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Old 06-08-2010, 04:22 PM #1
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Default Amitriptyline caused my neuropathy

I have taken Amtriptyline for 20 years started on it for insomnia. I then developed burning skin pain, and no one ever thought it was the Amit. I wouldn't have either, except, I was put on Remeron an other anti-depressant , and first developed numb feet, and the the itching skin and then after a few weeks the burning skin pain. I am no off the Remeron, and the pain is back to the normal level. Now what to do about going off Amit is very scary. It helps the pain, but yet is causing the pain. does that make any sense. Wouldlove to hear from anyone else .
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Old 06-09-2010, 08:30 PM #2
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I am not a fan of amitriptyline. I was on it a long time ago, and am no better off for being on it. All my problems started after I took that drug. That doesn't mean it caused it....but, I haven't ruled it out either.
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Old 06-09-2010, 09:33 PM #3
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I used to take this drug in the mid-1980's. I think it was prescribed a lot back then... may still be. I was on a hefty dosage of 100 mg.

I agree with Cyclelops statement:

"That doesn't mean it caused it....but, I haven't ruled it out either."

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Old 06-09-2010, 09:51 PM #4
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i take amitriptylene at night. it has helped with the stabbing pains and keeps me asleep once i get asleep. the only side effect i have noticed is its hard to stay awake for a while once i get up.
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Old 06-10-2010, 04:43 AM #5
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Lightbulb

This drug has some mixed history. It appears on lists from neuropathy sites as a "cause" of axonal neuropathy.

Here is an example:
http://www.wrongdiagnosis.com/t/toxi...line/intro.htm

However, I couldn't quickly find the studies that support this yet.
I'll look later in more detail.

Recently there have been studies showing amitriptyline actually enhances peripheral nerve regeneration.
Here is the link to that article:
http://neurotalk.psychcentral.com/sh...=amitriptyline

This might be dose dependent or a factor in those who do not metabolize this drug well. I do think this is very confusing.

Edit to add:
It appears that amitriptyline is being used as an injected anesthetic in some situations. So I found some neurotoxic in vitro (no in living subjects) on this subject. This would place the drug in high concentration near neurons:

Quote:
Eur J Anaesthesiol. 2007 Aug;24(8):702-8. Epub 2007 Apr 17.
Differential neurotoxicity of tricyclic antidepressants and novel derivatives in vitro in a dorsal root ganglion cell culture model.

Haller I, Lirk P, Keller C, Wang GK, Gerner P, Klimaschewski L.

Medical University of Innsbruck, Department of Anesthesiology and Critical Care Medicine, Innsbruck, Austria.
Abstract

BACKGROUND AND OBJECTIVE: Tricyclic antidepressants are commonly employed orally to treat major depressive disorders and have been shown to be of substantial benefit in various chronic pain conditions. Among other properties they are potent Na+ channel blockers in vitro and show local anaesthetic properties in vivo. The present study aimed to determine their differential neurotoxicity, and that of novel derivatives as prerequisite for their potential use in regional anaesthesia. METHODS: To directly test neurotoxicity in adult peripheral neurons, the culture model of dissociated adult rat primary sensory neurons was employed. Neurons were incubated for 24 h with amitriptyline, N-methyl-amitriptyline, doxepin, N-methyl-doxepin, N-propyl-doxepin, desipramine, imipramine and trimipramine at 100 mumol, and at concentrations correlating to their respective potency in blocking sodium channels. RESULTS: All investigated substances showed considerable neurotoxic potency as represented in significantly decreased neuron numbers in cultures as compared to controls. Specifically, doxepin was more neurotoxic than amitriptyline, and both imipramine and trimipramine were more toxic than desipramine or amitriptyline. Novel derivatives of tricyclic antidepressants were, in general, more toxic than the parent compound. CONCLUSIONS: Tricyclic antidepressants and novel derivatives thereof show differential neurotoxic potential in vitro. The rank order of toxicity relative to sodium channel blocking potency was desipramine < amitriptyline < N-methyl amitriptyline < doxepin < trimipramine < imipramine < N-methyl doxepin < N-propyl doxepin.

PMID: 17437653 [PubMed - indexed for MEDLINE]
from http://www.ncbi.nlm.nih.gov/pubmed/17437653

and this one :
Quote:
Toxicol Appl Pharmacol. 2006 Nov 15;217(1):100-6. Epub 2006 Aug 15.
A proposed mechanism for amitriptyline neurotoxicity based on its detergent nature.

Kitagawa N, Oda M, Nobutaka I, Satoh H, Totoki T, Morimoto M.

