![[dr. bob]](/dr-bob-sm.gif)
Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 32 to 56 of 106. Go back in thread:
Posted by SLS on December 14, 2008, at 8:26:15
In reply to Re: Treatment Resistant (Refractory) Depression, posted by CaptainAmerica1967 on December 13, 2008, at 15:33:09
> Did it work well for you?
As monotherapy, it produced episodic robust improvements, but proved to be an untenable therapy. I wish I were allowed by the NIMH protocol to add a therapeutic dosage of desipramine.
In my opinion, clorgyline, a specific MAO-A inhibitor, is the single most effective antidepressant in the world. It was considered by the NIMH to be their "ace-in-the-hole" when all else failed. Many people remained well on clorgyline for over a decade. Unfortunately, several people experienced cardiovascular events that convinced the NIMH to no longer support its use. It is unclear if these treatment-emergent events were caused by clorgyline.
Clorgyline is no longer manufactured for human consumption, but remains the paradigm for assaying MAO-A activity.
I don't think I would trust anyone to synthesize this particular chemical such that I would pass it down my throat. I wouldn't know how to find such a person, anyway.
- Scott
Posted by SLS on December 14, 2008, at 8:32:20
In reply to Re: Treatment Resistant (Refractory) Depression, posted by desolationrower on December 13, 2008, at 23:41:35
> and since you've basically done it already, MAOI+ssri?
That's about the only combination in psychiatry that will yield life-threatening effects at a rate nearing 100%. I have nothing against the idea of trying to potentiate the actions of antidepressants using drug combinations, but this one is really one that is dangerous.
- Scott
Posted by JadeKelly on December 15, 2008, at 12:14:29
In reply to Re: Treatment Resistant (Refractory) Depression » CaptainAmerica1967, posted by Racer on December 13, 2008, at 17:27:07
Hi Racer,
I have treatment resistant Dep for 2-3 yrs, was wondering about the articles you mentioned: Dexamethasone (never heard of it) and steroids. These are both used in trd? Were those articles on Babble or some where else? I'd love to take a look at those, or if easier can you give me a "brief" on how these work, and I can do my own research. I'm on Parnate. Thanks!
~Jade
Posted by CaptainAmerica1967 on December 15, 2008, at 16:18:53
In reply to Re: Treatment Resistant (Refractory) Depression » Racer, posted by JadeKelly on December 15, 2008, at 12:14:29
A good source to read from is www.biopsychiatry.com.
Dexamethasone suppression test involves giving cortisol to see if the depressed patient's body decreases or block it's own porduction as it should in normal non depressed individuals, but most hospitalized or refractory patients don't suppress their own production after the test. Excess cortisol blocks or interferes with serotonin.
CRF (corticotropin releasing factor) is secreted from the pituary but is faulty in depression and continues to be secreted to increase or stimulate cortisol production from the adrenal cortex despite a normal amount of cortisol in the body. Normally there's a feedback mechanism by which if you have normal levels in the blood stream then the pituary "recognizes" that one doesn't need more cortisol and suppresses CRF.
CRF antagonists (blockers) are being developed by pharmaceutical companies to treat depression.
www.biopsychiatry.com/crf1.htm
www.neurotransmitter.net/newdrugs/html
Posted by YOGI BRONX on December 16, 2008, at 16:23:03
In reply to Treatment Resistant (Refractory) Depression, posted by CaptainAmerica1967 on December 12, 2008, at 1:42:34
Dear Jeff,
We have something in common. I found that only extreme cardiovascular exercise alleviated my profound lifelong depression until Paxil in 1995. I have completed over twenty marathon foot races. (With a PR of 2:56! I try to squeeze in this fact regardless of the conversation.) High dosage Paxil, (90mg./day) worked for me for ten years. Subsequently, Lexapro at normal dosage did.
However, I still want more for myself and for others of whom I care whose depressions are still refractory.
