I have been having tests to see what pain meds work. Today I had a diagnostic epidural block and I was pain free for 4 hours. This hasnt happened in like 6 years.
I had a lapascopic cholysecectomy 6 years ago, and have had severe pain ever since, Worse when I eat, lie down and in the evening for which I take morphine.
They have tested morhine etc via IV in the last few weeks and other drugs and they havent shown to have helped in reducing pain via pain tests, where I do not know what they have used.
I had a nerve block 2 weeks ago and that didnt work. I have also had my splanchnic nerves cut previously. Up until now they have thought it has been Chronic Pancreatitis.
Last week the Pain Specialist said that he thought that my nerves had been imprinted calling it wind-up pain in his explanation my pain was nto treated properly and has ended up chronic and imprinted?
Today they injected 5 differnt things via the epidural inserted and the 5th one caused my arms, body from breast height to below my navel to be numb and the pain disappeared.
I dont quite know quite what this means and whether, it means tha they can put a block? epidural catheter or somethignm else in to stop the pain.
Does anyone know what this could mean?
I go for another test next week, but today I was so happy at last something that stopped my pain
Not sure where to from here, would welcome input, below is what they did on the test
it took him 75 minutes to get the epidural needles in with misses you wouldnt believe he calle din
my old pain med guy rob, got my old files i told him it took rob 90 minute to do it when he was
half way though and so they grabbed all files and sure enough I was right
well test 1 I reckon was saline I started at 5 no change
test 2 no change
test 3 worse went to a 6 point felt in right then 5 then 4 then 5
test 4 pain 5 pain to left and no change
test 6 well I was over the moon took 4 hours for the block to work off. on test 5 though was pain free/ totally numb breast to below navel and arms for 4 hours and no ****ing pain eg 0/10
I had no feeling eg totally numbed across arms and body ...and this means um................?
I have no idea what this means....with the block working or what it was in it? any ideas? and what
this means for treatment? eg maybe a spinal stimulator or implant pain pump? your thoughts?
Hi Deb, It sounds like you and friar jen have the same doc, where they just dig blindly with a needle untill they think they have it. That was not uncommon 15 years ago, I had a half dozen esi done blindly by anesthesiologist at the hospital. They do epidural blocks for surgery and child birth and don't have time and don't want to radiate a new born with flouoscopy so some docs do get very proficient at finding the spot by feel, But you also have accidents like going to far and nicking the dura which causes a spinal fluid leak and headache, out of 6 ESI's, I eneded up nicked twice requiring blod patches to reparir the holes in the Dura from going to deep . Spinal fluid has little to no clotting ability on it's own so as you lose fluid your brain rest downon your boney skull and the headache islike no other. Bloinded by lihgt and target vomitting. Laing flat helps rlieve the headahe but the quick fix is a blood patch. They inject blood right next to where they punctured the cord, as the blood trickles out of the two holes you have now it slowly clots the leak and tps off the lost fluid which puts an imediate end to a spinal headche.
Thre really is no advantage to doing a blind ESI unless your pregant and don't want o radiate a baby. Floro is the standard and why docs don't use it is part EGO, part ignorance, and when you have physical medecine docs/PM docs or any ther specialty that hasn't done hundreds of these as part of their daily practice in surgery or the maternity ward it's a huge risk and you end up taking 45 minutes to do a 10 minute procedure. Personally I would find somehwere else to have ESI's done under flouoscopy, you too friar Jen. It's not worth experincving even one spinal headache or catching spinal meningitis.
I explained the gatewy theory, phantom pain and pain imprinting to TK in her post the other day, It's still on page one and is long, here is a shortened version/excerpt from my post.
There is this theory called the gateway theory, It's pretty well accepted and explains things like phantom pain, RSD and many othr chronic pain conditions. YOu mentioned nerve imprinting in your other post and that's a component of the thory. The theory goes ruffly like this. You stub your tow, signals are sent to your brain through a number of gates "nerve branches" to the spine and eventually your brain. Normally the gate opens and closes as the stubbed toe will cause the gate to open and close as it swells up, throbs and becomes more painful, your brain gets the signal and you experience pain. Eventually that swelling stops, and the signals deminish and everything goes back to normal except when you catch that toe on the carpet and sheets and you get a few more burst of electic signals through the nervous sytem, wich open the gates again but they normally close like a door after the signal stops. This is normal/acute pain and how it's interpreted.
