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PostPosted: Thu Aug 13, 2009 4:52 am 
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i responded to a post today in regards to klonopin. here's what i wrote. just some info... thought it might be helpful.

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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PostPosted: Thu Aug 13, 2009 12:47 pm 
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Aren't you taking Klonopin right now?

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PostPosted: Thu Aug 13, 2009 1:47 pm 
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Not anymore.


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PostPosted: Thu Aug 13, 2009 1:48 pm 
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Not anymore.


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PostPosted: Thu Aug 13, 2009 1:58 pm 
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Holy wall-of-text MD...you need to make friends with the return key.

Question - my doctor is talking about me going on Lyrica for my fibro pain. I know it works @ gaba receptors also...is it like a benzo? Cause I don't want to get involved with that.

Thanks!

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 Post subject: Lyrica
PostPosted: Thu Aug 13, 2009 3:31 pm 
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Sorry didn't mean to post that previous post twice.

And point taken, enter key will definitely be used more frequently. See...

Anyway, how long have you had fibromyalgia? And what trigger points provide the most discomfort for you? How much Lyrica does your doctor want to start you with, like 75mg twice daily?

Lyrica, Pregabalin, is in a class of drugs known as anticonvulsants, which house numerous different kinds of medications. It's primarily used for neuropathic pain, especially in patients with diabetic neuropathy. It's used as adjunct therapy for partial seizures and in some places (Europe I believe) used for generalized anxiety disorder. It has recently been approved by the FDA specifically for the treatment of fibromyalgia. It's main competitor is Cymbalta, which gained FDA approval last year for treatment of fibromyalgia.

Pregabalin shares the same mechanism of action as other drugs in it's class, such as Neurontin (Gabapentin). Lyrica works by binding to voltage-dependent calcium channels on neurons in the central nervous system (brain and spinal cord). These channels are permeable to the ion calcium. Neurons that have been excited (in my previous post, depolarized), have an action potential running from the head of the cell (dendrite) all the way down to it's tail (axon). When an action potential reaches the end of the axon (the synapse), it gets depolarized (excited) which causes these calcium channels to open. Since there is more calcium outside neurons than inside them, by diffusion, calcium begins to influx into the axon at the synapse. Calcium in the synapse (terminal end of an axon) plays an important role because it binds to vessicles located in the axon terminal. These vessicles, you can think of them as little water balloons, contain specific neurotransmitters. These could be excitatory ones, like glutamate and norepinephrine, or inhibitory ones, like GABA. As the concentration of calcium increases in the synapse, these vessicles containing neurotransmitters get activated and begin to fuse with the end wall of the synapse, and eventually they get released into an open space called the synaptic cleft. The neurotransmitters that were released from the vessicles are now in the synaptic cleft and they now can carry out their desired effects on the next neuron (which is called the post synaptic neuron). If the neurotransmitter is norepinephrine, glutamate, or dopamine, it will cause this post synaptic neuron to be excited (depolarized) and another action potential will result. As the action potential reaches the terminal end of the neuron (axon's synapse), the same thing will happen: synapse gets depolarized (excited) --> causes voltage gated calcium channels to open --> increased concentration of calcium in synapse --> fusion of vessicles containing neurotransmitters to terminal end of axon --> release of neurotransmitter in synaptic cleft --> all over again.

So going back to Lyrica. The drug binds to a certain subunit on these voltage gated calcium channels on neurons within your brain and spinal cord. The binding of Lyrica to these channels causes the channel to be impermeable to calcium, thereby dramatically reducing the amount of calcium entering the axon. End result, low low levels of calcium leads to less vessicle activation leading to less neurotransmitter release (primarily the excitatory ones like glutamate and norepinephrine). You would think that the neurotransmitter GABA would also be decreased by this mechanism, and indeed it is, if the Lyrica is bound to calcium channels on neurons containing GABA vessicles. However, there is a specific enzyme called glutamic acid decarboxylase (GAD), and this enzyme converts the excitatory neurotransmitter glutamate into the inhibitory neurotransmitter GABA. Lyrica, through some complicated mechanism, greatly increases GAD's activity, thereby producing more GABA. So in answer to your question, Lyrica itself doesn't really work at GABA receptors. It increases the activity of the enzyme GAD which increases the amount of GABA, and it's this increased amount of GABA that works at the GABA receptors. For this reason, Lyrica can greatly potentiate benzodiazepines. So if you're on one while on Lyrica, talk with your Dr. about it.

The concept of pain management coming from a drug like Lyrica is that conditions like fibromyalgia and other neuralgias have hyperexcited neurons that are contributing to the neuropathic pain. By binding to the voltage dependent calcium channels on these hyperexcited neurons, calcium influx is decreased which significantly reduces excessive excitatory neurotransmitter release ==> calming effect on these hyperexcited neurons ==> decreased pain sensation.

