Re: NCCP 's - Debbie's Article- Chest pains, heartburn, acid reflux, spasm pains, NCCPs...

[Guest guest]

workgreat post on NCCP in achalasia.

just one caveat, however:

one can drive and work on opioid analgesics. in fact these meds, when properly

titrated to effect, improve life functions.

steve

> >

> > My son will be 17 in Aug. He had a Heller myotomy when he was 6. Been

getting NCCP's for years. He's not on any meds. GI doc wants to put him on

something. He is going to scope him and do a biopsy of lining of the E. this

summer ..,....just wondering

> > What others thought?? son doesn't want to be on any meds

> >

>

>

>

>

>

[Guest guest]

There's a difference between using narcotics for chronic pain management and

occasional use for occasional flare-up pain. Likewise, there's a difference

between using narcotics for situations like osteoarthritis versus neuropathy.

To treat neuropathy with narcotics, you pretty much have to be high to take the

pain away -- the pain remains, but you're too high to care about it.

If you're in the emergency room for an NCCP, they're not going to give you a

narcotic if you don't have someone to drive you home.

Debbi in Michigan

>

> workgreat post on NCCP in achalasia.

>

> just one caveat, however:

>

> one can drive and work on opioid analgesics. in fact these meds, when properly

titrated to effect, improve life functions.

>

> steve

[Guest guest]

I doubt most people prescribed opioid analgesics in treatment of chronic pain

management are " too high to care about their pain. " Those meds merely make the

pain more tolerable, after they are titrated-to-effect. One minimized side

effect is euphoria.

Steve

> > >

> > > workgreat post on NCCP in achalasia.

> > >

> > > just one caveat, however:

> > >

> > > one can drive and work on opioid analgesics. in fact these meds, when

properly titrated to effect, improve life functions.

> > >

> > > steve

> >

> >

>

>

>

[Guest guest]

Good post, notan.

In terms of a first choice, pain management just isn't going to happen with

opioid analgesics, because of all the medical resistance to opioids, regulatory

and criminal threats and opioignorance.

The frustration many achalasians have is they are fundamentally forced to

undergo the traditional treatments GIs want, whether they're safe and

efficacious for a given patient. Most GIs won't even recognize or adequately

treat pain their procedures produce. With my HM w/ fundo, I was given Tramadol

which had virtually no effect on pain relief. If you " suggest " you're still in

pain - and every patient has a different pain threshold/tolerance - you're

likely to be pegged as a " drug seeker. "

The dr-pt relationship becomes extremely distorted under these conditions,

affecting what choices are available.

Steve

> >

> > ... To treat neuropathy with narcotics, you pretty much have to be

> > high to take the pain away -- the pain remains, but you're too high to

> > care about it. ...

> >

>

> When I had my myotomy I was on a morphine pump but I had terrible

> feelings in my hand from neuropathy. I had damaged a nerve in my

> shoulder during the surgery by having my arm behind my head for too

> long. The feeling in my hand was like the worst case of a hand waking up

> from being " asleep " I ever had. It was much worse than the other pain

> from the surgery. The morphine seemed to be doing nothing for it. It

> slowly went away over three months. When I was injured last summer I was

> extremely drugged with a number of drugs after the surgery but because

> of the neuropathy in my feet I could not tolerate the feeling of even a

> bed sheet touching my toes. The drugs did help with the other pain. I

> would start begging for more long before they could give me more. Then

> it would be much better again when I finally got some more but not the

> neuropathy, except that it put space between my consciousness and the

> neuropathic pain and I was sleepy enough I could sleep.

>

> Not all achalasia NCCP are purely neuropathic though. Some are spasm

> related and while the spasms may possibly be reduced by some other

> medications the pain caused by the contractions may respond to

> narcotics. Some NCCP are probably triggered by real events, such as

> acid, that simulates sensory nerves but the signal from them is

> distorted by neuropathy either as pain or in causing a spasm. A narcotic

> may make the sensory nerves less sensitive so they don't trigger the

> neuropathic response or stops them after they have started to signal.

>

> If it were me I would want to try other options first. Some people don't

> seem to find anything that works. I have to feel better about those that

> are helped by narcotics than those that are helped by nothing. Just

> wouldn't be my first choice. If narcotics for NCCP is the devil casting

> out the devil then I am still for it.

>

> The best thing about pain is the people who bring comfort. I count you

> and your famous NCCP post in that context.

>

> notan

>

>

>

>

>

>

[Guest guest]

notan wrote:

The best thing about pain is the people who bring comfort. I count you

and your famous NCCP post in that context.

