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The New Neuropsychology of Sleep: Commentary by

Allen Braun (Bethesda, MD)
a

Allen Braun M.D.

a

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e-mail:
Published online: 09 Jan 2014.

To cite this article: Allen Braun M.D. (1999) The New Neuropsychology of Sleep: Commentary by Allen Braun (Bethesda,
MD), Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences, 1:2, 196-201, DOI:
10.1080/15294145.1999.10773260
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Allen Braun

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The New Neuropsychology of Sleep

Commentary by Allen Braun (Bethesda, MD)

Allan Hobson has presented what is essentially a modification of his activation-synthesis model; Mark
Solms reviews this and presents a novel and interesting model of his own. In some sense this debate might
have been far more lively five years ago, for there is
now much room for common ground between these
two. Nevertheless there is an air of contentiousness
evident which I will argue may be simply due to the
specter of Freud, who is never far from the center of
this dialogue.

Meaning, Appetite, and Dopamine

There are some problems with Hobson's new model:
activation-input-mode (AIM) appears to treat the conditions it uses to define states of consciousness-levels
of activity, sensitivity to internal vs. external outputs,
and neuromodulation-as if they were orthogonal. In
fact they undoubtedly interact in complex ways that
make this linear model a bit too simple. Nevertheless,
the model, at least as it is used to illustrate REM in
Figures 3 and 4, is much more flexible than activationsynthesis and, with respect to "activation" in any
case, is no longer entirely brainstem based, but acknowledges a more complex and active role for the
forebrain. At the same time, in much of what he writes,
Solms seeks to show that dreams can be uncoupled
from REM in order to liberate the dream process from
brainstem mechanisms. I suspect that this essentially
represents a response to the initial activation-synthesis hypothesis-in which the dream was a secondary
attempt by the forebrain to "synthesize," i.e., create
order out of its regular but chaotic activation by the
pontine reticular formation. Dreams were in essence
meaningless and psychologically empty.
In the present version-modified in light of
Solms's own clinico-anatomical data and PET studies
conducted by us, as well as by Maquet's group in
Belgium (Maquet et aI., 1996), Nofzinger's in Pittsburgh (Nofzinger et aI., 1997), and Madsen and coworkers in Denmark (Madsen, 1993)-Hobson no
Allen Braun, M.D., is Acting Director, Language Section, Voice
Speech and Language Branch, National Institute on Deafness and Other
Communication Disorders, National Institute of Health, Bethesda, MD.

longer dismisses dream content as vacuous. The' 'synthetic" process is informed by what is known about
the functional neural architecture of REM-particularly patterns of neocortical and paralimbic activity-and the possibility that there is meaning in dream
content (not disguised, rather on the surface) is recognized. Hobson now suggests that salient memories and
emotions serve as the primary shaper of dream plots
rather than playing a secondary role. That is, he seems
to acknowledge a rather more complicated participation of forebrain mechanisms in dream generation-not simply a secondary senseless response to
chaotic brainstem events. If orthodox Freudian theory
were not the bone of contention here, both authors
might acknowledge a conceptual overlap between
Hobson's "emotional salience" and Solms's "motivated mental state." While uncoupling the dream process from the brainstem mechanisms may no longer
be necessary to salvage the idea that dreams have
meaning, Solms continues to vigorously argue this
point. He makes his strongest case by simply pointing
out that dreams-indistinguishable from REM reports--can occur during NREM sleep. A bit more detail would be useful, however. The fact that Foulkes
and Vogel (1965) found sleep-onset hallucinosis to be
statistically indistinguishable from REM reports may
say more about their methods than the qualitative features of NREM dreams.
The curious thing is that, after describing the phenomenology of complex partial seizures and making
a case that forebrain structures must play a critical
role in the dream system, Solms ends up by suggesting
that it is the dopaminergic afferents to these regions
that represent Freud's "capitalist"-thereby placing
the dream instigator back in the brainstem, where the
origins of the mesolimbic and mesocortical projections are found in the ventral tegmental area (VTA)
and medial portions of the substantia nigra pars compacta. In any case, Solms argues that the occurrence
of vivid dream mentation during NREM sleep means
that it has to be possible to effect the direct engagement of the dopaminergic "capitalist" in the brainstem and the cognitive "entrepreneur" in the
forebrain, independent of the physiological events
manifest during REM. There is indeed a mechanism
by which this might occur: direct projections from the

