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J. Allan Hobson and Edward Pace-Schotts Response:

Commentary by Mark Solms (London)
a

Mark Solms
a

Academic Department of Neurosurgery, 4th Floor, Alexandra Wing, Royal London

Hospital, London E1 1BB, England, e-mail:
Published online: 09 Jan 2014.

To cite this article: Mark Solms (2000) J. Allan Hobson and Edward Pace-Schotts Response: Commentary by Mark Solms
(London), Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences, 2:2, 193-201, DOI:
10.1080/15294145.2000.10773305
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193

ONGOING DISCUSSION

J. Allan Hobson and Edward Pace-Schott's Response

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Commentary by Mark Solms (London)

I will respond here to the major points made by Braun

and Reiser and Hobson and Pace-Schott regarding my
commentary on Hobson's target paper (1999). I will
start with some general issues before moving on to
more specific ones.

The Ghost of Freud

Both Reiser (1999) and Braun (1999) lament Hobson's
and my preoccupation with "whether or not Freud
was right"; they argue that "perhaps Freud need not
be the central issue any longer" (Braun, 1999, p. 200).
Certainly, I agree that Freud need not be the central
issue any longer for modern scientists seeking to understand the brain mechanisms of dreaming. I accept
too that the narrow question, Was Freud right?, places
unnecessary constraints on fresh theoretical possibilities. However, Hobson was specifically asked by the
editors of Neuro-Psychoanalysis to comment on the
implications for psychoanalysis of recent developments in the neuroscientific understanding of dreams.
We were interested in Hobson's views on this issue
for the reason that his earlier research findings with
respect to the brainstem mechanisms of dreaming were
widely interpreted as disproving Freud's dream theory
(including by Hobson himself; e.g., Hobson and
McCarley, 1977; Hobson, 1988). If recent findings in
neuroscience have now cast doubt on the validity of
Hobson's earlier findings, then it is necessary, and
only fair, for us to reevaluate his criticisms of Freud
in the light of the new data. Naturally, in other contexts (in a journal dealing only with neuroscience, for
example) it would be less appropriate for our discusMark Solms is Lecturer, Department of Psychology, University College, London; Hon. Lecturer, Academic Department of Neurosurgery, St.
Bartholomew's and Royal London School of Medicine; Associate Member
of the British Psycho-Analytical Society.

sion to revolve around Freud's dream theory (cf.

Solms, in press, a; Hobson, 2000).
As Hobson has always appreciated (e.g., McCarley and Hobson, 1977) the pivotal place that Freud's
dream theory occupies in relation to psychoanalytic
theory as a whole makes it a matter of no small importance for psychoanalysts whether or not his dream theory incorporated significant errors. Any new evidence
that calls for a major revision of Freudian dream theory would probably necessitate a radical reappraisal
of Freud's conceptualization of the functional organization of the mind as a whole. Since Freud's basic
concepts continue to inform contemporary psychoanalysis in a fundamental way, the question as to
whether or not they remain scientifically tenable cannot, in all conscience, be ignored.
I hope it goes without saying that our responsibility to reevaluate Freudian dream theory in light of the
new evidence is not synonymous with attempting to
"rescue [it] by retrofitting it onto new data" (Hobson
and Pace-Schott, 1999, p. 208). We do psychoanalysis
no favors by insulating it from scientific progress. A
central purpose behind the neuro-psychoanalytic endeavor is to discover the neural correlates of our basic
psychoanalytic concepts, so that we might open
Freudian metapsychology to all the benefits that modern neuroscientific research methods can provide
(Solms, 1997b, 1998b, 1999; Kaplan-Solms and
Solms, in press, a). It is quite apparent, I think, that
metapsychology has begun to reach its limits. Insofar
as it relies exclusively on the psychoanalytic method,
we need new ways of advancing our basic psychoanalytic models-of deciding between rival points of
view, clarifying obscure questions, getting beyond impasses-and modern neuroscientific methods provide
an array of powerful tools for doing just that. But
before we can subject psychoanalytic concepts to neuroscientific scrutiny we need to determine the physical
correlates of those concepts; to do otherwise is to risk

194

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testing apples by measuring pears (Solms and Nersessian, 1999). That is one major reason why it is useful
for us to attempt to translate Freud's functional models
into modern neuroscientific terms. Establishing correlations of this kind is no armchair affair; it is a complicated empirical task that requires the development of
appropriate interdisciplinary methods (Kaplan-Solms
and Solms, 2000; Solms, 1998b, 1999). In the process
of establishing these correlations, it should come as no
surprise that some aspects of Freud's psychoanalytic
models cannot be reconciled with our unfolding
knowledge of the functional organization of the brain.
That is precisely how weak points in the models can
be exposed.

