Narcotic (Opioid) Pain Medications Relieve Some of my Neurological ME/CFS Symptoms

[heapsreal]

[/QUOTE

]Endorphins though, seem to be targeting this neural sensitivity from a different angle. It's too bad they're laden with all sorts of other issues.

LDN is used for this purpose and has less side effects than narcotics.

 

[acrosstheveil]

are there any other ways to raise endorphins that we haven't discussed yet?

 

[heapsreal]

are there any other ways to raise endorphins that we haven't discussed yet?

i think there is a connection between endorphins and dopamine??

 

[acrosstheveil]

i wish my doctor was more open to prescribing opiates. I have tried all the alternatives. Antidepressants, memantine, gabapentin, and even benzos and they all have TERRIBLE withdrawal. I have taken lots of opiates in the past and they all help but the withdrawal is never bad. This gabapentin crap I've been described is HORRIBLE. I feel like I'm losing my mind and now I am becoming a social recluse to the debilitating anxiety. Is there any other alternative I can ask for at the next appointment? I'm seriously losing my mind over this stuff.

 

[Dufresne]

i wish my doctor was more open to prescribing opiates. I have tried all the alternatives. Antidepressants, memantine, gabapentin, and even benzos and they all have TERRIBLE withdrawal. I have taken lots of opiates in the past and they all help but the withdrawal is never bad. This gabapentin crap I've been described is HORRIBLE. I feel like I'm losing my mind and now I am becoming a social recluse to the debilitating anxiety. Is there any other alternative I can ask for at the next appointment? I'm seriously losing my mind over this stuff.

Have you tried LDN or baclofen? I've gone down the benzo, DM, gravol trail and not been favourably impressed in the long run. But baclofen was a breath of fresh air. I've found tapering down over two to three weeks brings with it absolutely no problems.

Baclofen works as a sedative and a stimulant at the same time. The stimulating effect can cause problems if you can't handle it energetically. I find that when my brain can't handle the increase in energy, what I believe must pertain to oxidative stress, my system will push back against the drug. So instead of feeling the antidepressant effect and increased libido, I experience the opposite, which is terribly unpleasant. That said I'm lucky enough to have discovered the other factors for this complication to develop.

It's a terrific drug for treating anxiety and depression. Who really does all that well on SSRI's? Certainly not me. You hear the same things from people for whom these actually do have a positive effect: it's not a miracle cure, you still need to work on yourself, and there are side-effects. Baclofen can actually give someone zest and passion, and instead of crippling you sexually it turns you into a teenager again, and then some. As a kid I could hardly maintain eye contact, with baclofen I often feel energized by social interaction. The medical profession has really overlooked this one, in my opinion, though I suppose indications other than as a muscle relaxant need to be studied further. Thanks to @Marco for writing those blogs that led me to try it.

Don't even get me going on benzos.

 

[Wayne]

Hey @Dufresne,

Remarkable post! Thanks for your most interesting perspectives.

Wayne

 

[acrosstheveil]

what dose of baclofen is effective for you? and what does DM stand for?

 

[Dufresne]

what dose of baclofen is effective for you? and what does DM stand for?

You really just have to build up the dose until you know you're taking too much and then cut back to discover where you get the best results at the minimum dose.

Dextromethorphan.

 

[Marco]

@Dufresne

Good to hear it's working for you!

 

[knackers323]

Hi everyone, what an interesting thread. I haven't been able to read through the whole thing yet so I hope I'm not covering old ground but is this the general idea of what is going on.

LDN, baclofen and opioids help some people by way of raising endorphins which in turn reduce cytokines and brain inflammation?

If so has anyone been able to work out who they will likely have a positive effect on in regards to what started the illness to begin with or what is driving it? Eg. Does it tend to work better in those with known current infections etc.

Are there any Drs or researchers that have or are looking into this?

And the big question of course is what is causing these problems in the brain to begin with?

Ongoing infection or something like Dr Lloyds proposal that he just spoke on about people's genes/immune systems reacting to an event or infection that may have already past?

 

[Wayne]

LDN, baclofen and opioids help some people by way of raising endorphins which in turn reduce cytokines and brain inflammation? ...... If so has anyone been able to work out who they will likely have a positive effect on in regards to what started the illness to begin with or what is driving it?

Hi Knackers, I've had an eye on this thread for quite some time, and I think your understanding is better than mine on some of the key points. What I can say from experience, is I've long noticed I felt better after taking a Tylenol 3 for headache pain relief--Tylenol 3 is half Tylenol and half codeine. Until I saw this thread, I had always assumed the benefits were from the pain relief. I now consider that a small part of my feeling better, and feel the majority of the benefit derives from the codeine effect on my brain.

I used to take half a Tylenol 3 to get this effect, but have recently gotten a prescription for Tylenol 4, which is 3/4 codeine and 1/4 Tylenol. This works even better (with less Tylenol). I discovered this past week that I can take 1/6 tablet of Tylenol 4 before going to bed at night, and consistently feel better in the morning. So far I've only done it every other night, as I have a concern that the benefits might decrease if I start doing it daily. I don't know the details about how or why this works, but can relate this simple protocol that has worked for me.

My doctor didn't hesitate a bit to give me the prescription for the Tylenol 4. He even gave me refills, which should last for years based on my current usage. I think I paid about $25 for 30 tablets.

 

[Dufresne]

Hi everyone, what an interesting thread. I haven't been able to read through the whole thing yet so I hope I'm not covering old ground but is this the general idea of what is going on.

LDN, baclofen and opioids help some people by way of raising endorphins which in turn reduce cytokines and brain inflammation?

If so has anyone been able to work out who they will likely have a positive effect on in regards to what started the illness to begin with or what is driving it? Eg. Does it tend to work better in those with known current infections etc.