If you were to park the car on your foot and not pull it out, the messages to your brain would be continually sent keeping the gates open, basicly retraining the gates to stay open and be more effecient, the signal of pain is constant and millions of pain signals are sent to your brain, IF you leave your foot in there long enough and don''t cause total nerve death, there is a chance that once removed the gates will stay open and continue to send the exact pain signal. With the gates wide open and milions of signals having passed through those nerves, the signal can become engrained in nerve tissue too, making your brain think your foot is still under the tire when it's not. LIke phantom pain
Your brain continues to get the same signal and it's response is to dump endorphins continously and you start having dramatic changes in brain chemistry and the perceptin of pain. Please read Dr brookoffs artcile, It explains the difference between chronic pain and acute pain on the most basic levels involving chemical changes, changes in neurotransmitters,The part of the brain interpreting pain, creation of new bio chemicals that actualy cause more pain due to the neuro inlamatory response from these new chemicals or excess chemicals now being constantly produced.
Read this now. Copy, and cut and paste the addy into your search engine or browser.
http://www.hosppract.com/issues/2000/07/brook.htm
reply continued on next post
The same can happen if post op pain is not treated and the patient sufffers terribly, or in war often care came very late and eventual ampuation removed the injured leg but didn't stop the nuero chemical process of sendng that signal that your in pain. It's not just chemical changes that occur, but an entirley different part of your bran starts recieving and interpreting those pain signals
So the gates stay open even after the problem is corected, They may never close or you may develop RSD where your entre nervous system starts going nuts and you have pain where you never even had an injury an your brain is prodcung so many neuro toxic agents you develop a shingle like condition that an be seen , can't be touched without extreme pain and although RSD or CRPS is still controversial, you can't argue with what you see in front of you as far as discolerinng, inflamation and the shingle like leasions caused by neurotransmitters that actually cause inflamation of all the nerves in an affected area.
This isn't something unique that just happened to your deb r Jen, Acute pain that isn't treatd orlast for a rpolonged cange eventually becomes chronic and all the changes occue that I mentioned and the article mentioned, The article is a must read and has diagrams of noormal and chronic pain pathways and exlains in detail what the difference is, how it occurs and why it occurs. Ecerone with itractable pain with a problem that can't be fixd will rech this point of completely diffrntesponses to pain that acute pain would cause. With those gates open, you also able to interpret and process mor than one pain genertor. Acue pain s overrridden by te most painfl injury other injures will go un noticed until the owst problem is adressed. Bt CP patints can feel and interpret mor than onepain generator and acutepain focuses on that one big Ouchie that's sending the loudest sugnal to yorur barin.
But everyne with CP goes through these changes, so ymany of us have pain engrained into nerve tissue, have all the negativ consqunces of chronc painhapening and have the ability to percieve mor than one source of pain. The artcile is realy mportant to read, reread and understand for all this to make sense.
Evn though pain has been engraind and our gates stay open and we create thenurtransnittes and transformation that occurs with CP, It doesn't mean it can't be treatd. Thre are sevral methods, starting with anti depressants and anti seizure drugs to reduce substance P and to distrt the pain signal.
The test you had done sound lietrials ofor an implanted intrathecal pump to deliver meds drctly to th sit of pain, but lack of response really shows it's mor f a nerve problem thatay be better suitd for nrve stimiulation. Doa seacrg on nerve stim, there are 3 vbasic types, the spinal cord stim where a specific nerve root is wired to distort the pain signal, It's a much more adbvanced method of TENS. There is also Vega nrve stim which would handle aproblem like pancriatitis and other maladies caused by organ problams that use the vega neere to transmit the pain signal. The Veag nerve runs down through the toracic cavity and why heart attacks and reflux can be hard to distnguish alone via sympyoms, they both send the signal op the vag nerve and our grain doe's knowq if it's your hard, stmoach or pancreas. Th implant a device like a pacemaker and rap a lead around the Vga nerve and ou have the ability to contol the strnght, duration and amplitude of the elctrical signa l your using to drown out apain carrid by the veaga nerve. The thrid stim unit is s the same acemaker but leads are implanted in your brain and while your awake tthey test diffeent sites to drown out the pain and stop the formayion of the chemicals assciated with CP.
