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Neuropsychoanalysis: An Interdisciplinary Journal

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The New Neuropsychology of Sleep: Commentary by

Mark Solms (London)

Mark Solms

Academic Department of Neurosurgery, Royal London Hospital, London E1 1BB, United

Kingdom, e-mail:
Published online: 09 Jan 2014.

To cite this article: Mark Solms (1999) The New Neuropsychology of Sleep: Commentary by Mark Solms (London),
Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences, 1:2, 183-195, DOI:
To link to this article: http://dx.doi.org/10.1080/15294145.1999.10773259


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Commentary on The New Neuropsychology of Sleep

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Witte, E. A., Gordon-Lickey, M. E., & Marrocco, R. T.

(1992), Pharmacological depletion of catecholamines
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sleep induction zone in the anterodorsal pontine tegmentum: Spontaneous and drug-induced neuronal activity.
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pontine tegmentum: Locus of the sensitized region. Neurosci., 39:295-304.

Zadra, A. L., Nielsen, T. A., & Donderi, D. C. (1998),
Prevalence of auditory, olfactory and gustatory experiences in home dreams. Percep. & Motor Skills,
J. Allan Hobson

Laboratory of Neurophysiology
Massachusetts Mental Health Center
74 Fenwood Road
Boston, MA 02115

The New Neuropsycholog)r of Sleep

Commentary by Mark Solms (London)

Allan Hobson is the leading authority on the neurophysiology of REM sleep dreaming, and his work has
dominated this field for more than twenty years
(McCarley and Hobson, 1975; Hobson and McCarley,
1977). Recent findings concerning the neuropsychology of dreaming, however, as Hobson himself acknowledges, need to be reconciled with the old
physiological findings, and this is ushering in a new
era in this field.
In his paper, Hobson has covered a vast area of
knowledge. It will not be feasible for me to address
all of the points that he raised. I will focus selectively
on one or two things that I think are of central importance. This omits a lot else that is also of interest. I
am going to structure what I have to say around six
questions which I would like to pose to Professor
I don't have any disagreement with Hobson's understanding of the essential physiological mechanisms
underlying the sleep-waking cycle, including the
mechanism of REM sleep. However, I do disagree
with his understanding of the psychology of dreams
based on those physiological mechanisms. Obviously,
psychology is what interests psychoanalysts most.
There has always been an uncomfortable gap between
the psychological approach to dreams, as remembered
The present commentary is a lightly edited version of a discussion
of Hobson's presentation to the Neuro-Psychoanalysis Center of the New
York Psychoanalytic Institute, November 7, 1998:"The New Neuropsychology of Sleep: Implications for Psychoanalysis."
Mark Solms is Hon. Lecturer, Academic Department of Neurosurgery, S1. Bartholomew's and Royal London School of Medicine; and Associate Member of the British Psycho-Analytical Society.

subjectively by patients, and the physiological approach to dreams, as manifested objectively (apparently) by REM sleep. However, it is now possible to
bridge this gap, using the insights that modern neuropsychological methods and neuro-imaging techniques
can provide into the neural organization of all higher
mental functions.
REM sleep is a state with many components, including a forebrain component, but until recently, only
the brainstem component has been well understood.
The recent developments in the neuropsychology of
dreaming that I am going to refer to (clinico-anatomical studies of human patients and functional imaging
of the dreaming human brain)-which also form the
basis of Hobson's most recent revisions of his own
model-are beginning to elucidate the forebrain component, and thereby starting to bridge the uncomfortable gap just referred to (Madsen, 1993; Maquet et aI.,
1996; Braun et aI., 1997, 1998; Nofzinger, Minturn,
Wiseman, Kupfer, and Moore, 1997; Solms, 1997). In
this gap, new insights are now being gained into the
neural correlates of dreaming itself, and these insights
are casting a different light on the issues that confront
us (Solms, in press).
What, then, are the issues that confront us? Many
analysts might be tempted to dispute the accuracy of
Hobson's presentation of Freud's dream theory (or
indeed of his remarks about psychoanalysis as a
whole). I am not going to take up those polemics here.
I am going to recall just one aspect of Freud's (1900)
theory, one that brings us to what I think is the central
issue at stake in these deliberations. Freud believed
that there is an ongoing mental process during sleep.

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Although that process is not identical with waking
mental activity, it is also not synonymous with dreaming. The mind is simply active-preconsciously active-during sleep, as it is during waking life. But
something special happens during sleep; we enter the
hallucinatory, quasi-delusional state called dreaming.
This happens, according to Freud, because the sleeper
becomes aroused by what he called' 'libidinal" drives
(what would nowadays be called appetitive drives)
which are especially powerful due to the weakened
(sleeping) state of the ego's inhibitory functions. These
disinhibited drives threaten the ego's state of sleep
because intense needs motivate goal-directed activities, which lead to consummatory behaviors, which
are certainly incompatible with the state of sleep. Consequently, in order to protect sleep, these drives (experienced as "wishes") cannot be satisfied in the real
world and they must be dealt with in some other way.
For this reason, according to Freud, the sleeper imagines such wishes as being fulfilled in an hallucinatory
fashion, and in this way temporarily fends off the demands of the underlying, ascendant drives. That, in a
nutshell, according to Freud, is the core mechanism
of the dream process; that is why our sleeping thoughts
are punctuated every night by the vivid, hallucinatory
experiences that we call dreams. So, according to
Freud, the crucial factor that distinguishes thinking
during sleep from dreaming proper is the intervention
ofdisinhibited appetitive drives during sleep. If it were
not for this disinhibition of the drives, the ongoing
thought processes that occur during sleep would not
be transformed into hallucinations. Thus, on Freud's
view, dreaming only becomes possible once appetitive
interest (a highly excited state of an instinctual kind)
attaches to and intervenes in our ordinary nocturnal
thought processes.
Freud used the analogy of the relationship between an entrepreneur and a capitalist to illustrate this
central aspect of his theory. He said that the ordinary
mental processes that occur throughout sleep (memories, volitions, perceptions, etc.) are only the "entrepreneurs" of dreams-they trigger the process which
eventually leads to a dream-but that the dream itself
only occurs if and when the mental processes initiated
by the entrepreneur attract the interest of a "capitalist" (the libidinal drives). Without capital the entrepreneur's idea will not be transformed into a reality
(hallucination). This analogy usefully captures the
central problem that Hobson has posed for us.
At first sight one might be inclined to argue, in
the light of this analogy, that Hobson's activation-synthesis theory of dreaming is not fundamen-

