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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 7 of 7. This is the beginning of the thread.
Posted by shellie on October 4, 2000, at 21:53:45
Andrew, I did read one small (N=7) ketamine study on medline and read what Dr. Goldstein had to say about it.
But explain to me why I might have an interest in it.
1. adderall, ritalin, and dexadrine all increase dopamine and all have bad effects on me.
2. codeine reduces dopamine and has a great effect on me.
Ketamine (apparently?) increases dopamine.
So based on the above, maybe my body just doesn't want any more dopamine stimulated.Where has my logic gone awry here? Or am I making this too simplistic? Also, is something else becoming wrong with my brain that I am even thinking about neurotransmitters? What happened to the person who went to a new pdoc and was relieved to put it in his hands?
(It was only last week!)Shellie
Posted by SLS on October 5, 2000, at 8:56:22
In reply to ketamine drops ------ AndrewB, SLS, posted by shellie on October 4, 2000, at 21:53:45
Dear Shellie,
> Also, is something else becoming wrong with my brain that I am even thinking about neurotransmitters?Shellie, can you be more specific about your concerns here?
> Andrew, I did read one small (N=7) ketamine study on medline and read what Dr. Goldstein had to say about it.What was the title of the study you found on Medline? I'd like to take a look at it.
> But explain to me why I might have an interest in it.
> Ketamine (apparently?) increases dopamine.
> So based on the above, maybe my body just doesn't want any more dopamine stimulated.I am afraid to draw any conclusions as to what exactly ketamine does that might help with depression. It does so many things. One thing I read indicates that the increase in dopamine release provoked by initial dosing of ketamine is attenuated with continued dosing. Ketamine has in common with PCP (angel's dust?) the ability to block NMDA receptors. Ketamine is sometimes used experimentally to produce schizophrenic, psychotic, and dissociative symptoms in healthy human volunteers for study. Does Dr. Goldstein mention this? Ketamine is used frequently as a recreational drug and has significant abuse potential.
I would like to see a study of the use of ketamine in depressive illness that is conducted for a period longer than 72 hours.
> 1. adderall, ritalin, and dexadrine all increase dopamine and all have bad effects on me.Sedation?
> 2. codeine reduces dopamine and has a great effect on me.
Can you describe in what ways codeine makes you feel better? How long does this improvement last for? Can you extend the improvement by taking subsequent dosages, or does the effect disappear regardless of further dosing?
Naltrexone produces sedation in you, right? Do you feel activated when you take codeine?
> Where has my logic gone awry here?
It hasn't.
> Or am I making this too simplistic?
Yes, as are we all.
> What happened to the person who went to a new pdoc and was relieved to put it in his hands?
> (It was only last week!)Who?
- Scott
Posted by AndrewB on October 5, 2000, at 12:30:43
In reply to Re: ketamine drops ------ AndrewB, SLS » shellie, posted by SLS on October 5, 2000, at 8:56:22
Dear Scott and Shellie,
I noticed that both of you have responded to lamotrigine and temporarily to an MAOI and little else. (Doesn't Anita have a similar profile?). Do you think that possibly you are birds of a feather, sharing, at least in part, a similar underlying dysfunction?
Concerning Ketamine, it can be a very dangerous drug. It causes schizophrenic, psychotic and disassociative states as well as amnesia. It also is a street drug, some people enjoy the disassociative state it seems. It also has an important use as an anesthesia.
As you know, some drugs act very differently at low doses than high, so we shouldn’t immediately condemn ketamine because of its effects at higher doses.
Is it an AD and arousal agent at lower doses? Dr. Goldstein claims that for many it is, and these effects are not just short term. He also hasn’t noted a tendency for his patients to increase their doses and abuse the drug. The one person I have corresponded with who takes the low dose ketamine nasal spray confirms that it is an arousal agent, AD and cognition enhancer for him. But he also says it is fickle. There is a fine line between an effective dose and too much. Besides a couple of very short term studies, there are only these anecdotal reports indicating it can help with depression. I will try it in a week or so and let you know what I think. Its effects are short enough in duration that I don’t think I am risking much in trying it.