Censorship-Disguise
In Freud's dream theory, the function of "censorship"
is a case in point. While the bulk of Freud's dream
theory seems readily reconcilable with our understanding of the neuropsychological mechanisms involved (Solms, 1997a), the neuroscientific data do not
seem to require the hypothesis of an active distorting
agency. Braun and Hobson and Pace-Schott have accordingly suggested that the bizarre quality of REM
dream imagery and cognition might be explained more
simply as being a consequence of the release of limbic
and posterior cortical (affective, mnestic, and perceptual) mechanisms from the constraining influence that
dorsolateral prefrontal (executive) mechanisms normally impose on them. In this view, translated into
Freud's terminology, the bizarre quality of dreams
(and the forgetting of dreams) would be solely attributable to the release of the sleeping ego from the reality
principle and secondary process constraints.
This certainly seems plausible, and it is therefore
a possibility that we must seriously entertain. What
it seems to suggest (among other things) is that the
activation of a particular memory-motive network at
the limbic level might generate underconstrained perceptual imagery at the posterior neocortical level,
without the active intervention of a distorting agency
between the two levels. (I fail to see, incidentally, how
this possibility does away with the distinction between
latent and manifest content, as Braun and Hobson and
Pace-Schott seem to believe it does.)
This hypothesis is probably only directly testable
by psychoanalytic methods, and I would like to invite
our analytic readers to contribute data (in the form of
dream reports together with associations) that might
help us to decide the issue. Does the transformational

Mark Solms
process between the (reconstructed) late::.lt dream
thought and the manifest dream content merely involve an inadequately constrained representational
mechanism or does it seem to require the additional
hypothesis of an active, tendentious censorship mechanism? This question probably cannot be answered
conclusively by the psychoanalytic method alone, primarily due to the interpretational vagaries of reconstruction. But the question can also be addressed
indirectly by clinicoanatomical methods. I have previously observed that the functions traditionally attributed to Freud's "censorship" (among other things) are
profoundly disrupted by damage in the ventromesial
frontal quadrant of the forebrain (Kaplan-Solms and
Solms, 1996, 2000; Solms, 1998a). This implicates
ventromesial frontal cortex (including anterior cingulate gyrus), some basal forebrain nuclei, and possibly
some components of the thalamus and basal ganglia-all of which are known to be involved in selective attentional and other gating functions-in the
censorship function. (I do not see why Braun and Hobson and Pace-Schott have difficulty in distinguishing
between these structures and the mesocortical-mesolimbic dopaminergic fibers that project onto them and
serve an entirely different function.) Since these structures seem to be highly activated during dreaming
sleep (at least during REM dreams), I have suggested
they might yet turn out to be the anatomical correlate
of Freud's censorship functions (or rather, an important component in the network of structures that
would subserve that complex function).
A theoretical caveat is required here: Braun
seems to believe that the cerebral tissues subserving a
censorship function should be more activated during
sleep (or during REM sleep) than during waking. The
opposite is in fact the case (I am grateful to Calvin
Yu for pointing this misunderstanding out to me). Although the censorship function in Freud's dream theory remains active during sleep, it is nevertheless
relatively weakened (Freud, 1917, p. 225: "we have
every reason to suppose that in sleep the censorship
between the Pes. and the Ues. is greatly reduced, so
that communication between the two systems is made
easier"). This relative weakening might well correlate
with the observed inactivation of the dorsolateral prefrontal convexity and other frontal structures (e.g., orbital cortex).
I have observed and reported elsewhere (Solms,
1997a), that damage to the ventromesial frontal structures mentioned above produces a striking syndrome
characterized by excessively frequent and intense
dreaming, and a breakdown of the distinction between

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Ongoing Discussion: J. Allan Hobson and E. Pace-Schott

thought and reality. This observation is consistent with
the possibility that these structures contribute to the
(residual) censorship function hypothesized by Freud.
On this basis, two predictions might be made, which
I would like readers with access to suitable clinicoanatomical material to test. (1) The dreams of patients
with lesions in the structures mentioned above should
be less distorted; that is, more self-evidently wish fulfilling (childishly, ruthlessly, instinctually driven),
than those of controls. (2) With reference to the phenomena that Freud sometimes attributed to the "failure" of censorship, we may predict that these patients
should also have more nightmares (and perhaps more
awakenings or microawakenings) than controls.
I hope that these suggestions will be taken up so
that we might bring some appropriate empirical data
to bear on Braun's and Hobson and Pace-Schott's belief that it is no longer necessary for us to postulate a
"censorship" function to account for dream distortion.