Mark Solms
tally incompatible with Freud's entrepreneurcapitalist theory. A good few decades ago Foulkes
(1962) demonstrated empirically-by awakening experimental subjects at various points during the sleep
cycle (not only during REM sleep)-that there is indeed ongoing mental activity throughout sleep, just as
Freud claimed. This mental activity is not dreaming,
it is "thinking" (or something like thinking). Then,
every 90 minutes or so, a radical change occurs in
the form of this mental activity. It becomes bizarre,
affectively charged, hallucinatory, and delusional; this
is the dream proper-a very different type of mental
activity. This type of mental activity is highly correlated with the physiological state known as REM.
As Hobson and others have demonstrated moreor-less conclusively, this state is caused by pontine
brainstem release (aminergic demodulation) of cholinergic activation. On this theory, it is cholinergic activation of the forebrain during sleep that is unique to
dreaming. It is the cholinergic activation of REM sleep
that transforms ordinary thinking into the unique mental process that is the dream proper. Might not cholinergic activation, therefore, be the "capitalist" (the
libidinal drives) of Freud's theory?
One can see why, at first sight, psychoanalysts
might wish to equate libidinal drive with cholinergic
REM activation. Through this simple equation, the
whole of Freudian dream theory would be brought into
line with the findings of contemporary dream research.
But there are many problems with this equation. For
example, why does the "capitalist" appear on the
scene every 90 minutes or so with such monotonous
regularity? Why should it appear automatically, by
way of a simple brainstem switch which is activated
so predictably, no matter what the sleeper has been
thinking about, in fact, regardless of any mental state,
wishful or otherwise?
These disparities could still perhaps be reconciled
with the Freudian theory. It is possible, for example,
that libidinal drives do simply become active every 90
minutes or so during sleep, due perhaps to an automatic disinhibitory process, or some other intrinsic
rhythm of instinctual control (cf. Wassermann, 1978).
But this kind of ad hoc theorizing ultimately strikes a
rock: if we are going to respect the scientific facts, we
have to admit that there is nothing about the cholinergic systems of the brain that would justify the hypothesis that they are the physiological correlate of what
Freud called the t t libidinal drives." Acetylcholine
simply is not the command neurotransmitter of appetitive interest; and none of the cholinergic pathways
leading from the brainstem to the forebrain has ever

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Commentary on The New Neuropsychology of Sleep

been shown to mediate this function. Cholinergic activation is therefore not a viable candidate for the role
of the "capitalist" in Freud's dream theory. Instead,
as Hobson has pointed out, cortical acetylcholine
seems to participate primarily in selective attentional
processing. (It contributes to many different complex
functions, of course, but one of the fundamental physiological effects of cortical acetylcholine seems to be
an improvement in discriminative mental processes.)
I do not see how we can validly construe this focusing
function as the neural equivalent of an instinctual urge.
Some might still want to dispute that, but I cannot
agree with them and I do not think they will succeed.
If it is at all legitimate to seek a single neurotransmitter system which might be the neurophysiological correlate of what Freud called libidinal drive,
then it would probably have to be part of the mesocortical-mesolimbic dopamine systems of the brain-the
"curiosity-interest-expectancy" circuit of Panksepp
(1985), about which I will have a lot more to say later.
If contemporary Freudians are seeking a command
neurotransmitter system which might be equated with
their "capitalist," it would have to be this one, rather
than the cholinergic systems identified by Hobson.
Here, then, is the nub of the problem we are discussing. This is the main point of divergence between
Hobson's viewpoint-and the whole paradigm of
work that has developed around his discoveries and
theories-and the older, Freudian viewpoint. In Hobson's view, what distinguishes dreaming proper from
the ongoing, banal mental processes that occur during
ordinary (non-REM) sleep is not an appetitive
urge-not a libidinal drive or a "wish"-but rather a
"motivationally neutral" upsurge in cholinergic activation (McCarley and Hobson, 1977, p. 1219). And
this upsurge, as Hobson has so elegantly shown, results from the simple, mechanical release of brainstem
(and possibly basal forebrain) cholinergic nuclei from
the modulatory constraints imposed on them during
non-REM sleep by a network of reciprocally interacting brainstem serotonergic and noradrenergic
That is the essence of Hobson's post-Freudian
model. On the basis of this model, Hobson has drawn
various conclusions about the psychology of dreams,
including the claim that the reciprocal interactions between cholinergic and aminergic brainstem nuclei explain not only the causation of dreams, but also their
formal characteristics. In Freud's model, the causation
and hallucinatory-delusional quality of dreaming was
explained by the libidinal wish-fulfillment hypothesis.
However, various subsidiary hypotheses were required

to explain other cardinal features of dreams, such as
the hypothesis of "censorship," which was invoked
to explain some of the bizarre content of dreams, the
fact that some dreams are unpleasurable and unsatisfying experiences, and the fact that we forget dreams
so readily. On Hobson's theory, all of these characteristic features of dream psychology can be explained
with reference to a simple oscillatory switch in a tiny
part of the brainstem (Hobson, 1992). Therefore, according to Hobson, all of the complicated mental
mechanisms that Freud proposed can be removed like
a scruffy beard with Ockham's razor.
The problems with Hobson's theory start here.
The unique state of mind that we call dreaming, with
all those special mental features that Hobson reduces
isomorphically to the neurochemistry of the REM
state, does not occur during REM sleep alone. Precisely the same state of mind occurs at other points in
the sleep cycle, which have different neurochemical
properties. In fact, a full 20 percent of all dreams occur
during non-REM sleep.l This is a conservative estimate (see Cavellero, Cicogna, Natale, Occhonero, and
Zito, 1992). I am referring here to REMlike dreaming;
not thoughtlike dreaming or thinking. Hobson himself
has conceded that these non-REM dreams' 'are indistinguishable by any criterion from REM dreams"
(Hobson, 1988, p. 143). But I think he does not make
enough of this fact. I think that it really poses a fundamental problem for his theory.
Let me spell out its implications as I see them.
If, as Hobson suggests, the whole of dream psychology can be accounted for by the physiology of REM
sleep-by cholinergic activation coupled with aminergic demodulation-then why does exactly the same
mental state occur in the absence of that mechanism?
If the REM state has a unique neurochemical basis,
which is absent by definition during the non-REM
state, then the existence and formal characteristics of
non-REM dreams cannot be accounted for by the
unique physiology of the REM state (Vogel, 1978).
This implies either that REM dreams and these nonREM dreams are governed by two entirely different
physiological mechanisms (which seems highly unlikely in view of the equivalence of their formal characteristics), or alternatively, dreams in general are
caused and regulated by something other than the sim1 Hobson (1988, pp. 142-143) concedes that 5 to 10 percent of nonREM dreams are indistinguishable by any criterion from REM dreams.
This constitutes approximately 20 percent of all dream reports if the number of reports are weighted for sleep-stage duration; 5 to 10 percent of nonREM sleep (which occupies 75 percent of total sleep time) is equivalent to
roughly 15 to 30 percent of total sleep.