Scott, I have been corresponding with Shellie and I want to fill in a few details about her drug responses (I hope you don’t mind Shellie) and ask you whether she may have dopaminergic dysfunction (hypofunction?)
On Adderall (and also ritalin and dexadrine) she felt her body pulsating and felt drugged. These stimulants of course also act on NE. Do the above symptoms indicate either excess dopamine or NE?
Here are Shellie’s reactions to other drugs:
Tricyclics completely fog her
Hydrocodone energizes her
Naltrexone after one day made her feel awful
Risperadone, one dose made her body stiff and speech slurred.
Seroquel, one dose of it kept her up all night
Amisulpride, one dose of only 25mgs completely fogged her head and gave her a shaky feeling.Scott, I suggested to Shellie that, like another person I am corresponding with, she may be supersensitive to amisulpride. The symptoms to me resemble an overdose of amisulpride. I suggested she try taking 6.25mg taken twice daily. The other person I mentioned seems to be doing well (time will tell) at 12.5 taken twice a day. I am thinking she may be even more sensitive.
So what do you make of all this Scott. Are there any clues here as to her dopaminergic function.
Best wishes,
AndrewB
Posted by SLS on October 5, 2000, at 13:53:17
In reply to Shellie, Scott, posted by AndrewB on October 5, 2000, at 12:30:43
Hi guys.
I think I'm battling the flu on top of the usual energy and concentration stuff, so you'll have to pardon the brevity of my response.
Shellie - I want you on my team.
Andrew, I think you may be right regarding DA hypersensitivity.
One thought - not much.Without knowing very much about it, I would say that there may be some problems with opioid/dopamine balance interactions.
Simplistically speaking (the best I can do), if opioid receptor stimulation is decreased, I believe that some dopaminergic pathways with which opioid receptors and neurons interact might become hyperactive. Too much dopamine. More accurately, perhaps, too little control over the throttle and bad brakes.
Evidence:
Hydrocodone (opioid agonist) - feels good and is activating.
Naltrexone (opioid antagonist) - feels crappy.The hydrocodone (an opioid) may be functioning to stabilize and attenuate DA activity in various regions, including the nucleus accumbens. There may be some alterations in the ratios of specific opioid subtypes.
I bet Dr. Goldstein has something regarding this. He seems to have some keen insights into this sort of thing. I don't know what opioid (mu-type?) agonists are available to try.
As far as dopamine receptor ligands are concerned, if low-dose antagonsists hurt (amisulpride), maybe low-dose agonists (bromocriptine) would help. Simplistic.
I've never tried codeine. It might be an interesting experiment.
Andrew, I agree with your posture on a trial of ketamine. Good luck.
- Scott
> Dear Scott and Shellie,
>
> I noticed that both of you have responded to lamotrigine and temporarily to an MAOI and little else. (Doesn't Anita have a similar profile?). Do you think that possibly you are birds of a feather, sharing, at least in part, a similar underlying dysfunction?
>
> Concerning Ketamine, it can be a very dangerous drug. It causes schizophrenic, psychotic and disassociative states as well as amnesia. It also is a street drug, some people enjoy the disassociative state it seems. It also has an important use as an anesthesia.
>
> As you know, some drugs act very differently at low doses than high, so we shouldn’t immediately condemn ketamine because of its effects at higher doses.
>
> Is it an AD and arousal agent at lower doses? Dr. Goldstein claims that for many it is, and these effects are not just short term. He also hasn’t noted a tendency for his patients to increase their doses and abuse the drug. The one person I have corresponded with who takes the low dose ketamine nasal spray confirms that it is an arousal agent, AD and cognition enhancer for him. But he also says it is fickle. There is a fine line between an effective dose and too much. Besides a couple of very short term studies, there are only these anecdotal reports indicating it can help with depression. I will try it in a week or so and let you know what I think. Its effects are short enough in duration that I don’t think I am risking much in trying it.
>
> Scott, I have been corresponding with Shellie and I want to fill in a few details about her drug responses (I hope you don’t mind Shellie) and ask you whether she may have dopaminergic dysfunction (hypofunction?)