Forebrain and Brainstem

Hobson and Pace-Schott consider it necessary to ask
rhetorically whether the forebrain is ever free of the
brainstem, and to opine that my "effort to liberate the
forebrain from the brainstem [is] ill-advised, misguided, and doomed to failure" (p. 217). Braun, for
his part, is also puzzled by my effort to "liberate the
dream process from brainstem mechanisms" (p. 196),
especially in view of the fact that the source cells of
the dopaminergic system (which I suggest is the instigator of dreaming) are brainstem neurons. This is all
the more puzzling to Braun in light of the fact that
Hobson now "seems ready to acknowledge a rather
more complicated participation of forebrain mechanisms in dream generation-not simply a senseless
secondary response to chaotic brainstem events" (p.
196).
I have obviously not made my argument clear
enough on this score. There are two issues. First, of
course, I do not believe that the forebrain is ever
"free" of the brainstem. But the mere fact of this
obligatory and necessary coupling does not mean that
primary forebrain events are driven by primary brainstem events, which is what Hobson still seems to claim
with respect to dreams (see later). I accept that dreaming (a state of consciousness) is impossible to generate
without a certain degree of activation, which is usually
provided by consciousness-supporting core brainstem
structures (Damasio, 1999). But the same applies to

195

any state of consciousness. The coupling of forebrain

and brainstem therefore merely provides the background context necessary for all forms of conscious
experience; it tells us nothing about dreaming in particular. What I am claiming is the following:
1. The specific (cholinergic/aminergic) brainstem
mechanism that generates REM sleep is neither
necessary nor sufficient for dream generation.
Dreaming can also be instigated against a background of other (non-REM) consciousness supporting mechanisms.
2. In contrast to the various, nonspecific consciousness supporting mechanisms, none of which has a
unique relationship with dreaming, a mechanism
exists in the ventromesial quadrant of the anterior
forebrain which does appear to be uniquely necessary for dreaming. (If this mechanism is damaged,
dreaming stops completely, although consciousness
in general is preserved.)
3. Whatever this ventromesial forebrain mechanism
might be, and wherever its source cells might lie,
we know for certain that it can be activated' 'from
above." This has been empirically demonstrated in
the case of the focal forebrain events of complex
partial seizure activity, which can directly cause
complex dreams (nightmares) during non-REM
sleep. Normal equivalents may be inferred. In other
words, unlike what Hobson claims for the mechanism that drives REM sleep, the dream-generating
mechanism is not driven exclusively by the
brainstem.
4. On the basis of converging lines of evidence
(Solms, in press, a), I have suggested that the most
likely candidate for this dream-generating mechanism is the dopaminergic "SEEKING" system of
Panksepp (1998), which has its source cells in the
upper brainstem (rostral VTA, in a transitional zone
between mesencephalon and diencephalon), and
has reciprocal interconnections with a wide range
of forebrain structures (e.g., nucleus accumbens,
anterior cingulate gyrus, frontal cortex, amygdala).
5. What is crucial about this mechanism in the present
context is not the fact that it is located primarily
(although certainly not exclusively) in the forebrain, but rather (a) that its activity is independent
of the brainstem REM generator (indeed, its activity appears to be independent of the sleep cycle as
a whole) and (b) that it mediates motivational and
emotional states and is readily engaged by higher
mental processes (i.e., that it is not driven by
"senseless" and "chaotic" events).