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pie oscillatory mechanism that governs the REM/nonREM dichotomy. The fact that dreams occur during
non-REM sleep leaves open the possibility that cholinergic activation may interact with the mechanism that
is the "capitalist" of the dream process, but REM
sleep itself cannot be that "capitalist." In short,
dreaming must be governed by something other than
the brainstem mechanisms that govern REM sleep.
The new research that I want to mention has, I
believe, identified this other mechanism, which is the
true instigator of dreams. Before I describe this other
mechanism, however, I want briefly to review some
further data, derived from earlier research, which un~
derscore the dissociation I am drawing here between
dreaming and REM sleep. Then I will describe the
brain mechanism which I believe underlies dreaming
and show how it differs from the mechanism of REM
sleep. Finally, I will suggest how these two mechanisms might interact with each other, and explain the
high correlation that certainly exists between dreaming and REM sleep. In the process, I hope to show
that there is a complex relationship between the mental things called dreams which 'Freud studied (and
which other psychoanalysts study today), and the
brainstem things that Hobson and his colleagues have
traditionally studied.
I am going to argue, and present evidence for the
view, that even at the level of brain mechanisms, we
are in fact dealing with two entirely different things.
There is the brainstem mechanism of REM sleep and
there is the forebrain mechanism of dreaming. These
two things are frequently activated in tandem, or at
least they are highly correlated. But they are dissociable under certain conditions, and this makes it impossible for them to be one and the same thing. Dreaming
can occur without REM and REM can occur without
dreaming. This proves that cholinergic activation (the
mechanism of REM sleep) is neither necessary nor
sufficient for dreaming. Once we have established this,
we need to identify what the brain state could be that
is responsible for dreaming. We need to identify the
anatomical and chemical properties of the dream process, and distinguish them from the above-described
mechanisms of the REM process. Then, finally, we
need to understand why these two mechanisms are so
frequently activated together.
The first point that I have to convince the reader
of is that there are indeed two separate brain mechanisms for dreaming and REM sleep. This obviously
has fundamental implications for the sort of criticism
that Hobson has directed at Freud's theory.

Mark Solms
As I said earlier, during non-REM sleep, in the
absence of the unique state of cholinergic activation
that characterizes REM, the subject is usually in a state
of thoughtlike mentation. If one awakens a sleeping
subject during non-REM sleep, one has a 50 percent
chance of obtaining a subjective report of what he or
she was thinking about preconsciously. These are not
dreams. However, as already mentioned, sometimes
(in 5-10% of non-REM awakenings) one obtains
dream reports which are indistinguishable by any criterion from REM dream reports. As I have said already, although Hobson concedes this point, this is
where the main problem with his theory lies. How can
the same mental state occur regardless of the presence
or absence of the cholinergic mechanism that is supposed to generate it?
Even more important than the fact that 5 to 10
percent of non-REM reports are indistinguishable
from REM reports is the fact that these reports are
not randomly distributed through the non-REM
phases. There is a clustering of these reports at specific
points in the non-REM cycle. The best example of
this clustering occurs during descending stage I sleep
(sleep onset): at sleep onset, a full 70 percent ofawakenings elicit hallucinatory dream reports. The only
significant difference between these dream reports and
REM reports is that the sleep onset reports are shorter
(Foulkes and Vogel, 1965). In other respects (if the
factor of length is included) they are statistically indistinguishable from REM mentation, and they cannot
be described as anything other than "dreams." The
temporal location of this cluster of non-REM dreams
is especially telling. It lays to rest any lingering suspicion that non-REM dream reports are merely misremembered REM dreams (i.e., that the sleeper believes
that he or she has just been dreaming, but actually
they were dreaming a good twenty minutes ago during
the previous REM stage). Sleep onset dream reports
are elicited before any REM episodes have occurred.
So these dreams may safely be attributed to a mechanism other than the aminergically demodulated, cholinergic mechanism that Hobson postulated.
The same thing as occurs at sleep onset occurs,
to a lesser extent, at the other end of the sleep cycle.
Toward the end of a night's sleep, as the sleeper is
starting to stir (during the so-called rising morning
phase of the diurnal rhythm), progressively more and
longer dream reports are obtained during awakenings
from the non-REM sleep stages. This is called the
"late morning effect" (Kondo, Antrobus, and Fein,
1989). As with sleep onset, so with the rising morning
phase of the diurnal rhythm: non-REM dreams exist,

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Commentary on The New Neuropsychology of Sleep

and they are attributable to mechanisms other than the
cholinergic mechanism that Hobson claimed causes
dreaming during REM sleep.
There is something else about the temporal clustering of both REM and non-REM dreams that I want
to mention in passing. Please notice when these clusters occur: they occur just as one is falling asleep, at
sleep onset; then they occur in the highly excited state
of "paradoxical sleep" (as REM sleep used to be
called); then they occur again with increasing frequency as sleep starts to give way to renewed wakefulness. This pattern suggests that there might be some
sort of relationship between dreaming and arousal
states in general. So this might be the specific physiological correlate of dreams; perhaps dreams are provoked not only by REM arousal,2 but by any persistent
arousal state which occurs during sleep. This would
appear to account for all the facts I have reviewed
so far.
As it happens, Hobson himself has already suggested something like this to account for the (acknowledged) fact that some dreams occur during non-REM
sleep. His latest revision of his activation-synthesis
model (the AIM model) incorporates just such an explanation. It is unnecessary for me to recount the details of the AIM model; Hobson has summarized it
himself. But I do want to indicate a problem with it.
The revised model still assumes that all dreams
(whether REM or non-REM) can be explained in
terms of the dynamics of reciprocally interacting
brainstem aminergic and cholinergic systems. If this
assumption is correct, the existence of non-REM
dreams does nothing to diminish the challenge that
Hobson's original model posed to psychoanalytic
dream theory. If dreams (whether REM or non-REM)
are still reducible to cholinergic-aminergic brainstem
neurodynamics, then they still have nothing to do with
motivated mental states, which are principally mediated by forebrain mechanisms (localized mainly to the
limbic system and frontal lobes).
The problem with Hobson's revised model (or
any other model which reduces the causation of
dreams to brainstem mechanisms) is this. There is a
pathological state known as complex partial epilepsy,
in which seizures of a particular kind occur which are
2 There is interesting data to show that the cholinergic activation
which is characteristic of REM does indeed arouse the sleeper. If cholinergic agonists are introduced during non-REM sleep, they trigger REM sleep.
If cholinergic agonists are introduced during REM sleep, they provoke
waking. If cholinergic agonists are administered prior to sleep onset, they
induce insomnia (Sitaram, Wyatt, Dawson, and Gillin, 1976; Sitaram,
Moore, and Gillin, 1978).

