen receptors so that what is produced in your fat cells is suddenly sufficient to twart these symptoms. All this plus it activates the gene that protects against estrogen-mediated cancers like breast, uterus, ovaries, and prostrate. Good stuff. Just make sure the label says USP Progesterone and avoid all big pharma progestins. Oh, use cyclically, 3 wks on and 1 wk off and no more than 23 mgms/day. In perimenopause, day 1 is start of flow, use cream only on days 14-28. These are the recommendations of Dr. John Lee who was a pioneer in the use of topical progesterone, he started investigating his use for his breast cancer survivor patients who were developing osteoporosis and menopausal symptoms as they aged. Natural progesterone increases bone density.

PS in that Mt Everest Study, progesterone is one of the things that helped ameliorate the damages of the oxygen deprivation in altitude that mimics apnea.

[Muffy]

Interesting information, MI!

I started the Pristiq after that. Would I have even more hot flashes without it?

Well I ain't no statistician, but I'm lookin' and this data and sayin' "Huh?":

http://www.wyeth.com/news?nav=display&n ... 42616.html

A Placebo-Controlled Trial of Desvenlafaxine Succinate and Tibolone for Menopausal Vasomotor Symptoms

This 12-week, multicenter, randomized, double-blind, placebo- and active-controlled trial evaluated the safety and efficacy of Pristiq. The study included 451 postmenopausal women with 50 or more moderate-to-severe hot flashes per week, in multiple countries outside of the United States.

Results showed that at weeks four and 12, all groups experienced a decrease in the number and severity of hot flashes from baseline. There was no statistically significant difference between Pristiq and placebo; whereas, the difference between active comparator and placebo was significant.

When you look at the graphic presentation



it looks to me like placebo did pretty good. Maybe they should have increased the dose of placebo. Or just told the HF patients, "STOP THAT!!"

There was another study floating around at the same time.

The third study involved 508 women who were randomized to daily treatment with 100 mg desvenlafaxine, 2.5 mg tibolone, or placebo and were treated for 12 weeks. Tibolone (Xyvion), a synthetic hormone that is a selective estrogen-receptor modulator, is not approved for use in the United States but is approved for use in Europe and elsewhere. In this study, the 100-mg dosage of desvenlafaxine was not significantly different from placebo for reducing the frequency and severity of hot flashes and nighttime awakenings, and this dosage of desvenlafaxine was significantly worse than tibolone.

Muffy

[robertmarilyn]

Update

Haven't taken any Clonazepam or Nuvigil since Sept 12. During the middle of the night of Sept 15, our electricity when off, waking me up to horrendous stomach pains and bloating. With the urging of my husband, I have discontinued use of my CPAP machine for now. I may be back to where I started before I was given a CPAP machine at the beginning of March, but that place is a huge improvement over the severe stomach pain I have been feeling each night from using the machine. Now I will sleep for hours at a time before waking up with a sudden jolt rather than a full night of restless sleep/nonsleep.

Also my face is back to it's normal fair skinned healthiness rather than being irritated by the masks. So, I was waiting to see the neuro on Oct 5 but he called and asked me to come in on Sept 29 instead. My husband and I had a long talk with him as we went over the test results and records from my sleep doctor, endo doctor, and gastro doctor reports together. He said he was going to call my sleep doctor and endo doctor to discuss things with them. His main concern is the flat line on the chart below, accompanied by the what the brain waves are doing at that time.



So Monday morning I go into his his office for a "sleep deprived EEG". When I get up on Sunday morning, I don't get to sleep again until after my EEG test on Monday morning. Hyperventilation and lights will be used while I sleep hooked up to electrodes, to see how my sleepy deprived brain responds to the stimulation. After that I may or may not be sent to a clinic in another city, where I would be monitored over night or longer. Our city doesn't do this type of testing although he has tried to get the sleep clinic from which my current sleep doctor works, to provide such a service...at this point the owner of the clinic isn't prepared to do that.

