![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 25 of 77. This is the beginning of the thread.
Posted by btrout on March 16, 2002, at 13:36:15
Hi everyone,
I've been a frequent lurker and an infrequent poster. I've been through med after med over the last several months and I'd really like some comments or suggestions. I was originally diagnosed with CFS, and I have overt immune dysfunction with lots of food allergies that make me depressed. My depression is very anhedonic and apathetic, but not very anxious. Feeling sick and being depressed go hand in hand for me, always. I am on 10 mg Celexa currently, plus 2 mg reboxetine. More Reboxetine gives me insomnia and makes me feel like I have ADD. More Celexa makes me feel really sick with extreme insomnia if I take it at night and makes me very fatigued and sick-feeling if i take it durig the day. This dose of reboxetine gives me more energy but no depression relief and this dose of Celexa does nothing for me. The only times I have really felt well since I started the medication odyssey were when I was reducing my celexa dose from 40 mg in 10 mg increments. When I reduced the dose, I would feel sick for several days and then awesome,almost euphoric for several days. Then back to depression, but not as sick as I felt on the higher dose of Celexa. I also would have brief periods of feeling better as my next dose of celexa became slightly overdue.
I have tried the following and they have made me feel sick:effexor - never got above 37.5 mg
30mg remeron
1.25mg Zyprexa
2.5 mg Mirapex- not nauseated just depressed and sick
amantadine
Naltrexone 25 mg.- better for two days, then more depressedAfter I stopped the Zyprexa,I felt really good and energetic and happy for 3 days, and also could not sleep a wink. I feel good on occasional doses of caffeine. I'm thinking about trying amisulpride because I am still suspicious that what I need is more dopamine, judging from my response to SSRI's, but I'm afraid of having a bad response to it like I had with Zyprexa. I suspect part of the problem, though, with both zyprexa and remeron are these drugs' binding to adrenergic receptors. I do not think I handle adrenegic antagonist drugs well because of the CFS. I would really appreciate some suggestions, I'm feeling really rotten.
Thanks,
btrout
21 yo female
Posted by crepuscular on March 16, 2002, at 14:31:06
In reply to treatment resistant depression -Suggestions?, posted by btrout on March 16, 2002, at 13:36:15
maybe zoloft or wellbutrin would be worth a trial...
> Hi everyone,
> I've been a frequent lurker and an infrequent poster. I've been through med after med over the last several months and I'd really like some comments or suggestions. I was originally diagnosed with CFS, and I have overt immune dysfunction with lots of food allergies that make me depressed. My depression is very anhedonic and apathetic, but not very anxious. Feeling sick and being depressed go hand in hand for me, always. I am on 10 mg Celexa currently, plus 2 mg reboxetine. More Reboxetine gives me insomnia and makes me feel like I have ADD. More Celexa makes me feel really sick with extreme insomnia if I take it at night and makes me very fatigued and sick-feeling if i take it durig the day. This dose of reboxetine gives me more energy but no depression relief and this dose of Celexa does nothing for me. The only times I have really felt well since I started the medication odyssey were when I was reducing my celexa dose from 40 mg in 10 mg increments. When I reduced the dose, I would feel sick for several days and then awesome,almost euphoric for several days. Then back to depression, but not as sick as I felt on the higher dose of Celexa. I also would have brief periods of feeling better as my next dose of celexa became slightly overdue.
> I have tried the following and they have made me feel sick:
>
> effexor - never got above 37.5 mg
> 30mg remeron
> 1.25mg Zyprexa
> 2.5 mg Mirapex- not nauseated just depressed and sick
> amantadine
> Naltrexone 25 mg.- better for two days, then more depressed
>
> After I stopped the Zyprexa,I felt really good and energetic and happy for 3 days, and also could not sleep a wink. I feel good on occasional doses of caffeine. I'm thinking about trying amisulpride because I am still suspicious that what I need is more dopamine, judging from my response to SSRI's, but I'm afraid of having a bad response to it like I had with Zyprexa. I suspect part of the problem, though, with both zyprexa and remeron are these drugs' binding to adrenergic receptors. I do not think I handle adrenegic antagonist drugs well because of the CFS. I would really appreciate some suggestions, I'm feeling really rotten.
>
> Thanks,
> btrout
> 21 yo female
Posted by btrout on March 16, 2002, at 15:33:36
In reply to Re: treatment resistant depression -Suggestions?, posted by crepuscular on March 16, 2002, at 14:31:06
> maybe zoloft or wellbutrin would be worth a trial...
>
>
Several years ago, I gave Wellbutrin SR a 10 week trial at 150 mg with no effect. Do you think it is worth it to try again at a higher dose?Btrout
Posted by polarbear206 on March 16, 2002, at 16:59:03
In reply to treatment resistant depression -Suggestions?, posted by btrout on March 16, 2002, at 13:36:15
> Hi everyone,
> I've been a frequent lurker and an infrequent poster. I've been through med after med over the last several months and I'd really like some comments or suggestions. I was originally diagnosed with CFS, and I have overt immune dysfunction with lots of food allergies that make me depressed. My depression is very anhedonic and apathetic, but not very anxious. Feeling sick and being depressed go hand in hand for me, always. I am on 10 mg Celexa currently, plus 2 mg reboxetine. More Reboxetine gives me insomnia and makes me feel like I have ADD. More Celexa makes me feel really sick with extreme insomnia if I take it at night and makes me very fatigued and sick-feeling if i take it durig the day. This dose of reboxetine gives me more energy but no depression relief and this dose of Celexa does nothing for me. The only times I have really felt well since I started the medication odyssey were when I was reducing my celexa dose from 40 mg in 10 mg increments. When I reduced the dose, I would feel sick for several days and then awesome,almost euphoric for several days. Then back to depression, but not as sick as I felt on the higher dose of Celexa. I also would have brief periods of feeling better as my next dose of celexa became slightly overdue.
> I have tried the following and they have made me feel sick:
>
> effexor - never got above 37.5 mg
> 30mg remeron
> 1.25mg Zyprexa
> 2.5 mg Mirapex- not nauseated just depressed and sick
> amantadine
> Naltrexone 25 mg.- better for two days, then more depressed
>
> After I stopped the Zyprexa,I felt really good and energetic and happy for 3 days, and also could not sleep a wink. I feel good on occasional doses of caffeine. I'm thinking about trying amisulpride because I am still suspicious that what I need is more dopamine, judging from my response to SSRI's, but I'm afraid of having a bad response to it like I had with Zyprexa. I suspect part of the problem, though, with both zyprexa and remeron are these drugs' binding to adrenergic receptors. I do not think I handle adrenegic antagonist drugs well because of the CFS. I would really appreciate some suggestions, I'm feeling really rotten.
>
> Thanks,
> btrout
> 21 yo femaleHi!
I think your main med should be a mood stabilizer. You probably have an underlying bipolar depression. There is a broad spectrum to mood disorders. When you find the right mood stabilizer you probably won't have any problems with the antidepressants working. You need to find a balance with the both.