by definition focal forebrain events. These seizures
typically manifest in the form of what Hughlings Jackson called "dreamy states." They almost always arise
from limbic and frontal lobe structures-and they
never spread to the brainstem structures which Hobson
claims are the primary instigators of dreams. If they
did spread to those structures they would be neither
complex nor partial seizures; they would be something
completely different. This type of seizure commonly
occurs during sleep, and to be more specific, it typically occurs during non-REM sleep (Janz, 1974; Kellaway and Frost, 1983). This type of seizure is
associated with a distinctive dream phenomenon: recurring stereotyped anxiety dreams (Epstein, 1964). It
was demonstrated long ago, conclusively, that these
recurring anxiety dreams are seizure equivalents-that
they are merely complex partial seizures occurring
while the patient is asleep (Penfield, 1938; Penfield
and Erickson, 1941; Penfield and Rasmussen, 1955).
Penfield was actually able to trigger these seizures,
these dreams, experimentally by stimulating the affected area of the temporal lobe. So these dreams, at
least, which typically occur outside of REM sleep, are
instigated by a mechanism which is completely unrelated to the oscillatory brainstem mechanism that Hobson described. These dreams are without a shadow of
doubt caused by a (highly specific) forebrain mechanism.
The first major problem with Hobson's activation
synthesis model is that many dreams occur outside of
REM sleep. The second is that some non-REM dreams
are certainly caused by forebrain mechanisms. This
leads to the first of the six questions that I would like
to ask Professor Hobson: How does he account for
non-REM dreaming in general and for the recurring
nightmares that are associated with complex partial
seizure disorders in particular?
Now I want to introduce a third line of evidence,
one that begins to suggest that in fact all dreams might
be generated by forebrain mechanisms. For obvious
reasons, the research program that Hobson has followed for the past thirty years was conducted not with
human subjects but rather with lower mammals-principally the domestic cat. The REM state in humans
was discovered more than forty years ago, and once
it was established that an identical physiological state
occurs in almost all mammals, it seemed reasonable
to study the neuroanatomy and neurophysiology of the
REM state in animals, on the assumption that this
would teach us something about the anatomy and
physiology of its equivalent in humans. Although this
generalization seemed reasonable enough with respect

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to REM sleep, it rested on somewhat shakier foundations when it came to the correlation between REM
sleep and dreaming.
It is true that the high correlation between REM
sleep and dreaming is firmly established in humans,
but it is impossible to determine whether or not this
correlation holds good for cats; indeed it is impossible
to know whether cats ever dream (during REM sleep
or at any other time). Thus, when Hobson and his
colleagues performed ablation, stimulation, and recording experiments on cats in order to determine their
effects on REM sleep, the simultaneous effects of
these experiments on the cats' dreams remained quite
unknown. This applied even at the most basic level of
correlation. For example, when Jones (1979) demonstrated that ablation of a large portion of the paramedian pons completely obliterates REM sleep in cats, he
had no way of knowing whether or not these REMdeprived cats still dreamed. In this way, Hobson and
his animal-research colleagues have had to carry over
a large unknown factor into all their theoretical formulations about dreams, and their inferences about the
neuropsychological mechanisms of dreaming in humans could not be directly tested.
For more than one hundred years, the standard
empirical method of establishing mind-brain correlations in humans has been the clinico-anatomical
method. By this method it is very easy to test hypotheses about the neural correlates of mental functions of
the kind that Hobson has advanced with respect to
dreaming and the brainstem. If one believes that a
particular mental function is intrinsically related to the
physiological activity of a particular part of the brain,
then this predicts what should happen to that mental
function when that part of the brain is damaged. For
example, Broca justified his belief that the production
of speech was a function of the third frontal convolution of the left cerebral hemisphere by demonstrating
empirically that damage to that part of the brain resulted in a loss of expressive speech. Thus, if Hobson
is justified in his belief that the generation of dreams
is a function of the paramedian pontine tegmentum,
then it should be possible for him to demonstrate that
damage to that part of the brain results in a loss, not
only of REM sleep, but also of dreaming.
Nature has provided science with human subjects
with discrete lesions in this part of the brain. 3 Twentysix such patients, human cases, have been reported
3 Contrary to Hobson's statement, which in general is true, some of
these patients are conscious and alert enough to be able to state whether
they dream or not.

Mark Solms

in the neurological literature; twenty-six patients with

pontine brainstem lesions, who no longer had REM
sleep (Adey, Bors, and Porter, 1968; Chase, Moretti,
and Prensky, 1968; Feldman, 1971; Markand and Dyken, 1976; Cummings and Greenberg, 1977; Osorio
and Daroff, 1980; Lavie, Pratt, Scharf, Peled, and
Brown, 1984). In only one of these twenty-six cases
was it demonstrated that there was a cessation of
dreaming (Feldman, 1971); in all other cases the correlation between loss of REM and loss of dreaming was
either absent or it was not even considered by the authors.
The one positive case suffered a traumatic occlusion of the basilar artery. Since this case report was
published in 1971, before the advent (or at least, before the widespread use of) CT imagery, we do not
know the precise extent of the lesion that produced
the combined loss of REM sleep and dreaming in that
case. A diagnosis of massive pontine damage was
made on purely clinical grounds. Although the evidence for that diagnosis was good, there is little in the
published report to reassure the clinical neuroscientist
that this patient did not also sustain damage to the
forebrain. Certainly, given what we know about the
pathological anatomy of basilar artery infarctions, it
is in fact highly likely that this patient did also have
abnormalities in the region of the posterior cerebral
circulation-that is to say, forebrain damage. So, for
scientific purposes, we can more-or-less exclude even
the one case among the twenty-six human brainstem
patients where it was demonstrated that loss of REM
sleep was accompanied by loss of dreaming.
It is true that the neuropsychological investigation of patients with pontine lesions presents difficulties. These patients are few and far between, they are
very ill, consciousness is often clouded, and so on. I
readily accept that this is an area that needs further
investigation. Nevertheless, it is very striking indeed,
considering the huge amount of scientific interest that
has been devoted to REM sleep precisely because of
its correlation with dreaming, that this standard requirement of neuropsychological correlation has never
been met-that it has never been demonstrated that
brainstem lesions cause cessation of dreaming. The
failure to meet this rudimentary clinico-anatomical
standard greatly undermines any theory which would
reduce the neuropsychology of dreams to brainstem
But in clinico-anatomical research, negative evidence (absence of a correlation) is seldom as telling
as positive evidence (presence of a correlation). The
following line of evidence is therefore still more un-

