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PostPosted: Mon Mar 30, 2009 10:37 pm 
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I have been on percocets for 2 yrs now for severe back pain and now I have been free of them for 4 months with the help of a little suboxone,maybe 1mg a day for the 4 months of being off the percs.It helps very much for my back pain.Is this wrong?I'm also on klonopin 2mg for 25 yrs and find that impossible to get off of.Anyone have any suggestions on what to do with the little suboxone that I take and the klonopin to get off of.thanx eddie


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PostPosted: Fri Apr 03, 2009 10:54 pm 
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Hi, I am new to this site but I have been taking Suboxone for my back pain for 7 months now. I've had back problems for 7 years total and eventually I got sucked into the painkiller trap. I eventually got addicted and became very dependant. After failed attempts to quit the painkillers due to unrelenting back pain from withdrawl, I visited a Addiction doctor in my area and he put me on the suboxone 8mg 3 times a day. I was nervous at first that my back would start killing me and that It would be another failed attempt to get off painkillers. But it was actually a very smooth transition and my lower back pain never got worse. I've read numerously that Suboxen is not intended for pain management but my prescribing doc said that if it relieves my pain and keeps me off the opiates, then why can't it be used to treat your pain? And 7 months later I agree. It still works for my pain and it has kept me off the opiates for 7 months without any relapse. It has made life with chronic back pain much more tolerable. I don't know anything about Klonopin though. I hope this helps on the pain part though.


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 Post subject: re: klonopin
PostPosted: Thu Aug 13, 2009 12:42 am 
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Hi,

Hope your pain is being controlled with the Suboxone. My addiction (not disease) started when I was put on Percocet after a serious leg operation, and since then have been in chronic pain. At the end of 16 months, I was taking up to 600mg qd of oxycodone, and I'd say that was 10% for the pain and 90% because I was hooked. Long story short, went to rehab, got off the oxy's, 8 months clean, relapsed on Vicodin and went on a binge for about 10 weeks before I decided to get help. Went to a detox facility where they put me on Suboxone and slowly tapered me from 32mg to 2mg in about 10 days. While I was on it, I was shocked at how well my pain was controlled. I decided to stay on Suboxone for at least two months, and I'm taking 16mg qd. My pain is virtually gone because of the Suboxone. Buprenorphine is a very potent analgesic and many hospitals back in the day used to give it IM or IV for pain control. I feel that being on Suboxone will alleviate a lot of your pain, just as the Percs were doing.

