New and on the manic side yet depressed still (triggers ?)

Well, as I said, I'm new here, at least I think I am, right now I really don't know where I have been

I'll start off with a bit of an introduction about myself.

I was diagnosed as Bipolar with Schizoaffective Disorder so needless to say, my life has been a bit crazy (hopefully that dosen't offend anyone) maybe I should say interesting at times.

I was diagnosed around 10 years ago and at first it was a really rocky road in finding the right meds for me but then over the last two years I've been really stable. That is until now. More about that later.

I live on a small farm, I have 1 dog, 2 rabbits, 3 cats, 4 goats and 22 chickens that I take care of. Having to be responsible for their care helps me, expecially my dog. He is my best friend and I don't know what I would do without him. He comforts me, makes me feel safe.

I'll also be turning 40 this June and am really looking forward to it. That may suprise some people but the fact is that I was told that I wouldn't live to 18 with the things that I was doing so to reach 40, I think I've done pretty good, I've survived all the things that I have done to myself, sometimes it was pretty close and almost didn't make it.

Right now I am going through something that I can't remember ever having experienced before.

At the beginning of Feb I tried to quit smoking and that put me into a depression which surprised me because every other time that I had tried to quit, I'd gone to the mania side. I had not been taking any anti-depressants because the SSRI's caused mania, Lithium left me where I couldn't remember anything at all and didn't even know that and the old anti-depressants gave me nightmares.

But I decided that I would go on Welbutrin at 75mg. I started bouncing up and down, rapid cycling. But then I hit a low again, lower than what I had been before and even had thoughts of self-injury though I have not done that for quite some time (I'm a cutter and I cut very deep which is why I almost didn't make it a few times).

Well I decided that I would start taking Sudafed because I knew that it also had a tendency to cause mania in me. I had to do something, I absolutely could not function except on a very minimal level. I didn't hit mania which was good but I did get to where I could function better.

My Pdoc raised the Welbutrin to 150mg and as far as I can tell, its done nothing for the depression. I still feel it and I only keep going because of the Sudafed.

However I have now been heading toward mania, I knew it was a fine line that I was walking by taking the Sudafed but I had to do it and I still do or I am going to fall back into that deep dark empty lonely hole. I can't go back there, I just can't do it.

I have never before that I remember felt both the depression and mania at the same time. I may have already said that already, I'm a bit on the flakey side because of this. I'm not sleeping well at all even though I take Seroquel.

I want to crawl into bed and hide away from the world and all my responsibilities yet I am also compelled to go out and work my bum off with all the chores that need to be done around here. It takes alot of work to keep 15 acres in shape. I getting completely confused . I have no idea which direction I am going and I don't have any idea of how to handle this.

Anyone have any suggestions? I'm seeing my counselor on the 19th and my Pdoc again on the 22ed so those are covered.

Please help if you can.

Thankyou,
Jeanette

Jeanette, it sounds like you have slipped into a mixed state. Both depression and mania are present.

When you tried to quit smoking it sounds like your dopamine levels went up.

One of the neurotransmitters playing a major role in addiction is dopamine. Many of the concepts that apply to dopamine apply to other neurotransmitters as well.
As a chemical messenger, dopamine is similar to adrenaline. Dopamine affects brain processes that control movement, emotional response, and ability to experience pleasure and pain.

Dopamine



Regulation of dopamine plays a crucial role in our mental and physical health. Neurons containing the neurotransmitter dopamine are clustered in the midbrain in an area called the substantia nigra . In Parkinson's disease, the dopamine- transmitting neurons in this area die. As a result, the brains of people with Parkinson's disease contain almost no dopamine. To help relieve their symptoms, we give these people L-DOPA, a drug that can be converted in the brain to dopamine.


Drugs can stimulate or fail to stimulate dopamine receptors
Some drugs are known as dopamine agonists. These drugs bind to dopamine receptors in place of dopamine and directly stimulate those receptors. Some dopamine agonists are currently used to treat Parkinson's disease. These drugs can stimulate dopamine receptors even in someone without dopamine neurons.
An example of agonist drug action



In contrast to dopamine agonists, dopamine antagonists are drugs that bind but don't stimulate dopamine receptors. Antagonists can prevent or reverse the actions of dopamine by keeping dopamine from attaching to receptors.

Dopamine antagonists are traditionally used to treat schizophrenia and related mental disorders. A person with schizophrenia may have an overactive dopamine system. Dopamine antagonists can help regulate this system by "turning down" dopamine activity.
Cocaine and other drugs of abuse can alter dopamine function. Such drugs may have very different actions. The specific action depends on which dopamine receptors the drugs stimulate or block, and how well they mimic dopamine.