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Commentary on The New Neuropsychology of Sleep

dermining of Hobson's brainstem conception of
It has been demonstrated that certain brain lesions, highly focal brain lesions, do cause cessation
of dreaming, but these brain lesions are in an entirely
different part of the brain from the brainstem location
of the mechanism which regulates the sleep cycle. The
lesions in question are localized in two parts of the
higher brain. Patients with damage in either of these
areas experience a total cessation of dreaming, and
their retrospective reports in this regard are confirmed
by REM sleep awakening (Solms, 1995, 1997). These
patients simply do not dream anymore. The REM cycle is unaffected in these cases; they still have normal
REM episodes, despite their complete inability to
dream. This confirms the dissociation between dreaming and REM sleep.
Such cases have been reported in their hundreds.
Only one case with a dubious focal pontine brainstem
lesion has been reported with cessation of dreaming in
association with cessation of REM sleep. By contrast,
literally hundreds of cases with unequivocal focal
forebrain lesions have been reported with cessation of
dreaming in association with completely normal REM
sleep. This leads to the second question I want to pose
to Professor Hobson: How does he account for the
demonstrable dissociation that exists between REM
and dreaming, using the standard clinico-anatomical
paradigm of brain-behavior correlation?
What, then, are these forebrain lesion sites that
are associated with loss of dreaming (as opposed to
loss of REM sleep); and what do they tell us about the
brain mechanisms of dreaming (as opposed to those of
REM sleep)? There are, as already mentioned, two of
them. First, lesions of either hemisphere in the region
of the parieto-temporo-occipital (PTO) junction
(where the parietal, temporal, and occipital lobes converge) lead to a cessation of dreaming during the acute
phase of the underlying neurological illness (dreaming
usually recovers within one year). Why should lesions
in this highly evolved part of the human forebrain lead
to an acute cessation of dreaming? Due to the high
number of available cases, it is possible to answer
this question by multivariate analysis of the cognitive
deficits that coincide with the loss of dreaming in these
patients. The results suggest that the loss of dreaming
in these cases is due to an abnormality of spatial cognition, or to be more precise, of what cognitive psychologists call the "visual cache" of working memory.
These patients are defective with respect to visuospatial working memory and related functions, and they
are therefore unable to construct (or maintain) in con-

sciousness a stable "mental space." Since dreams are
fundamentally grounded in such a space, it is perhaps
not surprising that these patients are unable to dream.
I am sure that Hobson would agree that the fact
that these patients do not dream does not represent
compelling evidence against his theory that dreams
are generated by pontine brainstem mechanisms. No
matter where the process of generating dreams may
begin, at some point it would have to engage these
higher spatial mechanisms in order to produce a complex hallucinatory experience grounded in the conscious "mental space" of working memory. The fact
that dreaming ceases following PTO junction lesions,
therefore, does not mean that dreams are actually generated in the PTO junction; the process could merely
culminate there. So the involvement of this part of the
brain in the dream process is, so to speak, merely the
tip of the neuropsychological iceberg.
However, here it is necessary to digress for a
moment, in order to make the point that although even
the activation-synthesis model would have predicted
that the neocortical structures subserving visuospatial
working memory must somewhere be involved in the
dream process, it would not have predicted the specificity of the involvement of these structures that has
actually been observed (Solms, 1997; Braun et aI.,
1998). In the activation-synthesis model, pontine
brainstem aminergic mechanisms demodulate ascending brainstem cholinergic mechanisms, resulting
in widespread cortical activation (this is the' 'activation" aspect of activation-synthesis). The activated
forebrain then "synthesizes" the meaningless brainstem stimulation, thereby producing the conscious experience of the dream itself. The dream itself, then,
according to the activation-synthesis model, is ultimately an attempt by the cortex to synthesize all of
the meaningless images that are generated by a diffuse
autoactivatory process.
In the light of this model, it is important to note
that only a very specific part of the great expanse
of imagery-producing perceptual and motor cortex is
implicated in the dreaming process by the clinico-anatomical evidence. It is only with lesions in the few
square centimeters that constitute the region of the
PTO junction that dreaming stops completely. Lesions
anywhere else in the whole of the vast expanse of the
cerebral cortex do not have this effect. 4
4 Recent PET findings reported by Braun et aI., (1997, 1998) suggest
that the critical lesion site for cessation of dreaming might, in fact, be the
insula (which lies immediately beneath the PTa junction) or the posterior
aspect of the superior temporal gyrus (which is immediately adjacent to
the PTa junction), rather than the PTa junction itself. Nevertheless, the
specificity of the structures identified by Braun support the point being
made here.