Department of Anesthesiology, Tsuruta Orthopedic Clinic, Ushizu, Saga 849-0306, Japan.
Abstract

Although amitriptyline has gained attention as a potent local anesthetic, recent animal studies showed that it can cause irreversible neural impairment. We hypothesized that nerve membrane disruption caused by solubilization, a common detergent property, accounted for amitriptyline neurotoxicity. We used a two-phase approach to test our hypothesis. Firstly, we determined (1) the molecular aggregation concentration of amitriptyline, (2) the concentration of amitriptyline that disrupts artificial lipid membranes and (3) the concentration of amitriptyline that causes hemolysis. Secondly, we compared these levels with neurotoxic concentrations determined from assessment in a rat model of spinal anesthesia using changes in cutaneous stimulus threshold (CST). Amitriptyline concentrations that caused molecular aggregation, model membrane disruption and hemolysis were 0.46%, 0.35% and 0.3%, respectively. Animal study showed a significant increase in CST at >or=0.3% of amitriptyline, indicating neurological impairment. Since amitriptyline caused model membrane disruption and hemolysis at the molecular aggregation concentration, solubilization plays a role in the destruction of artificial membranes and erythrocytes. Furthermore, these concentrations are also in good agreement with the minimum concentration causing neurological injury. Therefore, while additional studies, including histopathology, are necessary to clarify this observation, amitriptyline neurotoxicity appears to be associated with its detergent nature.

PMID: 16978678 [PubMed - indexed for MEDLINE]
and this one:
http://www.ncbi.nlm.nih.gov/pubmed/16717317

All involving injection as an anesthetic.

I am still looking for oral studies...

There are studies about SSRIs causing neuronal cell death...these have been around for few years. This paper includes amitriptyline with prozac (which has been most studied so far):
http://www.ncbi.nlm.nih.gov/pubmed/11996893
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Last edited by mrsD; 06-10-2010 at 06:10 AM.
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Old 06-10-2010, 06:15 PM #6
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Now what do I do. Is there a doctor some place that knows about this link. I am decreasing the Remeron, and the depression is increasing, but the burning pain is less. This is such a catch 22 situation.


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Old 06-16-2010, 10:18 PM #7
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The following article suggests that "tricyclic antidepressants might deplete the body of coenzyme Q 10 (CoQ 10)." Perhaps a mechanism by which amitriptyline could cause neuropathy. BTW I have been taking it for a few years, mainly 25 mg/day, and it helps with my pain level. If it were slowly making it worse, I might never know. You can find alternatives, there are many drugs used to relieve painful neuropathy. It seems one of the premier ones is gabapentin (Neurontin).

I can't post links yet, so go to **
and search for "Tricyclic Antidepressants"

"Coenzyme Q10(CoQ10)

Preliminary evidence suggests that tricyclic antidepressants might deplete the body of coenzyme Q 10 (CoQ 10), a substance that appears to be important for normal heart function.1,2 Based on this observation, it has been suggested (but not proved) that CoQ 10 supplementation might help prevent the heart-related side effects that can occur with the use of tricyclic antidepressants."

Good luck
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Old 06-17-2010, 08:44 AM #8
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Boy, this has me really PO'd.

I was on amitriptyline 150mg WITH zoloft back in the 90's when that was what they used for pain.....or 'fibro' and its concomittant 'depression'. And those dipsh#ts never took a blood level of the amitrip. I would ask, and they would say....'you don't need it'. This was the same HMO linked clinic that I was with for 11 years and left, only to be diagnosed with neuropathy and SjS.

I could never prove a case and at this stage, it would not be worth the stress, since litigation is horrible on one's health.

It makes me wonder about the whole thing on drugs...consume at your own risk, I guess.
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Old 06-17-2010, 09:05 AM #9
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We must take an active role in our health care. Sometimes we expect too much of doctors. We have to trust them to some degree, but they don't know everything. We can't expect them to know every interaction between all drugs & supplements. And then each person is different too. I sure hope Drs begin to learn more about supplements in medical school.

And be careful, just because you were taking a particular drug at the time you developed neuropathy, doesn't mean the drug caused the neuropathy. Because two things happen at about the same time does not mean that one caused the other.
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Old 06-17-2010, 09:26 AM #10
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Lightbulb

Basically doctors are poorly trained on drugs. They have a short course on them once in college.

They are predominately trained in observation, anatomy and labeling of illness. They then consult therapeutic manuals, many of them way out of date (because they are expensive to buy), on how to treat what they have just diagnosed.
For example methylcobalamin and oral supplements of B12 are typically not in their manuals, and it never occurs to them to look elsewhere for newer information.

I read an interesting critique of medical school in US recently that likened medical training to a cult indoctrination. I can't find that exact article but this one is similar:
http://www.naturalnews.com/021922_ju..._medicine.html

If you Google Is medicine a cult? You will find more.
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