The FDA was supposed to act on the approval of a drug named, "Ixel, (Milnacipran)", by the end of last October. Its an SNSRI, a Selective Norepinephrine Serotonin Reuptake Inhibitor". It inhibits the reuptake of noephinephine/serotonin at a ratio of 3/1. The other drugs curretly on the US market that inhibit reuptake of these neurotransmitters, (Effexor & Cymbalta), inhibit the uptake of serotonin/norepinephine at the rate of 33/1. The effect increases the availability of norephinephrine at a massively higher rate, and, obviously, at a more even pace with serotonin.
It is the only truly NEW drug for depression of which I know, rather than a reformulation of an existing drug or family of drugs.
The FDA failed to meet the October deadline and, instead, sent out a notice to that effect without posting a new deadline.
Thereupon, I ordered the drug from Great Britain. I'm not sure of the legality of this. If it hasn't been designated a prescription drug in the US, is one prohibited from buying it?
Various health product websites in Great Britain sell it openly to US residents, but not the residents of GB or the EU where it has been prescribed for ten years.
My experience, in the one day that I took it earlier this month, at a dosage of 25 mg. in the morning and 25 mg. at night, (half the normal adult dosage), was that in that one day I experienced a significant improvement in energy alertness, and, "drive", (for want of a better word), in the afternoon, a problem time for me. (I can't judge its specific antidepressant effect because I am doing OK on Lexapro at the moment. However, I find Lexapro's sexual side effect to be annihilating even to the concept of sex.) I was pleased and hopeful.
However, after taking the second 25 mg. dosage at bedtime, I experienced terrible ischuria all night long, having to get up to urinate every ninety minutes. Each time, I was able to coax just enough urine out to stop my bladder from hurting before returning to bed and repeating the entire drill 90 minutes later. It was a long, long night.
I took no more Milnacipran and the ischuria disappeared gradually the next day.
Upon further research, I have learned that this is a not uncommon side effect, (although the literature states that it affects only 2.7% of patients), that it can be alleviated with, "Flomax", and that patients have found success with it at as low a dosage as 15 mg./day, (v. 100 mg./day according to the patient instruction sheet).
One member on this board said that he used it successfully, after a refractory depression that defeated every drug in the world AND a failed course of ECT, at 6mg, 3X daily.
The same poster said that he actually didn't know of anyone who DIDN'T benefit from the drug, those people who discontinued it having to do so because of side-effects, (principally hypertension, dysuria, and what I would describe as hypertense, staring uselessness.)
He also said that the dysuria went away over time.
I haven't recommenced the drug yet but I intend to do so at the 6 mg. 3 x daily dose rate initially. Currently, I am trying to figure out how to divide, conveniently, one 25 mg. capsule into four 6 mg. doses at a bulk level. I am also waiting until the time feels absolutely right to do begin again.
Hope you find this helpful and that I am not carrying coals to Newscastle.
Cordially,
YOGI
Posted by West on December 16, 2008, at 16:45:14
In reply to Re: Treatment Resistant (Refractory) Depression » CaptainAmerica1967, posted by YOGI BRONX on December 16, 2008, at 16:23:03
I hope i'm not letting anyone down (yogi) by saying i am proof that milnacipran doesn't work for everyone. Proper doses are hard on the heart and orthostatic hypotension was as bad as i've ever experienced. Pity, as it did seem promising at the lower end of the dosage range. I'm not sure how reliable it's thought to be in terms of efficacy.
W
Posted by YOGI BRONX on December 16, 2008, at 16:55:04
In reply to Milnacipran, posted by West on December 16, 2008, at 16:45:14
Dear West,
Rats! But the poster did say that people discontinued it because of unmanageable side effects rather than because of lack of efficacy.
Cordially,
YOGI
Posted by CaptainAmerica1967 on December 16, 2008, at 20:39:02
In reply to Re: Treatment Resistant (Refractory) Depression » CaptainAmerica1967, posted by YOGI BRONX on December 16, 2008, at 16:23:03
Hi YOGI,
Thanks for your input and experience.
Yes, I've tried Ixel (milnacipran)and have researched it extensively, but like most other meds except the MAOI (type A's), milnacipran was a failure. It may be approved (clinicaltrials.gov) for fibromyalgia soon in the USA. I purchased it via www.antiaging-systems.com in Great Britian.