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Moreover, it can be demonstrated that the imagery generated in some of these other parts of the cortex
is positively preserved in dreams, despite massive
damage to the structures concerned. What this suggests is that dreaming is not merely a synthetic manifestation of diffuse cortical arousal; rather, it appears
that highly complex representational and rerepresentational mechanisms are actively involved in the cognitive construction of dream images. For example,
lesions in the somatosensory and motor cortex-which produce dense hemiplegia in waking
life-are not accompanied by hemiplegic imagery in
dreams. Hemiplegic patients experience intact somatosensorimotor functions in their dreams. There is a very
poignant description of this in an early report by Mach
(1906), where he tells how he dreamed of himself
playing the piano and thinking he was normal again,
only to wake up and find that his hemiplegia was
still there.
If the simple, isomorphic relationship that Hobson postulated really existed between the excitation of
motor cortical elements and the dream experience,
then one would not expect this kind of dissociation to
occur between lesions of the cortical motor system
and motor imagery in dreaming. The same applies to
the other unimodal cortical structures. For example,
lesions in the visual cortex which produce hemianopia
in waking life are not accompanied by hemianopia in
dreams. These patients, despite losing half their visual
field in waking perception, experience normal vision
in their dreams. This demonstrates that the perceptual
and motor images we experience in our dreams are
not simple, isomorphic products of nonspecific activation of perceptual and motor cortex during sleep;
highly complex, heteromodal representational mechanisms appear to be involved in the active construction
of the manifest dream.
Now we can return to the main theme. I said
that cessation of dreaming was associated with two
forebrain lesion sites. The first of these was the region
of the PTO junction. The second lesion site is the
white matter of the ventromesial quadrant of the frontal lobes (the fibers immediately surrounding and inferior to the frontal horns of the lateral ventricles).
Bilateral lesions in this highly specific area lead to a
cessation of dreaming-permanent, global cessation
of dreaming. Again, despite the demonstrable absence
of dreams in these cases, REM sleep is completely preserved.
What is the function of this second part of the
brain which is so crucial for dreaming? This is precisely the part of the brain that the psychosurgeons

Mark Solms
targeted in the modified prefrontal leucotomy procedure that was so extensively performed in the fifties,
sixties, and early seventies for the treatment of severe
mental illness (Bradley, Dax, and Walsh, 1958). This
procedure produced large numbers of patients with
bilateral lesions in the part of the brain just mentioned.
In my own clinico-anatomical study (1997) I collected
only nine nondreaming cases with lesions in this area
(which is seldom damaged bilaterally through natural
causes). However, I was very struck by the similarity
of this lesion site to the site of the old prefrontalleucotomies; so I went back to the psychosurgical literature
and, 10 and behold, completely unnoticed by all of us,
there they were reported in the hundreds-very large
series of prefrontalleucotomy cases, with a 70 percent
incidence of loss of dreaming following the procedure
(Frank, 1946, 1950; Partridge, 1950; Piehler, 1950;
Schindler, 1953; Jus et aI., 1973). And again, REM
sleep was preserved, despite the loss of dreaming (Jus
et aI., 1973).
This begins to suggest what the functional contribution of this part of the brain, so crucial for dreaming,
might be. At the same time as these patients lost whatever it was that generated their psychiatric symptoms,
they also lost the ability to dream. A common side
effect of prefrontalleucotomy was adynamia-loss of
spontaneous interactive interest in the world. This
points to the fact that this part of the brain is crucially
involved in motivation. In fact, there is a major motivational system in this sector of the frontal lobes, the
core of which is a pathway that connects dopaminergic
nuclei in the upper ventral tegmental area, via the lateral hypothalamus, with the amygdala, septal area and
nucleus accumbens, anterior cingulate gyrus, and ventromesial frontal cortex. This system, which is richly
interconnected with the limbic temporal lobe structures that were discussed earlier, forms part of the
mesocortical-mesolimbic dopamine system. The specific portion of this system which seems to be crucial
for dreaming has been described as the' 'curiosity-interest--expectancy" system (Panksepp, 1985) or the
"seeking" system (Panksepp, 1998) or the "wanting"
system (Berridge, 1999). This system is engaged with
all appetitive behaviors; it drives our interactive interest in the world. It is especially active in states of
craving (such as occur in addiction). The fact that lesions along this pathway cause a cessation of dreaming is very interesting in light of the Freudian dream
theory, for it suggests that dreams are indeed-no less
than the excited cravings of the drug addict-motivated mental states.

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Commentary on The New Neuropsychology of Sleep

I have already mentioned that the psychosurgical
procedure of prefrontal leucotomy targeted this system. On this basis, it has long been suggested that
the therapeutic benefit of prefrontal leucotomy was
attributable to the amotivational state that such lesions
produce (Panksepp, 1985); these patients simply lost
interest in the world, and all the excitement that fueled
their psychiatric symptoms was lost along with it. The
link between cessation of dreaming and improvement
of positive psychotic symptoms will therefore also be
of interest to psychoanalysts, in view of the theoretical
parallels that Freud always drew between dreams and
mental illness.
Modern psychopharmacological treatments of
schizophrenia target the "curiosity-interest-expectancy" system, too, no less than the old psychosurgical
approaches did. Antipsychotic medications are dopamine blockers, and they are thought to act on precisely
the pathway that was described above (Role and Kelly,
1991). This coincidence has even lead some authors
to suggest that antipsychotic medications are merely
"chemical leucotomies" (Breggin, 1980). This view
would certainly be consistent with the view that the
primary therapeutic effect of these medications is a
reduction of interactive interest in the world (Lehmann
and Hanrahan, 1954). One might therefore expect that
drugs which excite the dopaminergic motivational systems of the brain would artificially stimulate psychotic
symptoms and dreaming. This is precisely what drugs
which have an excitatory action on this system do:
L-dopa, cocaine, and amphetamine intoxication, for
example, all induce psychotic symptoms, together with
excessively vivid dreaming and nightmares. Again, the
increased frequency and vivacity of dreaming is not
associated with similarly increased REM frequency
and density (Hartmann, Russ, Oldfield, Falke, and
Skoff, 1980). This putative causal link between dopaminergic activity and dreaming is further supported by
the fact that excessive dreaming (and other psychotic
symptoms) can be successfully treated by the administration of dopamine blockers.
What all of this provides, I think, is a firm base
of evidence for the conclusion that this pathway, the
dopaminergic pathway in the ventromesial frontal region (this motivational system of the brain, the appetitive interest command system) is involved causally in
the instigation of dreams and dreamlike mentation. So
here we have a specific relationship between dreaming
and a brain mechanism which coincides quite closely
with the fundamental hypothesis of Freud's dream theory: namely that dreaming is generated under the direct influence of a highly motivated, wishful state of