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196
The implication of all this for psychoanalysis is
that statements to the effect that the causal stimuli for
dreaming arise "from the brainstem and not in the
cognitive areas of the cerebrum" (Hobson and
McCarley, 1977, p. 1347) and that the dream process
has "no primary ideational, volitional, or emotional
content," and that dreams are driven by "motivationally neutral" mechanisms (McCarley and Hobson,
1977, p. 1219) are no longer empirically supportable.
These are the viewpoints that Braun believes Hobson
has now abandoned.
This leads to the second point. I can see why
Braun gained the impression that Hobson no longer
believes that dreaming is simply "a secondary attempt
to 'synthesize', i.e., to create order out of its regular
but chaotic activation by the [brainstem]" and that he
now "seems to acknowledge a rather more complicated participation of forebrain mechanisms in dream
generation" (p. 196). I too gained the impression at
some points that "Hobson now suggests that salient
memories and emotions serve as the primary shaper
of dream plots rather than playing a secondary role"
(p. 196); but on closer reading it becomes apparent
that Hobson's viewpoint is highly ambivalent (to say
the least) in this respect. For example, in his target
article he still defines the causal mechanism of dreaming as follows:
Dreaming is a state of consciousness arising from the
activation of the brain in REM sleep. The brain activation which underlies dreaming is, like that of waking,
a result of the excitation of forebrain circuits by impulses arising in the ascending activation systems of
the brainstem (e.g., pontine and midbrain reticular
activating systems) and basal forebrain (e.g., cholinergic Nucleus Basalis of Meynert). This activation process prepares the forebrain to process data with
associated cognitive awareness.... The mechanism
of the brainstem triggering of forebrain activation involves the spontaneous excitation of cholinergic neurons in the pontomesencephalic LOT and PPT nuclei
[po 171].

And with respect to the psychological function

and "sense" of dreaming, Hobson still believes:
[D]reaming is epiphenomenal with respect to the most
fundamental biological adaptations of REM sleep....
[D]ream content might be quite irrelevant, telling us
only what a subject's mental state might be like if he
or she were to become delirious. In this sense, the
interpretation of dreams in terms of unconscious mo-

Mark Solms
tives would make about as much sense as interpreting
the ravings of an alcoholic in the throes of delirium
tremors or the demented ramblings of an Alzheimer's
disease victim [po 174].

I fear that Braun is perhaps being overoptimistic when

he concludes that' 'Hobson no longer dismisses dream
content as vacuous" (p. 196).

Dreaming versus REM Sleep

Many of the criticisms that Braun and Hobson and
Pace-Schott direct at my arguments are based on their
continual conflation of dreaming with REM sleep. For
example, Braun's appraisal of my dopamine hypothesis does not differentiate between dopaminergic influences on REM and dopaminergic influences on
dreaming. Hobson and Pace-Schott's review of the
pharmacological literature fails to distinguish between
indirect (REM-mediated) effects of drugs and direct
(REM-independent) effects of drugs on dreaming. I
placed the emphasis on the acute effects of L-DOPA
in normal subjects precisely because (to my knowledge) no other drug has been shown to increase dream
prevalence and intensity without having any simultaneous effects on REM frequency, duration, and density (Hartmann, Russ, Oldfield, Falke, and Skoff,
1980). Likewise, I was especially interested in the PET
study of Heiss, Pawlik, Herholz, Wagner, and Wienhard (1985) because it was the only such study that
compared dreaming and nondreaming sleep rather
than REM and NREM sleep. Great caution must be

exercised when interpreting the results of studies that

do not distinguish between direct dream effects and
indirect REM effects.
Rather than detail all the instances where Braun
and Hobson and Pace-Schott have made this conceptual error, I would ask the reader to consider this complication wherever they feel a telling argument has
been raised against me. Before reaching an independent conclusion, ask the question: Does the argument
rest on evidence about REM sleep or does it concern
dreaming per se? This distinction is absolutely critical.
I suspect that Braun and Hobson and Pace-Schott's
conflation of these two things in their critiques of my
arguments reflects the fact that they still do really believe (explicitly or implicitly) that dreaming and REM
sleep are one and the same thing. The erroneous assumption that dreaming sleep is synonymous with
REM sleep has gravely distorted neuroscientific theorizing about the brain mechanisms of dreaming for

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Ongoing Discussion: J. Allan Hobson and E. Pace-Schott

more than 30 years. There is no excuse for perpetuating it any longer.
I think that Braun misunderstands and underestimates the evidence with respect to NREM dreaming.
Nobody seriously claims that REM dreams and
NREM dreams are "statistically indistinguishable"
(p. 196). Only some NREM dreams are indistinguishable from REM dreams; the average NREM dream is
distinguishable from the average REM dream. But the
fact that some NREM dreams are indistinguishable
from REM dreams is not under dispute. Braun is
wrong to suggest that this claim might be due to methodological errors. Even Hobson accepts that 5 to 10%
of NREM dreams' 'are indistinguishable by any criterion from REM dreams" (Hobson, 1988, p. 143). Correcting for the fact that NREM sleep occupies 75% of
total'sleep time, what this means is that 15 to 30% of
all dreams are generated by NREM mechanisms. For
this reason alone, the view simply can no longer be
sustained that dreams are generated by the unique
physiological properties of the REM state.
Braun avers that "the fact that the overwhelming
majority of dreams do occur during REM cannot be
ignored" (p. 197). Hobson and Pace-Schott go further
and claim that "since REM provides the most favorable physiology for dreaming, its physiology is the
most relevant set of neurobiological data available
with which to understand dreaming" (p. 210). This is
faulty reasoning. Would they not accept that although
the overwhelming majority of babies cry when they
are hungry, and the state of hunger therefore provides
the most favorable physiological conditions for crying
in babies, data about the physiological mechanism of
hunger do not help us to understand the physiological
mechanism of crying? The fact that hungerlike crying
(' 'indistinguishable by any criterion" from hungry
crying) can also occur independently of the state of
hunger suffices to prove that these two phenomena-hunger and crying (and their underlying physiological mechanisms)-are distinct states, no matter
how often they may occur together.

