This is discussed in that online book that
@btdt linked too
https://static1.squarespace.com/static/54059cd8e4b09fa759f4c83f/t/5416a202e4b00f3a4f0de025/1410769410474/Killing Us Softly 1.3.pdf
Mark Donohoe writes about nurses noticing a distinct breathing abnormality in the Multiple Chemical Sensetivities and CFS patients in a hospital ward and they seemed to have periods of over and underbreathing. In the book he sees both the MCS and CFS as cases of neurological damage, but I cannot remember the details.
I had a day where I was clear enough to listen to the book last week and then a couple of nights with little or no sleep. So no or little consolidation of memories.
I would suggest that if this is a feature of ME/CFS it may have a different cause and ideal treatment to sleep apnea in the general population. (The lesson I keep forgetting and having to relearn: research on "normals" may not tell us anything about pwme/cfs.)
found it for you
This is a quote from his online book... linked in the quote
"I recall attending a wonderful lecture by Jaques Benveniste in Nevada in 1988. During this inspiring talk, he told us in a delightfully tortured French accent, “there are some things which are totally obvious. You do not need a double blind, prospective crossover clinical trial to determine which is taller, a man or the Eiffel Tower. You use your eyes and common sense. I call it the ‘bloody obvious test’.”
What is obvious is not always true, so we went through the process of graphing out the differences. It was not only that there were longer gaps between the breaths measured for the multiple chemical sensitivities patients, there was a whole different phenomenon occurring during sleep (Fig 1).
Because the monitors discarded data on gaps between breaths of less that six seconds, we were left wondering about the extent of the compensatory hyperventilation (which we could determine was happening simply by looking at sleeping patients). The apnoeic periods, however, were undeniable. Reworking the figures, we learned that in an average night’s sleep of eight hours, nearly two hours was spent in apnoea, presumably with a compensatory hyperventilation after each apnoeic episode. No wonder people woke feeling unrefreshed in the mornings!
In addition, we realised that this was evidence of brain injury at a fairly profound level, interfering with the normal neurological mechanisms controlling respiration during sleep. We have yet to really follow this aspect of the illness up, but I believe that it may yet provide some critical insights into the illness.
I will be prepared to bet that the sleep clinics will grab this finding, and make it really pay, especially as the adult sleep apnoea falls out of fashion.
• Central evoked response testing Another test of neurological function, the Auditory Evoked Response Potential test, proved bimodal in a way similar to that of the immunology. This is a simple,cost effective test of neurological function, often used to determine the degree of neurotoxic damage from solvents in the workplace. The critical single figure was the P3 latency, a measure of the time taken for the “peak” of the recognition wave to occur.
The average for the population is a value of around 308 milliseconds, or just under a third of a second following the sound. The spread of the healthy population is a normal distribution, sometimes known as the “Bell Curve” (Fig 2). The average for our multiple chemical sensitivities sufferers was 328 milliseconds, but there were two distinct groups (Fig 3). One group showed a delay in the P3 wave, averaging over 340 milliseconds. The other, smaller group, showed a speeding of the P3 wave, averaging around 275 milliseconds. There were very few of our multiple chemical sensitivities patients where the peak would be expected, around the 308 millisecond mark
. There are a few points to make here about the Auditory Evoked Response Potential test, and all of them, I believe, lead to some insights into the disease process.
KUS • Dr Mark Donohoe (internet Creative Commons release 2008) 21
The first is that although there were two distinct groups, individuals did not move from one group to the other. Their AERP responses were, in fact, quite stable and were among the best descriptors/predictors of the degree of disability.
That is, the more abnormal the AERP was, the more neurologically disabled the person tended to be (there are some subtleties to this, for not everyone is neurologically damaged in multiple chemical sensitivities, but this will do for now).
As well, recovery of the AERP was the single best predictor of good outcomes in multiple chemical sensitivities. Those with stable, abnormal AERPs tended to recover poorly, while those with improving (even slowly improving) AERPs tended to do well.
There is a strange aspect to this recovery, however, and if it is not understood, it can lead to all sorts of problems in management. Severely abnormal AERPs are associated with severe neurological impairment, but not always with many complaints from the sufferer. It is more the family and friends who notice the problems. Why? My own guess is that at this level of damage, the brain becomes an unreliable auditor of its own function and disability"
I call this too dense to know your dense... I have had it and hope I am one of the ones that can recover more easily even after being dense... very dense. Others may call this brain fog... I wish these testing ideas were more wide spread. Still wonder what he does as treatment.