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Commentary on The New Neuropsychology of Sleep

medial prefrontal cortex to the VTA exist (Kalivas and
Nakamura, 1999). These are glutamatergic, apparently
excitatory, and could account for activation of the
VTA in NREM sleep. Whether such activation would
result in the widespread paralimbic and extrastriate
activation which appears to characterize REM is an
open question. Solms goes on to suggest that it may
be elevated levels of arousal per se (manifest at sleep
onset and prior to waking as well as during REM) that
may couple ongoing mentation to firing of the VTA,
resulting in activation of the ventromedial prefrontal
cortex. I would be interested in hearing Hobson's response: indeed, would a slight modification of AIM
accommodate this if dopamine were simply added to
the monoaminergic soup? But perhaps too much is
ultimately made of the fact that dreams can occur during NREM sleep. 'As noted, coupling of dreaming with
REM no longer carries the stigma implicit in the initial
version of activation-synthesis. And, more importantly, the fact that the overwhelming majority of dreams
do occur during REM cannot be ignored. And it turns
out that the VTA also receives direct projections from
the lateral dorsal tegmental nucleus (Oakman, Faris,
Kerr, Cozzari, and Hartman, 1995), one of the cholinergic nuclei that project to the pontine reticular formation and initiate REM. Thus, direct coupling subserved
by this pathway may provide a seamless integration
of REM physiology and dopamine (DA) mediated
dreaming.
That dopamine may play a critical role in sleep
and dreaming is an intriguing notion (one of the shortcomings of the reciprocal interaction hypothesis is that
it is limited to three neuromodulators, ignoring many
other endogenous compounds that regulate sleep).
Such a role seems reasonable, not only in terms of
effects of mesolimbic DA on appetitive drive but the
role played by the transmitter in general mechanisms
of attention and arousal (Robbins, Granon, Muir, Durnatou, Harrison, and Everett, 1988) and the well-established effects of DA agonists and antagonists on
sleep architecture (Thaker, Wagman, Kirkpatrick, and
Tamminga, 1989; Monti, Fernandez, and Jantos,
1990). In addition, the impact of REM or REM deprivation on DA receptor sensitivity (Brock, Hamdi,
Ross, Payne, and Prasad, 1995), the effects of MPTP
on REM (Pungor, Hajnal, Kekesi, and Juhasz, 1993),
the prevention of REM rebound by MFB self-stimulation in rats (Steiner and Ellman, 1972) all make a role
for DA quite plausible.
Hobson makes much of the fact that the
pons-and therefore perhaps the cholinergic and cholinoceptive pontine nuclei-were activated during

REM in the PET studies cited. The midbrain-source

of dopaminergic cortical and limbic afferents-was
significantly activated as well. In addition, the lateral
habenula, a nucleus within the forebrain, may also play
a role in REM by integrating information from the
limbic system, basal ganglia, and monoaminergic nuclei and projecting back to these nuclei within the
brainstem. It may serve as a direct link, within the
forebrain, between the dopamine and serotonin systems; interestingly, it receives direct projections from
the VTA and represents the major source of input to
the dorsal raphe nucleus. Activity within the LH is
significantly coupled to REM and REM deprivation
(Goldstein, 1983; Peder, Lindroos, Laakso, PorkkaHeiskanen, and Johansson, 1986). Because it represents a testable hypothesis, I don't believe the proposed role for dopamine would be rejected out of hand
by Hobson.
One might evaluate the activity of single units in
the VTA or dialysis methods could be used to measure
the release of DA in the cortex, during REM, or at
other times, i.e., at sleep onset. PET-imaging methods
in humans (e.g., C-l1 raclopride/amphetamine) could
be used to evaluate pre- and postsynaptic DA function
throughout the sleep-wake cycle. Clinical correlations
should be possible: levodopa toxicity in Parkinson's
disease is associated with formed visual hallucinosis
that is phenomenologically similar to hallucinations
occurring at sleep onset. Controlled PET or tMRI
studies of these patients might be revealing.