An example of antagonist drug action




Drugs can act directly or indirectly on dopamine receptors
Drugs such as cocaine and amphetamine produce their effects by changing the flow of neurotransmitters. These drugs are defined as indirect acting because they depend on the activity of neurons. In contrast, some drugs bypass neurotransmitters altogether and act directly on receptors. Such drugs are direct acting.

Use of these two types of drugs can lead to very different results in treating the same disease. As mentioned earlier, people with Parkinson's disease lose neurons that contain dopamine. To compensate for this loss, the body produces more dopamine receptors on other neurons. Indirect agonists are not very effective in treating the disease since they depend on the presence of dopamine neurons. In contrast, direct agonists are more effective because they stimulate dopamine receptors even when dopamine neurons are missing.


MAO affects dopamine levels
Once returned to the sending neuron by the reuptake system, dopamine is subject to an enzyme named monoamine oxidase (MAO). MAO usually breaks down dopamine.

If no other factors were at work, MAO would keep the amount of "used" dopamine fairly low. However, dopamine taken back into the nerve ending can return to the vesicle for storage. Once inside the vesicle, dopamine is protected from MAO.

A drug named reserpine prevents the reuptake of dopamine and some other neurotransmitters. Administering reserpine causes dopamine to remain exposed within the cell and broken down by MAO. This profoundly reduces the available dopamine.

Changing the action of MAO can help us treat diseases that involve dopamine transmission. For instance, the drug deprenyl inhibits MAO. This increases the stores of dopamine and slows the progression of Parkinson's disease. In higher doses, deprenyl enhances the effects of dopamine on behavior.

Interestingly, one form of MAO actually protects dopamine. This form of MAO, found in dopamine neurons, acts on substances in the neuron other than dopamine. Here MAO protects the "purity" of neurotransmission by breaking down other neurotransmitters. Inhibiting this form of MAO can increase levels of neurotransmitters such as serotonin, which seems to help people diagnosed with depression.


Drugs can also affect dopamine levels
Dopamine binds to its receptors quickly. This neurotransmitter is also quickly removed from its receptors as long as dopamine levels in the synapse are sufficiently high.

However, drugs can affect dopamine levels. Some drugs increase dopamine by preventing dopamine reuptake, leaving more dopamine in the synapse. An example is the widely abused stimulant drug, cocaine. Another is methylphenidate, used therapeutically to treat childhood hyperkinesis and symptoms of schizophrenia.

It's interesting that amphetamine and cocaine produce affect behavior and heart function in similar ways. Furthermore, both drugs increase the amount of dopamine in the synapse. However, cocaine achieves this action by preventing dopamine reuptake, while amphetamine helps to release more dopamine. So, these drugs with similar effects produce their actions through entirely different processes. In turn, addiction to the two drugs may call for somewhat different types of treatment.


Neurons can become sensitized or desensitized to dopamine
One important aspect of drug addiction is how cells adapt to previous drug exposure.

For example, long-term treatment with dopamine antagonists increases the number of dopamine receptors. This happens as the nervous system tries to make up for less stimulation of the receptors by dopamine itself. Likewise, the receptors themselves become more sensitive to dopamine. Both are examples of the same process, called sensitization.

A type of sensitization.


An opposite effect occurs after dopamine or dopamine agonists repeatedly stimulate dopamine receptors. Here overstimulation decreases the number of receptors, and the remaining receptors become less sensitive to dopamine. This process is called desensitization.


Desensitization is better known as tolerance, where exposure to a drug causes less response than previously caused. Tolerance reflects the actions of the nervous system to maintain homeostasis -a constant degree of cell activity in spite of major changes in receptor stimulation. The nervous system maintains this constant level in an attempt to keep the body in a state of equilibrium, even when foreign chemicals are present.
Sensitization and desensitization do not take place only after long-term understimulation or overstimulation of dopamine receptors. Both sensitization and desensitization can occur after only a single exposure to a drug. In fact, they may develop within a few minutes.

A type of desensitization.



Disease and drugs can produce faulty sensitization
Sensitization or desensitization normally occur with drug exposure. However, addiction or mental illness can tamper with the reuptake system. This disrupts the normal levels of neurotransmitters in the brain and can lead to faulty desensitization or sensitization. If this happens in a region of the brain that serves emotion or motivation, the individual can suffer severe consequences.