The only thing beyond the MAOI(A)+TCA+Psychostimulant+Lithium that I feel will provide relief to those with severe TRD is the deep brain stimulation device that Dr. Helen Mayberg founded showing that virtually all of those with depression suffer from an overactive (PET scans) part of the brain in the prefrontal cortex called Brodmann Area (25). Broadmann Area always returns to normal or becomes less active upon recovery from depression, but those who never or only partially recovery from depression continue to show overactivity in this specific spot. I tried to enter one of the studies being done in Dallas, but since I had several seizures while receiving trazodone and ECT (70 of them) in 1986, I was unable to participate in the study. Those wishing to learn more can visit www.BroadenStudy.com.
The other hopeful meds in the pipeline can be viewed on www.neurotransmitter.net/newdrugs/html.
Thanks,
Jeff
Posted by CaptainAmerica1967 on December 16, 2008, at 20:42:07
In reply to Milnacipran, posted by West on December 16, 2008, at 16:45:14
I experienced the same cardiovascular reactions as you had. Studies show that milnacipran is now more and maybe even less effective than the time tested standard TCA imipramine.
Posted by desolationrower on December 16, 2008, at 21:56:34
In reply to Re: Treatment Resistant (Refractory) Depression, posted by CaptainAmerica1967 on December 16, 2008, at 20:39:02
> The only thing beyond the MAOI(A)+TCA+Psychostimulant+Lithium that I feel will provide relief to those with severe TRD is the deep brain stimulation device that Dr. Helen Mayberg founded showing that virtually all of those with depression suffer from an overactive (PET scans) part of the brain in the prefrontal cortex called Brodmann Area (25). Broadmann Area always returns to normal or becomes less active upon recovery from depression, but those who never or only partially recovery from depression continue to show overactivity in this specific spot. I tried to enter one of the studies being done in Dallas, but since I had several seizures while receiving trazodone and ECT (70 of them) in 1986, I was unable to participate in the study. Those wishing to learn more can visit www.BroadenStudy.com.
>
> The other hopeful meds in the pipeline can be viewed on www.neurotransmitter.net/newdrugs/html.
>
> Thanks,
>
> JeffThe new somatic treatments do look quite interesting. transcranial mag stimulation as well, even outside affective disorders, it has potential for autism, or even for inducing creative and altered states of consciousness at the touch of a button. It woudl be facinating to sit down and become extrondinarily creative or experience a different personality. There is also ultrasound treatment on the horizon that promises a more accurate targeting of brain region for stimulation. Its too bad you can't try out a new treatment.
Also, looking at your combination, only Li directly affects the glutamate system. I think that might be the area where new drugs become availible. have you tried adding something glu related, like a supplement like acetyl cysteine or aniracetam to MAOI(A)+TCA+Psychostimulant+Lithium? I really believe that for the hardest disorders, multifactorial approach is needed. Even one flat tire is a problem, even if you've got the other 3 aired up.
-d/r
Posted by JadeKelly on December 16, 2008, at 23:03:36
In reply to Agomelatine -) 67 days before EMEA decision., posted by CaptainAmerica1967 on December 15, 2008, at 16:18:53
Posted by Neal on December 17, 2008, at 2:28:44
In reply to Treatment Resistant (Refractory) Depression, posted by CaptainAmerica1967 on December 12, 2008, at 1:42:34
I would like to hear from others and what they've found to be effective in dealing with tough to treat refractory depression.
Effective for me was the usual ADs + bupernorphine
Posted by SLS on December 17, 2008, at 5:29:10
In reply to Re: Treatment Resistant (Refractory) Depression, posted by CaptainAmerica1967 on December 16, 2008, at 20:39:02
I would like to add that a treatment strategy that can be very effective is to add an atypical neuroleptic, of which Abilify and Geodon are emerging as the most effective.
