If our brains were simple, we would be too simple to understand them.



Hence we can predict the neural correlates of these conscious states of dreaming, assuming that
there is a connection with the NCC of similar awake states. If this prediction turns out to be true, we
can reasonably assume that these underlying brain states somehow determine the features of
REM sleep dreaming. At least we have stronger reasons to believe that there are lawful
connections between specific conscious states and neural states.

Table 1: Neuropsychology of dreaming. = increase of metabolism, Ψ = decrease.

phenomenal features of REM sleep dreaming

neurophysiological correlates____________

vivid visual hallucinosis

spatial imagery construction
motoric hallucinosis

bizarreness (incongruity, discontinuity, uncertainty)
delusion (being duped into believing to be awake)
deficits of self-reflective awareness, directed
thought, insight in illogical and impossible
experience, and memory ("dream amnesia")
strong emotions (especially anxiety, fear, anger,
elation)

extrastriate cortices
primary visual cortex Ψ
right parietal operculum
basal ganglia
frontal cortex (dorsal, orbital)
Ψ
aminergic demodulation (noradrenergic and
serotonergic neurotransmitter
Ψ)

(para)limbic system

amygdala
anterior cingulate
temporal pole ____________________________

The latest PET studies provide a consistent and coherent picture indeed. Table 1 gives some
examples. It lists the well-known phenomenal features of dreaming and the recently discovered
neurophysiological correlates. Their anatomical locations were already known as necessary for the
summarized mental features or their undisturbed functioning of awake persons. These studies led
to the hypothesis that dreaming is a result of (1) a functionally isolated loop between the extrastriate
cortices and the (para)limbic system including the amygdala, largely disconnected from sensory
input and motor output due to inhibition of the striatum and frontal cortex respectively, (2) a chaotic
autoactivation process within the extrastriate cortices and the (para)limbic system, triggered by an
increased input from the brainstem and the basal forebrain, and (3) the absence of top-down
control because of an inhibited frontal cortex. The effects of brain lesions on dreaming strengthen
this proposal. Lesions which are correlated with deficits or accentuations of dream experience
remarkably complement the studies of brain metabolism. For example, PET studies revealed an
increase of activation of pontine tegmentum, limbic structures, extrastriate cortex and right parietal
operculum in REM sleep while lesions of these areas decrease dreaming or have no effects; and a
decrease of metabolism in striate cortex and dorsolateral prefrontal cortex measured by PET
correspond to no changes of dreaming after lesions of these areas.

Of course, PET studies provide only an indirect, approximate insight into NCC with spatial and
temporal resolutions of a few millimetres and seconds, averaged over many experiments or
individuals. But they give us important information about the functional architecture of our brains and
demonstrate that different aspects of our mental life depend on different areas of the brain. And
there are other, more sensitive methods like EEG, MEG and psychophysical experiments that
unveil temporal constraints of conscious experience, which sometimes contradict what we find by
introspection, or are at least not accessible in this way. This leads me to my next point.

I.2. "The Times, They Are A Changing" - NCC On Stage

NCC can account for phenomenologically opaque facts - the temporal structure of
consciousness, for instance (see Dennett and Kinsbourne, 1992, Metzinger, 1995, and Vaas,
1997). The phenomenal temporal continuity and homogenity is in a sense an illusion, because there
are discrete "temporal units of consciousness", e.g., a succession of temporal windows of
conscious perception and action, each about two to three seconds long, and a succession of



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