Consider an example. Cocaine prevents dopamine reuptake by binding to proteins that normally transport dopamine. Not only does cocaine "bully" dopamine out of the way-it hangs on to the transport proteins much longer than dopamine does. As a result, more dopamine remains to stimulate neurons, which causes a prolonged feelings of pleasure and excitement. Amphetamine also increases dopamine levels. Again, the result is over-stimulation of these pleasure-pathway nerves in the brain.

REsource: http://www.utexas.edu/research/asrec/dopamine.html

AD's make me rapid cycle, and do nothing for my depression. When you feel that depression run thru your veins, hug your dog. It calms you. I have 4, and try to take a few day for yourself. Take an hour at a time if you have to , this too shall pass. But tell your doc. It may be the wellbutrin.

When I took trileptal, mood stabilizer, I felt much better. Ad's don't work on us bipolars, regardless of the research. I've lived it.

You'll find most bipolar drink when manic, to become depressed, subconsciencely, and they may do drugs to stimulate themselves, i.e. meth, sinus meds, coffee overdrinking. Exercise, diet and sleep are the only true home remedies.

I hope this helps you. Exercise helps too, it helps to release endorphines. They may have been mentioned above, but they are little happy chemicals. And also help reduce pain.

Thank you ddee for your response. I knew when I tried to quit that it changed something in my brain. I had been perfectly fine, quite stable in fact compared to what I use to be like. I liked my life, and then it all changed that day.

When I was younger I use to use the alcohol and drugs (meth in fact) in order to try and control the symptoms I suppose. I did a lot of rapid cycling which is rough. Now I'm older, I no longer drink but I sure do take the meds my Pdoc gives me to try and bring myself down. This is actually the first time that I have used the sinus meds in order to bring myself up. I've avoided them like the plague, that is when I finally put 2+2 together and it was clear that they hyped me up.

Right now though, it is the only thing that is keeping me going, getting me up out of bed and functioning enough to get by, sometimes even a little ahead of the game. Yesterday was a good day for me. Todays not so good so far but hey, its early here so theres hope that it will turn around.

The AD is definately not working for me and when I see my Pdoc I'm going to tell her that. I had hoped that it would pick me up but it didn't so there is no use for me to continue taking it. I thought that maybe changing to a different one may make a difference but I don't know if I want to even try, I have strange reactions to meds much of the time.

Right now I take Neurontin, Trileptal, Welbutrin, Vistaril, Klonopin, Seroquel (to sleep and help with the schizoaffective aspects I have) and Sinemet which is an anti-parkison's drug used in my case to treat Restless Leg Syndrome. Then of course there is the sinus meds I use, both Sudafed and Benedril. I use to use only the Benedril for my allergies but I have actually found now that the combination of both allergy meds helps with the allergies better than just one alone being that they have different active ingredients.

As for exercise, I hike every so often but most of the time my exercise comes from all the work that I do around the house. Its heavy labor most of the time mixed with light work like weeding. I'm always on the move somehow except for a few breaks a day to get on the computer or watch a bit of tv. I'll work from sun up to sun down when I'm feeling good. I wanted to try something new to get my heart rate going so I had my daughter bring her bicycle out and I'm going to give that a try. Its been a long time since I've rode a bicycle. Might be fun.

Well, thank you again for your response. Yeah, it will change and I'll be good as gold again. I just have to be patient and wait for it. I can't force it as we all know.

Jeanette

<<<<<Right now I take Neurontin, Trileptal, Welbutrin, Vistaril, Klonopin, Seroquel (to sleep and help with the schizoaffective aspects I have) and Sinemet >>>>>

wow, neurontin and wellbutrin. The wellbutrin, helps with the dopamine, but you are on two AD's/. I'm on xanax and that's all right now. I set them all down to find the real me, to see if the meds all these years were tweaking me out. Many bipolar have to take benzo(Klonopin) for their whole life, but they are so addictive.

You may definetly need a med adjustment. Trileptal is a good med, with little side affects.

I do see that you are subconsciencely substituting with the benedryl, and sudafed(the active ingredient in black market meth)

You need to concentrate on a low stress level and mood stablizers.

How long has it been since you 've had pyschosis? I only take seroquel when I go into psychosis, for the sleep, as I go into it when I am off the scale. To find out what is going on , would you be interested in a mood chart , to give your doc, to see what might be causing this, the info helps them so much. I think the link is in the top of the forum, it is a pdf file. I think you'll like it. http://www.psychiatry24x7.com/bgdisplay ... =mooddiary


my best