mind. More about that later. For now, I would like to
ask Professor Hobson my third question: What does
he make of the causal relationship that appears to
exist between mesocortical-mesolimbic dopaminergic
stimulation and dreaming and dreamlike mentation?
This leads to another digression. There is something that always puzzled me about the cholinergic
hypothesis of dreaming. As I have said already, I do
not dispute the mass of evidence that Hobson has presented in support of his cholinergic hypothesis of REM
activation, but there is something that does not add up
about the cholinergic hypothesis of dream activation.
I mentioned earlier that increased cortical acetylcholine in waking mental life produces an increasedfocusing of mental powers. One of the reasons why people
like to smoke, for example, is because smoking improves concentration and sharpens selective attention-an effect which is mediated by acetylcholine via
nicotinic receptors. But according to Hobson's hypothesis, excitation of cholinergic neurons should induce dreamlike mentation in waking cognition. It
certainly does not do that; if anything it does the very
opposite. It is drugs with the opposite action---anticholinergic agents-which induce dreamlike states in
waking life. That is what has puzzled me: I can't understand why forebrain cholinergic activation during
sleep leads to dreaming whereas in waking life it has
the opposite effect. This, then, is my fourth question:
I would be interested to know how Hobson accounts
for this disparity between the effects on waking and
sleeping mentation of cholinergic activation.
What I make of it is that either pontine cholinergic activation (or aminergic deactivation) has an inhibitory effect on forebrain cholinergic activity (which is
certainly not what Hobson has hypothesized, but see
below) or some intermediate link between the cholinergic activation and the mental effect is
needed-something that intervenes between the cholinergic activation and the REM dream state. This intermediate mechanism would account for the mental
characteristics of the REM state, since they cannot be
accounted for by cholinergic activation itself. I am
proposing that this intermediate link is provided by the
dopaminergic mechanism described above.
That dopaminergic mechanism does not have an
exclusive relationship with REM; it can eq\lally be
triggered by other arousal stimuli. REM is just one of
the many things that is apt to arouse the interest of
the dopaminergic appetitive systems; other things
which have the same effect are the various sources
of non-REM arousal discussed above: the relatively
aroused state of sleep onset, the relative arousal of

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late-morning sleep, the various stimulant drugs, and
the complex partial seizures.
My proposal, therefore, is this: dreaming can occur as a result of anything that arouses the sleeper,
but only if the arousal stimulus in question attracts
appetitive interest. In other words, anything that excites the motivational systems of the forebrain and
thereby initiates a goal-directed intention-which is
by definition incompatible with the state of sleep----ean
stimulate the dream process proper. The final common
path leading from all these various different types of
arousal (sleep onset, stimulant drugs, REM, seizures,
late-morning effect, etc.) to dreaming is the dopaminergic "curiosity-interest-expectancy" system in the
ventromesial quadrant of the frontal lobes. The final
common path from all of these things to dreaming is
the excitement ofappetitive interest. If appetitive interest is stimulated, then dreaming can occur; if it is not
then dreaming does not occur. That is why dreams
cannot occur (despite the persistence of normal REM)
when this pathway is bilaterally damaged.
This is my main point. Before I close, however,
there are two other questions I want to ask Professor
Hobson. He spoke about censorship and he spoke
about the function of dreams. I will quickly address
each of these issues in turn.
First, if I may transgress for a moment the restrictions I imposed earlier on my own discussion of
Freudian dream theory, I would like to correct Hobson's reading of that theory on one small point. In
Freud's dream theory, the bizarreness of the dream is
not attributable to censorship alone; in fact, it is attributed to two different factors which act in combination.
The first factor is what Freud (1900) described as the
decathexis (i.e., deactivation) during sleep of the motor and perceptual systems of the ego-the withdrawal
of the ego from reality into the narcissistic state of
sleep. This represents a massive weakening of the ego
(the executive system of the mind), resulting in a regression to primary-process activity, which is what
dominates in sleep (and especially in dreaming): the
displacements, condensations, regression, and so on,
which are so characteristic of dreams. These are positive symptoms of a relative shift in the dynamics of
the mind, a weakening of the ego in favor of the ide
The withdrawal from contact with reality is a withdrawal from the fundamental principle that determines
the ego's domination of waking mental life-the reality principle. Taking account of reality is what the ego
is for. Once that function is relinquished, there is a
release from inhibition of the other great principle of
mental life-the pleasure principle-and the feeble

Mark Solms
ego is thenceforth dominated by the wishful type of
thinking that governs the id: "I want it, I want it now,
therefore I have it now." This type of thinking, which
does not recognize the constraints of reality, accounts
for a good deal of what might be called the bizarreness
(the irrationality and so on) of dreaming-and it does
so quite independently of the censorship.
The hypothesis of censorship states that something more happens, in addition to the irrationality that
flows naturally from the type of thinking that is released from the constraints of the reality principle.
Some of the wishes that are activated and hallucinatorily gratified in dreams under the influence of the pleasure principle cause great anxiety to the ego (the
enfeebled sleeping ego). That is why the ego censors
those wishes. Censorship is a very crude, rough-andready way of rendering the wishful hallucinations generated under the influence of the id tolerable to the
sleeping ego. It simply chops them up and changes
them about in order to make them more acceptable to
itself. This too, like the dream as a whole, ultimately
serves the purpose of sleep protection: that is
Freud's theory.
So in Freud's theory, censorship does not account
for the whole of the bizarreness of dreams. Much of
it is accounted for simply by the withdrawal of the
ego from reality; and this, I think, would seem to be
the equivalent of what Hobson described-his hypothetical demodulation by aminergic systems, i.e., the
depletion of cortical serotonin and noradrenaline, and
the resultant inactivation of the dorsolateral prefrontal
lobes (the executive' 'scene of action" of normal waking cognition) and other higher cortical structures. The
pattern of deactivation that is observed during sleep,
and accentuated during REM sleep (Braun et aI., 1997,
1998) would be more compatible with what is described in Freud's theory as the withdrawal of cathexis
from the reality-oriented perceptual and executive systems, than with the withdrawal of censorship.
We do not yet know what the specific neural correlates are of the mental functions that Freud described as censorship, but on the basis of our own,
initial clinico-anatomical observations (Solms, 1998),
we have at least been able to determine that ventromesial frontal cortex (the very cortex that the "curiosity--expectancy-interest" system projects onto) is
crucial for the maintenance of that function. The integrity of ventromesial frontal cortex, more than any
other region of the brain, seems to be necessary for
the function of executive inhibition, in other words,
for the broader function of which censorship is a special variety.