Posted by shelliR on March 16, 2002, at 17:11:51
In reply to treatment resistant depression -Suggestions?, posted by btrout on March 16, 2002, at 13:36:15
Hi Btrout,
I noticed that you left out a whole group of drugs-namely mood stabilizers. Some people also benefit by adding stimulents (ritalin, dexadrine, etc) to their mix. I have seen a lot of people on this board be success with lamictal. I don't think you've yet tried enough meds to be labeled treatment resistant. BTW, lamictal is the only drug I've had success with after trying over 20, and I had many many good years on nardil before it pooped out for me a few years ago.
Shelli
Posted by mike21 on March 16, 2002, at 19:01:16
In reply to treatment resistant depression -Suggestions?, posted by btrout on March 16, 2002, at 13:36:15
Maybe st. johns wort would be worth a try. It usually has few if any side effects. (One occasional side effect is upset stomach which can be remedied by taking it with food). There is also evidence to suggest it affects the immune system by lowering levels of interleukin-6. It could be that your allergies are causing your immune system to induce some of your depression by raising levels of cytokines. This is the article I read about sjw and the immune system:
http://www.hypericum.com/hyp40.htm
This is another interesting article about depression and the immune system:
http://www.biopsychiatry.com/immunesystem/
Good luck and keep us posted,
Mike
> Hi everyone,
> I've been a frequent lurker and an infrequent poster. I've been through med after med over the last several months and I'd really like some comments or suggestions. I was originally diagnosed with CFS, and I have overt immune dysfunction with lots of food allergies that make me depressed. My depression is very anhedonic and apathetic, but not very anxious. Feeling sick and being depressed go hand in hand for me, always. I am on 10 mg Celexa currently, plus 2 mg reboxetine. More Reboxetine gives me insomnia and makes me feel like I have ADD. More Celexa makes me feel really sick with extreme insomnia if I take it at night and makes me very fatigued and sick-feeling if i take it durig the day. This dose of reboxetine gives me more energy but no depression relief and this dose of Celexa does nothing for me. The only times I have really felt well since I started the medication odyssey were when I was reducing my celexa dose from 40 mg in 10 mg increments. When I reduced the dose, I would feel sick for several days and then awesome,almost euphoric for several days. Then back to depression, but not as sick as I felt on the higher dose of Celexa. I also would have brief periods of feeling better as my next dose of celexa became slightly overdue.
> I have tried the following and they have made me feel sick:
>
> effexor - never got above 37.5 mg
> 30mg remeron
> 1.25mg Zyprexa
> 2.5 mg Mirapex- not nauseated just depressed and sick
> amantadine
> Naltrexone 25 mg.- better for two days, then more depressed
>
> After I stopped the Zyprexa,I felt really good and energetic and happy for 3 days, and also could not sleep a wink. I feel good on occasional doses of caffeine. I'm thinking about trying amisulpride because I am still suspicious that what I need is more dopamine, judging from my response to SSRI's, but I'm afraid of having a bad response to it like I had with Zyprexa. I suspect part of the problem, though, with both zyprexa and remeron are these drugs' binding to adrenergic receptors. I do not think I handle adrenegic antagonist drugs well because of the CFS. I would really appreciate some suggestions, I'm feeling really rotten.
>
> Thanks,
> btrout
> 21 yo female
Posted by btrout on March 16, 2002, at 19:46:55
In reply to Re: treatment resistant depression -Suggestions?, posted by mike21 on March 16, 2002, at 19:01:16
Hi everyone,
thank you for the suggestions. I'm so pleased. I had been thinking along similar lines about trying stimulants (probably adderal), mood stabilizers (currently trying nimodipine), and just before I read Mike's post about SJW, I had been researching the IL-6 connection on medline. I think it is very likely I have elevated IL-6 levels because of the delayed type hypersensity that characterizes my food allergies. I think SJW is also interesting in that it appears to inhibit the uptake of serotonin, noradrenaline, and dopamine equally. I do wonder about how powerful the stuff is because it has only been shown to work for mild to moderate depression, and mine is more like moderate to severe. Has anybody heard any stories about good responses to SJW on this board?
With regard to the mood stabilizer, I recently took 700mg of Neurontin over a 3 hour period (per Jay Goldstein's protocol) with no apparent effect, good or bad. Does this response indicate anything to anyone? Does anyone have any info about Gabitril?
You guys are so generous for responding. YOu've given me a lift tonight. Thank you.btrout
Posted by Darby on March 17, 2002, at 0:36:11
In reply to treatment resistant depression -Suggestions?, posted by btrout on March 16, 2002, at 13:36:15
btrout --
I'd agree with most of what's been said. There are far too many meds/combinations you haven't tried to be labelled TR. I'd stay with an SSRI as a foundation, only switch to one that tends to be less sedating like Prozac (10 or 20 mg). A mood stabilizer/ anti-convulsant like Lamictal or Gabitril (again less sedating) would be excellent. Small am dose of stimulant might help.
After 12 years of searching (and trying every almost major psych med), I'm doing 20mg of Prozac and 8mg (b.i.d)of Gabitril and have never felt better in my life. I took Prozac (by itself) at a much higher dose many years ago, with mixed results. Taken with Gabitril, there seems to be a synergy that's given me unbelievable relief. Lamictal worked very similarly when I took it with Celexa.
This SSRI/GABA approach has worked wonders for me.
Good Luck,
Darby
Posted by Blue Cheer 1 on March 17, 2002, at 2:11:19
In reply to Re: treatment resistant depression -Suggestions?, posted by Darby on March 17, 2002, at 0:36:11
Hi, btrout. I know it's easier said than done, but you need to find a psychopharmacologist who will go through your psychiatric history, family history, etc., like a detective, correctly diagnose you, and devise a systematic treatment plan tailored for your needs. Also, psychotherapy during pharmacotherapy (or when you're able to benefit from it) is helpful. I agree that you might try higher doses (or the maximum tolerable doses of the drugs you try).
Good luck,
Blue
Posted by SLS on March 18, 2002, at 8:10:56
In reply to Re: treatment resistant depression -Suggestions?, posted by Darby on March 17, 2002, at 0:36:11
Hi Darby.
> After 12 years of searching (and trying every almost major psych med), I'm doing 20mg of Prozac and 8mg (b.i.d)of Gabitril and have never felt better in my life. I took Prozac (by itself) at a much higher dose many years ago, with mixed results. Taken with Gabitril, there seems to be a synergy that's given me unbelievable relief. Lamictal worked very similarly when I took it with Celexa.
Your Gabitril story is exciting. How long did it take for it to start working? What side effects are there?I'm curious as to how you would describe the depression you suffered from. I'm sort of bipolar, and the main features of my depression include extreme fatigue, a burdonsome heaviness and weakness in my limbs, and a general lack of energy and motivation to move, even to get off a chair to go to the bathroom. Also, my memory is impaired and I can't read more than a few sentences before I have to stop - and then only with minimal comprehension.
Would you considered to be treatment-resistant? What drugs had you tried in the past.
I would really appreciate any information you can provide me with.
Thanks.
- Scott
Posted by petters on March 18, 2002, at 10:26:48
In reply to Re: treatment resistant depression -Suggestions? » Darby, posted by SLS on March 18, 2002, at 8:10:56
Dear Scott!!
Have you tried amantadin yet,to you current mix?