Are there any Drs or researchers that have or are looking into this?

And the big question of course is what is causing these problems in the brain to begin with?

Ongoing infection or something like Dr Lloyds proposal that he just spoke on about people's genes/immune systems reacting to an event or infection that may have already past?

It's primarily that opioids clear the head and prevent PEM. LDN works as a step in this direction, at least for me. GHB does just as well as opioids if not better, as it also counters excitotoxicity by working on the GABA system. Baclofen can be a useful drug but it doesn't have the same effect as these.

I've at leasat a couple tick-borne infections, primarily borrelia and babesia. I understand there are those out there who'd question this, but I'll just say I'm absolutely convinced of this. Does this pertain to my response to endorphins? I don't know.

I suspect endorphins are neuroprotective. So whether one is suffering hits from infection, toxins, auto-immunity, etc the endorphins act to cool the inflammation.

I was just listening to the Jared Younger presentation at Stonford the other night, and he goes into the correlation between leptin and levels of fatigue, and explains how microglia become hyperexcitable. He suggests essentially all the above as possible hits. Interestingly he also mentions longterm opioid use as being able to prime microglia. I wonder if it's not the addiction to opioids and subsequent withdrawal that leads to primed microglia. This might suggest it can work the other way around and opioids can calm irascible microglia. At least that's my guess. That could explain what some of us are experiencing.

I also think his leptin correlation might suggest something like the CIRS Shoemaker talks about might be more common than we'd thought in our population. I know it certainly applies to me. I'm intrigued by Dr Younger's finding that if one pretreats with leptin the response to LPS on microglia is far greater. To me, again, this is hugely suggestive of CIRS and would correspond to my anecdotal observations.

 

[melamine]

I wonder has anyone ever looked at GAD antibodies or glutamate transporters in ME/CFS. The problem in the Wired and Tired type may be either due to impaired conversion of glutatmate to GABA or impaired clearance of extracellular glutamate.

Marco - I realize this is old, but in response to your question, I was tested for GAD antibodies and tested negative in spite of having developed a history of acute episodes of excitotoxic nerve injury, as well as a more chronic course of the same. The most identifiable source of acute (CNS/spinal cord) symptoms followed by permanent nerve injury has been MSG in food.

 

[Marco]

Marco - I realize this is old, but in response to your question, I was tested for GAD antibodies and tested negative in spite of having developed a history of acute episodes of excitotoxic nerve injury, as well as a more chronic course of the same. The most identifiable source of acute (CNS/spinal cord) symptoms followed by permanent nerve injury has been MSG in food.

Thanks for the feedback melamine.

Struck out on that one but I'm more inclined to agree with @Hip that elevated (potentially extracellular) glutamate results from chronically activated microglia rather than a systemic problem of GAD antibodies as per stiff person syndrome.

 

[melamine]

but I'm more inclined to agree with @Hip that elevated (potentially extracellular) glutamate results from chronically activated microglia rather than a systemic problem of GAD antibodies as per stiff person syndrome.

Funny you should mention stiff person syndrome as it was one of the things I was looking into a couple years ago. Not just because of my muscles being chronically stiff now, nor the feeling of them seizing up that signal another excitotoxic insult. As it is, I am experiencing just that since about an hour ago and am trying once again to identify a potential culprit.

 

[Marco]

Funny you should mention stiff person syndrome as it was one of the things I was looking into a couple years ago. Not just because of my muscles being chronically stiff now, nor the feeling of them seizing up that signal another excitotoxic insult. As it is, I am experiencing just that since about an hour ago and am trying once again to identify a potential culprit.

I wish I had an answer for you. Although the absence of GAD antibodies doesn't definitively rule SPS out it is an exceptionally rare disease.

 

[melamine]

[Idea's, theories, links, on the cause of the NMDA excitoxicity or Glutaminergic storm, in me/cfs?/QUOTE]

No theory but here is a broad clue maybe: My excitotoxic symptoms increased to the point of identification as such, following two events: immune function test vaccines and a severe flu-like infection with symptoms (again) of brain damage/encephalopathy. The infection began within weeks of the vaccines, which may or may not have had anything to do with the highly unusual nature of it, or the new symptoms it initiated or that permanently worsened.

 

[melamine]

I wish I had an answer for you. Although the absence of GAD antibodies doesn't definitively rule SPS out it is an exceptionally rare disease.

Well I'm actually in the process of getting at least a partial answer that is probably at least as rare, especially since I am neither in the male population that dominates the diagnosis nor quite the age of those who are more likely to be diagnosed. The neuropathy appears to be related to IgM MGUS - monoclonal gammopathy of undetermined significance. But in my case it is not of undetermined significance. How all these things and more fit together is a mystery. Anti-MAG antibodies, which I have not yet been tested for, are found in about 50% of those with the Dx. I do have positive ANA since about 2010, low levels of antibodies to the standard AI diseases, immune deficiencies, and sicca syndrome.

I have experienced a very noticeable increase in excitotoxic activities and fatigue since the last three dental surgeries. The main things involved have been pain, NSAIDs/Advil, amoxicillin, and dental anesthetic. Also fermented foods and probiotics. All must be considered, particularly since I have experienced increased excitotoxicity with use of certain (probably overly immune-stimulating) probiotics. It seems that once sensitized, a certain tolerance is broken or weakened to things that were not noticeably problematic. It takes many months to settle back but there is a progression in the nerve damage that prevents a return to baseline in that respect.

 

[Marco]

Good to hear that you're getting somewhere.

The rest of it is beyond me I'm afraid.

 

[knackers323]

I don't suppose having these favourable results with these medications really points us any closer to knowing what the underlying cause is, possible follow up investigations that may be usefull or other treatments that may work even better than these ones?