Hope it wasn't too "jargoned". Don't know much about abuse potential, but I'll look into it. My assumption is that if it's increasing the amount of GABA being produced, then more GABA receptors will be produced which may then lead to tolerance. So I would assume if you were to stop the medication, a taper may be necessary.

Cheers


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PostPosted: Thu Aug 13, 2009 3:57 pm 
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Thanks for the neurochemistry lesson.

I was dx with fibro like 5 years ago. I personally don't think I have it. When I went to pain management about 6 months after I was dx, they told me I have "a fibromyalgia-like syndrome." Huh.

I think I have MPS. I have actual knots in my muscles that can be massaged away and I have inflammation. NSAIDS help my pain, which is not supposed to happen with fibro. Opiates also helped my pain, which is not supposed to happen with fibro. None of the fibro drugs they gave me helped my pain and most of them made me feel worse.

So I basically gave up on getting any help from the medical profession regarding my pain. I treat myself with trigger-point therapy, yoga, meditation, hot soaks, ibuprofin and the occasional curse-laden ranting fit against your profession. Nothing personal. But really, how many times can you tell your doctor: I am in such pain that it has made my life miserable, and have them say: are you exercising, yes? taking hot baths, yes? Well, just keep that up and hope for the best. O RLY????

I tried lyrica once already, 50mg 3xs a day for a week. Didn't do anything and that was the end of the sample pack, so, yeah.

I'm really out of options I guess. I could ask for a referral to a specialist, but I'm tired of jumping through hoops. For now I can push through it most days. It just sucks not to be able to dance or hike or play with my kid without pain.

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PostPosted: Thu Aug 13, 2009 4:15 pm 
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I totally understand with what you're saying. Many docs forget, the number one priority of a physician is to alleviate a patient's pain. Many have lost this idea.

How much Suboxone are you on and is that helping at all? I know opiates don't really do much for fibromyalgia, but you said you had some experience before using opiates for the fibro pain. I suffer from chronic leg pain after a complicated surgery and being on suboxone has virtually eliminated the pain.

Trigger point therapy, yoga, acupuncture have all shown to work well with some people. Has your doctor talked to you about Cymbalta? Has similar properties to Lyrica but some studies show that it has much better pain relieving qualities, especially for neuropathic pain.

Also, wouldn't hurt seeing a pain management doc. Now stop, breathe, and realize that's not exactly what I mean. What I mean is, seeing an INTERVENTIONAL pain management doc. These docs do wonders, especially for pt's w/fibro. They do a lot of joint and muscle injections with local anesthetics, steroids, etc. Might want to give it a shot. But remember the interventional part. You don't want to see a regular old pain management doc, who's just going to give you a script for a 100 percocet, even though he/she knows opiates don't touch fibro pain. gotta love them pain docs!

Feel better.


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PostPosted: Thu Aug 13, 2009 7:23 pm 
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Dude, I WENT to a pain mgmt doc and they didn't give me shit. That's why I started buying my pain pills illicitly.

I'm not on Suboxone anymore. I'm done. It helped my pain quite a bit, but my insurance only covers it for a year and I can't afford to buy it.

The pain mgmt clinic wouldn't even give my physical therapy - because they didn't think I was in enough pain. Because I still work and do all the things I do. But I'm on medicaid, so that's probably why they don't want dick to do with me.

Yes, I am a little bitter. But whatever. I'll figure it out, I always do.

As far as cymbalta, me and SNRI's don't get along. Too bad.

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PostPosted: Thu Aug 13, 2009 8:31 pm 
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Sorry to hear. Have you tried neurontin (gabapentin)? The other one that comes to mind is amitryptiline, which is a tricyclic antidepressant, but has has potent effects on pain fibers. I'm assuming advil or tylenol round the clock isn't touching the pain. You might ask about a more powerful NSAID, toradol, but it's really toxic to your kidneys, shouldn't be on it for more than a few days. But wow, in my experience, it's always provided the best analgesia for me.

Fibromyalgia is such a debilitating disease because it leaves individuals like yourself in chronic pain. You might want to keep trying the Lyrica, since it is the number one drug of choice these days for fibro, and you usually have to wait a couple weeks for it to reach therapeutic levels in the body. Meaning, they usually start you on it pretty low, like 75mg BID, then increase over two weeks or so to 150 to 250 and even 400mg.

I know this may sound bad, but keep shopping around for another pain specialist. Try and find ones that have a background in PM&R (physical medication and rehabilitation). Anesthesia pain docs are usually the ones that just prescribe narcs or refuse to do anything. Many of the PM&R trained pain specialists are interventional ones as well. You can also see a pain doctor that has a neurology background, which might really help in your case, considering the big role the nervous system plays in fibro. Point being, there's usually three avenues in how pain docs become pain docs and it's all through fellowships. Either from anesthesia (script writers), PM&R (interventional mostly), and neurology. So I would advise to do some research and get some background info on a couple docs that interest you. There is hope. Oh and lastly, have you tried sitting in a dry sauna? Feel better.


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