I don't know about the phrase night time discomfort. But sleep
discomfort would be a powerful incentive to bad dreams. At least
anecdotally I have always been able to cure nightmares simply by
curing the discomfort.

However, meaning is another matter. If we're looking to decipher
dreams the way Freud did, that involves meaning. But looking for the
physiological cause at least for bad dreams would seem to be what
neurophysiology ought to be interested in.

Kinda depends on your orientation. I would expect dreams to follow
whatever orients and preoccupies you. I think the real key here is
that dreams (ast least bad dreams) are not random walks down memory
lane but directed along specific paths by the dreamer in verbal terms.

But that's exactly what I think does happen. There may or may not
be a definite script, but successions of bad dream situations are
definitely cued in my own anecdotal experience. To me that makes the
dreamer an active participant although not at the level of conscious
control. He's just trying to get at what's causing the discomfort.

Regards - Lester

It's interesting you mention heat, John H. At one time I considered it
the only cause for nightmares because it seemed to be so for me. (For
example, I could invariably cure a nightmare by throwing off a
blanket.) But I subsequently found others whose nightmares had other
sources, including one who considered himself possibly insane on the
basis of the nightmare.Yet they turned out to have concrete discomfort
sources. All anecdotal, of course.

Yeah, John H. I would agree there is no or at best a very limited
paradigm for understanding dream content. However, let me point out
that I am not especially interested in psychiatry. I am interested in
mental effects in terms of mechanical causation, but what little I
think I know about dreams is an anecdotal product of my own
experiences and a handful of conversations I've had with others.

Having said which I think there are very circumscribed generalities
that can be applied, but as I've already indicated primarily to bad
dreams and nightmares. Preoccupation seems to be a possible key as far
as subject content is concerned. I think I know how and why dreams
come about, but that doesn't really explain content or associations.

Regards - Lester

That's it, even when I tried writing down dreams to look for patterns the
emotional content was nearly absent. For the most part I'm just grateful my
brain can generate entertainment for me while asleep. Even last night I
nearly got killed twice through reckless driving but no sweat I just kept
driving like a maniac(in my younger days I nearly got killed several times
on the bike). In one situation it was physically impossible for me to avoid
the accident but somehow I managed to retrieve control yet thought nothing
of it. Last night was a typical example of my current dreams, lots of
exploration with an old friend as we explored some new territory and figured
out how to make it work to our advantage. In dreams I am typically on the
move, usually on some adventure or solving some practical problem(never
conceptual problems). No-one dies in my dreams, I'm not even sure really bad
things happen to anyone. However, I am a freak so I am not surprised that my
dreaming experience is different from others.

What might be interesting is to contrast dreams that occur during REM and
NREM sleep. NREM dreams are much harder to assess but there is more research
being conducted in this area. The Hobson et al text I am reading states that
considerable controversy still exists in regard to these two dreaming
states. (What about day dreams, where we still are monitoring the
environment? Not nearly as bizarre, if bizarre at all.)  The authors also
make this important point:
Hobson et al ...

The sleep laboratory itself constitutes a second major methodological
problem. Anyone who has ever slept in a sleep laboratory (as all of us
have!) knows that it is an inhospitable and unnatural setting which makes
sleep more difficult and less deep than is possible in more naturalistic
settings.
---
Additionally, how people report their dreams is contingent upon certain
features of their cognition. Eg. Vivid images usually require more words to
be described, so verbal reports of such accounts are much longer than
accounts of mundane images in dreams and may reflect a reporting bias. REM
dreams are more vivid because of greater cortical activation, reporting of
NREM sleep may be hindered by failure to remember the same. NREM dreaming is
active but we remain largely unaware of it. There are important differences
in these types of dreams but is this a matter of reporting or of actual
differences in these dream states:

Hobson et al ...
Therefore, we conclude that
while some NREM dreams approach REM dreams in length, vividness,
dreaminess and bizarreness (Cicogna et al., 1998; Foulkes & Schmidt 1983;
Herman et al. 1978; Nielsen, 1999) and while "dream-like" versus
"thought-like" mentation may predominate in some NREM reports (Foulkes
1962; Nielsen 1999; Rechtschaffen et al. 1963a; Zimmerman 1970), NREM
reports are far more likely than REM reports to be short, dull and
undreamlike (Nielsen 1999; Rechtschaffen et al. 1963).

---

Some studies have indicated the exercise of being asked to recall dreams
changes reports over time. Thus people interested in their dreams may often
generate differing reports than those who simply remember some dreams but
are not too interested in the exercise. The conscious attention to dreaming
changes the reporting, I suspect it also changes the dreaming. Now that's a
problematic  confounder.

Another problem is that memory is severely degraded in sleep and just prior
to sleep, thus making verbal recall problematic. What is remembered and
reported may at best be a very fragmentory and misleading account of dreams:
...
All of the above findings can be regarded as being caused by the failure of
recent episodic memory (as defined by Tulving 1994) in sleep. And as we
have noted, recent episodic memory is weak across wake-sleep and
sleep-wake transitions as well as within sleep itself (Pace-Schott et al.
1997a). We believe that a deficiency of memory in dreaming may go a long
way toward explaining such distinctive and robust dream phenomena as
orientational instability, loss of self-reflective awareness, and failure of
directed thought and attention.
---
With many caveats regarding the technologies employed, the authors offer
these neurophysiological observations:
...
Instead of the global,
regionally nonspecific picture of forebrain activation that has been
suggested by EEG studies, all of these new imaging studies indicate a
preferential activation of limbic and paralimbic regions of the forebrain in
REM compared to waking (Braun et al. 1997, 1998; Maquet et al. 1996;
Nofzinger et al. 1997). One implication of these discoveries is that dream
emotion may be a primary shaper of dream plots rather than playing a
DREAMING and the BRAIN: Toward a Cognitive Neuroscience of Conscious States
http://home.earthlink.net/~sleeplab/bbs/BBS.html (40 of 222) [1/6/2000
2:48:02 PM]
secondary role in dream plot instigation.
---