Brain surgery to implant this device has it's own set of risks, the brain has no feeling itself do being awake is neccesary to report changes and crect lead placement. That's abut the most radical method of dealing with intractable pain that won't repond to any other method of pain relief.
But imprinting can be fooled and the gates can be closed with drugs lie Ketamine where they place you in a comma for a few days and this is supsed to reset those gates and your threshold and tolerance to pain.
Th fact you didn't repond well to epidural opiates doesn't suggest an intrathecal morphine pump is the way to go. Yu really ned t reach 50% relief with the pump trials or you may be wasting your time . There is another poster waiting to have her pump removed but she never had a succesful trial. At best one test showed sligt imporvment, that's a long way from 50% in ost eples book and the pump never shuld have beenimplanted without asuccesful trial. That's what they did, a pump trial testing different opiates in the epi space.
As faras the total block, obviously you can't funtion with a block from the nipple line down. could do a TKR after that bolck and you wouldn't ave flinched because evrything was numbd with bupivicaine, marcaine o lidocaine, same stuff they use to numb teeth before an extraction.
I would imagine the next tests would be for tha spinal cord stim, try to isolate what nevr root the pain is traveling through and disrupt th signal wit electral impulses. Nerve pain simply dosn't respond to opiates as well as say somatic ain or incisional pain, Neoro pain is the hardest to treat.
I didn't quite folow all the numbers, was the scond numbe te pain score after the injection, a 5 should represent a 5% reduction in pain if your constantly floating betwen *09 I rarely use 10 because most of the time the pain I experince isn't the worst pain I have ever expereinced.
But ain imprintin is something many CP patients have to dal with along with the changes froma cute to chronic the article explans, please read it and likly the understanding light bulb will go off. something doesn't make sense or you don't undertsand, just ask.
Hang in ther, the doc hasn't condemened you to a life of pain, ZZPain imprintin can be dealt with and overcome, the neurochemical changes can be controlled with other meds like baclofin and clonodine, but the testing of meds you went thogh via the epidural space was simply a trial they do for all perspective pump patients. But not getting significant relief means they either need to use much higher doses or you may not be a candidate for the pump but still a candidate for one of the nerve stim techniqes.
Do stay away from unguided needles into your spine, there is just too much risk and if the dc doesn't have a fluro he can send you somewhere that does, It's greed and arrogance for that 1100 hundred dollar ESI that has him taking a chance on your spine.
Simply ask him what the next step is, stronger epi meds/doses or an SCS stim trial of the nerve roots. But they need to be able to isolate what nerve root is involved for an SCS to be succesful. Again the goal is 50% reduction in pain, Pumps and stims aren't cure alls, just one of many tools.
Goodluck and let me know what you thought of the article.
Take care, Dave
PS also checkout TKs thread regarding surgery not an option. There must have been a PM conference somwhere that suddenly all these docs are using the corect terms and explainng the gateway theory and nerve memeory and engraining all in one week.
Dave I Have been suffering pain requiring morphine an dsvredol for 6 years, I have had visits in hospital where it has been weeks at a time on fentanyl and the only way I got out was when they put in epidurals with fentanyl andf ketamine, they allowed me to get on top of the pain
I have had Multiple surgeries starting with a laproscopic cholyscectomy, they found small gall stones but then my pain got worse, I couldn’t eat lie down pain went up . they then did 2 ERCP’s with spincteromtoies my pain after that went to a 10 and I was there for 4 weeks in severe pain on fentanyl. I only got out after they also did a laparotomy with a feeding tube
I have had the epidural more then once and feeding tubes. Due to the pain my speclaislit used w working diagnosis of Chornic Pancreatitis caused by unknown causes , but I have never had a definitive test to prove that an dits been 6 years.
I have suffered pain ever since
The other day they put in a epidural trial , they had perveiously done trials of drugs via IV which had no response on me
I Have explained what my tests were more below.
Dave they injected drugs, , saline or whatever through the epidural to test effects below is what I felt re pain score a
well test 1 I reckon was saline I started at pain score of 5 an dno change in pain score happenedno change
test 2 no change stayed at pain score of 4
test 3 Pin was worse on injection went up to a score of 6 points, with sharp pain felt in right nabdomen then down to 5 then down to 4 then up to 5
test 4 pain 5 pain to left and no change
test 6 well I was over the moon took 4 hours for the block to work off. on test 5 though was pain free/ totally numb breast to below navel and arms for 4 hours and no ****ing pain eg 0/10
Dave
you said that pain imprinting can be overcome with things like Baclofen. What is that ?