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Commentary on The New Neuropsychology of Sleep

For this reason, it is important to note that the
PET studies which Hobson used to support his argument that the "censoring" part of the brain is inactive
during sleep, actually report that ventromesial frontal
cortex is highly activated during REM sleep. So I think
that it is plausible to say that the available PET evidence is at least compatible with the Freudian "censorship" hypothesis, although I readily accept that it
does not by any means prove that hypothesis. Further
investigations-focused more specifically on this neuropsychological question-are obviously required.
But at this stage I would be interested to know what
Hobson's interpretation is of the ventromesial frontal
cortical activation that Braun and others have observed during REM sleep. That is my fifth question.
As for the function of dreaming, I'll just say this.
It may be true that the function of dreaming is memory
consolidation. It may be that this is the function of
dreaming, but it may also be true that it is not; and it
may equally be that the function of dreaming is just
what Freud said it was-the protection of sleep. The
important point at this stage, I think, is that we need
to differentiate between the function of REM sleep
and the function of dreaming. They are not the same
thing. The REM state triggers the dream state, but
dreaming can also be triggered by many other things.
So understanding the function of REM sleep is something separate from understanding the function of
dreaming. The time has now come for us to study the
function of dreaming directly. We have not done this
in the past, and as a result, the effects of dream deprivation have always been conflated with the effects of
REM deprivation and those of sleep deprivation.
I'll give an example of the sort of research I have
in mind. We know that cortical lesions in the PTO
junction of either hemisphere lead to a cessation of
dreaming with preservation of REM sleep. Likewise,
bilateral ventromesial frontal white matter lesions are
associated with cessation of dreaming and preserved
REM sleep. So if we want to understand something
about the function of dreaming, as opposed to the
function of REM sleep, we should focus our efforts
on a study of these two groups of patients. Here we
have the possibility of performing a critical test of any
hypothesis concerning the function of dreaming-the
sleep protection hypothesis included.
If dreams protect sleep then the sleep of patients
who are unable to dream due to brain lesions (but who
nevertheless have intact REM sleep) should be more
disturbed; they should have more frequent awakenings
and they should have quantitatively less sleep than
neurological patients who are able to dream. That

would be a simple, controlled study of one of the central hypotheses of the whole Freudian dream theory.
This is the sort of experiment that really needs to be
done, as I think Hobson was suggesting, if we want
to take psychoanalysis forward into the twenty-first
century. And here is an opportunity to do so. I hope
I have made myself clear. The important point is that
hypotheses like this can now be tested (neuropsychologically) and I do not believe they have been adequately tested before. So this is my final question to
Professor Hobson: Does he not agree, in view of the
conflation in the past of the REM state with dreaming,
that the sleep protection theory of dreaming has not
yet been adequately tested?
I want to conclude by describing an alternative
to Hobson's model of how the dreaming brain works.
It is this: there is an ongoing thought process in sleep.
During this process, something happens which arouses
the sleeper. This might be due to the thought process
itself, or it might be due to an external stimulus, or it
might be due to REM, or to something else. This activates the sleeping brain and threatens to awaken the
sleeper. Then, if and only if the arousal stimulus attracts appetitive interest-if it excites the dopaminergic "seeking"
system of the ventromesial
forebrain-then the dream proper begins. Appetitive
interest normally instigates goal-directed activity
which terminates in a motivated act. But this outcome
is incompatible with the maintenance of sleep. This,
perhaps, is why the executive systems of the
brain-together with spinal motor systems-are deactivated during sleep. As a result of these systems being
unavailable for action, the emotion and memory systems (which have been activated by the appetitive interest) prime the perceptual systems to the point of
hallucination. Instead of motor action, a regressive
hallucinatory process occurs; and that is the basis of
the dreamwork proper. From the ventromesial frontal
motivational systems there is a regressive activation
of, first of all, the emotional and episodic memory
systems of the mesial temporal lobe, then, second, the
associative semantic processing and spatial representational systems of the PTO junction; and then, finally,
backwards from there onto unimodal visual systems
in the ventral occipitotemporal region (which represents the conscious visual experience of the manifest
dream). This hallucinatory experience is mistaken for
a real event, due to the inactivation of dorsolateral
frontal reflexive systems, but not only because of that.
This leads to a last point, which I have touched
on once already. Another reason why the hallucinatory
experience of the dream is uncritically accepted as a

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real event is perhaps because the basal forebrain nuclei are actively inhibited during dreaming sleep. I
suspect that this could be the specific effect of ascending pontine cholinergic activation during REM: it
inhibits the cholinergic basal forebrain. I have been
led to this suspicion by a curious finding. Lesions of
the basal forebrain-affecting, for example, the nucleus basalis of Meynert, the septal nuclei, and so on
(caused, for example, by aneurysmal rupture of the
anterior communicating artery)-provoke dreamlike
states in which the patient is unable to distinguish
thoughts from reality (Solms, 1997). In many respects,
these states are highly reminiscent of the effects of
anticholinergic medication. So lesions in the (cholinergic) basal forebrain nuclei, anticholinergic medication, and REM sleep all have the same consequence:
inability to distinguish between fantasy and reality
(once more, the very opposite of what one would expect on the basis of the activation-synthesis model).
That is why I believe that inhibition of the cholinergic
basal forebrain during REM sleep may be another reason why the sleeping ego mistakes dreams for real
So that is what I think happens in the dreaming
brain, based on the evidence that has emerged over
the last few years about the forebrain ~echanisms of
dreaming. And these are some of the main reasons
why I cannot accept Hobson's critique of the Freudian
dream theory. I think Freud's understanding of the
mental processes underlying the manifest dream are
as viable today as they ever were-perhaps even more
viable, scientifically, than they were before. I think we
are on the threshold of an exciting new era in dream
science, in which the neuropsychological mechanisms
of dreaming are finally going to be laid bare, and I for
one will not be at all surprised if we find that Freud's
understanding of those mechanisms was basically on
the right track all along.
I will close by restating my six questions to Professor Hobson:
1. How does he account for non-REM dreaming in
general and for the recurring anxiety dreams that
are associated with complex partial seizure disorders in particular?
2. How does he account for the demonstrable dissociation that exists between the REM state and dreaming, using the standard clinico-anatomical
paradigm of brain-behavior correlation?
3. What does he make of the causal relationship that
appears to exist between mesocortical-mesolimbic
dopaminergic stimulation and dreaming and
dreamlike mentation?

Mark Solms
4. I would be interested to know how he accounts
for the disparity between the effects of cholinergic
activation on waking and sleeping mentation.
5. I would like to know what his interpretation is of
the ventromesial frontal cortical activation that
Braun and others have observed during REM sleep.
6. Does he not agree, in view of the conflation in the
past of the REM state and dreaming, that the sleep
protection theory of dreaming has not yet been adequately tested?
I would like to thank Professor Hobson most sincerely for his willingness to participate in this dialogue.

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Mark Solms
Academic Department of Neurosurgery
Royal London Hospital
London E1 1BB, United Kingdom
e-mail: mlsolms@mds.qmw.ac.uk