>
> On Adderall (and also ritalin and dexadrine) she felt her body pulsating and felt drugged. These stimulants of course also act on NE. Do the above symptoms indicate either excess dopamine or NE?
>
> Here are Shellie’s reactions to other drugs:
> Tricyclics completely fog her
> Hydrocodone energizes her
> Naltrexone after one day made her feel awful
> Risperadone, one dose made her body stiff and speech slurred.
> Seroquel, one dose of it kept her up all night
> Amisulpride, one dose of only 25mgs completely fogged her head and gave her a shaky feeling.
>
> Scott, I suggested to Shellie that, like another person I am corresponding with, she may be supersensitive to amisulpride. The symptoms to me resemble an overdose of amisulpride. I suggested she try taking 6.25mg taken twice daily. The other person I mentioned seems to be doing well (time will tell) at 12.5 taken twice a day. I am thinking she may be even more sensitive.
>
> So what do you make of all this Scott. Are there any clues here as to her dopaminergic function.
>
> Best wishes,
>
> AndrewB
Posted by anita on October 5, 2000, at 21:07:27
In reply to Re: Shellie, Scott, posted by SLS on October 5, 2000, at 13:53:17
Hi all,
I do think that Scott and I are very similiar, given our reactions to meds. Interestingly, I think I might have a problem with general NE excess but DA mesocortical hypofunction -- I generally do worse on NE meds.
I thought that hydrocodone increased dopamine -- I remember researching this a while ago, but I don't have my notes in front of me now. I was pretty certain of this. I usually respond well to hydrocodone, decreasing anxiety and depression and social phobia especially, and it is a bit energizing (I can't sleep on it).
Andrew, where did you get the ketamine drops?
anita
>
> > Dear Scott and Shellie,
> >
> > I noticed that both of you have responded to lamotrigine and temporarily to an MAOI and little else. (Doesn't Anita have a similar profile?). Do you think that possibly you are birds of a feather, sharing, at least in part, a similar underlying dysfunction?
> >
> > Concerning Ketamine, it can be a very dangerous drug. It causes schizophrenic, psychotic and disassociative states as well as amnesia. It also is a street drug, some people enjoy the disassociative state it seems. It also has an important use as an anesthesia.
> >
> > As you know, some drugs act very differently at low doses than high, so we shouldn’t immediately condemn ketamine because of its effects at higher doses.
> >
> > Is it an AD and arousal agent at lower doses? Dr. Goldstein claims that for many it is, and these effects are not just short term. He also hasn’t noted a tendency for his patients to increase their doses and abuse the drug. The one person I have corresponded with who takes the low dose ketamine nasal spray confirms that it is an arousal agent, AD and cognition enhancer for him. But he also says it is fickle. There is a fine line between an effective dose and too much. Besides a couple of very short term studies, there are only these anecdotal reports indicating it can help with depression. I will try it in a week or so and let you know what I think. Its effects are short enough in duration that I don’t think I am risking much in trying it.
> >
> > Scott, I have been corresponding with Shellie and I want to fill in a few details about her drug responses (I hope you don’t mind Shellie) and ask you whether she may have dopaminergic dysfunction (hypofunction?)
> >
> > On Adderall (and also ritalin and dexadrine) she felt her body pulsating and felt drugged. These stimulants of course also act on NE. Do the above symptoms indicate either excess dopamine or NE?
> >
> > Here are Shellie’s reactions to other drugs:
> > Tricyclics completely fog her
> > Hydrocodone energizes her
> > Naltrexone after one day made her feel awful
> > Risperadone, one dose made her body stiff and speech slurred.
> > Seroquel, one dose of it kept her up all night
> > Amisulpride, one dose of only 25mgs completely fogged her head and gave her a shaky feeling.
> >
> > Scott, I suggested to Shellie that, like another person I am corresponding with, she may be supersensitive to amisulpride. The symptoms to me resemble an overdose of amisulpride. I suggested she try taking 6.25mg taken twice daily. The other person I mentioned seems to be doing well (time will tell) at 12.5 taken twice a day. I am thinking she may be even more sensitive.