This validates Dan's remark that dreams have high emotional content. What am
I then,  cloned Spock?! Lester is probably correct in asserting I am
sleeping lightly at present, hence not much REM sleep, which may explain
lethary, poor cognition, and easy awakenings; especially since I have been
taking the SSRI for sometime.
Especially given:
...
9) There is near universal suppression of REM sleep in humans by acute
dosage of serotonin and norepinephrine reuptake-inhibiting
antidepressants (Gaillard et al. 1994; Nicholson et al. 1989; Vogel 1975;
Vogel et al. 1990).
---
The SSRI I am taking is also a nore reuptake inhibitor ... .
...

Continuing with Hobson et al ...

In REM compared individually to delta NREM and to
pre- and post-sleep waking (see Table 2), these authors showed relative
activation of the pons, midbrain, anterior hypothalamus, hippocampus,
caudate, and medial prefrontal, caudal orbital, anterior cingulate,
parahippocampal and inferior temporal cortices (Braun et al. 1997). Based
on their observations, the Braun group then offered the following
speculations which are relevant to the neurology of dreaming:
1) Ascending reticular activation during REM as compared to waking may
favor a more ventral cholinergic route leading from the brainstem to the
basal forebrain over a more dorsal route via the thalamus.
2) Activation of the cerebellar vermis in REM may reflect input to this
structure from the brainstem vestibular nuclei. We note that these nuclei
also constitute an important potential source of neuronal activation
causing the unique vestibular features of fictive movement in dreams
(Hobson et al. 1997; Leslie & Ogilvie 1996; Sauvageau et al. 1998).

3) Noting both a particularly strong REM sleep-related activation of the
basal ganglia and the known connectivity of these subcortical structures,
Braun et al. suggest that the basal ganglia may play an important role in an
ascending thalamocortical activation network. They suggest that this
network extends successively from the brainstem to the intralaminar
thalamic nuclei, then to the basal ganglia, and back to the ventral anterior
and ventromedial thalamic nuclei, and thence to the cortex.
...
The role of the basal ganglia in the initiation of
motor activity may, in turn, be related to the ubiquity of motion in dreams
(Hobson 1988b; Porte & Hobson 1996).

...
5) The prominent decrease in the executive portions of the frontal cortex
(dorsolateral and orbital prefrontal cortices) contrasts with the
REM-associated increase in activation of the limbic associated medial
prefrontal area. This medial area region has the most abundant limbic
connections in the prefrontal cortex, has been associated with arousal and
attention, and disruption of this area has been shown to cause
confabulatory syndromes formally similar to dreaming. (Note also the
dream-wake confusional syndrome associated with anterior limbic cortical
lesions reported by Solms 1997.)

Nevertheless, it seems likely that considerable portions of executive and
association cortex active in waking may be far less active in REM leading
Braun et al. (1997) to speculate that "...REM sleep may constitute a state
of
generalized brain activity with the specific exclusion of executive systems
which normally participate in the highest order analysis and integration of
neural information" (p. 1190).
...
Not only is REM sleep chemically biased but the preferential
cholinergic neuromodulation is associated with selective activation of the
subcortical and cortical limbic structures (which mediate emotion) and
with relative inactivation of the frontal cortex (which mediates directed
thought). These findings greatly enrich and inform the integrated picture
of REM sleep dreaming as emotion-driven cognition with deficient
memory, orientation, volition and analytic thinking.

...

In addition to prominent thalamic deactivation, all three recent
studies have found regional deactivation during NREM in the pontine
brain stem, orbitofrontal cortex and anterior cingulate cortex (Braun et al.
...
In a second syndrome, "visual anoneria," bilateral medial occipito-temporal
lesions produce full or partial loss of dream visual imagery (again with
normal waking vision).
---
This suggests an important difference in Dream visual imagery and ordinary
seeing?
...

A second
concern is the often reported lack of emotion-related physiological arousal
accompanying dream events (e.g., violence) which would easily elicit such
arousal in waking (Perlis & Nielsen 1993). Such emotional "numbing" in
dreams could result both from a sleep-related dissociation of peripheral
and central autonomic activity (as with peripheral arousal in Stage 4)
combined with REM-related blockade of central readout to the periphery
and peripheral sensory feedback to the CNS.
---
Above touches on what I mentioned before about reduced affect being the
result of agents external to the CNS.
...
The left dorsolateral prefrontal cortex has been shown to be selectively
activated during human reasoning tasks (Goel et al. 1998). Its deactivation
could account for the illogical ad-hoc explanations offered for bizarre
occurrences (Williams et al. 1992). Similarly, the prefrontal cortices have
been consistently shown to activate during episodic and working memory
tasks (Brewer et al. 1998; Courtney et al. 1997; Cohen et al. 1997; Fletcher
et
al. 1997; Tulving et al. 1996; Wagner et al. 1998); their deactivation in
REM
may contribute to the prominent mnemonic deficits in dreaming noted
above in Section II.C.4.
---