Detailed Issues
I will deal with the remaining issues in the order that
they were raised in Braun's commentary and Hobson
and Pace-Schott's response. I have no remaining disagreements with Reiser's commentary.
1. While I agree that there is, as Braun argues,
"a conceptual overlap between Hobson's 'emotional
salience,' and Solms's motivated mental state' " (as

197

drivers of dream narratives) I would like to point out

that among the various basic emotional command systems that have been delineated in the human brain
(Panksepp, 1998) only the motivational SEEKING
system appears to be necessary for the generation of
dream narratives. Cessation of dreaming has never
been demonstrated with damage to the brain structures
subserving any of the other basic emotions.
2. Braun says that limbic processes are "unbridled" during sleep rather than disinhibited (p. 199).
There is no real disagreement here. I did not mean to
imply that limbic processes are literally disinhibited
in the neurophysiological sense by decreased dorsolateral frontal activation. I meant only what Braun himself accepts: that the' 'reality principle" is suspended
in favor of the "pleasure principle" and that this entails a functional' 'regression" (p. 199).
3. Braun asks "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?" Once again, there are two
issues here. First, Braun is right to suggest (as he does
by implication) that the experimental test of the sleepprotection hypothesis that I proposed in my commentary should by rights be limited to a comparison between the sleep patterns of PTO nondreamers and
dreamers. The bifrontal group does present additional
complications of the kind that Braun mentions. However (and this is the second issue), I should point out
that the SEEKING system is not the source of the
nocturnal "demands made upon the mind for work"
that disturb sleep; rather the SEEKING system is itself
activated by such demands. (Incidentally, I do not see
why Braun considers the question as to whether
dreams protect sleep or not as being "trivial, and of
interest only in a historical context" (p. 200). The
function of dreaming is, after all, still quite unknown.
I would like to say that I found Braun's commentary
to be well-informed, fair and reasonable throughout.
I want to thank him most sincerely for the careful
thought that he gave to this difficult interdisciplinary
dialogue.
I was disappointed that Hobson and Pace-Schott,
in their highly polemical response to the commentaries, chose not to answer some of the direct questions
that I asked Hobson. By ignoring some of the central
issues raised by Braun, too, they have deprived us
of an opportunity to resolve outstanding controversial
issues. Hobson and Pace-Schott, in turn, have raised
many questions of their own for psychoanalysis. I
hope that readers will take up these questions in the
course of this ongoing discussion. I myself will re-

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198

spond only to those questions that Hobson and PaceSchott directed at my own research and commentary.
1. Hobson's claim that "all you need to produce
dreamlike mentation" is brainstem activation plus
brainstem gating of input-output channels (p. 210) is
unsustainable in the light of some of the evidence I
summarized in my commentary. How can this claim
be reconciled with the fact that discrete lesions of
specific forebrain systems, which affect neither brainstem activation nor brainstem gating of sensorimotor
channels, obliterate dreaming? Also, if brainstem activation and input/output gating is all you need for
dreaming, then why is it so easy to demonstrate that
these two things can occur in the absence of dreaming?
Clearly the most essential "ingredient" for dreaming
lies elsewhere.
2. I have dealt elsewhere (Solms, in press, b)
with Nielsen's arguments--cited by Hobson and PaceSchott (p. 210)-to the effect that NREM dreams are
in fact "phantom REM" dreams. Rather than repeat
my criticisms of the phantom REM concept, the interested reader is referred to the detailed discussion of
this concept (by myself and others) that will appear
very shortly in a special issue of the journal Behavioral and Brain Sciences (BBS) devoted to current
controversies in sleep and dream science.
3. This also gives me an opportunity to respond
to Hobson and Pace-Schott's astonishing claim that I
have not subjected my dream research findings to peer
review. As Hobson well knows, since he has written
a commentary on it, a paper setting out my main findings was accepted for publication many months ago in
the above-mentioned issue of BBS-a highly respected
journal with the most stringent peer review procedures
(Solms, in press, a). As Hobson and Pace-Schott also
must surely realize, my 1997 book was published in
a peer reviewed behavioral neuroscience monograph
series. No academic publisher nowadays would publish a specialist neuroscientific text like mine without
first subjecting it to peer review. The reason why I
published my findings in monograph form (rather than
break them up into a series of journal articles) was
not to avoid peer review, but rather to do justice to
the scope and complexity of the clinicoanatomical
data that needed to be presented, analyzed, and digested by the reader. Hobson and Pace-Schott seemed
to appreciate all this when they reviewed my book in
1998 (quite favorably, I thought) in the journal Trends
in Cognitive Science. Readers who are not familiar
with my book should also be made aware that almost
all the observations I reported there have been replicated by other investigators, who independently de-