Reciprocal Interaction and the Forebrain

Neurochemical PET methods also exist for evaluation
of other systems (e.g., 5HT and ACH) and could be
used to test Hobson's hypothesis that forebrain events
in REM mirror changes in monoaminergic activity. Is
the dissociated pattern of cortical activity noted in the
PET blood flow studies due to monoaminergic deactivation and cholinergic activation? If so, patterns of
release of these neurotransmitters should match the
characteristically dissociated CBF patterns. Reciprocal inhibition is a mechanism for which there is abundant evidence in the brainstem, but it may be naive to
think we can explain the patterns cortical activity on
this basis; the functional cortical architecture in
dreaming may not represent the one-to-one mapping
of brainstem neurochemistry onto the forebrain. However, it should be noted that distribution of ChAT and
AchE in two macaques (Mesulam, Volker, Marquis,
Mufson, and Green, 1986) showed greatest concentra-

Downloaded by [Gazi University] at 22:21 17 August 2014

198
tion of these enzymes in core limbic areas, paralimbic
zones, and cingulate cortex, and less in primary sensorimotor regions and neocortical association areas. This
is quite similar to the distribution of regional cerebral
blood flow during REM. Interestingly, there were very
low levels of the enzymes in the dorsolateral prefrontal
cortex (DLPFC), frontal pole, inferior parietal lobule,
and primary visual cortex-all regions which were not
activated during REM. On the other hand, Mesulam
et al. also showed low levels of the enzymes in extrastriate regions-and these were, on the other hand,
regions in which activity was significantly elevated
during REM. I think things will prove to be more complicated than this: forebrain mechanisms-the dissociated pattern of activity described in all PET
studies-will probably not be explained solely by
changes in cholinergic tone. Indeed, it isn't at all clear
what role ACH plays in the forebrain during REM.
The pedunculopontine and lateral dorsal tegmental nuclei-which represent the major cholinergic input to
the mPRF-are active at REM onset. But there is no
evidence as far as I know, that ascending projections
mediating transfer of information to the diencephalon
and forebrain are themselves cholinergic (cells of the
mPRF clearly are not). Direct projections from brainstem cholinergic nuclei to the neocortex are rare; the
principal targets of these nuclei are thalamus, basal
forebrain, subcortical limbic structures, and other portions of the brainstem. But even if effects upon the
forebrain were mediated by direct ascending projections of the PPN/LDT nuclei themselves, it still isn't
clear that the most critical synapses are cholinergic.
Indeed, 50 percent of cells in PPN/LDT are noncholinergic (70% of these are glutamatergic). This is also
the case for the cholinergic nuclei that do project to
cortical structures; e.g., the magnocellular basal nucleus, nucleus of the diagonal band and septal nuclei.
Noncholinergic cells projecting from these nuclei innervate as widespread an array of targets within the
forebrain as do their cholinergic counterparts. And
while single unit studies show that neurons in these
nuclei are active during REM, it is not possible to
tell whether the active cells are cholinergic, or even
whether they project to the cortex (since antidromic
stimulation is difficult).
Indeed the only direct evidence for cholinergic
release in the cortex during REM comes from very
early studies using "cortical cups" in rats and cats,
and it was never shown that the ACH measured was
not due to leakage from intrinsic cholinergic cells
within the cortex found in these species. With respect
to cholinergic transmission during REM, Solms poses