Oh, that is so sweet! Thank you, notan!

We can all hope and pray that the day will come that NOBODY will need

that information ever again, but in the meantime I'm so glad that people

have found it to be helpful. I can't even imagine going through this

stupid disease without the comfort that we've been able to get through

this support group. Thank goodness we have access to the internet these

days!

Debbi in Michigan

[Guest guest]

Steve wrote:

I doubt most people prescribed opioid analgesics in treatment of chronic

pain management are " too high to care about their pain. " Those meds

merely make the pain more tolerable, after they are titrated-to-effect.

One minimized side effect is euphoria. Steve, I don't know what your

problem is, but it appears that you have either a chip on your shoulder,

or you have reading comprehension issues. Heck, maybe it's both.

NOBODY IS SAYING THAT NARCOTICS ARE EVIL. Please stop acting as if

we're insulting everyone who uses narcotics for chronic pain management.

Nothing could be further from the truth.

What we are saying, is that MANY occurrences of NCCPs are related to

problems with the nerves sending " false/bad " signals to the brain,

rather than from actual " painful incidents " that are occurring in the

esophagus. That's why we're using the term " Non-Cardiac Chest Pain "

(NCCP) rather than " spasms " -- in many, many, many cases, the

feeling/sensation of having a " spasm " is not actually caused by a muscle

in the esophagus that is actually in spasm. It FEELS LIKE a spasm, but

there is no cramped muscle.

In these situations, the pain sensation comes from the fact that the

brain doesn't understand what the screwed up nerves in the esophagus are

saying. In my own particular case, I'm likely to experience NCCPs when

I bend over (pressures change in my chest when I bend over, and the

nerves try to say " increased pressure in the chest because of bending

over " but it comes out as " omvtrsdrf [trdditr om yjr vjrdy nrvsidr pg

nrmfomh pbrt " . (I just moved my fingers over one key on the home row

and typed the same sentence... makes a HUGE difference in comprehension,

doesn't it?) When the brain gets the jumbled message, it has no clue

what is going on -- it just knows that the esophageal nerves are talking

mumbo-jumbo, so it assumes that the esophagus has been gravely injured

and it " sounds the attack " in the form of a PAIN!!!!! message. When I

sneeze, instead of sending a message that says, " Hey, we just sneezed

down here, just letting you know! " , the message that gets sent is likely

to be, " Hru. er kidy dmrrxrf fpem jrtr. kidy ;ryyomh upi lmpe@ " and the

brain is thinking, " WTF is going on down there???? SEND THE ALERT! PAIN

ATTACK!!!! "

With this type of neuropathic pain, there is no *actual pain event* in

the form of tissue damage, etc., that is happening. And the

nerve-message that is being sent isn't actually " PAIN! " like it would be

in the event of an actual pain event. While your beloved opioids are

often successful at intercepting actual pain messages to alleviate the

sensation of actual pain events, they are not very successful at

intercepting the garbled mumbo-jumbo messages that the brain INTERPRETS

as a pain event message.

So someone has a Pain Attack, takes a narcotic, and still has pain. So

they take another narcotic, but still have the pain. So they take

another narcotic, and while they still have the pain, they don't CARE

about the pain anymore because they are spaced out on narcotics. This

is the type of thing that notan was talking about with his major trauma

to his legs. The nerves were damaged and sending out garbled messages,

and no amount of narcotics would stop those messages from coming through

to his brain.

This is why there are special classes of drugs specifically for

neuropathic pain. Science is still learning about this whole

phenomenon, and new drugs are being discovered and old drugs are being

repurposed.

In my case, just 5mg of Paxil (paroxetine) per day is enough to keep the

NCCPs away. Interestingly enough, 5mg of paroxetine is only 25% of what

is considered the minimum therapeutic dose for its intended purposes

(depending on use, it's prescribed at 20-60mg/day). Interestingly

enough, my itty-bitty dose of Paxil does not alleviate ANY other kind of

pain in my body: pain from sinuses acting up because of allergies,

bumps/bruises, muscle strains, etc., are all the same as always. When I

had my knee surgery and my sinus surgery years ago, I used narcotic pain

relievers, and they worked great. I wasn't high as a kite and my pain

was manageable (although I did have to change my dosing regimen to

alleviate the sedating effect during the daytime -- half as much but

twice as often worked great at keeping me on an even keel).