I have seen one case similar like yours, with bipolar depression and letargi, heavyness and some atyptical features. This person had a med mixture similar like yours, if my memory is not a fault. She had tried almost everthing.When amantadin was added, to her mix the depression, that she had for year, disapperad.
She had almost tried everthing before.
I will look for memantine (wrong spelling?) in my country, and in Germany. I know you would like to make a trial on it.
Take care of your self...//Petters
Posted by btrout on March 18, 2002, at 12:08:29
In reply to Re: treatment resistant depression -Suggestions?, posted by Darby on March 17, 2002, at 0:36:11
Can you describe more how you felt on an SSRI with and without the addition of a mood stabilizer? Have you ever tried Neurontin? Is Neurontin a mood stabilizer? How long does it take to respond to a mood stabilizer?
My nimodipine (as mood stabilizer) trial continues. This is my third day. I seemed to be more relaxed and happy yesterday, but I will have to see if this continues.btrout
> This SSRI/GABA approach has worked wonders for me.
>
> Good Luck,
>
> Darby
Posted by shelliR on March 18, 2002, at 20:39:09
In reply to Re: treatment resistant depression -Suggestions? » Darby, posted by SLS on March 18, 2002, at 8:10:56
" I'm sort of bipolar, and the main features of my depression include extreme fatigue, a burdonsome heaviness and weakness in my limbs, and a general lack of energy and motivation to move, even to get off a chair to go to the bathroom. Also, my memory is impaired and I can't read more than a few sentences before I have to stop - and then only with minimal comprehension."
Hi Scott,I'm not someone who thinks that everyone has chronic fatigue syndrome, but your symptoms of not being able to get up seem so much like people's description of CFS. Is that something you and your doctor have discussed? Also, I do not usually tout the use of opiates--I see them as a last resort. But I'm curious what your reaction has been if you've ever tried them. I wondering because some people feel tired on them; other people like me find them very energizing. You've been in very bad shape for a long long time. I wonder if opiates (including buprenorphine) might give you your life back until you can find a medication that works for you. (They did give me back my life.) I do know that buprenorphine set off a psychotic mania when Zoe tried tried it with a diagnosis of BPII. But I do know others with BPII who found it lifted them up and did not cause a manic episode.
But if not opiates, focusing on building up your immune system. Maybe the answer for you is not in mood stabilizers or ADs. I know that Lorraine has lots of information on the immune system and depression and fatigue. She had the same problem as I did, trying several dozen drugs and not finding any that she could tolerate AND that helped. (I do think provigal is helping her to some extent.)
Wishing you the best,
Shelli
Posted by btrout on March 18, 2002, at 22:13:49
In reply to treatment resistant depression -Suggestions?, posted by btrout on March 16, 2002, at 13:36:15
Hi,
Wanted to post an update on the nimodipine trial. It seems to make me more energetic... but increases my anxiety to very surprising levels considering I am not typically very anxious. It also has been making me increasingly nauseated. I read an abstract that said that nimodipine inhibits the release of GABA. I'm going to try gabitril next...btrout
Posted by allisonm on March 19, 2002, at 7:08:05
In reply to Re: treatment resistant depression -Suggestions?, posted by btrout on March 18, 2002, at 22:13:49
How closely are you working with your pdoc? What is his or her plan for next steps should your current combo not work? Does your doctor talk with you about side-effects? Other than the Celexa, have you tried these other drugs for descent lengths of time (several weeks up to 6-8)?
Have you ever seen an algorithm such as Harvard's (http://www.mhc.com/Algorithms/). I have found it interesting and helpful in seeing how doctors proceed in trying to help people with depression.
My psychiatrist, whom I see once a week, has diagnosed me with chronic refractory depression. We believve I have had this for many years -- perhaps as early as the mid-1970s. I was diagnosed a little more than 4 years ago and have taken in various combinations and amounts Zoloft, Effexor XR, Remeron, Lithium, Wellbutrin SR, Neurontin, Celexa, Serzone, and on occasion, Ativan. I have found that a combination of Wellbutrin SR (300mg per day) and Serzone (300mg per day) work best so far.
As the others have said, don't give up. There are lots and lots of drugs out there. If you have a good doctor who knows his pharmacology and is up-to-date with what's new, he/she should be your best guide.
I also think it's important to remember that instant miracles are rare. It can take years to find the right combo if you are treatment-resistant. I also have found that my improvement came slowly. It was not overnight. I didn't wake up one morning deciding that I felt terrific. It can take months of work before you can look back and see whether there really has been a change for the better.
I have found that good psychotherapy with good drug therapy works best. I am lucky to have one person for both. During our weekly apppointments, he sees things about me that I don't. He can see patterns and declines in my moods and suggests changes in drug therapy accordingly. I would not be here were it not for him.
Good luck. It may be a long road, but many find the right answers on the way.
Posted by Ron Hill on March 19, 2002, at 11:55:00
In reply to Re: treatment resistant depression -Suggestions?, posted by btrout on March 16, 2002, at 19:46:55
Ms. Brook Trout;
You sound like an intelligent young lady. Two things came to my mind when I read your original post in this thread. First, like others, I wondered if a mood stabilizer might help you and, second, I wonder if SAM-e may be of benefit to you. I (a layman) agree with you that your anergic symptoms are due to dopamine problems. Please read the following two posts in order to more fully understand what I am referring to.
http://www.dr-bob.org/babble/20020313/msgs/97982.html
http://www.dr-bob.org/babble/20020318/msgs/98710.html
Let me know if I can help!
-- Ron
-----------------------------------------------> Hi everyone,
> thank you for the suggestions. I'm so pleased. I had been thinking along similar lines about trying stimulants (probably adderal), mood stabilizers (currently trying nimodipine), and just before I read Mike's post about SJW, I had been researching the IL-6 connection on medline. I think it is very likely I have elevated IL-6 levels because of the delayed type hypersensity that characterizes my food allergies. I think SJW is also interesting in that it appears to inhibit the uptake of serotonin, noradrenaline, and dopamine equally. I do wonder about how powerful the stuff is because it has only been shown to work for mild to moderate depression, and mine is more like moderate to severe. Has anybody heard any stories about good responses to SJW on this board?
> With regard to the mood stabilizer, I recently took 700mg of Neurontin over a 3 hour period (per Jay Goldstein's protocol) with no apparent effect, good or bad. Does this response indicate anything to anyone? Does anyone have any info about Gabitril?
> You guys are so generous for responding. YOu've given me a lift tonight. Thank you.
>
> btrout
Posted by Ron Hill on March 19, 2002, at 12:26:05
In reply to Re: treatment resistant depression -Suggestions? » Darby, posted by SLS on March 18, 2002, at 8:10:56
>I'm sort of bipolar, and the main features of my depression include extreme fatigue, a burdonsome heaviness and weakness in my limbs, and a general lack of energy and motivation to move, even to get off a chair to go to the bathroom. Also, my memory is impaired and I can't read more than a few sentences before I have to stop - and then only with minimal comprehension.
-------------------------------Scott,
A lot of people on this board care about you very much. I am one of them. You are a very giving person.