> >
> > So what do you make of all this Scott. Are there any clues here as to her dopaminergic function.
> >
> > Best wishes,
> >
> > AndrewB
Posted by shellie on October 5, 2000, at 23:27:48
In reply to Re: ketamine drops ------ AndrewB, SLS » shellie, posted by SLS on October 5, 2000, at 8:56:22
Hey Scott, sorry you're sick. I don't have time to answer all your questions now, but I did find the article on medline:
TITLE: Antidepressant effects of ketamine in depressed patients.
AUTHORS:
Berman RM; Cappiello A; Anand A; Oren DA; Heninger GR; Charney DS; Krystal JH
AUTHOR AFFILIATION:
Abraham Ribicoff Center Clinical Neuroscience Research Unit of the Connecticut Mental Health Center, New Haven 06519, USA.
SOURCE: Biol Psychiatry 2000 Feb 15;47(4):351-4
CITATION IDS: PMID: 10686270 UI: 20153964
ABSTRACT:
BACKGROUND: A growing body of preclinical research suggests that brain glutamate systems may be involved in the
pathophysiology of major depression and the mechanism of action of antidepressants. This is the first
placebo-controlled, double-blinded trial to assess the treatment effects of a single dose of an N-methyl-D-aspartate
(NMDA) receptor antagonist in patients with depression. METHODS: Seven subjects with major depression completed 2
test days that involved intravenous treatment with ketamine hydrochloride (.5 mg/kg) or saline solutions under randomized, double-blind conditions. RESULTS: Subjects with depression evidenced significant improvement in
depressive symptoms within 72 hours after ketamine but not placebo infusion (i.e., mean 25-item Hamilton Depression Rating Scale scores decreased by 14 +/- SD 10 points vs. 0 +/- 12 points, treatment).
CONCLUSIONS: These results suggest a potential role for NMDA receptor-modulating drugs in the treatment of depression.Hope you feel better soon,
shellie
p.s., do we need a team uniform?
Posted by SLS on October 7, 2000, at 21:40:42
In reply to Re: ketamine drops ------ SLS, Andrew B, Anita, posted by shellie on October 5, 2000, at 23:27:48
Thanks Shellie.
This sort of study reminds me of procaine challenges performed at the NIMH. It is not so much that procaine was being considered as a clinical antidepressant, but rather, that it served as a biological probe to help illucidate the neurochemistry of affective disorders.
- Scott
> ...but I did find the article on medline:
>
> TITLE: Antidepressant effects of ketamine in depressed patients.
> AUTHORS:
> Berman RM; Cappiello A; Anand A; Oren DA; Heninger GR; Charney DS; Krystal JH
> AUTHOR AFFILIATION:
> Abraham Ribicoff Center Clinical Neuroscience Research Unit of the Connecticut Mental Health Center, New Haven 06519, USA.
> SOURCE: Biol Psychiatry 2000 Feb 15;47(4):351-4
> CITATION IDS: PMID: 10686270 UI: 20153964
> ABSTRACT:
> BACKGROUND: A growing body of preclinical research suggests that brain glutamate systems may be involved in the
> pathophysiology of major depression and the mechanism of action of antidepressants. This is the first
> placebo-controlled, double-blinded trial to assess the treatment effects of a single dose of an N-methyl-D-aspartate
> (NMDA) receptor antagonist in patients with depression. METHODS: Seven subjects with major depression completed 2
> test days that involved intravenous treatment with ketamine hydrochloride (.5 mg/kg) or saline solutions under randomized, double-blind conditions. RESULTS: Subjects with depression evidenced significant improvement in
> depressive symptoms within 72 hours after ketamine but not placebo infusion (i.e., mean 25-item Hamilton Depression Rating Scale scores decreased by 14 +/- SD 10 points vs. 0 +/- 12 points, treatment).
> CONCLUSIONS: These results suggest a potential role for NMDA receptor-modulating drugs in the treatment of depression.
>
> Hope you feel better soon,
>
> shellie
> p.s., do we need a team uniform?
This is the end of the thread.
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