Opioid pain medications are great for their intended purposes, but they

do NOT successfully treat all kinds of pain. And if someone's

experiencing achalasia-related NCCPs that are neurogenic rather than

spasm-related, opiods are not going to stop the pain even at extremely

high doses -- they are simply going to make the person so spaced out

that they don't care about the pain.

You can titrate your arse off for all I care, you're not going to

alleviate many NCCPs with opioids. Neuropathy is a different kind of

animal -- you need to think outside the box on this one.

Debbi in Michigan

Successfully PREVENTING 99.99% of NCCPs for over 10 years with minimal

daily doses of Paxil.

[Guest guest]

> >

> > one can drive and work on opioid analgesics. in fact these meds, when

> > properly titrated to effect, improve life functions.

> >

>

> Even if they had no effect on my driving I would not want to have to

> defend myself in the state of AZ if police decided I had a problem being

> on them while driving.

>

> notan

>

>

>

>

>

[Guest guest]

What I objected to was your pejorative terminologies of " spacing out "

or " getting high " when opioids are administered for neuropathic pain. That isn't

an accurate characterization or symptom of opioid therapy for the treatment of

chronic pain, including neuropathic.

Most pain modulation occurs with the GABA pathways within the brain, where the

endogenous opioids - naturally occurring - control sensitivity threshold to pain

stimuli. The human brain doesn't allow one to 'space out' in response to

endogenous opioids mediating pain relief; and chronic administration of

exogenous opioids titrated to effect would also not produce disorientation.

That's my point.

I'm fully familiar with the differences from pain signal transmission resulting

from tissue damage and nerve damage, as well as the mechanisms of nociception

and antinociception.

It's important to recognize that alterations in the brain have also been

demonstrated following nerve injury. For example, phantom limb pain has been

shown to be associated with re]organization of the cortex of brain. There is a

considerable degree of re]organization of spinal cord in response to peripheral

nerve injury. It's also well know that the dorsal horn is the site where most

pain signals are processed.

GABA pathways form a major inhibitory neurotransmitter system in the central

nervous system - pathways in which opioids mediate pain relief. Suppression of

this pathway by a GABAA receptor antagonist is associated with allodynia (a

neuropathic condition). GABA receptor levels in the spinal cord are decreased

with nerve damage, probably as a result of degeneration of the primary neurons.

This suggests a role for GABA in modulating the response to nerve injury.

Opioids play a crucial role in modulating the perception of pain.

Central nervous system sensitization might be contributed to by a decrease in

the efficacy of GABA pathways. Decreased efficacy of GABA pathways is known to

contribute to neuropathic allodynia.

Co]administration of a NMDA receptor antagonist and morphine has also been

demonstrated to attenuate pain in trigeminal neuralgia.

But tricyclic anti]depressants only achieve clinically significant(greater than

50%) pain relief in less than 50% of patients and are associated with

sub]optimal side effect profiles

Your Paxil shares the common side effects and contraindications of other SSRIs,

with high rates of nausea, somnolence and sexual side effects.

The physiology of nociception involves a complex interaction of peripheral,

central nervous system and brain structures. The pathophysiology of chronic pain

shows alterations of normal physiological pathways of the brain, giving rise to

hyperalgesia or allodynia.

The two most important systems in modulating nociception and antinociception are

the NDMA and opioid receptor systems; while activation of NMDA receptors has

been found to contribute to the hyperalgesia associated with nerve injury or

inflammation.

Opioids remain an effective tool for alleviating neuropathic pain, without the

adverse effects presented by other adjuvants.

In regards to NCCP, opioids certainly reduced its episodes and severity in my 33

year experience with achalasia.

When available, opioids decreased the severity of most of my achalasia symptoms

and allowed a much higher quality of life - for well over 15 years. After

successful treatment is summarily withdrawn by an overzealous DEA, and my life

is essentially gone, one tends to have a " chip " on one's shoulder.

Steve

> I doubt most people prescribed opioid analgesics in treatment of chronic

> pain management are " too high to care about their pain. " Those meds

> merely make the pain more tolerable, after they are titrated-to-effect.

> One minimized side effect is euphoria. Steve, I don't know what your

> problem is, but it appears that you have either a chip on your shoulder,

> or you have reading comprehension issues. Heck, maybe it's both.

> NOBODY IS SAYING THAT NARCOTICS ARE EVIL. Please stop acting as if

> we're insulting everyone who uses narcotics for chronic pain management.

> Nothing could be further from the truth.