I will see my sleep doctor Oct 13...and we can discuss my CPAP situation then. I wouldn't have discontinued the use just for my skin problem...I am willing to continue trying to make things better. I do need to be able to sleep with the machine and using the machine has not helped me sleep better at all when it causes stomach pain and bloating. And I am willing to stop taking the Pristiq too. I asked the neuro if he thought the Pristiq or Allegra D could be causing me sleep problems and he seemed confused about why I would think so. (I think he is looking at this from the angle of brain seizures...not so much from the angle of sleep hygiene.) But I also wanted to have some time between not taking the Nuvigil and the Clonazepam before stopping other meds just so I could have a better chance of seeing what might make a difference or not. Really though, I would prefer to take as few meds as possible.

As I just mentioned, I think the neuro is looking at this as a brain seizure situation that is disrupting my sleep. He said we are 'winging it' for now...he'd like to see if the "sleep deprived EEG" will show anything although something is much more likely to show up with an overnight or longer monitoring situation. We'll take one day at a time and go from there. It does look like he wants to work closely with my sleep doctor...he regards both my sleep doctor and endo doctor highly...he said my endo doctor is a "real" endocrinologist...he's a very good one to be treating me and my sleep doctor detected a patient having neuro problems from a conversation she was having with the patiend over the phone...she referred the patient to my neuro and they were able to help the patient with the problem...like I said, he regards both doctors highly and welcomes their input on what might be going on.

mar

[Muse-Inc]

Oh Mar, I hope they find a resolution for you! Pretty sad it's been so long without good answers, but it sounds like you've got a trio of great docs now. Got my fingers crossed they come up with some answers. Sorry you haven't been able to do the long rides, I know you must miss them. Keep us posted, rooting for you!

[Muffy]

Yo, mar.

Can you contrast that .jpg to try to reveal the THO and ABD a little better? I think something's backwards.

Muffy

[robertmarilyn]

Yo, mar.
Can you contrast that .jpg to try to reveal the THO and ABD a little better? I think something's backwards.
Muffy

Will do, I'll get on it now.
mar

[robertmarilyn]

Here you go Muffy,



mar

[Muffy]

His main concern is the flat line on the chart below, accompanied by the what the brain waves are doing at that time.

OK, to highlight a couple of things:



some of the things that may be happening here are:

There appears to be a reduction in airflow, which, since the effort bands are also somewhat reduced, suggest that this is central in nature;

It doesn't appear to be associated with anything, however...

As noted by another forum member, the leak rate is a little high relative to that pressure, so the waveform may simply be blunted secondary to the leak;

That heart rate pattern is confusing, but what I think is occurring is that there is a cortical arousal (marked in C4) that has an accompanying autonomic arousal (the corresponding tachycardia). Rather than two separate tachycardic events, it should be considered to be a single cardiac event that has 2 missed P-waves.

Based on the data you've presented, you've got a lot of missed P-waves.

All the waveforms should go up on inspiration and down on expiration, so inverting flow would make more sense--



Although this may be academic.

Muffy

[ozij]

Muffy,
Can you explain a bit more what you mean by "All the waveforms should go up on inspiration and down on expiration, so inverting flow would make more sense--"? Is that something you see on the chart?

And what is this about an academic discussion?

O.

[-SWS]

So Mar, are those the same brain and heart wave patterns that your sleep doctor said happened incessantly throughout your sleep study? If so, does your doctor still qualify these as highly unusual mini-seizures?

Also, Mar, what progress have your neurologist and sleep doctor made regarding an interpretive diagnosis and/or proposed treatment---including any experimental treatment(s)? Or do you or your doctor(s) now consider that your symptoms are successfully treated?

That heart rate pattern is confusing, but what I think is occurring is that there is a cortical arousal (marked in C4) that has an accompanying autonomic arousal (the corresponding tachycardia). Rather than two separate tachycardic events, it should be considered to be a single cardiac event that has 2 missed P-waves.