Allen Braun
an interesting question: Why do anticholinergics exert
"twilight" or dreamlike effects? Solms speculates
that the ascending pontine cholinergic projections actively inhibit the basal forebrain during REM, thus
decreasing cortical cholinergic tone. There is some
indirect evidence for this: LDT projections to the basal
forebrain synapse on noncholinergic neurons which
may be inhibitory internuncials (D. B. Rye, personal
communication). So I suspect that while AIM and reciprocal inhibition are useful as heuristic models they
are probably not in themselves sufficient to account for
the complexity of cerebral activity patterns associated
with dreaming. It is instead possible that the pattern
of activity in the cortex is driven by differential patterns of information transfer between cortex and thalamus, perhaps coordinated by the reticular nucleus. The
basal ganglia are in a position to gate ascending reticular information from the intralaminar thalamus, and
to orchestrate activity within the cortex through their
projections back through nonspecific thalamic nuclei.
Or the pattern may be "set" within cortical neural
networks themselves. That is, rather than an attempt
by the cortex to "synthesize" order out of chaos, networks may be activated that possess order in themselves. The dream' 'agenda" may be set by the cortex.

Amnesia and Memory Consolidation

I cannot directly comment on Hobson's notion that
amnesia for dreams may be due to the deactivation of
monoamines (since these modulators normally activate signal transduction processes necessary to store
record of events mediated at the postsynaptic membrane). I would only say that it seems to me that amnesia for dreams is atypical amnesia-dream content has
in fact been encoded. We know this because it can
return spontaneously during the day through association to visual objects or emotions which are connected
to the dream. I think that amnesia, in this case, may
represent a defective search function which could be
attributed to inactivity of the prefrontal cortex during
REM. The DLPFC, in addition to supporting sustained
attention, logic, and self-monitoring, plays an executive role in working l1l;emory systems which normally
provide a coherent context for the ongoing flow of
thought, emotion, or sensory experience. It may be that
the context provided by working memory-if active at
the time of encoding-may provide a mechanism for
deliberate search and retrieval of episodic memories.
Thus one can ask, "What did I have for breakfast this
morning?" and conduct a coherent search (I woke up,

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Commentary on The New Neuropsychology of Sleep

spoke with my wife, picked out a shirt, made coffee
and eggs), but cannot ask, "What was I dreaming at
4 A.M. this morning?" and expect to come up with
anything. In the absence of the context provided by
working memory, no systematic search can be organized. Paradoxically, while amnesia or failure to retrieve dream content is typical, REM is felt to play a
critical role in long-term memory processing, in consolidation of long-term memories or pruning of unwanted memory from "overloaded" long-term
memory circuits (as hypothesized by Crick and Mitchison). The unusual situation which seems to be manifest in the brain during REM-i.e., activation of
mesial temporal regions such as the hippocampus,
which are felt to be involved in long-term memory
processing, and deactivation of frontal regions involved in short-term or working memory-may actually support these functions. That is, REM may
provide a situation in which long-term memory traces
can be processed off-line, either consolidated or
pruned, while the brain is not actively processing information generated during REM itself.

Dream Work
Finally, with respect to classical psychoanalytic theory: Solms thoroughly discusses appetitive drive and
I think his dopamine hypothesis may adequately account for the motivational features of dreams. It is this
portion of Solms's thesis that is congruent with the
neuroimaging work. But Solms never really adequately addresses what Hobson refers to as "censorship and disguise," and indeed seems to minimize
these features in his discussion of Freud's model. This
represents a major failure in his argument (and his
defense of Freud). Intervention of appetitive drive during sleep, investment of libido in "seeking" behaviors, whether mediated by DA or not, would be
considered consistent with the results of most PET
studies, which show widespread activation of the limbic system and relative inactivity in the dorsolateral
and orbital prefrontal regions during REM. As noted,
this now appears to be integrated into Hobson's model
and considered a cardinal feature of REM: activation
of the limbic system, in the absence of top-down control by the frontal cortex, provides a context in which
salient memories and emotions are manifest. I should
add here that I do not see the decrease in frontal cortical activity as evidence of disinhibition of limbic structures. The DLPFC does not play such a role. Instead
it is normally involved (in addition to working mem-

