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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 6 of 6. This is the beginning of the thread.
Posted by k23d on July 21, 2002, at 19:31:33
Hi Folks,
Posted a few weeks ago regarding potential treatments I was considering for my long term social anxiety / panic. Unfortunately my pdoc does not agree. (First time we met so perhaps a bit hasty on my part). He's very benzo phobic, as in he said there is no way he will ever prescribe me a benzo (even long HL clonazepam). He even told me I have mild depressive symptoms even though no other pracitioner or other person has ever seen this. I agree that perhaps paroxetine has given me mild depressive symptoms but off SSRI's I'm one of the most positive people around so that's no excuse for an anti benzo stance...
Anyway, he has given me the choice of effexor (not sure whether xr but assume yes) or mirtazapine to treat my condition.
I was previously on aropax(paroxetine) and hated the anorgasmia, weight gain and apathy/lethargy.
The way he explains it is that mirtazapine is opposite to paroxetine in all these effects and effexor is somewhere in between.What are other people's thoughts / experiences?
Thanks,
KD
Posted by Shawn. T. on July 21, 2002, at 23:21:14
In reply to Paxil - Effexor - Remeron Social Anxiety / Panic, posted by k23d on July 21, 2002, at 19:31:33
I have been on Paxil and Remeron. I have not taken Effexor, but I have a friend who was on it. Effexor is more or less an SSRI until you start taking amounts of the drug that are much too high in my opinion. Taking large amounts of Effexor very often leads to unacceptable side effects. Remeron has a much more favorable side effect profile than Effexor. I have observed study after study showing that Remeron is the best antidepressant currently available. Effexor is one of the antidepressants that I most dislike. I am consistenly baffled by the FDA. I would like to see a Senate investigation into their practices. They are permitting drug companies to get away with things that I believe are blatantly unacceptable when our current knowledge of neuroscience is taken into account. Benzodiazepines are a dying breed these days; you are lucky that your pdoc does not like them. I'll provide one study comparing Remeron (mirtazapine) and Effexor (venlafaxine).
http://www.biopsychiatry.com/mirtazvvenlaf.html
Basically, Remeron prevents upward spikes in noradrenaline, dopamine and acetylcholine levels in response to stressors by blockading 5-HT2a and 5-HT2c serotonergic receptors.
Remeron's proven efficacy in treating anxiety:
http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=26459011"One of the main sequelae to prolonged stressful situations is the development of depressive illness, which is usually accompanied by sexual dysfunction, insomnia and anxiety. The SSRIs that are used to treat depression may themselves aggravate these symptoms further and so delay recovery from the 'stress-illness vicious circle'. These problems would appear to be considerably less with the newer sedative antidepressant drugs, such as nefazodone and mirtazapine."
http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=18759394
Remeron's effects upon dopamine spikes:
http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=16273293Remeron's effects upon acetylcholine spikes:
http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=30151309Remeron's effects on noradrenalin spikes:
http://www4.infotrieve.com/newmedline/detail.asp?NameID=11746735&loggedusing=M&Session=&SearchQuery=mirtazapine++AND+GABA&count=3The evolution of antidepressant thought:
http://www4.infotrieve.com/search/databases/detailsNew.asp?artID=26459015You need not read the rest; I only provide it as an explanation of the above. I'll provide you with a model that shows how Remeron can effectively help to prevent anxiety and panic attacks. I'm going to use auditory stimuli as an example. My explanation of the auditory pathway in the brain is taken from Joseph E. LeDoux's "Emotion, Memory, and the Brain." See pages 105-117 from The Scientific American Book of the Brain, copyright 1999.
Sound waves enter the ear canal and trigger responses in an auditory nerve (the frequency of the waves probably affects the rate at which the auditory nerve is stimulated). The signal is transmitted to the auditory midbrain, which directs it to the auditory thalamus. If a learning process called long term potentiation has taken place across the route upon which the auditory stimulus travels, the signals will travel more quickly. Long term potentiation allows a person to adapt more quickly to dangerous situations. Louder sounds will also increase the rate of signal transfer; they imply a more immediate danger.
After the auditory input reaches the auditory thalamus, it is transferred to the lateral nucleus in the amygdala. This location is very important in the process of fear conditioning. Next, the input is sent to the basal nucleus in the amygdala. From there, it is transferred to the central nucleus, which is also in the amygdala. This nucleus is connected to the subiculum, a region of the hippocampus. The hippocampus is an area of the brain that is very important in memory formation and retrieval. In the subiculum, contextual information pertaining to a person's surroundings is used to determine the emotional significance of the auditory input. The signal may be increased or decreased depending on the nature of the current environment. From here, the signal is transferred back to the central nucleus.
