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a
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
To link to this article: http://dx.doi.org/10.1080/15294145.2000.10773305
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ONGOING DISCUSSION
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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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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].
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].
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
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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
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(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
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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