- Scott
Posted by SLS on December 17, 2008, at 5:43:01
In reply to Re: Treatment Resistant (Refractory) Depression, posted by desolationrower on December 16, 2008, at 21:56:34
I understand that lithium is thought to directly inhibit the reuptake of glutamate, but I am still unclear as to how it can stabilize and limit glutamatergic excitation. I recall something involving NMDA receptors, but I don't know if lithium acts directly to change the conformation of the transporter molecule. What else does lithium do to influence glutamate activity? How might protein kinase-C inhibition affect glutamate?
Thanks.
- Scott
Posted by CaptainAmerica1967 on December 17, 2008, at 10:05:57
In reply to Re: Treatment Resistant (Refractory) Depression, posted by desolationrower on December 16, 2008, at 21:56:34
Thanks for your response.
"acetyl cysteine or aniracetam"- yes I tried both of these; I've been into holistic health for years (Life Extension Foundation) and have taken acetyl cysteine before.
I've tried aniracetam and some other "smart drugs" after reading the book "Smart Drugs & Nutrients years ago by Ward Dean, M.D..I've been very interested in NMDA receptor antagonists after the news of ketamine having such a profound and lasting effect on TRD and looked into going to the NIMH in Bethesda, MD, for a ketamine study on treatment resistant depression but it would have meant having to go off the antidepressant I was taking at the time or any antidepressant for that matter for a washout time and I get severely non functional just after being off them for two days. I've tried memantine without any benefit and have thought about trying the med for ALS(Lou Gehrig's Disease) called Riluzole which is also a potent glutamate blocker or NMDA receptor antagonist (clinicaltrials.gov), but the cost is phenomenol at $10-$20 per pill and the dose of at least two per day.
I thought about trancranial magnetic stimulation (TMS), but since I failed a course of 70 ECT treatments, the TMS wouldn't likely to anything.
I'm also interested in cortisol blockers being studied.
Jeff
Posted by SLS on December 17, 2008, at 10:18:43
In reply to Re: Treatment Resistant (Refractory) Depression, posted by CaptainAmerica1967 on December 17, 2008, at 10:05:57
I suffered a negative reaction from taking Provigil. Nevertheless, I am suspicious that it might make a good adjunct to MAOIs.
By the way, what treatments are you aware of that you have not yet tried?
- Scott
Posted by CaptainAmerica1967 on December 17, 2008, at 20:18:14
In reply to Re: Treatment Resistant (Refractory) Depression, posted by SLS on December 17, 2008, at 10:18:43
"By the way, what treatments are you aware of that you have not yet tried?"
Deep brain stimulation-hopefully it will continue to show promise in treating severe treatment resistant depression and will be approved even though I don't like surgery as there's always a risk.
Other than that, there's not much I haven't tried except some drugs going through clinical trials.
http://neurotransmitter.net/newdrugs.html
or www.clinicaltrials.gov
-CRF antagonistsI'm still really interest in ketamine (NMDA antagonsit), but cannot or will not get off my current meds (was out) in order to be able to participate in the study. http://clinicaltrials.gov/ct2/show/NCT00088699?cond=%22Depression%22&rank=35
Riluzole(an inhibitor of glutamate release)-indicated for ALS, but studies on going like ketamine.
Also meds that increase brain-derived neurotrophic factor (BDNF) as antidepressants and physical exercise increase levels in the brain and those with depression have reduced levels.
Cysteamine bitartrate (Cystagon), an FDA approved med for the treatment nephropathic cystinosis, has been shown to increase BNDF in neuronal tissue, and to stimulate cell growth.
Posted by SLS on December 17, 2008, at 20:55:15
In reply to Re: Treatment Resistant (Refractory) Depression, posted by CaptainAmerica1967 on December 17, 2008, at 20:18:14
I did not respond to riluzole. Nothing good - nothing bad.
I also tried mifepristone. I did not like it. I felt very washed-out at the end of the week, and less well overall.
Did you ever combine Provigil with an MAOI?
- Scott
Posted by CaptainAmerica1967 on December 17, 2008, at 21:11:43
In reply to Re: Treatment Resistant (Refractory) Depression, posted by SLS on December 17, 2008, at 20:55:15
No, I haven't used Provigil with an MAOI. I used Provigil with other meds such as Cymbalta but I still felt sleeply most of the time, however, I was taking so many other meds at the time too such as pindolol, thyroid, various amphetamines, Lamictal.