I also take clonidine, nortrtytiline, for pain as well as voltaren and panadeine.
I didn’t quite understand what you meant by the below, and it may apply to the tests above on some of the inectiosn above they only slightly decresed my pain, and some increased. What would they be to increase?
, ZZPain imprintin can be dealt with and overcome, the neurochemical changes can be controlled with other meds like baclofin and clonodine,
I also need to point out that due to the pain I have suffered in the first year they severed my splanchnic nerves via a Thorascopic splancnicnetomy.
My pain didn’t decrease, I am not sure if it stopped increasing it as I cant tell, 2 weeks ago this same pain doc did a block and he said that I do nto have pain from my pancreas or that region as his test showed that. My question to him has been and still is. Why is my pain worse when I eat, lie down and worse at night? Why does it sometimes get to the point where I have to be admitted to hospital for it? They also 3 years ago admitted me due to severed constipation, they gave me 2 drinks of pic prep to cleam me out, what happened was that I then eneded up in such severe pain that I was on a PCA fentany; and letamien pain pump for 6 weeks. They inserted a feeding tube and I was there in terrible pain until they put in the epidural which after 1 week I was able to get off all the fentanyl and bring my pain back down. I still don’t know what eating caused me pain and why the epidurals work
I thank you soo much for your help, I am in New Zealand and have been this way for 6 years being passed from specialist to specialist.
My other main question is . is this nerve damage likely to be due to the operations or treatment injury from the initial surgeries? And is it likely I could prove it
You are awesome, hugs
Debs
PS what is an ESI? I am doing a test this fridya again not sure if its a block he sai dit was hard to do on my back as its so bony???? is that common and that he may use a fluoroscope
Hey Debs, An ESI is an epidurl steroid injection, Used to reduce inflamaton around the nerve roots. A total block like they did at the end relieved all your pain, they pump numbing agents into the epidural space and it simply numbs everything down, just like they do for child birth and surgery on your lower extemeties. They relplaced my moms knee using an epidural block and mild sedation, the numbing agents totally numb the nerves and nothing is felt or transmitted. If they can block the pain of sawing your femor off to replace with an articical knee it will pretty much block any pain from the site of the epidural down.
It's like when they do a block in the back of your jaw and it causes you to go numb from where they blocked you to the tip of your nose and tip of your chin, They could yank every tooth and you wouldn't feel pain. So relief through a total nerve block isn't a surprise if they can replace knees, reconstruct ankles after doing an epidural block in the lumbar area. It also makes child birth mcuch less traumatic when you can't feel the severe pain of teraing and bones spreading. My wife actually broke ger ankle during child birth, we all heard the snap as she was pulling on one and I was on the other side, but due to the block she felt nothing at the time.
Unfortunatly you can't live with a continous block. You wouldn't be able to walk and you wouldn't haven't control of your bowels or bladder. Blocking nerves isn't anything new, they ave been doing nerve blocks for procedures for as long as they have used novacaine or marcaine in dentistry and have done epidurals on women during child birth. With info gathered from the last block thay can at least determine the pain is real, you didn't respond to blind/placebo injections but did respond when they used the actual numbing agents. Your response to pain meds is hard to gage becuase it looks like you under rate your pain. We use a 1-10 scale in the US, and if you went to the ER and said you pain was a 5 , you might get some Motrin and sent on your way, but when a 5 requirs a Ketamine coma and a fentanyl drip, that number doesn't jive with the amount of pain your reporting. Perhaps you guys use a
1-5 scale down under and 5 is the worst you can report, that would exlpain the desperation of living with 5 pain.
