ME/CFSウェブセミナー第４弾　MEと睡眠障害

broadcast on November 23th, 2012

Most ME-patients suffer from sleep disorders and many of them remember that at the onset of the disease they slept too much. At least twelve hours a day, where they used to sleep eight hours a day. It’s normal that these sleep disorders slowly evolve into a sleep disorder which is characterized by lack of deep sleep, where one often wakes up at night. And usually another problem is added to it. One has to get up to urinate in the night, so sleep really becomes fragmented.

This is caused by blood flow disorders of the brain, and also by the effect of cytokines. These are substances which are formed by our white blood cells. But we suspect the so-called gas neurotransmitters CO, H2S en NO to play a part in it too. Because they function like a neurotransmitter, and in normal circumstances we can’t do without. Yet in too large quantities they’re causing problems with the neurotransmitters. Moreover there’s also a disruption of the normal balance of neurons in the brain. All this can lie at the basis of sleep disorders. Unfortunately in this context not much research has been done.

Yet we know for example that one of those cytokines, interleukin-6, comes with too much sleep. Interleukin-6 is an inflammatory cytokine, which occurs at the onset of the disease, because the onset of this disease is usually accompanied by an infection, an infection that does not go away. In this way the presence of the interleukin-6 may account for the occurrence of hypersomnia.

Still another cytokine, interleukin-10, is associated with sleep disorders. Interleukin-10 probably originates from an inflammatory reaction, because a cytokine actually is an anti-inflammatory particle. In the USA the association of interleukin-10 with sleep disorders has been demonstrated. That’s not the whole story: low blood flow occurs in the brain as well. In general with some patients the blood pressure is extremely low during the night. It can drop to about 85 over 60, and we also know that certain parts of the brain receive less blood. There is an explanation for these sleep disorders, but that isn’t limited to one single phenomenon. Most probably they depend on several factors. We know that the studies done are partly too contradictory to serve as an explanation. Just because no thorough studies have been done. There are no thorough studies, in which patients have also been compared to normal people or twins have been studied. Those would be the best studies to demonstrate the possible mechanism of these sleep disorders.

As for the treatment of these sleep disorders, we have noticed that an EEG can be abnormal with these patients. And that an abnormal delta wave occurs. That’s something which may lead us towards a treatment. We also know that there is little stage 3 and 4 REM sleep. A delta wave is one of the waves seen on an EEG. Normally this is an individual wave, but with ME patients we observe an alfa-delta intrusion. So we notice an amalgamation of waves and also very little power in this delta wave. In English this wave is called delta power, and it differs from normal people.

This is one of the few scientific, objective evidences. This research has been done in the Brugmann hospital in Brussels. It is the first time that a clear relationship between sleep disorders and ME has been shown with patients. This is determined by highly specialized EEG research. And it more or less justifies the treatment we’ve been applying for more than twenty years. Formerly, it wasn’t actually justified, however the last twenty years we apply treatments based on anti-epileptic drugs. Short acting anti-epileptic medication is being used, which is active for six hours at the most, and they ensure a better quality of sleep. Anti-epileptic drugs are no longer appropriate for epilepsy, because in fact it’s difficult to coerce people to take a medicine 4 to 5 times every 24 hours. That’s difficult indeed. Yet already from the early nineties onward we’ve been noticing that a certain anti-epileptic drug is highly suitable to enhance the quality of sleep. There are still some other drugs in the repertory of sleep medication that might be helpful, but in general they don’t improve the quality of sleep. We notice minor stage 3 and 4 sleep, minor REM sleep, so there is little recuperation.

The impact of many hormones which has to decrease intensively during the night, doesn’t do so. For example we note that with these patients in the morning less cortisol and less growth hormone are being formed, where actually it should be at its peak. Normally such hormones have a peak very early in the morning, but this is not reached. Studies, 24-hours hormone-measurements studies have been done, which show an abnormal rhythm. That again has to do with poor quality of sleep. And these drugs, the names of which I won’t mention, can provide an artificial sleep. But they won’t very frequently correct the defect or lack of stage 3 and 4 sleep. One has been sleeping all right, but one is as tired in the morning as when one fell asleep. This is an important issue that I should mention: one can ensure the sleep- and daily rhythm will be more or less maintained.

Because ME patients feel better in the evening, they often go to sleep later and later. They eventually create a circadian rhythm where they end up having to take dinner at three a.m. Which is extremely problematic for the rest of their families and for leading a normal life.