199
ory) in self-monitoring, categorization, rationalization, temporal organization of goal directed behavior,
judgment, as well as semantic or symbolic processing.
Limbic activation in the absence of prefrontal activity
simply represents an unusual circumstance in which
memory, emotion, and appetite may be expressed in
the absence of the rational context provided by the
prefrontal cortex. Limbic processes are unbridled,
without being examined, categorized, rationalized, ordered. Rather than disinhibition, this could represent,
in psychoanalytic jargon the suspension of the' 'reality
principle" in favor of the "pleasure principle" - ' 'regression" if you will.
Nevertheless, certain of our PET findings-specifically the persistent inactivity of dorsolateral prefrontal and orbital cortices-are inconsistent with
other central tenets of Freudian dream theory. They
provide no clear mechanism for some of the secondary
processes proposed by Freud; that is, screening of impulses emerging from the unconscious, censoring these
impulses or wishes, and encoding them in obscure but
acceptable dream symbols. Surprisingly, Solms gives
short shrift to the issues of censorship and symbolic
transformation in his discussion of the theory. He
treats the issues tangentially and characterizes them in
a rather simplistic fashion: "chopping it up and changing it about in order to make it more acceptable"
doesn't seem to capture the embedded levels of meaning that Freud seems to attribute to manifest "symbois" in the dream. Although I am no expert, my
reading of The Interpretation ofDreams (Freud, 1900)
suggests that this is a far more critical process, that
condensation and distortion represent the crux of the
"dream work"-camouflaging threatening material
by transferring the latent into the manifest content.
This process should require considerable mobilization
of the brain's symbol-making machinery. And if there
is any single region of the brain felt to be essential for
self-monitoring, abstraction and symbolic encoding, it
would be the dorsolateral prefrontal cortex-a region
in which activity plummets at sleep onset and in which
functional inactivity is destined to persist throughout
the entire sleep cycle. Furthermore, other heteromodal
areas that play an established role in semantic processing and might be expected to participate in Freud's
secondary dream work-perisylvian regions including
the posterior middle temporal gyrus and the inferior
parietal lobule-are relatively inactive during REM as
well. Like the dorsolateral prefrontal cortex, activity
in the inferior parietal lobule is reduced at sleep onset
and does not recover until waking. It is not clear what

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200

relationship the posterior perisylvian regions have to

the sites of Solms's PTO junction lesions.
In order to account, in part, for Freud's secondary
processes, Solms cites activation of "ventromedial"
frontal regions in our PET study as evidence for an
active censor. We did see two distinct areas of activation in the frontal paramedian cortex, when REM was
contrasted with deep NREM sleep (rather than waking). The first of these was deep in the posterior frontal
midline, in Brodmann area 25, which we considered
to be in the basal forebrain, and which is posterior
to medial orbital regions typically described (e.g., by
Damasio or Luria), as responsible for disinhibited behavior in patients with frontal lesions. (Activity in the
medial orbital regions did not differ significantly from
levels observed during NREM sleep and was in some
instances lower in REM than during waking). We also
saw increased activity in dorsal portions of the medial
prefrontal cortex, Brodmann area 10 in the superior
frontal gyrus. Interestingly, we see activation of this
region in PET studies of waking subjects who are generating a narrative, recounting a series of events from
memory. It is possible that these regions are responsible for the attempt to tether the visual images which
appear in the course of the dream into a narrative
form. This medial prefrontal region also appears, in
other neuroimaging studies, to be active during the
generation of self initiated or stimulus independent
thoughts (McGuire et aI., 1996). In any case, this is
not the portion of the medial prefrontal cortex that
inhibits behavior. This raises the issue of exactly what
region Solms is referring to as "ventromesial frontal
cortex." In some instances, this seems to represent
the region to which the VTA projects and that constitutes a central element of Panksepp's "wish" or
"seeking" system. But Solms seems to equate this
region with the "censoring" part of the brain, as well.
It seems odd that he places the seat of appetitive drives
and craving in the same tissue as the behavioral censor.
He does so on the basis of clinicopathological observations, citing his 1998 monograph. What exactly is the
evidence for this? Moniz's leucotomy patients are typically described as flat and devoid of appetitive interest rather than disinhibited. Were Solms's (1997)
bifrontal patients both adynamic and disinhibited?
Finally, Solms's suggested experiment for evaluating sleep disturbances in patients with PTO or bifrontal lesions is puzzling. His argument seems to be
that if dreams protect sleep, then the sleep of patients
unable to dream should be disturbed. Why should this
be? Again, as I read Freud it should be patients with
the' 'seeking system" engaged who are unable to cam-

