Effects of Epilepsy on REM Sleep

James Michael Howard jmhoward at sprynet.com
Mon Apr 3 10:55:10 EST 2000


Re: Arch Neurol. 2000;57:363-368

Effects of Seizures on REM Sleep

Re: Arch Neurol. 2000;57:363-368

Results: "Daytime seizures reduced REM from 18% 1% to 12% 2% (P = .003). Night
seizures reduced REM from 16% 1% to 6.8% 2% (P<.001). Night seizures also
significantly reduced stages 2 and 4 while increasing stage 1 sleep. Night
seizures, but not day seizures, significantly reduced sleep efficiency,
increased time to first REM period, and increased drowsiness as measured by the
maintenance of wakefulness test."

Bazil, et al., found that seizures reduce REM sleep.  I suggest
dehydroepiandrosterone (DHEA) produces REM during sleep.   Seizure activity
stimulates DHEA production, which is then reduced in availability for later REM.
This is explained in the following paragraphs.

I produced an explanation of sleep and an explanation of epilepsy that is
supported by the findings of Bazil, et al., (Arch Neurol. 2000;57:363-368).  At
the most basic, I think dehydroepiandrosterone (DHEA) and melatonin produce
consciousness when DHEA is high during the day and sleep when melatonin is high
when melatonin is high at night.  This is effected because of the brain
stimulating activity of DHEA and the reduction of DHEA produced by melatonin.
This occurs as a cycle: at morning, DHEA is produced in high amounts which
stimulate the brain.  Consciousness occurs.  One aspect of that stimulation is a
tonic stimulation of the pineal, via the superior cervical ganglia, which
inhibits melatonin production.  As DHEA production declines throughout the day
and reaches lower amounts in the evening, this tonic restriction of melatonin is
reduced and melatonin is released.  Meltaonin release reduces prolactin
production, which is a direct stimulator of DHEA, and DHEA production is reduced
to background levels.  Sleep occurs.  This first sleep period is the deepest
because melatonin is highest and DHEA lowest (stage 1).  As sleep progresses,
melatonin and DHEA cycle so that DHEA stimulation of the lower parts of the
brain does not decline to lethal levels.  Therefore, DHEA rebounds slightly in
response to stage 1 sleep; this cycling produces the following stages of sleep
until pineal melatonin is exhausted, prolactin increases to fully stimulate DHEA
production and consciousness occurs, again.  REM sleep is caused by the rebound
productions of DHEA that increase throughout the night as stage 2, etc.  REM
sleep is a rebound to keep the brainstem functioning.  (This is available at
http://www.naples.net/~nfn03605/dheaslee.htm, © copyright, 1985)

This is my explanation of epilepsy from my page,
http://www.naples.net/~nfn03605/dheamig.htm, (© copyright, 1997).  "With the
foregoing in mind, it should be easier to explain epilepsy with the MLT - DHEA
cycle. MLT is high in epileptic people. 'Melatonin production in untreated
patients with active epilepsy is increased and had a circadian pattern with a
phase difference as compared with that of normal subjects.' (Epilepsia 1995; 36:
75). In the paragraph, just above, I demonstrated how MLT can induce the
production of DHEA. During the day, my sleep mechanism suggests that the larger
production of DHEA is involved in inhibiting synthesis of MLT from the pineal
gland (where MLT is made). This means that once DHEA is 'used up' during the
day, there is not enough DHEA to keep the pineal from making MLT. When MLT
production occurs, the shut down of PRL occurs and DHEA is reduced to even lower
levels. This is how the sleep - wake cycle occurs.

Sleep deprivation keeps MLT from being released. This has been determined. 'It
was found that the melatonin levels were increased after sleep deprivation...'
(Sleep 1988; 11: 362). A much later study found that MLT was not increased by
sleep deprivation, but that 'Prolactin was higher on the post-sleep deprivation
and control nights but did not rise on the deprivation night.' (Journal of
Pineal Research 1996; 20: 7). Sleep deprivation increases the build up of the
thing that stimulates DHEA, i.e., prolactin. Since increased sleep is a
consequence of sleep deprivation, I suggest MLT increases. Since it is the PRL
that stimulates DHEA production, both of these studies say, essentially, the
same.

There is another way of seeing this. I have suggested that DHEA stimulates the
nerves that inhibit synthesis of MLT. I suggest that electroconvulsive shock
exerts its effects by stimulating DHEA. In the following quotation, I suggest
the reduced production of MLT is due to increased DHEA, inhibiting the pineal
gland. 'In ECS [chronic elctroconvulsive shock]-treated rats, both pineal and
serum melatonin levels after isoproterenol administration were significantly
lower than those in sham-treated animals and in rats receiving subconvulsive
shock.' (Psychiatry Research 1994: 53: 185).

I suggest that the opposite mechanism explains epilepsy. I suggest the increased
melatonin found in untreated epileptics builds up and is released so that nerves
are shut down. Individuals susceptible to epilepsy must have entire sections of
the brain shut down so much that they 'rebound' and call up a large response of
DHEA. It is this rebound response that is the large area of stimulated nerves
that cause the seizures. Once the brain has stimulated sufficient DHEA, then the
seizure stops."

James Michael Howard
Fayetteville, Arkansas, U.S.A.





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