Do you think your symptoms (extreme fatigue, a burdonsome heaviness and weakness in limbs, and a general lack of energy and motivation to move) are related to dopamine problems? To understand more fully what I am getting at, please read the following post:
http://www.dr-bob.org/babble/20020318/msgs/98710.html
Also, I think I remember that you were taking SAM-e last year and finding some benefit from it. Am I remembering this correctly? If so, please tell me about your SAM-e experience. Did you take plenty of B-6, folic acid, and sublingual B-12 with the SAM-e.
-- Ron
Posted by Dave1 on March 19, 2002, at 19:42:56
In reply to Re: treatment resistant depression -Suggestions? » SLS, posted by Ron Hill on March 19, 2002, at 12:26:05
Hi,
I recently had some success with anafranil and lithium after many failures on other drugs. Be sure to have your lithium blood level checked.
Good luck,
Dave
Posted by SLS on March 19, 2002, at 20:48:39
In reply to Re: treatment resistant depression -Suggestions? » SLS, posted by Ron Hill on March 19, 2002, at 12:26:05
For Petters, ShelliR, Ron, and others,
I really appreciate your concern and contributions. I can't reply to your posts right away because it takes me so long to read through them - I guess you know that already.
Thanks again.
As for the involvement of dopaminergic neurotranmission in depression, particular anergic/anhedonic depression, I first focused my attention on it in 1983. I have always suspected that it plays a central role in my case. I just don't know what to do about it.
And again.
- Scott> >I'm sort of bipolar, and the main features of my depression include extreme fatigue, a burdonsome heaviness and weakness in my limbs, and a general lack of energy and motivation to move, even to get off a chair to go to the bathroom. Also, my memory is impaired and I can't read more than a few sentences before I have to stop - and then only with minimal comprehension.
> -------------------------------
>
> Scott,
>
> A lot of people on this board care about you very much. I am one of them. You are a very giving person.
>
> Do you think your symptoms (extreme fatigue, a burdonsome heaviness and weakness in limbs, and a general lack of energy and motivation to move) are related to dopamine problems? To understand more fully what I am getting at, please read the following post:
>
> http://www.dr-bob.org/babble/20020318/msgs/98710.html
>
> Also, I think I remember that you were taking SAM-e last year and finding some benefit from it. Am I remembering this correctly? If so, please tell me about your SAM-e experience. Did you take plenty of B-6, folic acid, and sublingual B-12 with the SAM-e.
>
> -- Ron
Posted by Ron Hill on March 19, 2002, at 21:40:32
In reply to Re: treatment resistant depression -Suggestions?, posted by SLS on March 19, 2002, at 20:48:39
Scott,
What about your past exeriences, if any, with SAM-e and the associated B viaimins. Answer at your leasure.
-- Ron
Posted by SLS on March 20, 2002, at 8:45:38
In reply to Re: treatment resistant depression » SLS, posted by Ron Hill on March 19, 2002, at 21:40:32
> Scott,
>
> What about your past exeriences, if any, with SAM-e and the associated B viaimins. Answer at your leasure.
>
> -- Ron
Hi Ron.About a 1 1/2 years ago, I was "in between" drugs. I was in real bad shape. I was hoping to use something as a bridge to get me through the waiting period between a change in doctors. I had spent most of the summer in a very strange state of a worsened depression that seemed to have mutated in conjunction with exposure to a combination of lamotrigine + gabapentin + sulpiride + modafinil. It was an unfamiliar state to me, and I can't remember a time when my consciousness was so dampened and numbed. Things seemed real strange, and I couldn't figure out how to do the simplest things. It was at this point that I decided to try taking S-AMe, hoping that it would help me to avoid committing suicide (or some such thing).
After the very first dose (200mg I think), I perceived an increase in mental energy, but it felt somewhat uncomfortable. I was terrified to continue with it because I was afraid that it might screw-up my brain function more than it already had been by the previous drug trial. I take a vitamin B-Complex 50 every day, along with a multi-vitamin, vitamin-C 1000mg., and vitamin-E 800mg.
Thanks, Ron.
Sincerely,
Scott
Posted by petters on March 21, 2002, at 2:03:23
In reply to Re: treatment resistant depression » Ron Hill, posted by SLS on March 20, 2002, at 8:45:38
Hi Scott..
I really hope your shape is not to bad. You are really a supportive and giveness person, with a lot of warmth in your personality. It is really an resources to have you on a site like this.
Your knowelles about affecitve disorders are really impressive. You have more to say than many of the pdoc I have met during a couple of years. I really mean this, with no thought of trying to flatter you. I know one have to have knowless if one have an refractary affective disorders of any kind.
Good news in my cases. I have started olanzapin for four days ago. 5 mg at night. I have a very nice result. My depression have lifted, and my sleep is greath. I alwas respond very fast, when a drug worked for me. But I`m very scared for the dam-d poop out. I pray that this not occure for me this time. I know you are also make a trial on olanzapin once with temporary benefites, unfortunately.
My current mix:
T. venlafaxin 225 mg
T. lamotrigine 100 mg
T. litium ( serum level, 0,5 )
T. olanzapine 5 mgI give you my best wishes, and take care of yourself, and please don´t give up, there is allway new med options. I´t is like having an winning ticket, when the right meds are found for you, and finaly kick in.
Petters.
Posted by SLS on March 21, 2002, at 10:55:52
In reply to Re: treatment resistant depressionSLS, posted by petters on March 21, 2002, at 2:03:23
Hi Petters.
> Good news in my cases. I have started olanzapin for four days ago. 5 mg at night. I have a very nice result. My depression have lifted, and my sleep is greath. I alwas respond very fast, when a drug worked for me. But I`m very scared for the dam-d poop out. I pray that this not occure for me this time.I will pray too.
More good news (I hope):
I have not seen anyone experience a poop-out of the antidepressant effects of olanzapine (or any of the other atypical neuroleptics), once a good response has been established for 3 or 4 weeks. I hope this is true for you also.
I have discontinued venlafaxine. I have determined that it reacts badly in combination with tricyclics in me. It makes things worse. I am going back to try nortriptyline again at 100mg. Imipramine affects my memory and cognition too much. It is probably the result of the anticholinergic effects. www.biopsychiatry.com calls imipramine "the stupid drug". Imipramine is not too bad at dosages of 200mg and less. Unfortunately, I need 300mg for it to have any beneficial effect. Perhaps taking an acetylcholine cholinesterase inhibitor drug like donepezil would help mitigate the cognitive side effects.
My current medications:
lamotrigine 300mg
nortriptyline 100mgI will give this a few weeks before making any changes. I am encouraged by what I feel. However, it has only been 3 days at 100mg.
> I know you are also make a trial on olanzapin once with temporary benefites, unfortunately.
I added olanzapine to Parnate + desipramine. I started at 2.5mg. I felt an improvement during the first 3 days, but it faded. The improvement did not disappear completely, though. When I raised the dosage to 5.0mg., I experienced significant cognitive side effects that required me to discontinue it. My mind felt numb - "zombie" and "foggy". I felt disconnected from the things around me. I could not think clearly. When driving a car, I would forget where I was. Things were not familiar. It was too much. This also happened with risperidone and ziprasidone.
I think I will probably need another drug. I might choose Nardil (phenelzine) to add next. If necessary, I might then try again to add either olanzapine, ziprasidone, or aripiprazole. I will also consider adding pramipexole.