If the auditory signal is one that has created fear in the past, an autonomic conditioned response is elicited. The signal is sent from the amygdala to the brain stem. The body will likely exhibit the fight or flight stress response. The hypothalamic-pituitary-adrenal axis
will adjust hormone levels to deal with the
potentially dangerous situation. For example, cortisol (the primary stress hormone) levels will be increased. Upward spikes in neurotransmitter levels (dopamine, noradrenaline, acetylcholine, and possibly others) will occur in the brain's cortical regions. The potential for increased neurotransmission should allow a person to quickly make a decision on how to react to the situation. I should mention that serotonergic 5-HT2 receptors are often implicated in the modulation of neurotransmitter and hormonal levels.While all of this was happening, the signal was also being sent from the auditory thalamus to the auditory cortex. The autonomic stress response takes place very quickly, so the auditory cortex is likely to be already flooded with neurotransmitters, thus allowing a faster conscious interpretation of the auditory stimulus. If it is perceived to be harmless, the stress response should be diminished.
One of the problems that a person with an anxiety disorder has to deal with is an adaptation that their hormonal system has made to chronic stress. The negative feedback loop between cortisol and the hypothalamus is basically severed. Everytime that a person adapts to a new stressor, their hormonal stress threshold is lowered for the next stressor. Neurons in the brain alter their gene expression to compensate for chronic stress. Cortisol is less able to turn off the hormonal stress response when it reaches the hypothalamus. The body is more or less in a state of constant preparation for fight or flight.
Alterations in 5-HT2 receptor functions could also lead to a situation where the brain is unable to effectively modulate, in this case turn off, the levels of its neurotransmitters. A combination of hormonal feedback mechanism dysfunction and the alteration of certain serotonin receptors is the most likely explanation for anxiety disorders.
Some people are more apt to have their stress threshold lowered than others, based on their genetic makeup. They may have a hormonal system dysfunction or an altered number of serotonin and noradrenaline receptors. I will consider what probably occurs in a person with major depression that does not have a bipolar disorder and experiences excessive anxiety. This person is likely to have an excess of serotonin receptors (evidence is somewhat inconclusive in my opinion). They likely have hyposensitive 5-HT1a receptors and hypersensitive 5-HT2 receptors. Their alpha-2-adrenergic receptors are also probably hypersensitive. So, hypothetically, activating 5-HT1a receptors and blockading problematic 5-HT2 and alpha-2-adrenergic receptors should solve the problem. 5-HT1a receptors control the release of serotonin and indirectly affect the levels of other neurotransmitters in the brain. Alpha-2-andrenergic antagonism serves to indirectly increase the activation of 5-HT1a presynaptic receptors.
A person with an excess of 5-HT2 receptors that have been hypersensitized will experience a greater release of cortisol, because these receptors are implicated in cortisol release (5-HT2c specifically). Dr. Herbert Y. Meltzer has done a number of experiments on 5-HT2 receptor functions. If there is enough serotonin in the synapse (as there would be in response to a powerful stimulus), a large number of the 5-HT1a and 5-HT2c receptors in the brain will be activated. This creates a much larger release of cortisol than a person with a relatively normal number of unsensitized receptors would experience.
Consider the initial increase in anxiety seen in people beginning SSRI treatment (still taking a person with major depression and an anxiety disorder into consideration). The activation of their hypersensitive 5-HT2 receptors by serotonin will create a large hormonal response (Maes and Meltzer 1995). After a while, a person taking an SSRI will have the sensitivities of their receptors somewhat normalized. The brain's negative feedback mechanisms lead to this result.
This is when the person begins to see an improvement in their depression. A combination of 5-HT1a and 5-HT2c activation is less likely to result in an increase in ACTH, GH, cortisol and prolactin secretion (Anand et al. 1994 and Quested et al. 1997). As a person taking an SSRI experiences more and more stress over time, the delicate balance achieved by their serotonergic receptors will be upset. Their antidepressant has "pooped out."Remeron does not rely nearly as much on receptor sensitivity to achieve its results as antidepressants such as the SSRI's and Effexor do. It blocks the 5-HT2 receptors responsible for the stress response, which serves to alleviate the problem of an altered cortisol feedback loop in those who have endured chronic stress. Because both 5-HT1a and 5-HT2 receptors require activation for a hormonal response, the indirect activation of 5-HT1a receptors by Remeron does not result in increased hormonal secretion. 5-HT1a activation serves to alter monoamine levels in certain areas of the brain, which compensates for the brain's reduced reaction to stressors. Remeron's antagonism of 5-HT3 receptors may also play a role in its anxiety relieving effects. More research needs to be done on 5-HT3 receptors to illuminate its exact actions. Many of the symptoms of depression are hormonal in nature, so Remeron effectively and durably alleviates the negative effects of depression with anxiety. Remeron can be improved upon, but until that happens, it is the best available antidepressant option.