I know we don't want to sem like we are exagerating pain and you don't want to claim 10 pain if it's not the worst pain you have experienced, but reportng 5 pain woudn't likely get you the treatment you have been getting or someone even considering a pump implant with what the US idea of 5 pain is. 5 pain doesn't send you to the ER and is managable with OTC meds or milder short acting opiates,
Flouro is the absolute standard of care for spinal injections, particluarly when It's not an anesthesiologist dong the Injection. The thoracic area is boney on everyone, that's where ribs attach, but with flouro that small gap needed to insert a needle can be found without going through what seems like a bone biopsy from catching bone everytime they insert the neeedle. That's not common and shouldn't happen, using flouroscopy would prevent it. To schedule another without flouro is even more rediclous after your last experience.But if that's the standard in in Nw zealand, you may have to do some shopping or addiment insisting that your not going to let him dig around your spine untill he feels like it's in the right spot.
I'm guessing you didn't read or couldn't find the article. Use your IE browser and cut and paste the addy in, It's almost 20K characters with illustrations. I can cut and paste pieces of the article but the illustartions certainly help understand the gateway theory and the huge difference between the way your body responds to chonic pain Vs acute pain and that's what your trying to understand.
Excerpt from article you must read.
http://www.hosppract.com/issues/2000/07/brook.htm Chronic Pain Pathways
Chronic pain is not just a prolonged version of acute pain. As pain signals are repeatedly generated, neural pathways undergo physiochemical changes that make them hypersensitive to the pain signals and resistant to antinociceptive input. In a very real sense, the signals can become embedded in the spinal cord, like a painful memory. The analogy to memory is especially fitting since the generation of hypersensitivity in the spinal cord and memory in the brain may share common chemical pathways.
Activation of NMDA Receptors. The main neurotransmitter used by nociceptors synapsing with the dorsal horn of the spinal cord is glutamate, a versatile molecule that can bind to several different classes of receptors. Those most involved in the sensation of acute pain, AMPA (alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic-acid) receptors, are always exposed on afferent nerve terminals. In contrast, those most involved in the sensation of chronic pain, NMDA (N-methyl-D-aspartate) receptors, are not functional unless there has been a persistent or large-scale release of glutamate. Repeated activation of AMPA receptors dislodges magnesium ions that act like stoppers in transmembrane sodium and calcium channels of the NMDA receptor complex. The conformational change in the neuronal membrane that makes these receptors susceptible to stimulation is the first step in central hypersensitization (Figure 3) and marks the transition from acute to chronic pain.
Activation of NMDA receptors can also cause neural cells to sprout new connective endings. This neural remodeling can add new dimensions to old sensations. The emotional component of pain may be increased, for example, if the new connections channel more of the pain signal to the reticular activating system of the brain. When that occurs, the signal's pathway into the cerebral cortex is more splayed and the pain signal more diffuse and difficult to localize.
Neural remodeling may also precipitate the destruction and loss of cells. Some of the brain damage that occurs during strokes is believed to be caused by the torrents of glutamate released from injured presynaptic cells, which overstimulate NMDA receptors on adjacent postsynaptic cells and effectively burn them out. The same phenomenon may occur in parts of the spinal cord receiving persistent pain signals. There is also evidence that NMDA receptor activation can stimulate normal apoptotic mechanisms. Although some of the details have yet to be elucidated, the data obtained thus far suggest that chronic pain is a destructive process that requires timely treatment in order to limit the damage that it causes.
Activation of NK-I Receptors. A further effect of NMDA-receptor activation is that it causes nociceptors to release the peptide neurotransmitter substance P, which binds to neurokinin-1 (NK-1) receptors in the spinal cord. Activation of these particular receptors amplifies the pain signal and also stimulates nerve growth and regeneration. It is thus interesting to note that the one chemical abnormality repeatedly documented in controlled studies of patients with fibromyalgia syndrome is an elevated level of substance P in the spinal fluid.
In animal models of chronic pain, substance P binding to NK-1 receptors induces production of the c-fos oncogene protein, which in many respects can be regarded as a biochemical footprint of chronic pain. The presence of c-fos protein in spinal cord cells is a marker for central hypersensitization. At first, it is detectable in afferent spinal cord cells actively receiving pain signals. With persistence of the pain, the protein spreads to progressively higher levels of the spinal cord until it eventually reaches the thalamus, at which point the pain is virtually untreatable.
This model explains why patients who have had uncontrolled pain for months or years often find that their pain has spread beyond the originally affected organ or dermatome. In these cases, physicians who are not familiar with the concept of neural plasticity are apt to conclude that the pain is psychogenic, because it does not conform to their preconceived map of the nervous system.