What do you think of aripiprazole (Abilitat)? Is it available in Europe?
> My current mix:
>
> T. venlafaxin 225 mg
> T. lamotrigine 100 mg
> T. litium ( serum level, 0,5 )
> T. olanzapine 5 mgI will also consider taking lithium at low dosages like you. How much do you take? What blood-levels are necessary? I don't like the way I feel when I take lithium at dosages of 600mg. and higher. I feel apathetic. I lose my sense of myself (ego). I want lithium because of its neuroprotective and neurotrophic potential. It is supposed to promote plasticity. Maybe this would help to restore the size and function of the hippocampus. What do you think? Depression has greatly impaired my memory.
> I give you my best wishes, and take care of yourself, and please don´t give up, there is allway new med options. I´t is like having an winning ticket, when the right meds are found for you, and finaly kick in.Thank you, my friend.
STAY WELL !!!
Sincerely,
Scott
Posted by Ron Hill on March 21, 2002, at 16:33:03
In reply to Re: treatment resistant depressionSLS » petters, posted by SLS on March 21, 2002, at 10:55:52
Scott,
I want to help you! You have been in pain too long, and you are too nice of a guy for me to just dismiss.
For six years I went from one drug trial to the next never finding long term relief for the depressive side of my BPII. Thanks to a pdoc that does more than just listen to what the drug company reps tell him, I now have my solution; 600 mg/day Lithobid and 200 mg/day SAM-e. (B-6, folic acid, and SUBLINGUAL bioactive B-12 must also be taken. I also add some phosphatidylserine and phosphatidylcholine 'cause they feel good in my brain.
For you, it might be 300 mg/day Lamictal and 400 mg/day SAM-e (or as high as 1600 mg/day SAM-e if needed). Start by using 100 or 200 mg/day of SAM-e as an add-on to your current cocktail, then play it by ear to see if you can discontinue your AD.
PLEASE read the very well written and technically informative SAM-e article (posted previously by davex) linked below. All I can do is put out the bread; it's up to you to decide whether or not to eat.
-- Ron
P.S. I know it is currently difficult for you to read. I am so sorry that you are in so much pain. Just take your time, resting as needed.
-----------------http://www.immunesupport.com/news/SAMe2txt.htm
S-Adenosylmethionine (SAMe): Fast-Acting Natural Antidepressant
SAMe is a substance synthesized in the body from the amino acid, methionine. An enzyme called methionine S-adenosyltransferase (MAT) catalyzes a reaction between methionine and ATP to form SAMe. SAMe has numerous actions within the body: its importance has been demonstrated in numerous published studies.
SAMe has three important actions:
1. Methylation-SAMe is a "methyl donor" for the synthesis of neurotransmitters, DNA, RNA, protein, and phospholipids;
2. Transsulphuration-SAMe is the precursor for cysteine, glutathione and taurine;
3. Polyamines-SAMe and Arginine catalyze the synthesis of spermine, spermidine and putrescine, which are essential for cell growth and differentiation.A Methyl Donor
SAMe "donates" methyl groups to other molecules in order to stimulate biochemical reactions that transform these molecules into bioactive substances. For example, when methyl groups are transferred from SAMe to certain phospholipids, phosphatidylcholine is produced. This important lipid is found in all cell membranes. Its presence or absence affects how cells react to stimuli from the outside environment because it controls accessibility of the cell membrane to signals from the outside.Phosphatidylcholine makes cell membranes pliant. The other lipid in cell membrane-cholesterol-makes them stiff. Stiff membranes do not transmit signals as well as pliant membranes because more receptors are exposed in pliant membranes. There is also evidence that there may be distortion in the receptors of overly viscous cells. Receptors and molecules that occupy them are like parts of a jigsaw puzzle. With a malformation, and the piece may fit into its "receptor", but the fit will be imperfect. And any signal between the two pieces will be impaired. Cells with an overabundance of cholesterol simply "don't get the message."
Aging causes "hardening" of cell membranes. With age, the ratio of phosphatidylcholine- to-cholesterol decreases, and cholesterol becomes predominant. Decreased methylation which occurs with age plays a part in this lipid alteration. This is one area where the increased methylation that SAMe causes, protects and enhances cell integrity.
Methylation of DNA is another area where SAMe goes into action. The methylation of DNA causes the activation or inactivation of genes. Activated genes transcribe proteins. Without the proper transcription of proteins, cells cannot grow or function optimally. Activating or inactivating genes can stop tumor growth.
Other important processes that involve methylation are the suppression of viruses, the activation of heat shock proteins, and the synthesis and signaling of cytokines.
Transsulphuration
SAMe is the precursor for the sulfur amino acids cysteine and taurine, as well as the tripeptide glutathione. SAMe is first transformed into S-adenosylhomocysteine, which is then converted into cysteine and taurine. Sulfur compounds are so important that it has been written that "under conditions of absolute deficiency of sulfur, there is no living material." Every cell in the body contains sulfur compounds.The end products of the transsulphuration pathway-free radical scavengers-are important. Glutathione is the most important substance in the liver. The liver's principle function is to break down damaging substances the body encounters. These may be drugs, or the body's own products. Liver malfunction- whether caused by alcohol, viral infection or other disorder-is invariably accompanied by glutathione depletion. When glutathione is depleted, the liver simply can't do its job. Glutathione is also found in other organs. It inihibits the deleterious effects of inflammation throughout the body. And it is an extremely potent free radical scavenger in the eye, where it protects against cataracts caused by UV sunlight. By providing the building blocks of glutathione, SAMe contributes to maintenance of this important natural antioxidant.
Polyamines
These biochemical bombshells bind DNA and regulate gene expression. They make cell membranes act younger (more fluid), and repair DNA. We will be telling you much more about the importance of polyamines in future issues.Natural Antidepressant
The most compelling clinical evidence for SAMe is the hundred-plus published studies regarding its benefit in depression. SAMe is the most well-documented non-drug antidepressant available today.According to the latest data from the Center for Disease Control's (CDC) National Center for Health Statistics (NCHS), suicide is the 9th leading cause of death in the U.S., after AIDS, which ranks 8th. In people aged 25-44, it is the 5th leading cause of death; and in those aged 15-24, it is the 3rd leading cause of death, following accidents and homicides. In 1995, the number of suicides exceeded the number of homicides in the U.S. Clearly suicide is a major health problem.
It was estimated that successful suicides and suicide attempts cost over $16 billion in 1994-in lost earnings, hospitalizations, and the like. This year, thousands of Americans will suffer a serious bout of depression, which is the Number One cause of suicide! It has been reported that every American will suffer at least one bout of depression during their lifetime. People with serious physical illness are often depressed, and it is occurring with greater frequency in the elderly and in young adults.
Antidepressant drugs are part of a billion dollar psychopharmacology industry that, according to some physicians, churns out dangerous, addictive products. While antidepressants work in most patients, there are drawbacks. According to statistics from the Substance Abuse and Mental Health Services Administration (SAMSHA), 53% of drug-related admissions to emergency rooms are due to overdose. People frequently overdose on tricyclic antidepressants during the lag time between the time the drug is prescribed, and when it starts working. In 1994, 90% of emergency room visits related to tricyclic antidepressants were for overdose (intentional and unintentional).