Now about the Klonopin. 25yrs is a LONG time. Have you been taking 2mg qd since the beginning, or did your dose recently go up to 2mg in the last year or two? Klonopin's (clonazepam) is a benzodiazepine, a powerful set of drugs that work on specific receptors on your neurons, called the GABA(a) receptors. In very simple terms, your brain is a web of many many neurons, all of which communicate with other neurons, and this communication may be excitatory or inhibitory. Neurotransmitters such as norepinephrine and glutamate produce excitatory effects by depolarizing the post synaptic neuron (the next neuron in the chain). Pretty much all comes down to two ions, sodium and chloride. Influx of sodium into neurons is caused generally by excitatory neurotransmitters, and that sodium influx in the post synaptic neuron causes it to "fire", sending the signal down it's axon to the end of the neuron where it can do the same thing again. These are called action potentials, and they occur when neurons become depolarized past a certain threshold. GABA, on the other hand, is an inhibitory neurotransmitter, which causes instead of depolarization, hyperpolarization of the post synaptic neuron. This means that instead of sodium influx, there is chloride influx. Chloride influx thus causes the neuron to hyperpolarize, thereby unable to "fire" an action potential. This is why GABA is an "inhibitory" neurotransmitter. Now remember, this is at the molecular and cellular level. But when you look at this model grossly, neurons that are not firing are not sending excitatory signals. This reduces the communication between neurons and therefore has a calming effect on many of the functions of the brain, hence why benzo's are used for anxiety. But they're used for a number of other things as well, such as seizures. Going back the cellular level, it's kind of cool how benzo's actually work. So what Klonopin actually does is that it binds to the GABA receptor on your neurons. There are many other sites on this receptor that other chemicals bind to, one being GABA the neurotransmitter itself. Once the GABA receptor is bound by GABA neurotransmitter, a chloride channel opens in the receptor which allows an influx of chloride to the next neuron in line. The Klonopin binds to a specfic site on the GABA receptor and locks the receptor into a certain conformation. This new conformation of the receptor, caused by the binding of Klonopin, increases the affinity of the site on the receptor that actually binds the GABA neurotransmitter. So because there is more "attraction" for GABA neurotransmitter to its respective binding site on the GABA receptor, the FREQUENCY of that chloride channel associated with that GABA receptor greatly increases. So now there's much more chloride getting into the post synaptic neuron because the channel's frequency of being open has increased, due to the binding of GABA neurotransmitter at its binding site on the GABA receptor. End result, instead of depolarization, there is hyperpolarization of the next neuron from the chloride, which leads to an inhibitory effect, leading to sedatory and anxiolytic effects. Think of a water faucet as a GABA receptor, like a sink, with two handles: one for cold one for hot. The cold handle is a GABA neurotransmitter binding site, and let's say GABA neurotransmitter is your left hand. The right handle is a benzodiazepine binding site and Klonopin in this example is your right hand. And now let's say the spout of the sink is the chloride channel and the water coming out of it are chloride ions. So this is what happens, Klonopin (your right hand) grabs the right sink handle. It doesn't turn the sink on or anything, but what it does in some magical way is that it automatically like a reflex causes your left hand (GABA neurotransmitter) to grab the left sink handle. Now once that GABA is bound, the channel opens up, and the water (chloride) comes pouring out. The stronger that GABA is attached to that left sink handle, the frequency of that spout being open increases. So the Klonopin is indirectly making any GABA neurotransmitter that's available bind to that GABA receptor like crazy, thus making more and more chloride flow through, thus causing more and more inhibitory effects.

So now here's the problem, you've been on Klonopin for 25yrs. This means that the number of Klonopin binding sites on those GABA receptors has increased, and that's how you develop tolerance. You have to take more to get the desired effect. My point is, if you suddenly just stop taking the Klonopin, you'll have all these unoccupied benzo binding sites. You're neurons are so used to having these inhibitory effects, and now it's not getting the stimulation (Klonopin) to be inhibited. So what happens... withdrawal. Most symptoms of benzo withdrawal are due to this imbalance of GABA and glutamate in the brain. A chronic benzo user has way more GABA activity than glutamate activity. The body tries to balance this by increasing glutamate activity. More benzo's you take and for longer of a time, more and more glutamate is produced, to counter the effects of the "GABAergic" benzo's. So when you take away the benzo, you have all this glutamate activity that's not being countered by GABA. There is a huge imbalance now, and this is the cause for many of the withdrawal symptoms. They can range from insomnia, gastric problems, tremors, agitation, spasms, irritability, depression, sweating, psychosis, delirium tremens, and most lethal... seizures. That's why it is absolutely imperative that if you want to stop your Klonopin use, please discuss this with your doc so he/she can taper you off it slowly. Benzo withdrawal is one of the worst things anyone can go through, so please take the time and address this fully. When I detoxed from the opiates just a couple weeks back at a detox facility, I met a girl there who was on Klonopin 1.5mg qd for 2 yrs. She was going through hell, and from such a small dose and not that long of a time period. Taper nice and slow, and you'll be okay.

Wow, I have absolutely no idea why I went into all the details of this, maybe it's the suboxone I'm on. Anyways, sorry. But hope it was a bit informative. Oh, and if I've made any errors or mistakes, please correct.

Wish you all the best!


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Fond Du Lac Psychiatry
Dr. Jeffrey Junig, M.D., Ph.D.

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