Mark Solms

scribed precisely the same phenomena (Solms, 1997a,

pp. 4-70). Hobson and Pace-Schott know all of this
very well. Their insinuation now that I am trying to
hide something by "side-stepping peer review" (p.
214) is therefore unfair and totally uncalled
for.
4. More appropriately and pertinently, elsewhere
in their response Hobson and Pace-Schott accept that
the crucial observations I reported in my 1997 monograph were "real and robust" (p. 212) but go on to
dispute my interpretation of those observations. First,
they point out that not all patients with deep bifrontal
lesions report global cessation of dreaming, that some
report less extensive attenuation of their dreams, and
that some recover. There is nothing unusual about any
of this. The same applies to all clinicoanatomical correlations, including the most well established. Such
variations are normally attributed to variability in the
lesion site and type and individual differences in functional anatomy (Kertesz, 1983; Damasio and Geschwind, 1985; Frederiks, 1985; Damasio and Damasio,
1989). Second, Hobson and Pace-Schott "vonder
whether the deficits in dream recall associated with
modified prefrontal leucotomy in schizophrenics
might not be at least partly attributable to the' 'weakening of cognitive capacity in chronic schizophrenics"
(p. 212). This is plausible but unsustainable as a criticism of the basic correlation in question for the reason
that the same phenomenon (cessation of dreaming)
has been observed in nonschizophrenic patients with
naturally occurring deep bifrontal lesions (Solms,
1997a). Third, Hobson suggests that my clinical methodology might have distorted the reported phenomena.
This too is a fair question but fails to take account of
the fact that precisely the same correlations have been
observed using the alternative methods that Hobson
and Pace-Schott suggest (REM awakening, dream diary; see Solms, 1997a, for review). Fourth, Hobson
and Pace-Schott present detailed anatomical arguments against my conclusions; these are dealt with
below.
5. They assert that "interruptions of these deep
medial [frontal] fiber tracts must diminish the influence upon the medial forebrain of the pontomesencephalic [cholinergic] systems that we have
emphasized as well as the dopaminergic ones" (p.
212). Whilst this statement is theoretically plausible,
the empirical fact is that lesions to medial forebrain
cholinergic structures lead to increased dreaming and
dreamlike mentation, not less dreaming as Hobson's
theory would have predicted. This is consistent with
the fact that anticholinergic drugs increase dreaming

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Ongoing Discussion: J. Allan Hobson and E. Pace-Schott