Europe's Best-Kept Secret
In the 1970s, while testing SAMe as a treatment for schizophrenia, Italian researchers discovered that their patients were becoming less depressed. This set off a wave of studies that continues to the present. In study-after-published-study, SAMe is equal, or superior, to tricyclic antidepressants. Not only is it usually more effective, it works faster, and without significant side effects.SAMe has been proven effective in every type of depression, and seems particularly good for the endogenous form, where people are depressed without any apparent external cause. Even people with depression so severe they were contemplating electroshock therapy (ECT), have been "saved" by SAMe. Bipolar depression (manic depressive) may be an exception to SAMe's otherwise good record. SAMe can cause some people with this type of depression to switch from depression to mania. This effect does not always occur.
SAMe's anti-depressant effect begins anywhere from immediately to 5 weeks. Most patients benefit within 4 days, which is faster than most antidepressant drugs.
Clinical Studies Support Efficacy, Safety and Quick Action
In 1987, the University of Alabama and the University of Trieste (Italy), along with BioResearch S.A. (which manufactures SAMe) sponsored a symposium on SAMe. The purpose of the meeting was to gather all the data together on using SAMe as a treatment for neuropsychiatric disorders. Among the papers presented were the results of a study done at the University of California at Irvine on 18 patients hospitalized for depression. In this study, intravenous SAMe was compared to oral imipramine (Tofranil). The researchers found that 67% of the SAMe patients had 50% or greater improvement by the 14th day of the study, compared to only 22% of the patients given imipramine.A larger study by DeVanna and Rigamonti confirmed these results in a placebo controlled, double-blind study using oral SAMe. In this study, patients with major depression were given 1,600 mg of SAMe per day. In order to reduce the "placebo effect", DeVanna and Rigamonti gave the patients a placebo for a week before beginning the real trial. Patients who felt better after taking the sugar pill were excluded from the study.
Using four different depression scales to measure response, the researchers found that by day 10, SAMe had decreased depression 27% versus imipramine's 18% on the Hamilton Rating Scale for Depression. On day 20, the anti-depressant effect of SAMe and imipramine were similar, although SAMe had a clear advantage on the anxiety scale. On day 42, imipramine surpassed SAMe. More patients dropped out of the study due to side effects from imipramine than SAMe.
SAMe has also been compared to desipramine (Norpramin), amitriptyline (Elavil), and chlorimipramine in placebo-controlled, double-blind studies. According to one meta-analysis of these studies, 92% of patients responded to SAMe, compared to 85% for the tricyclics. SAMe has also been compared to amoxapine (Asendin), maprotiline (Ludiomil), and trazadone (Desyrel).
Depression Caused by Organic Disease
SAMe has been tested for depression caused by a variety of diseases, including Parkinson's Disease (PD), fibromyalgia, cancer, cardiovascular disease, and rheumatoid arthritis. And researchers have used SAMe successfully in conjunction with drug and alcohol withdrawal.Parkinson's Disease (PD)
The incidence of depression in PD patients is about 46%. It is interesting to note that In one recent study, 32% of PD patients had a lifetime history of depression. Unfortunately, there is only one published double-blind, placebo-controlled study on using SAMe for depression in PD patients. That study, conducted in Italy (where SAMe is manufactured) shows a definite improvement in depressive symptoms. Importantly, SAMe did not affect L-Dopa treatment. (Ed. note: L-Dopa is the precursor to dopamine, which is the standard treatment for PD). The most significant side effect was that three patients complained of elation during the first days of treatment.L-dopa (the treatment for PD) depletes SAMe. In rodents, SAMe bounces back in the brain after L-dopa, but doesn't in the liver. It has been suggested that L-Dopa may cause damage to organs such as the liver, where SAMe disappears after L-Dopa treatment. This theory has never been proven or disproven.
It has been suggested by one research group that since L-Dopa depletes SAMe, excess SAMe maybe the cause of PD. The researchers attempted to prove their theory by injecting huge amounts of SAMe directly into the brains of rodents so as to produce PD-like symptoms. One problem with the study is that such huge amounts of any substance injected directly into an organ can cause severe damage. Many different substances can create PD symptoms by depleting dopamine in the brain. Manganese chloride is one of those substances. Iron is another. Another is MPTP, which is used by researchers in studies to create PD in animal models.
The one published study on giving SAMe to PD patients does not support the theory that SAMe is detrimental to PD patients. On the contrary, the results of that study show a beneficial effect. The fact that no patient had to increase their dose of L-Dopa suggests that SAMe does not interfere with L-Dopa therapy.
New and exciting research is being published on the real cause of PD. Scientists are once again focusing on the role of serotonin in dopamine production. Researchers at Sandoz have shown that the part of the brain affected by PD-the substantia nigra-contains serotonin-related receptors. This part of the brain is always associated with dopamine, and since the discovery of L-Dopa, research into PD has centered around dopamine. But researchers have shown that serotonin raises dopamine, and dopamine lowers serotonin in certain parts of the brain. This see-saw relationship between serotonin and dopamine ensures that neither substance gets too high. Since dopamine can become toxic to neurons, the interplay between serotonin and dopamine can't be ignored.
L-Dopa and Serotonin
In a recent study from the National Institute of Neuroscience in Japan, researchers demonstrated that the serotonin inhibitor, para-chlorophenylalanine (PCPA) decreases dopamine activity, which L-Dopa does not restore. However, intravenous serotonin does restore dopamine activity after PCPA therapy. This study implicates a completely new pathway in dopamine production and maintenance that L-Dopa does not affect. It opens a new avenue of PD research. It does not mean that PD patients can cure themselves by taking serotonin- PD is an extremely complicated disease which involves free radicals, among other things-but it does open up exciting possibilities.Research shows that L-Dopa quits working after about 4 years. Some of the new research on the interaction between dopamine and serotonin seems to indicate that the ultimate failure of L-Dopa may relate to its depletion of serotonin. In a study in Neuroscience Letters in 1993, it was shown that PD patients have significantly decreased levels of dopamine and serotonin in their cerebral spinal fluid. Patients treated with L-dopa have even less serotonin than untreated patients (although they have increased dopamine). The depression that a lot of PD patients have may be a result of the loss of serotonin, both from the disease itself and from L-Dopa treatment. It is important to note that the drug Selegiline (Deprenyl), which is often used in PD patients to keep L-Dopa effective longer, increases serotonin.