Currently I'm taking Parnate, Nortriptyline, Lithium Orotate and amineptine.
Vigorous physical exercise can make feel completely normal for temporary afterwards as can total sleep deprivation.
Posted by desolationrower on December 17, 2008, at 23:01:12
In reply to Re: Treatment Resistant (Refractory) Depression, posted by CaptainAmerica1967 on December 17, 2008, at 21:11:43
If you haven't tried buprenorphine or lowdose naltrexone, i think that would be the obvious thing. I think they either could be taken with current regimine.
Dextromethorphan has some similarities to ketamine. It has strong affinity for the SERT (i think, info is hard to come by) so definatly not something you can take with parnate. I think it has some specific dopaminergic activity as well, and sigma. Of course, i have no idea if this would be benefical long-term, but it is another easily avilible uncompetitive NMDA antagonist
Did you try the memantine with the current drugs, and did you take at least 40mg? It seems to be more effective at higher doses. I'm asking again as some of the studies show subtherapeutic mem+tca or other AD results in full antidepressant effect.
Also, have you tried adding NAC to your current drugs.
Scott, you've mentioned modafinil+MAOI as synergistic, any particular reason? I haven't noticed any strong effect from adrafinil with parnate and my other stuff, n=1. Oh and wherever it was mentioned, i don't know about specific Li/Glu interaction or PCK. I believe it increases glu uptake chronically. Given Mgs role in the NMDA receptor, i'd think it interacts in some fashion.
-d/r
Posted by CaptainAmerica1967 on December 18, 2008, at 4:06:01
In reply to TRD --SLS, CPTAmerica, posted by desolationrower on December 17, 2008, at 23:01:12
Thanks for your feedback.
I haven't tried buprenorphine, but have been interested in it as I'm interested in almost anything that could bring about a better life. I'm not sure about the drug interaction with Parnate and would have to do some more research on it. I have a gut feeling my depression could be related to some sort of malfuncition with the hypothalamus-pituitary-adrenal axis (hot flashes or feeling warm all the time)-cortisol, endorphins, neurotransmitters. Obviously exercise affects mood as a result from many different physiological mechanisms, but it's only the intense physical exercise that produces the slight euphoria and antidepressant effect I feel which could be attributed to endorphins hence buprenorphine or naltrexone might help. Also, my father got "hooked" on heroin the first time he tried it in 1972 and died from an accidental overdose (sad to know that the following day he was suppose to go in for treatment, but never made it) so this could point to my depression as having some type of opioid dysfunction. Dextromethorphan would be interesting to try too if I weren't on an MAOI.
I cannot recall the dose of memantine (10mgs twice day or whatever the dose was BID). NAC is in my life extension multivitamin mix and I've used it for years.
Regards,
Jeff
Posted by SLS on December 18, 2008, at 6:37:51
In reply to TRD --SLS, CPTAmerica, posted by desolationrower on December 17, 2008, at 23:01:12
> Scott, you've mentioned modafinil+MAOI as synergistic, any particular reason?
Not really. I just remember that, during the first few days of modafinil treatment (added to imipramine and Lamictal), I felt some pretty good stuff, and just wondered if it might not be a great augmenter of an MAOI. Unfortunately, toward the end of the first week, I deteriorated; an increase in the severity of my depression that lasted for weeks after the discontinuation of modafinil. Was there a glutamatergic antagonism by modafinil of Lamictal that caused this? I can't be sure.
If one really thought they could hand-pick drugs based on their properties, I guess there would be no concrete rationale that I am aware for why there might be a synergistic effect between the two drugs. I am still not convinced that modafinil is fully understood, and that dopamine reuptake inhibition explains its wake-promoting effect. If anything, it might help with vigilance. Wake promotion seems to be the result of orexin (hypocretin) interactions in the hypothalamus and reticular formation. One wouldn't necessarily think of this as being important in the etiology of depression. I have yet to read about just where and how dopaminergic flow is enhanced by modafinil.