Posted by k23d on July 22, 2002, at 1:46:50
In reply to Arguments in favor of Remeron over all other AD's » k23d, posted by Shawn. T. on July 21, 2002, at 23:21:14
Thanks for that wealth of info Shawn. I've got a full copy of some of the extracts you mentioned and I'll have a read through these over the next few days.
You also mentioned you previously took paxil. Not sure if you moved straight from one to the other but if so or if you know, what's the changover like. I'm expecting just to start mirtazapine and slowly withdraw from paxil once I'm clearly getting an effect.
Also, any thoughts on dosage. I see mentioned on the boards that mirtazapine becomes more activating at doses around 60mg. Does more activating mean a potential increase in anxiety / avoidance as well or just "more activating"?
I would so love an activating med after paxil and if it helped with anxiety as well... Baby! Yeah!
Anyway, here's hoping...KD
Posted by Shawn. T. on July 22, 2002, at 3:11:32
In reply to Re: Arguments in favor of Remeron over all other AD's » Shawn. T., posted by k23d on July 22, 2002, at 1:46:50
I really don't know about switching from Paxil to Remeron. If someone doesn't reply about this issue, I'll search the net for some information tomorrow. My recommendation to you is that you start very low: either 7.5mg/day or 15mg/day. If you start out at 30mg, you will very likely not be feeling well for a couple weeks. Stick with the low dose for at least a month. Then go back and talk to your psychiatrist about increasing the dose. You don't need to increase it if you are feeling better and have an acceptable energy level. I really don't think that the high doses are necessary for most people. On a dose as low as 15mg/day, you should feel more alert and not so drowsy after a couple weeks. 60mg/day is much more likely to cause adverse effects than 15mg/day. I really need to explain why I believe this in a more in depth manner. I also need to type up some advice on fighting the potential weight gain that some people see in the first month. I'll try to do both of those things tomorrow. I got off of Paxil by taking Wellbutrin. The Wellbutrin agitated me a bit, so I added on 7.5mg/day of Remeron. The combination has worked extremely well for me; I've heard a lot of good things about it. You will definitely feel much better on Remeron than you did on Paxil. If you work during the week, you may want to switch over to the Remeron on a Friday night. The first couple days will be drowsy ones; I didn't have much of a problem though because of the low dose that I began on. The Wellbutrin helped as well. You're welcome... I usually don't mind answering questions at all, because they help me to learn more about myself and others.
Shawn
> Thanks for that wealth of info Shawn. I've got a full copy of some of the extracts you mentioned and I'll have a read through these over the next few days.
>
> You also mentioned you previously took paxil. Not sure if you moved straight from one to the other but if so or if you know, what's the changover like. I'm expecting just to start mirtazapine and slowly withdraw from paxil once I'm clearly getting an effect.
>
> Also, any thoughts on dosage. I see mentioned on the boards that mirtazapine becomes more activating at doses around 60mg. Does more activating mean a potential increase in anxiety / avoidance as well or just "more activating"?
>
> I would so love an activating med after paxil and if it helped with anxiety as well... Baby! Yeah!
> Anyway, here's hoping...
>
> KD
Posted by katekite on July 22, 2002, at 11:50:33
In reply to Paxil - Effexor - Remeron Social Anxiety / Panic, posted by k23d on July 21, 2002, at 19:31:33
I used to deal with a lot of social anxiety. The one drug that helped a lot was Neurontin. It is a little like a benzo I think.
I would try Remeron first over Effexor ONLY because if it doesn't work well and you want to get off of it Remeron is much easier to withdraw from. If you are not having trouble sleeping don't start higher than 7.5 mg or you will simply sleep through any social interaction you could have attended. Effexor has significant withdrawal that should not be taken lightly.
My personal experience with Remeron was negative: I think it is more apathy inducing than paroxetine, but everyone is an individual so its always worth trying.
Good luck == kate
Posted by Pattisun on July 22, 2002, at 18:50:51
In reply to Arguments in favor of Remeron over all other AD's » k23d, posted by Shawn. T. on July 21, 2002, at 23:21:14
I was just given Neurontin and told to stop my Klonpin. I have Fibromyalgia, depression, and a BAD panic disorder. (I also take Paxil and Prozac)
My rheumatologist told me Remeron was pretty effective in helping with pain control. I am scared to take the Neurontin because of its effect on the kidneys and water retention. Had a similar problem with Vioxx last year and ended up with congestive heart failure.
What do you think? Should I ask the psych to try me on Remeron instead?
Thanks,
Patti
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