Rheumatoid Arthritis
Fifty-nine RA patients participated in a study to measure the effect of SAMe on depression caused by RA. All the patients were experiencing major depression. They were given 200 mg SAMe per day by injection. Compared to placebo, patients receiving SAMe improved signficantly on the Hamilton Rating Scale for Depression (HAM-D).Osteoarthritis
A two-year study involving 108 patients (97 by the end of the study) was published in the American Journal of Medicine in 1987. It not only showed how SAMe alleviates pain, but also how it alleviates depression in people with osteoarthritis. Participants in the study were given 600 mg of SAMe per day the first two weeks, and 400 mg/day thereafter.Cardiovascular Disease, Cancer and Other Illnesses
A group in Italy tested the effects of SAMe on depression caused by different illnesses. Of the 55 patients tested, 40 were inpatients. All patients had moderate-to-major depression. Inpatients were given two 200 mg injections of SAMe. Outpatients took two 400 mg tablets of SAMe for 4 weeks. Besides cardiovascular disease and cancer, patients were suffering from alcohol-related liver disease, insulin-dependent diabetes, posttransfusion hepatitis, obesity, cerebro-vascular disorder, bronchial asthma, viral pneumonia, endocrine diseases, psoriasis, herniated disk, and congenital hip dislocation. Scores on the Beck's Depression Inventory were significantly improved in the patients receiving SAMe. Side effects were minimal, and none of the people treated dropped out of the study because of them.The authors point out that SAMe may be particularly beneficial in treating depression in heart disease patients because tricylics, MAO inhibitors, and second-generation antidepressants (such as Prozac, etc.) are contraindicated in these patients
.
There have been conflicting reports that some heart medications cause depression. In an effort to clear up the controversy, a researcher in Denmark recently reported the results of an analysis he did of 17,636 prescriptions. He found a correlation between angiotensin- converting enzyme (ACE) inhibitors, calcium channel blockers, and prescriptions for anti-depressants. Diltiazem (Cardizem) seemed particularly problematic. People who take these drugs should be aware that they may cause depression.The Dangers of Antidepressant Drugs
"Six depressed patients free of recent serious suicidal ideation developed intense, violent suicidal preoccupation after 2-7 weeks of fluoxetine (Prozac) treatment. This state persisted for as little as 3 days to as long as 3 months after discontinuation of fluoxetine. None of these patients had ever experienced a similar state during treatment with any other psychotropic drug."This report, from Harvard Medical School, set off a fire storm that raged in the pages of the American Journal of Psychiatry for two years. The issue of whether or not Prozac causes suicidal impulses is still not settled. One thing is for certain though-antidepressants turn up in drug-related overdoses almost as frequently as sedatives, which are used (along with alcohol) most frequently to overdose. The obvious reason is that people taking antidepressants are more likely to attempt suicide. Another, more subtle, reason is that antidepressants can take 4-6 weeks to work. A study in the British Medical Journal (which set off another fire storm) found that people who had been taking antidepressants for less than 30 days, and people taking high doses (which usually occurs in the beginning of therapy) were more likely to commit suicide.
Studies show that people who overdose on the older, tricyclic antidepressants are more likely to die than those who take the newer selective serotonin-reuptake inhibitors (SSRI). This makes Prozac, Paxil and others a safer choice-particularly for older people who can't metabolize the drugs well. The problem is that SSRIs don't work for everyone, and when they do, they sometimes have intolerable side effects.
The side effects of tricyclic antidepressants make up a long list. Dry mouth, weight gain/loss, constipation, blood sugar increase/decrease, insomnia/drowsiness, nausea, and sweating are some of the milder side effects. The SSRIs are noted for their inhibition of libido, anxiety, nausea, heart palpitations, and other central nervous system and gastrointestinal effects.
All antidepressants pose risks of life-threatening events including stroke, heart failure, and liver disease. Tricyclics cause liver damage through inhibition of Cytochrome p450 enzymes which are used by the liver to detoxify drugs. Recently, the MAO inhibitor, moclobemide was accused (in Lancet) of causing fatal liver cholestasis (stoppage of bile). The manufacturer, Hoffmann- La Roche, responded that the death was more likely caused by Prozac, which has been associated with liver abnormalities. The natural anti-depressant, SAMe, has been shown to be liver-protective in numerous studies.
The side effects of antidepressants relate to their interaction with certain receptors. No one knows exactly what antidepressants do to receptors. Furthermore, receptors that respond to antidepressants are located throughout the body-not just in the brain. For example, the gut problems associated with SSRIs probably relate to a serotonin receptor known as 5-HT3 found in the gut. At present, a dozen different types of serotonin receptors have been found-with more on the way. It will be years before scientists understand exactly what antidepressant drugs do in the body.
Patients who have been taking antidepressants for more than two months should never suddenly stop taking them suddently because severe withdrawal reactions have been reported. Garner, et al. reviewed some of the data on withdrawal from tricyclic antidepressants in The Annals of Pharmacotherapy. Some clinicians believe that withdrawal occurs because antidepressants down-regulate, and possibly reconfigure, receptor sites so that when the drug is removed, the body is left "crippled"-unable to respond with its own biochemicals.
Never combine different types of anti-depressants; anti-depressants and tryptophan; or anti-depressants and SAMe without first consulting a physician.
SAMe causes very few, if any, side effects. It has been given intramuscularly, intravenously, and orally with good results. It has been given to hundreds of patients with different types of depression-including patients debilitated from physical illness. It has been given to recovering drug and alcohol addicts to reduce depression and control drug cravings. Several authors have referred to it as the antidepressant for the '90s.
Dosage
The effective oral dose of SAMe for depression is 800-1600 mg/day. The Foundation recommends that people begin by taking two 400 mg tablets per day-once in the morning, and once in the afternoon. A third tablet should be added at noon, if the depression does not improve within 2 days. A fourth tablet in the evening may be necessary for some people. Severely depressed people have been given 1600 mg from the first day without significant adverse effect beyond dry mouth and nausea.Material for this article from LEF Magazine April 1997
REFRERENCES
Cole SA, Woodard JL, Juncos JL, et al.
Depression and disability in Parkinson's Disease. J Neuropsychiatry Clin Neurosci 8:20-5, 1996.Bottiglieri T, Hyland K and EH Reyonlds.
The clinical potential of ademetionine (s-adenosylmethionine) in neurological disorders. Drugs 48: 137-152, 1994.Van Kempen GM, Janjua R and RA Roos.
Effect of disease and drug treatment on blood serotonin and monoamine oxidase B activity in Parkinson's Disease. Clin Neurol Neurosurg 97: 131-3, 1995.Minabe Y, Emorik and CR Ashby Jr.
The depletion of brain serotonin levels by para-chlorophenylalanine administration significantly alters the activity of midbrain dopamine cells in rats: an extracellular single cell recording study. Synapse 22: 46-53, 1996.Jick SS, Dean AD and H Jick.
Antidepressants and suicide.
BMJ 310: 215-8, 1995.Teicher MH, Glod C and JO Cole.
Emergence of intense suicidal preoccupation during fluoxetine treatment.
Am J Psychiatry 147: 207-210, 1990.Mayeux R, Stern Y, Cote L and JB Williams.
Altered serotonin metabolism in depressed patients with Parkinson's disease.
Neurol 34: 642-6.Hallas J.
Evidence of depression provoked by cardiovascular medication: a prescription sequence symmetry analysis. Epidemiol 7: 478-484, 1996.Tohgi H, Abe T, Takahashi S, Takahashi J and H Hamato.
Alterations in the concentration of serotonergic and dopaminergic substances in the cerebrospinal fluid of patients with Parkinson's disease, and their changes after L-dopa administration.
Neurosci Lett 159: 135-8, 1993.Abramowski D, Rigo M, Duc D, Hoyer D and M Staufenbiel.