and dreamlike states. It is therefore difficult to understand why Hobson and Pace-Schott believe that the
loss of dreaming associated with deep medial frontal
lesions might be due to diminution of cholinergic influences (unless they accept my suggestion that the
net effect of these influences might be inhibitory!). I
pointed these facts out in my commentary and specifically asked Hobson how he accounted for them, but
this is one of the questions that Hobson and PaceSchott chose to ignore in their response.
6. Hobson and Pace-Schott seem to question
whether the "key disconnection" (p. 213) by which
modified prefrontal leucotomy alleviated psychiatric
symptoms involved the mesocortical-mesolimbic dopamine circuits I referred to. I cannot follow their reasoning here. Do they not realize that' 'a circumscribed
lesion just anterior to the frontal horn of the [lateral]
ventricle, in the lower medial quadrant of the frontal
lobe" (Walsh, 1994, p. 177) produced equally good
results as those obtained by the more extensive (older)
Freeman and Watts (1942) procedure they refer to,
and that some of these more circumscribed operations
were explicitly aimed at sparing the thalamofrontal
radiation? In his excellent review of psychosurgery,
Sweet (1973) concluded that the crucial therapeutic
lesion site was "the white matter of the posteromedial
orbital cortex just below the head of the caudate nucleus."
7. Hobson and Pace-Schott consider it "highly
illogical to single out a non-sleep-regulatory dopaminergic brainstem region (i.e., the VTA) to be more
causal than other clearly sleep-related limbic and
brainstem nuclei in the generation of normal dreaming" (p. 213). This argument from logical premises
ignores my main empirical observation: dreaming
simply is sometimes generated independently of sleepregulating brainstem mechanisms.
8. Next they ask whether I assessed any of the
cognitive functions in my nondreaming patients
which, if impaired, could lead to a false negative result
with respect to dreaming; for example, they ask: did
patients continue to dream but not know they did so?
My answer: yes, I did assess these functions, as Hobson and Pace-Schott should know (Solms, 1997a).
9. Their dismissal of the entire clinicoanatomical
research method (and with it, 150 years of behavioral
neuroscience!) on the grounds that "brain lesions are
not physiological" hardly deserves a response. The
same applies to their assertion that interpretation of
losses of function following brain lesions is "problematic." The interpretation of all forms of data is problematic. That is why it is prudent to check conclusions

199

derived from one method against those derived from

other methods (as already mentioned, this is the basic
rationale behind the whole neuro-psychoanalytic enterprise). Few indeed of our long-standing interpretations of lesion data have been called into question
by the "physiological" findings of modern imaging
techniques. The same applies to the findings of these
two methods with respect to the brain mechanisms of
dreaming; Hobson himself described the results derived from these two methods as "remarkably complementary" (Hobson, 1999, pp. 165-166).
10. Citing the fact thattJIe firing rates of VTA
neurons in rats and cats do not covary with global
state changes in the sleep-waking cycle (' 'they fire at
their usual high, regular rate no matter what state the
animal is in' '), Hobson and Pace-Schott assert that it is
"far-fetched" to suggest that this motivational system
instigates dreams, because "the system is always
wishing" (p. 214). Hobson and Pace-Schott might
therefore be surprised to learn that this is just what
Freudian theory predicts! The "wishing" system is
indeed always active and only generates dreams (hallucinatory fulfillment of wishes) under certain dynamic conditions (affecting interactions between the
"wishing" system and other systems), such as those
that prevail during sleep and in certain pathological
states. Of course this implies that a full account of the
mechanics of dreaming requires detailed consideration
of the dynamic interplay between the "wishing" system and the other systems that normally damp and
constrain its influence on the mental economy. However, I fail to see how and why this "throws us back
on REM physiology" (p. 214). The simple fact that
Hobson and Pace-Schott consistently fail to grasp (or
accept) is that dreaming and REM sleep are empirically dissociable. It is therefore simply disproven that
REM sleep is the "dream initiator" that they are
seeking.
I, Like Hobson and Pace-Schott, welcome the
positive suggestions that Allan Braun made for testing
my dopamine hypothesis. However, unlike them, I do
not think it at all "farfetched" that we might eventually discover that "REM or an adventitious stimulus
teams up with dopaminergic discharge to produce the
wish that [instigates dreaming]" (p. 214).
11. I cannot respond here to every point that
Hobson and Pace-Schott made in their detailed survey
of the pharmacological literature. I shall limit myself
to just one or two general points. The first point I have
made already, namely that Hobson and Pace-Schott
consistently fail to distinguish between REM mediated
effects on dreaming and direct effects on dreaming