- Scott
Posted by desolationrower on December 18, 2008, at 12:01:10
In reply to Re: TRD --SLS, CPTAmerica » desolationrower, posted by SLS on December 18, 2008, at 6:37:51
> > Scott, you've mentioned modafinil+MAOI as synergistic, any particular reason?
>
> Not really. I just remember that, during the first few days of modafinil treatment (added to imipramine and Lamictal), I felt some pretty good stuff, and just wondered if it might not be a great augmenter of an MAOI. Unfortunately, toward the end of the first week, I deteriorated; an increase in the severity of my depression that lasted for weeks after the discontinuation of modafinil. Was there a glutamatergic antagonism by modafinil of Lamictal that caused this? I can't be sure.
>
> If one really thought they could hand-pick drugs based on their properties, I guess there would be no concrete rationale that I am aware for why there might be a synergistic effect between the two drugs. I am still not convinced that modafinil is fully understood, and that dopamine reuptake inhibition explains its wake-promoting effect. If anything, it might help with vigilance. Wake promotion seems to be the result of orexin (hypocretin) interactions in the hypothalamus and reticular formation. One wouldn't necessarily think of this as being important in the etiology of depression. I have yet to read about just where and how dopaminergic flow is enhanced by modafinil.
>
>
> - ScottYeah, it seems to be one of the least understood meds. I think it also increase 5ht efflux in pfc, so that would make it one of the few meds with 5htergic properties that can be taken with an MAoi, although i guess a number have similar downstream effects. Also interesting the 'hibernation' theory of depression vs. antiD effects of sleep deprivation, hypocretin activation.
-d/r
Posted by desolationrower on December 18, 2008, at 12:26:42
In reply to Re: TRD --SLS, CPTAmerica, posted by CaptainAmerica1967 on December 18, 2008, at 4:06:01
> Thanks for your feedback.
>
> I haven't tried buprenorphine, but have been interested in it as I'm interested in almost anything that could bring about a better life. I'm not sure about the drug interaction with Parnate and would have to do some more research on it. I have a gut feeling my depression could be related to some sort of malfuncition with the hypothalamus-pituitary-adrenal axis (hot flashes or feeling warm all the time)-cortisol, endorphins, neurotransmitters. Obviously exercise affects mood as a result from many different physiological mechanisms, but it's only the intense physical exercise that produces the slight euphoria and antidepressant effect I feel which could be attributed to endorphins hence buprenorphine or naltrexone might help. Also, my father got "hooked" on heroin the first time he tried it in 1972 and died from an accidental overdose (sad to know that the following day he was suppose to go in for treatment, but never made it) so this could point to my depression as having some type of opioid dysfunction. Dextromethorphan would be interesting to try too if I weren't on an MAOI.Hm, given the relationship of opiods and your family tradegies i can see it being a complicated subject for you.
One more idea i thought of last night, stimulant-type drugs seem to help, have you ever gotten ahold of an H3 antagonist? Betahistine is the only one i think that is easily availible, its also a H1 agonist i think. Its used for some sort of ear dysfunction i think, but H3 antagonists are being tested for ADHD. Given its rather broad effects (h3 antongoism on heteroreceptors disinhibits a number of neurotransmitters) slow titration since you're on an MAOI would probably be wise although no reactions have been reported. Additionally, betahistine may be metabolised by MAO so much lower doses might be needed. -> THE METABOLISM OF BETAHISTINE IN THE RAT
L. A. STERNSON 1, A. J. TOBIA 1, G. M. WALSH 1, and A. W. STERNSON 1
ABSTRACT
The metabolism of betahistine, 2-(2-methylaminoethyl)pyridine, a bio-isostere of histamine, was studied in the rat. 2-Pyridylacetic acid, which had been previously isolated as a metabolite of betahistine from dog and rabbit urine, was isolated from rat urine as well as from rat liver homogenates. In addition, trace amounts of the N-demethylated product, 2-(2-aminoethyl)pyridine, was isolated from liver homogenates. In vitro studies revealed that the preponderance of betahistine oxidase activity originated in liver mitochondria and was attributable to monoamine oxidase (MAO). The participation of mitochondrial MAO in metabolism was corroborated by inhibiting betahistine oxidation with specific MAO inhibitors. Additional experiments ruled out the involvement of diamine oxidase in betahistine metabolism. The kinetics for the MAO-catalyzed oxidation of betahistine was studied and revealed that betahistine had a greater affinity for mitochondrial MAO (KM = 3.3 x 10-5 M) than did tyramine, serotonin, or benzylamine.Also, read this patent application for betahistine use-> http://www.wipo.int/pctdb/en/wo.jsp?wo=2007076140&IA=US2006049321&DISPLAY=DESC
Lots of stuff in there, they think it normalises HPA same as MAOIs.