> What we are saying, is that MANY occurrences of NCCPs are related to

> problems with the nerves sending " false/bad " signals to the brain,

> rather than from actual " painful incidents " that are occurring in the

> esophagus. That's why we're using the term " Non-Cardiac Chest Pain "

> (NCCP) rather than " spasms " -- in many, many, many cases, the

> feeling/sensation of having a " spasm " is not actually caused by a muscle

> in the esophagus that is actually in spasm. It FEELS LIKE a spasm, but

> there is no cramped muscle.

> In these situations, the pain sensation comes from the fact that the

> brain doesn't understand what the screwed up nerves in the esophagus are

> saying. In my own particular case, I'm likely to experience NCCPs when

> I bend over (pressures change in my chest when I bend over, and the

> nerves try to say " increased pressure in the chest because of bending

> over " but it comes out as " omvtrsdrf [trdditr om yjr vjrdy nrvsidr pg

> nrmfomh pbrt " . (I just moved my fingers over one key on the home row

> and typed the same sentence... makes a HUGE difference in comprehension,

> doesn't it?) When the brain gets the jumbled message, it has no clue

> what is going on -- it just knows that the esophageal nerves are talking

> mumbo-jumbo, so it assumes that the esophagus has been gravely injured

> and it " sounds the attack " in the form of a PAIN!!!!! message. When I

> sneeze, instead of sending a message that says, " Hey, we just sneezed

> down here, just letting you know! " , the message that gets sent is likely

> to be, " Hru. er kidy dmrrxrf fpem jrtr. kidy ;ryyomh upi lmpe@ " and the

> brain is thinking, " WTF is going on down there???? SEND THE ALERT! PAIN

> ATTACK!!!! "

>

> With this type of neuropathic pain, there is no *actual pain event* in

> the form of tissue damage, etc., that is happening. And the

> nerve-message that is being sent isn't actually " PAIN! " like it would be

> in the event of an actual pain event. While your beloved opioids are

> often successful at intercepting actual pain messages to alleviate the

> sensation of actual pain events, they are not very successful at

> intercepting the garbled mumbo-jumbo messages that the brain INTERPRETS

> as a pain event message.

> So someone has a Pain Attack, takes a narcotic, and still has pain. So

> they take another narcotic, but still have the pain. So they take

> another narcotic, and while they still have the pain, they don't CARE

> about the pain anymore because they are spaced out on narcotics. This

> is the type of thing that notan was talking about with his major trauma

> to his legs. The nerves were damaged and sending out garbled messages,

> and no amount of narcotics would stop those messages from coming through

> to his brain.

>

> This is why there are special classes of drugs specifically for

> neuropathic pain. Science is still learning about this whole

> phenomenon, and new drugs are being discovered and old drugs are being

> repurposed.

> In my case, just 5mg of Paxil (paroxetine) per day is enough to keep the

> NCCPs away. Interestingly enough, 5mg of paroxetine is only 25% of what

> is considered the minimum therapeutic dose for its intended purposes

> (depending on use, it's prescribed at 20-60mg/day). Interestingly

> enough, my itty-bitty dose of Paxil does not alleviate ANY other kind of

> pain in my body: pain from sinuses acting up because of allergies,

> bumps/bruises, muscle strains, etc., are all the same as always. When I

> had my knee surgery and my sinus surgery years ago, I used narcotic pain

> relievers, and they worked great. I wasn't high as a kite and my pain

> was manageable (although I did have to change my dosing regimen to

> alleviate the sedating effect during the daytime -- half as much but

> twice as often worked great at keeping me on an even keel).

>

> Opioid pain medications are great for their intended purposes, but they

> do NOT successfully treat all kinds of pain. And if someone's

> experiencing achalasia-related NCCPs that are neurogenic rather than

> spasm-related, opiods are not going to stop the pain even at extremely

> high doses -- they are simply going to make the person so spaced out

> that they don't care about the pain.

> You can titrate your arse off for all I care, you're not going to

> alleviate many NCCPs with opioids. Neuropathy is a different kind of

> animal -- you need to think outside the box on this one.

> Debbi in Michigan

> Successfully PREVENTING 99.99% of NCCPs for over 10 years with minimal

> daily doses of Paxil.

>

>

>

>

>

[Guest guest]

> > >

> > > one can drive and work on opioid analgesics. in fact these meds, when

> > > properly titrated to effect, improve life functions.

> > >

> >

> > Even if they had no effect on my driving I would not want to have to

> > defend myself in the state of AZ if police decided I had a problem being

> > on them while driving.

> >

> > notan

> >

> >

> >

> >

> >