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200
(independent of REM effects). I do not doubt that the
brain's REM mechanism interacts with its dream
mechanism; how else could one account for the very
high correlation between REM sleep and dreaming?
(All that I dispute is that the REM mechanism is synonymous with the dream mechanism; REM sleep is
neither necessary nor sufficient to generate dreaming.)
I therefore do not doubt that anything that affects REM
will indirectly affect dreaming, just as anything that
affects the hunger level of a baby is likely to affect
the intensity and frequency of its crying. But just as
this does not imply that the causal mechanism of crying behavior should be sought in appetite regulation
centers, so too the causal mechanism of dreaming
should not be sought in sleep regulation centers. This
leads me to my second point: the mesocortical-mesolimbic dopamine systems are dynamically interlinked
with other neurotransmitter and neuromodulator systems. (Incidentally, Hobson and Pace-Schott write as
if all dopamine systems and all dopamine receptors
were equal, I should therefore remind the reader that
I am only making a claim for one component of one
particular dopamine system.) It is extremely difficult
to interpret the pharmacological evidence for a particular neurotransmitter system in isolation. I therefore
fully concur with Hobson and Pace-Schott's remark
to the effect that' 'a wide variety of drug-induced disruptions of normal modulatory balance may lead to
alterations in dreaming" (p. 216). But this does not
mean that one is justified in rejecting a claim for one
particular system simply by muddying the waters. The
scientific task is to attempt to isolate the contribution
that each single system makes. For this reason, the
pharmacological literature has to be reconciled with
other forms of data (including anatomical data) before
any reliable conclusions can be reached. It is on the
basis of precisely this-multiple, converging lines of
evidence-that I have based my claim of a specific
role for Panksepp's SEEKING system in dream generation.
12. I am surprised that Hobson-who, like
Freud, always drew a close analogy between dreaming
and psychosis-now warns us to distinguish "the
dream effects of psychosis or its incipient onset" and
"[normal] dream induction" (p. 215) when extrapolating from L-DOPA effects. Hobson and Pace-Schott
seem to believe that since the vivid dreams and nightmares induced by L-DOPA and other dopamine agonists are sometimes part of an incipient psychosis, they
are not "real" dreams. I take quite the opposite view:
the fact that both dreaming and psychosis are simultaneously kindled by dopamine agonists tends not only

Mark Solms
to confirm the view that they share a common mechanism but, moreover, that the common mechanism is
in some crucial respect dopaminergically mediated.
13. Hobson and Pace-Schott's comment about
the preponderance of negative affects in dreams (fearanxiety in particular) disregards everything we know
about the dynamics of anxiety. They also ignore the
fact that the amygdala is a major destination for mesolimbic dopamine fibers.
In closing, I would like to say that I suspect that
Allen Braun is right to conclude (at the end of his
commentary) that, despite appearances, Hobson and I
are approaching common ground. I am less convinced
that it is the ghost of Freud that is getting in the way.
Perhaps it is the ghosts of both the warring parties
that divided our two disciplines throughout the century
now passed. In other words, it is the ghost of Meynert
(and all the subsequent reductionist anti-Freudians),
no less than that of Freud, that is getting in the way
of progress. It is not easy to let go of century-old
suspicions and antagonisms. However, there is much
in Hobson's revised AIM model that I can agree
with-certainly a lot more than in his original activation-synthesis model. There is still more that I can
agree with in the "integrated model" that Hobson and
Pace-Schott present at the end of their response to the
commentaries. It is only to be expected that important
differences of opinion remain. However, I for one am
certainly prepared to submit these differences to the
test of dispassionate observation and experiment.
Of course I cannot speak on behalf of an entire
discipline, but it is my sincere impression that many
psychoanalysts look to this journal-and the interdisciplinary collaboration it represents-to show the way
forward for psychoanalytic metapsychology in the
twenty-first century. We fully expect that we shall
have to give up some cherished theoretical assumptions. But we cannot be expected to abandon
them-our hard-won maps of the inner workings of
the mind-unless and until we are presented with new
theories that do equal justice to the complexities of
our subject. We are very much in awe of what has
been achieved in the neurosciences over the past few
years. But we also have not forgotten the many false
starts and oversimplifications of the past, and the
many contemptuous dismissals of (and refusals to understand) our own painstaking efforts to unravel the
mysteries of human subjective life. If Allan Hobson
and his colleagues are now ready to open their minds
to the possibility that they have been mistaken with
regard to some crucial aspects of dream theory (as
Braun suggests they are) then we are certainly no less

Ongoing Discussion: J. Allan Hobson and E. Pace-Schott

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ready than he is. All that we ask for is mutual respect,

a degree of humility in the face of the complexity of
our subject, and a genuine commitment to accepting
the empirical facts no matter how unpalatable they
may be. Nobody likes to admit that they were mistaken, or wants to abandon a theoretical viewpoint
they have vociferously defended for decades. This
must surely apply to Hobson no less than it does to
psychoanalysts.
I hope that the remainder of this dialogue will be
conducted in such a spirit, and that the outstanding
problems and disagreements will be tackled one by
one over the course of a long and fruitful interchange.

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Mark Solms
Academic Department of Neurosurgery
4th Floor, Alexandra Wing
Royal London Hospital
London E1 1BB, England
e-mail: mlsolms@mds.qmw.ac.uk