Hm, someone else had the same idea, i found this now: ongoing study -> http://clinicaltrials.gov/ct2/show/NCT00585585Quite promising.
-d/r
Posted by JadeKelly on December 18, 2008, at 18:04:23
In reply to Re: Treatment Resistant (Refractory) Depression, posted by CaptainAmerica1967 on December 17, 2008, at 21:11:43
Hi Jeff,
This is too long but IM DESPERATE!! I developed a tr/mdd about 3 years ago after a cluster of family tragedies struck in a very short time. It developed into apathy/numbness/not leaving my room/bed. I can't tolerate most a/d's, especially ssri's. I've been on Parnate for ten weeks and have been at 60mg for 3 days, wieght 125lbs. How high should I go? I got a week long reprieve/high following initial dose of 30mg, then 2-3 days of this when I increase dose. I honestly can't tell how well the A/d effect is because I am SO lethargic. It should be working by now, right? Whats the longest Parnate should take to work? I do think my mood is better. If I wasnt lethargic, I think the rest would fall into place. Was this your experience at all?
Our depresions sound similar, except I have never suffered from anxiety but am starting to as I lose hope with this catch 22 I seem to be in. I, too, get pretty intense high when I do a difficult workout. Don't know if thats everyone, or just some. Haven't done it for a while due to fatigue and fear of BP irregularities. I forgot to mention, BP always on the low side, but even when I can get it up to 120/80, I'm still lethargic. I need ritalin for a while as I'm very familiar with it and I can switch or add nortriptyline when fatigue/lethargy wears off.
Right now the only drug I take is 3mg klonopin, been taking it for years for a nerve injury in my neck. REALLY want to stop taking it and see if I still need it. Have no psychological dependence on it but don't want w/d's to interfere with Parnate benefit. Do you think I should taper off now? Or wait?
It makes sense to me, due to my ignorance in this subject, to copy your regimen (one that I was headed towards! I wanted ritalin or nortriptyline) and that advised to you by one of the leading tr/dep PDoc's, Dr. Gordon I think it is, in New york. I took Ritalin for 12 years for ADD, as diagnosed by only PDoc, and I responded to it beautifully. I don't have an addictive personality at all so I was able to go from original dose of 5mg 3x day to 5mg 5xday during those 12 years. (I often wonder if it wasn't working as a mild A/D also) Pdoc made me d/c with MAOI, will not talk about augment to get me up and moving. But no risk to bedridden 24/7??
My current problem, I have lost faith in my PDoc, he is not at all creative with despensing of meds, and I realize that he doesn't seem to care much that I've became deeply depressed, then onto apathetic and numb, in front of his very eyes. The only reason I'm on an MAOI is that I was following a poster (before I joined), RobertDavid, who was trying the patch. I took that and had the same immediate reaction (great). When I had to go up to 9mg patch it made sense to switch to Parnate.
So, I need Doc to prescribe first choice, low dose Ritalin (5mg 3-5x day), to get me up and moving, then maybe 2nd choice, nortriptyline or amitriptyline, and I noticed a 3rd you take Li??, would you recommend? It sounds like you are not in full remission, in what way: depression, fatigue, apathy, etc?
Finally, and most importantly, how does one go about getting much needed medication from a PDoc who is experienced enough to not be overly conservative, like the one you consulted with ? This is getting to be an emergency for me as I have to go back to work (not to mention the time of year) Do Docs scribe with phone consult? I've only had the one. ANY help appreciated.
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