Localization of the 5-hydroxytryptamine 2C receptor protein in human and rat brain using specific antisera.
Neuropharm 34: 1635-45, 1995.Konig B.
A long-term (two years) clinical trial with S-adenosylmethionine for the treatment of osteoarthritis.
Am J Med 83(5A): 89-94, 1987.Criconia AM, Araquistain JM, Darrina N, Navajas F and M Bordino.
Results of treatment with S-adensyl-L-methionine in patients with major depression and internal illnesses. Curr Ther Res 55: 666-674, 1994.Cibin M, Gentile N, Ferri M, et al. S-adenosyl-methionine (SAMe) is effective in reducing ethanol abuse in an outpatient program for alcoholics. In Kuriyama K, Takada A, Ishii M, eds.
Biomedical and Social Aspects of Alcohol and Alcoholism. Amsterdam: Elsevier, 1988:357-60.Lo Russo A, Monaco M, Pani A and D Fontanari.
Efficacy of S-adenosyl-L- Methionine in relieving psychological distress associated with detoxification in opiate abusers.
Curr Ther Res 55:905-13.Grassetto M and A Varotto.
Primary fibromyalgia is responsive to S-adenosyl-l-methionine.
Curr Ther Res 55:797-806.Dollow S.
[Antidepressant-associated fatal intrahepatic cholestasis].
Lancet 347: 1268-69.Berlanga C, Ortega-Soto HA, Ontiveros M and H Senties.
Efficacy of S-adenosyl-L-methionine in speeding the onset of action of imipramine.
Psychiatry Res 44: 257-62, 1992.Taylor KM and PK Randall.
Depletion of S-adenosyl-L-methionine in mouse brain by antidepressive drugs.
J Pharmacol Exp Ther 194: 303-10, 1975.Hietala OA, Laitinen SI, Laitinen PH, Lapinjoki SP and AE Pajunen.
The inverse changes of mouse brain ornithine and S-adenosylmethionine decarboxylase activites by chlorpromazine and imipramine. Dependence of ornithine decarboxylase induction on beta-adrenoceptors.
Biochem Pharmacol 32: 1581-5, 1983.
Posted by JohnX2 on March 23, 2002, at 0:24:09
In reply to Re: treatment resistant depressionSLS » petters, posted by SLS on March 21, 2002, at 10:55:52
I want lithium because of its neuroprotective and neurotrophic potential. It is supposed to promote plasticity. Maybe this would help to restore the size and function of the hippocampus. What do you think? Depression has greatly impaired my memory.
>Scott,
Sorry to budge in on your thread. I'm interested on your comment about lithium and its effects on plasticity in the hippocampus? Can you direct me to any information on this?
BTW, memantine has been shown to improve memory and cognition by improving ltp in the hippocampus.
I included some areas of application from the PDR
which they sent me translated into english, and a few abstracts I dug up (this was in demented patients, which you are not, but it does show clinical efficacy, i believe).(Hope the cut and paste doesn't suck).
Regards,
John--------------------------------------------------------------------------------
Akatinol Memantine Tablets/Drops (German Translated PDR)
4. Areas of Application
For the treatment of mild and moderate cerebral performance disorders with the following cardinal symptoms: concentration and memory disorders, loss of interest and drive, premature fatigue, reduced self-maintanance, motoricity disorders in routine activities and depressive mood (dementia syndrome) as well as in diseases which an increase in attention and alertness (vigilance) is required.
Cerebral and spinal spasticity such as , for example, as a result of infantile cerebral injury, craniocerebral trauma, multiple sclerosis, parapalegia, cerebral ischemia.
Parkinson and parkinson-like diseases (Parkinson syndrome).-----------------------------------------------------------------
ABSTRACTEffects of the uncompetitive NMDA receptor antagonist memantine on hippocampal long-term potentiation, short-term exploratory modulation and spatial memory in awake, freely moving rats. Eur J Neurosci 1996 Mar;8(3):565-71 (ISSN: 0953-816X) Barnes CA; Danysz W; Parsons CG
Arizona Research Laboratories Division of Neural Systems, Memory and Aging, University of Arizona, Tucson 85724, USA. Chronic treatment of adult male F-344 rats (9-12 months old) with therapeutically relevant doses of memantine (30 mg/kg/day in chow for > 8 weeks) increased the maintenance of long-term potentiation of field excitatory postsynaptic potentials from perforant path-granule cell hippocampal synapses recorded in the fascia dentata in vivo. In contrast, there was no effect of memantine on baseline synaptic responses or population spikes. Likewise, short-term exploratory modulation of these hippocampal evoked responses was not different between memantine-treated and control rats. Both groups of rats were able to learn the spatial version of the Morris water task equally well, but the memantine-treated group showed a strong tendency to show more selective spatial search patterns in the training quadrant of the water pool during a final probe trial. As such, these studies provide the first electrophysiological evidence that memantine can increase the durability of synaptic plasticity and provide preclinical confirmation of the cognitive improvement seen with memantine in the treatment of demented patients.-------------------------------------------------------------------------------------------
ABSTRACT
Memantine restores long term potentiation impaired by tonic N-methyl-D-aspartate (NMDA) receptor activation following reduction of Mg2+ in hippocampal slices. Neuropharmacology 1999 Sep;38(9):1253-9 (ISSN: 0028-3908) Frankiewicz T; Parsons CG
Department of Pharmacology, Merz and Co., Frankfurt am Main, Germany. This study compared the ability of memantine and (+)MK-801 to counteract deficits in the induction of long term potentiation (LTP) following reduction of Mg2+ in hippocampal slices--a model of increased synaptic noise due to tonic N-methyl-D-aspartate (NMDA) receptor activation. Decreasing Mg2+ from 1 mM to 10 microM for 60 min enhanced baseline field excitatory post-synaptic potential (fEPSP) slopes (87.2 +/- 10.6% above control) and impaired LTP (-4.1 +/- 9.8% compared to pre-tetanic levels). Long pre-incubations with memantine (1 microM), a concentration achieved in the CSF of dementia patients, almost fully restored the induction of LTP (to 43.4 +/- 8.4%) without changing the enhancement of baseline fEPSP slopes (84.1 +/- 11.6%). Memantine (10 microM) fully restored the induction of LTP (61.5 +/- 5.3%) and also decreased the enhancement of baseline fEPSP slopes (30.1 +/- 4.9%). In contrast, although (+)MK-801 (0.01, 0.1 and 1 microM) caused a concentration-dependent reduction in the low Mg2+ -induced enhancement of baseline fEPSP slopes, it was not able to restore the induction of LTP (3.0 +/- 9.8%, 16.3 +/- 5.7% and 4.8 +/- 6.7% respectively). These data indicate that memantine could produce symptomatological improvement in learning under conditions of tonic NMDA receptor activation such as those occurring in chronic neurodegenerative diseases whereas (+)MK-801 is likely to have only negative effects.
Go forward in thread:
Psycho-Babble Medication | Extras | FAQ
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.org
Script revised: February 4, 2008
URL: http://www.dr-bob.org/cgi-bin/pb/mget.pl
Copyright 2006-17 Robert Hsiung.
Owned and operated by Dr. Bob LLC and not the University of Chicago.