13 J. Allan Hobson and Edward Pace-Schott’s Response: Commentary by Mark Solms (London)

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J. Allan Hobson and Edward Pace-Schotts Response:Commentary by Mark Solms (London)Mark Solms

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aAcademic 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:

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93

ONGOING DISCUSSION

Allan Hobson and

dward

Pace-Schott s Response

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

BothReiser (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 un

derstand the brain mechanisms

of

dreaming. I accept

too that the narrow question, Was Freud right?, places

unnecessary constraints on fresh theoretical possibili

ties. However, Hobson was specifically asked by the

editors

of Neuro Psychoanalysis

to comment on the

implications

r psychoanalysis of

recent develop

ments 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 brainstemmechanisms

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 con

texts (in a journal dealing only with neuroscience, for

example) it would be less appropriate for our discus-

Mark Solms is Lecturer, Department

of

Psychology, University Col

lege, 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., McCar

ley 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 impor

tance for psychoanalysts whether or not his dream the

ory incorporated significant errors. Any new evidence

that calls for a major revision of Freudian dream the

ory would probably necessitate a radical reappraisal

of Freud s conceptualization of the functional organi

zation of the mind

as

a whole. Since Freud s basic

concepts continue to inform contemporary psycho

analysis in a fundamental way, the question as to

whether or not they remain scientifically tenable can

not, in all conscience, be ignored.

I hope it goes without saying that our responsibil

ity 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 en

deavor is to discover the neural correlates of our basic

psychoanalytic concepts, so that we might open

Freudian metapsychology to all the benefits that mod

ern 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 psychoana

lytic models of deciding between rival points of

view, clarifying obscure questions, getting beyond im

passes and modern neuroscientific methods provide

an array

of

powerful tools for doing just that. But

before we can subject psychoanalytic concepts to neu

roscientific scrutiny we need to determine the physical

correlates

of

those concepts; to do otherwise is to risk


3/10

94

testing apples by measuring pears (Solms and Nerses

sian, 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 corre

lations

of

this kind is no armchair affair; it is a compli

cated 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 under

standing

of

the neuropsychological mechanisms in

volved (Solms, 1997a), the neuroscientific data do not

seem to require the hypothesis

of

an active distorting

agency. Braun and Hobson and Pace-Schott have ac

cordingly 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 percep

tual) mechanisms from the constraining influence that

dorsolateral prefrontal (executive) mechanisms nor

mally impose

on

them. In this view, translated into

Freud s terminology, the bizarre quality of dreams

(and the forgetting of dreams) would be solely attrib

utable 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 per

ceptual 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 in

volve an inadequately constrained representational

mechanism or does it seem to require the additional

hypothesis

of

an active, tendentious censorship mech

anism? This question probably cannot be answered

conclusively by the psychoanalytic method alone, pri

marily due to the interpretational vagaries of recon

struction. But the question can also be addressed

indirectly by clinicoanatomical methods. I have pre

viously observed that the functions traditionally attrib

uted 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 cingu

late gyrus), some basal forebrain nuclei, and possibly

some components

of

the thalamus and basal gan

glia all of

which are known to be involved in selec

tive attentional and other gating

functions in

the

censorship function. (I do not see why Braun and Hob

son and Pace-Schott have difficulty in distinguishing

between these structures and the mesocortical-meso

limbic dopaminergic fibers that project onto them and

serve an entirely different function.) Since these struc

tures 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 im

portant 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). Al

though the censorship function in Freud s dream the

ory 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

es

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 pre

frontal convexity and other frontal structures (e.g., or

bital cortex).

I have observed and reported elsewhere (Solms,

1997a), that

damage

to the ventromesial frontal struc

tures 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

195

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 clinicoana

tomical 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 ful

filling (childishly, ruthlessly, instinctually driven),

than those of controls. (2) With reference to the phe

nomena that Freud sometimes attributed to the fail

ure 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 be

l ief that it is no longer necessary for us to postulate a

censorship function to account for dream dis

tortion.

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, mis

guided, and doomed to failure (p. 217). Braun, for

his part, is also puzzled by my effort to l iberate 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 insti

gator of dreaming) are r instem 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 mecha

nisms 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 brain

stem events, which is what Hobson still seems to claim

with respect to dreams (see later). I accept that dream

ing (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

any state of consciousness. The coupling of forebrain

and brainstem therefore merely provides the ck-

ground context necessary for all forms of conscious

experience; it tells us nothing about dreaming in par

ticular. 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 back

ground of other (non-REM) consciousness support

ing mechanisms.

2

In contrast to the various, nonspecific conscious

ness 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 neces

sary 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 mecha

nism 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 mecha

nism 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 i t is located primarily

(although certainly not exclusively) in the fore

brain, but rather (a) that its activity is independent

of

the brainstem REM generator (indeed, its activ

ity 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 motivation

ally 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 compli

cated 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 dream

ing

as

follows:

Dreaming is a state

of

consciousness arising from the

activation

of

the brain in REM sleep. The brain activa

tion which underlies dreaming is, like that

of

waking,

a result

of

the excitation

of

forebrain circuits by im

pulses arising in the ascending activation systems

of

the brainstem (e.g., pontine and midbrain reticular

activating systems) and basal forebrain (e.g., choliner

gic Nucleus Basalis

of

Meynert). This activation pro

cess prepares the forebrain to process data with

associated cognitive awareness

The mechanism

of the brainstem triggering

of

forebrain activation in

volves the spontaneous excitation of cholinergic neu

rons in the pontomesencephalic

LOT

and PPT nuclei

[po

171].

