ME/CFSウェブセミナー　第５弾　MEと痛み

broadcast on November 30th, 2012

 

The pains change during the disorder. Most patients who recall how they felt before the disease or in the run-up of the disease, remember they were free of pain in the beginning. The fatigue and the lack of recovery often occur before the start of the pain.

 

The various possible causes of pain are of a central nature. That is, cytokines, which are particles produced by our own white blood cells, can affect certain receptors and induce pain. This concerns mainly the so-called inflammatory cytokines, with one specific pointer to interleukin 1. They also occur in other disorders and animal models, and are accompanied by pain of central origin.

 

Bacterial neurotoxins also play a part. When the immune system has been seriously disrupted, all kinds of bacteria no longer can be eliminated. Or intestinal bacteria pop up, because the intestines are less capable of holding them back. Bacterial toxins can also cause central pain. Moreover there are a lot of other substances, such as nitrogen oxide, which play a role. We know for example that if we reduce the effects of nitrogen oxide, pain is also reduced. The same applies to a number of antibiotics that inhibit certain bacteria and also reduce pain.

 

There is also a problem with the opiate receptors. Endogenous opiates play a part in the brain, and with those receptors there seems to be a problem too. An English group is engaged in manipulating those opiate receptors, as to also reduce pain in patients.

 

Perhaps the most important cause of pain is metabolic pain, pain from the metabolism. It is caused by a poor delivery of oxygen to the organs and also by mitochondrial dysfunction. The mitochondria are responsible for the release of ATP to let all our organs function.

 

This is the most difficult pain to combat and the biggest problem, because there is no medicine for it. We can try to ensure the peripheral parts of the body getting more oxygen. We can do that artificially. But the release of several substances causing the large blood vessels to expand, automatically causes a contraction of the small blood vessels. Which is the cause of the cold feeling in the peripheral organs like fingers and feet, because the blood vessels themselves contract.

 

This is a result of an altered sympathetic nervous system that is more active as compensation, but still can’t prevent H2S, NO and other vasoactive substances to cause expansion of the large blood vessels. To such an extent that the small blood vessels are contracting. I think many organs suffer from a chronic oxygen shortage. And this will also cause a shortage of oxygen in the peripheral nerves – which contain blood vessels as well.

 

So we have a mixture of neuropathic and metabolic pain. In my experience metabolic pain is the biggest problem because you can’t cure it. Simply because there’s an imbalance in the blood circulation.

 

Then there are all kinds of other factors. With this condition the red blood cells aren’t functioning normally, and there is also a problem with oxygen supply. I could mention an entire list of different mechanisms which all come down to the same. We call them ischemic pains, due to a shortage of oxygen to form energy. The result, of course, is also the production of much lactic acid. We and others have found the concentration of lactic acid in the blood to be up to three times the normal value while resting. In normal blood 0.6 to 1 mmol lactic acid per litre is found. In a ME patient it is not uncommon to find 2 to 2.5 mmol per litre. And that’s a

broadcast on November 30th, 2012

The pains change during the disorder. Most patients who recall how they felt before the disease or in the run-up of the disease, remember they were free of pain in the beginning. The fatigue and the lack of recovery often occur before the start of the pain.

 

The various possible causes of pain are of a central nature. That is, cytokines, which are particles produced by our own white blood cells, can affect certain receptors and induce pain. This concerns mainly the so-called inflammatory cytokines, with one specific pointer to interleukin 1. They also occur in other disorders and animal models, and are accompanied by pain of central origin.

 

Bacterial neurotoxins also play a part. When the immune system has been seriously disrupted, all kinds of bacteria no longer can be eliminated. Or intestinal bacteria pop up, because the intestines are less capable of holding them back. Bacterial toxins can also cause central pain. Moreover there are a lot of other substances, such as nitrogen oxide, which play a role. We know for example that if we reduce the effects of nitrogen oxide, pain is also reduced. The same applies to a number of antibiotics that inhibit certain bacteria and also reduce pain.

 

There is also a problem with the opiate receptors. Endogenous opiates play a part in the brain, and with those receptors there seems to be a problem too. An English group is engaged in manipulating those opiate receptors, as to also reduce pain in patients.

 

Perhaps the most important cause of pain is metabolic pain, pain from the metabolism. It is caused by a poor delivery of oxygen to the organs and also by mitochondrial dysfunction. The mitochondria are responsible for the release of ATP to let all our organs function.

 

This is the most difficult pain to combat and the biggest problem, because there is no medicine for it. We can try to ensure the peripheral parts of the body getting more oxygen. We can do that artificially. But the release of several substances causing the large blood vessels to expand, automatically causes a contraction of the small blood vessels. Which is the cause of the cold feeling in the peripheral organs like fingers and feet, because the blood vessels themselves contract.

 

This is a result of an altered sympathetic nervous system that is more active as compensation, but still can’t prevent H2S, NO and other vasoactive substances to cause expansion of the large blood vessels. To such an extent that the small blood vessels are contracting. I think many organs suffer from a chronic oxygen shortage. And this will also cause a shortage of oxygen in the peripheral nerves – which contain blood vessels as well.

 

So we have a mixture of neuropathic and metabolic pain. In my experience metabolic pain is the biggest problem because you can’t cure it. Simply because there’s an imbalance in the blood circulation.

 

Then there are all kinds of other factors. With this condition the red blood cells aren’t functioning normally, and there is also a problem with oxygen supply. I could mention an entire list of different mechanisms which all come down to the same. We call them ischemic pains, due to a shortage of oxygen to form energy. The result, of course, is also the production of much lactic acid. We and others have found the concentration of lactic acid in the blood to be up to three times the normal value while resting. In normal blood 0.6 to 1 mmol lactic acid per litre is found. In a ME patient it is not uncommon to find 2 to 2.5 mmol per litre. And that’s a normal value in the blood of someone who’s running the marathon of Rotterdam at considerable speed. In ME patients this is a normal value when at rest. That lactic acid comes from tissues, which must convert all their glucose in lactic acid as a final product. With much less energy supply.

 

As we have shown in a publication on the other hand there are also intestinal bacteria which produce both left- as right-turning lactic acid. Often the disintegration of D-lactate (animal lactic acid) is more difficult with ME patients because they lack the enzymes to do so.

 

So there are a lot of factors which cause the aerobic metabolism to shift to a more anaerobic metabolism. And to me this is also an important element in the occurring pain. That’s why pain management must be performed with an overall vision on pain. Often one can’t cure this with one particular medicine, but with a more integrated approach one can usually cause a serious relief from the pains.