If I read Mar's earlier comments in this thread correctly, her sleep doctor seems to think these excessively-presented wave patterns adversely impact her architecture. And she seemed to agree about the patterns being highly unusual/confusing.

Based on the data you've presented, you've got a lot of missed P-waves.

A description of P-waves for those following along: http://www.madsci.com/manu/ekg_part.htm

All the waveforms should go up on inspiration and down on expiration, so inverting flow would make more sense--

...a bit more what you mean by "All the waveforms should go up on inspiration and down on expiration, so inverting flow would make more sense--"?

The waveform polarity/direction of the flow sensor appears inverted with respect to the other PSG wave forms---an academic point not really germane to diagnosis. At least that's my SWAG for the day...

[Muffy]

Based on the data you've presented, you've got a lot of missed P-waves.

And since the corresponding QRS is also missing, this phenomenon would be referred to as a "missed/skipped beat".

If you ask me, that particular epoch doesn't demonstrate EEG abnormality, but rather cardiac abnormality. If the whole night was like that, then "sick sinus syndrome" should be investigated.

I believe this is the one that may have triggered the "seizure" investigation:



but since it occurs during Wake, or in some semblance of Sleep Onset, I would have gone with "hypersynchronous theta" and left it at that (note that this opinion is not offered until after the EEG, of course).

Although this may be academic.

Academic in that no event was scored, but looking at the inverted waveform that I generated, flow now has a much less "flow-limited" appearance to it.

In addition to getting the original studies (to determine if she ever had SDB) perhaps we should get the raw data file and count up all the skipped beats.

Muffy

[Muffy]

Ooooh, I just saw a bad thing.

During the physician encounter, the abnormal EKG was not commented on. With those two tachycardic events circled, one would have assumed (and you know what happens when you assume) that they would have been looking at that a little more closely.



Maybe we'll have some use for those 50,000 rounds of ammunition after all.

Muffy

[-SWS]

Regarding Mar's arrhythmic cardiac waves: is the symptom purely a function of neurologically-disordered sleep or perhaps a diseased heart presentation? If heart disease, then there should also be a significant daytime presentation that cardiovascular diagnostics can flag. Supposedly heart disease can cause Mar's excessive fatigue. And her nocturnal hypopneic breathing patterns in that hypothetical case just might be secondary to heart disease and thus central in nature.

But again, regarding those same arrhythmic cardiac waves: is the symptom a presentation exclusive to sleep? And is this the wave pattern that Mar paraphrased her doctor earlier in the thread----as being both excessive and sleep-disruptive throughout the night? In that hypothetical case I would kind of wonder along the lines of hyper-arousability rather than classic hypopneic SDB---with that hyper-arousability perhaps presenting as concomitant episodes of cortical and autonomic arousals, and occasionally resulting in what are probably stimulus/response hypopneas.

I don't think the mini-seizures are sufficiently ruled out yet either...

So the big burning questions in my mind are: 1) which waveforms are the sleep-disturbing excessive ones, and 2) are the doctors stumped by what appears to be a highly atypical presentation?

[Muffy]

In attempting to analyze the available sparse data, there appears to be a great deal of Heart Rate Variability (HRV) that includes periods of sustained Wake:



Exceptions to that include REM (which would ordinarily make no sense, unless the REM is tonic), but apparently, that's not the only exclusionary criterion.

Besides, in analyzing HRV, you have to take out all the arrhythmia (including all the dropped QRS"s") so who knows what the heck that HR means. We really need to see the whole night EKG and count up all the missed beats. If there are only 6, then maybe NBD. If there are dozens to hundreds, then 24-hour Holter would seem appropriate.

I would love to see a HR night sans pseudephedrine.

My working hypotheses are: (1) there are no mini-seizures; and (2) there is no SDB.

Muffy