Allen Braun

ouflage the ensuing unacceptable wishes who should

awaken. Why shouldn't patients with deep bifrontal
lesions-who in Solms's model are unable to activate
the wish system in the first place-be able to sleep
quite peacefully?

Conclusions
I would suggest that not only does inactivity of the
DLPF and orbital cortices fail to provide symbolic
processing and condensation machinery necessary for
transformation of latent into manifest content, but that
inactivity of these regions can in and of itself explain
many of the cardinal features of dreams (loss of critical insight, inability to shift attention)-and that the
bizarreness of dream imagery (spontaneous changes
in orientation, narrative nonlinearity, shifting and
morphing of identities) could be easily attributed to
the disengagement of working memory mechanisms
and the resultant absence of a coherent context in
which the dream may take place.
The corollary of course is that there is no latent
content: that rather than metaphor or symbol, dreams
consist entirely of what is manifest on the surface.
This does not make dream content meaningless, chaotic, or random. The uncensored but distorted appetitive drives, memories, and attendant imagery may be
full of meaning, but it is mapped on the surface of the
dream, not disguised and in need of decoding. I am
inclined to agree with lung, who said: "I am doubtful
whether we can assume a dream is something other
than it appears to be. I am rather inclined to
quote ... the Talmud, which says, 'The dream is its
own interpretation' " (lung, 1937). The issue is important, and should dictate how dreams are dealt with
in a clinical context. And what should be most important to analysts is at what level dreams are meaningful and how they might represent a useful way of
understanding unconscious processes-salient emotions and memories or appetitive drives-that have
been accessed in the process. Next to this, the issue
of whether dreams protect sleep seems to me trivial,
and of interest only in an historical context; that is, it
simply comes down to the question of whether or not
Freud was right. Perhaps Freud need not be the central
issue any longer. Hobson may be correct, the debate
may be forever centered upon Freud himself: proponents may be driven by the tenacious adherence to
orthodox Freudian theory. But Hobson is not immune,
for his argument seems to be fueled by a rejection of
the "cult of Freud." Stepping back a short distance,

Commentary on The New Neuropsychology of Sleep

this is what I see: Hobson, a consummate biological
psychiatrist, now argues against reductionism and passionately advocates the study of subjective conscious
experience (Hobson, 1999). Solms, a psychoanalyst,
is attempting to recast dynamic psychology in neurochemical terms. It sounds to me like these gentlemen
are approaching common ground. Perhaps it is simply
the ghost of Freud that is getting in the way.

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Allen Braun, M.D.
Building 10, Room 5Nl18A
National Institutes of Health
Bethesda, MD 20892, U.S.A.
e-mail: abraun@pop.nidcd.nih.gov

The New Neuropsychology of Sleep

Commentary by Morton F. Reiser (New Haven)

One way to map mind onto brain is to search for neural

correlates of mental function. In regard to dreaming,
Morton Reiser, M.D., is Albert E. Kent Professor Emeritus of Psychiatry, Yale University School of Medicine, New Haven, CT: Training and
Supervising Analyst, Western New England Institute of Psychoanalysis.

the search should be for correlations between (1) the

content and process of the dreaming mind (including
the subjective experience of the dreamer), and (2) the
neurobiology (physiology and clinical anatomy) of the
dreaming brain. That may sound relatively straightforward, but the "mind-brain problem" and the enduring