And with respect to the psychological

un tion

and

s ns

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 s tate 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 hypothe

sis does not differentiate between dopaminergic influ

ences 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 knowl

edge) no other drug has been shown to increase dream

prevalence and intensity

without

having any simulta

neous effects on REM frequency, duration, and den

sity (Hartmann, Russ, Oldfield, Falke, and Skoff,

1980). Likewise, I was especially interested in the PET

study

of

Heiss, Pawlik, Herholz, Wagner, and Wienh

ard (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 concep

tual error, I would ask the reader to consider this com

plication wherever they feel a telling argument has

been raised against me. Before reaching an indepen

dent 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 be

lieve (explicitly or implicitly) that dreaming and REM

sleep are one and the same thing. The erroneous as

sumption that dreaming sleep is synonymous with

REM sleep has gravely distorted neuroscientific theo

rizing about the brain mechanisms of dreaming for


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Ongoing Discussion:

J.

Allan Hobson and E. Pace-Schott 97

more than 30 years. There is no excuse for perpetuat

ing it any longer.

I think that Braun misunderstands and underesti

mates 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 indistinguish

able from REM dreams; the

ver ge

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 meth

odological errors. Even obson accepts that 5 to 10

of NREM dreams 'are indistinguishable by any crite

rion from REM dreams (Hobson, 1988, p 143). Cor

recting for the fact that NREM sleep occupies 75 of

total'sleep time, what this means is that

5

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 favor

able 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 phenom

ena-hunger

and crying (and their underlying physio

logical

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 dis

agreements with Reiser's commentary.

While I agree that there is, as Braun argues,

a

conceptual overlap between Hobson's 'emotional

salience,' and Solms's motivated mental state' (as

drivers of dream narratives) I would like to point out

that among the various basic emotional command sys

tems 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 unbri

dled

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 dorsolat

eral frontal activation. I meant only what Braun him

self accepts: that

the

'reality principle is suspended

in favor of the pleasure principle and that this en

tails 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 sleep

protection hypothesis that I proposed in my commen

tary should by rights be limited to a comparison be

tween the sleep patterns of T nondreamers and

dreamers. The bifrontal group does present additional

complications of the kind that Braun mentions. How

ever (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 commenta

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

199

and dreamlike states. It is therefore difficult to under

stand why Hobson and Pace-Schott believe that the

loss of dreaming associated with deep medial frontal

lesions might be due to diminution of cholinergic in

fluences (unless they accept my suggestion that the

net effect of these influences might be inhibitory ). I

pointed these facts out in my commentary and specifi

cally asked Hobson how he accounted for them, but

this is one of the questions that Hobson and Pace

Schott 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 do

pamine circuits I referred to. I cannot follow their rea

soning 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 sp ring 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 nu

cleus.

7.

Hobson and Pace-Schott consider it highly

illogical to single out a non-sleep-regulatory dopamin

ergic brainstem region (i.e., the VTA) to be more

causal than other clearly sleep-related limbic and

brainstem nuclei in the generation

of

normal dream

ing (p. 213). This argument from logi l premises

ignores my main empiri l observation: dreaming

simply is sometimes generated independently of sleep

regulating 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 Hob

son 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 problem

atic. The interpretation

of

ll forms

of

data is prob

lematic. That is why it is prudent to check conclusions

derived from one method against those derived from

other methods (as already mentioned, this is the basic

rationale behind the whole neuro-psychoanalytic en

terprise). Few indeed of our long-standing interpreta

tions

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 de

rived from these two methods

as

remarkably com

plementary (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 t he 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 (hal

lucinatory fulfillment of wishes) under certain dy-

n mi 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 sys

tem and the other systems that normally damp and

constrain its influence on the mental economy. How

ever, 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 empiri

cally 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 eventu

ally 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 syn

onymous 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 cry

ing 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-meso

limbic dopamine systems are dynamically interlinked

with other neurotransmitter and neuromodulator sys

tems. (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 partic

ular 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 dis

ruptions

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 gener

ation.

2

I am surprised that

Hobson-who,

like

Freud, always drew a close analogy between dreaming

and psychosis-now warns us to distinguish t he

dream effects

of

psychosis or its incipient onset and

[normal] dream induction (p. 215) when extrapo

lating from L-DOPA effects. Hobson and Pace-Schott

seem to believe that since the vivid dreams and night

mares induced by L-DOPA and other dopamine ago

nists 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 simulta

neously kindled by dopamine agonists tends not only

Mark

Solms

to confirm the view that they share a common mecha

nism but, moreover, that the common mechanism is

in some crucial respect dopaminergically mediated.

3

Hobson and Pace-Schott s comment about

the preponderance

of

negative affects in dreams (fear

anxiety in particular) disregards everything we know

about the dyn mi s

of

anxiety. They also ignore the

fact that the amygdala is a major destination for meso

limbic 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 activa

tion-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 interdis

ciplinary 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 assump

tions. 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 un

derstand) 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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Ongoing Discussion:

J.

Allan Hobson

and

E. Pace-Schott

2 1

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 mis

taken, 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 Neurosurgery

4th Floor Alexandra Wing

Royal London Hospital

London

E

1BB England

e mail: [email protected]

13 J. Allan Hobson and Edward Pace-Schott’s Response: Commentary by Mark Solms (London)

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Transcript of 13 J. Allan Hobson and Edward Pace-Schott’s Response: Commentary by Mark Solms (London)