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The New Neuropsychology of Sleep: Commentary byMark Solms (London)Mark Solmsa

a Academic Department of Neurosurgery, Royal London Hospital, London E1 1BB, UnitedKingdom, e-mail:Published online: 09 Jan 2014.

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

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Commentary on The New Neuropsychology of Sleep

Witte, E. A., Gordon-Lickey, M. E., & Marrocco, R. T.(1992), Pharmacological depletion of catecholaminesmodifies covert orienting in rhesus monkeys. Soc. Neu­rosci. Abstr., 18:537.

Yamamoto, K., Mamelak, A. N., Quattrochi, J. J., & Hob­son, J. A. (1990a), A cholinoceptive desynchronizedsleep induction zone in the anterodorsal pontine tegmen­tum: Spontaneous and drug-induced neuronal activity.Neurosci., 39:279-293.

--------(1990b), A cholinoceptivedesynchronized sleep induction zone in the anterodorsal

The New Neuropsycholog)r of SleepCommentary by Mark Solms (London)

Allan Hobson is the leading authority on the neuro­physiology of REM sleep dreaming, and his work hasdominated this field for more than twenty years(McCarley and Hobson, 1975; Hobson and McCarley,1977). Recent findings concerning the neuropsychol­ogy of dreaming, however, as Hobson himself ac­knowledges, need to be reconciled with the oldphysiological findings, and this is ushering in a newera in this field.

In his paper, Hobson has covered a vast area ofknowledge. It will not be feasible for me to addressall of the points that he raised. I will focus selectivelyon one or two things that I think are of central impor­tance. This omits a lot else that is also of interest. Iam going to structure what I have to say around sixquestions which I would like to pose to ProfessorHobson.

I don't have any disagreement with Hobson's un­derstanding of the essential physiological mechanismsunderlying the sleep-waking cycle, including themechanism of REM sleep. However, I do disagreewith his understanding of the psychology of dreamsbased on those physiological mechanisms. Obviously,psychology is what interests psychoanalysts most.There has always been an uncomfortable gap betweenthe psychological approach to dreams, as remembered

The present commentary is a lightly edited version of a discussionof Hobson's presentation to the Neuro-Psychoanalysis Center of the NewYork Psychoanalytic Institute, November 7, 1998:"The New Neuropsy­chology of Sleep: Implications for Psychoanalysis."

Mark Solms is Hon. Lecturer, Academic Department of Neurosur­gery, S1. Bartholomew's and Royal London School of Medicine; and Asso­ciate Member of the British Psycho-Analytical Society.

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pontine tegmentum: Locus of the sensitized region. Neu­rosci., 39:295-304.

Zadra, A. L., Nielsen, T. A., & Donderi, D. C. (1998),Prevalence of auditory, olfactory and gustatory experi­ences in home dreams. Percep. & Motor Skills,87:819-826.

J. Allan HobsonLaboratory ofNeurophysiologyMassachusetts Mental Health Center74 Fenwood RoadBoston, MA 02115

subjectively by patients, and the physiological ap­proach to dreams, as manifested objectively (appar­ently) by REM sleep. However, it is now possible tobridge this gap, using the insights that modern neuro­psychological methods and neuro-imaging techniquescan provide into the neural organization of all highermental functions.

REM sleep is a state with many components, in­cluding a forebrain component, but until recently, onlythe brainstem component has been well understood.The recent developments in the neuropsychology ofdreaming that I am going to refer to (clinico-anatomi­cal studies of human patients and functional imagingof the dreaming human brain)-which also form thebasis of Hobson's most recent revisions of his ownmodel-are beginning to elucidate the forebrain com­ponent, and thereby starting to bridge the uncomfort­able gap just referred to (Madsen, 1993; Maquet et aI.,1996; Braun et aI., 1997, 1998; Nofzinger, Minturn,Wiseman, Kupfer, and Moore, 1997; Solms, 1997). Inthis gap, new insights are now being gained into theneural correlates of dreaming itself, and these insightsare casting a different light on the issues that confrontus (Solms, in press).

What, then, are the issues that confront us? Manyanalysts might be tempted to dispute the accuracy ofHobson's presentation of Freud's dream theory (orindeed of his remarks about psychoanalysis as awhole). I am not going to take up those polemics here.I am going to recall just one aspect of Freud's (1900)theory, one that brings us to what I think is the centralissue at stake in these deliberations. Freud believedthat there is an ongoing mental process during sleep.

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Although that process is not identical with wakingmental activity, it is also not synonymous with dream­ing. The mind is simply active-preconsciously ac­tive-during sleep, as it is during waking life. Butsomething special happens during sleep; we enter thehallucinatory, quasi-delusional state called dreaming.This happens, according to Freud, because the sleeperbecomes aroused by what he called' 'libidinal" drives(what would nowadays be called appetitive drives)which are especially powerful due to the weakened(sleeping) state of the ego's inhibitory functions. Thesedisinhibited drives threaten the ego's state of sleepbecause intense needs motivate goal-directed activi­ties, which lead to consummatory behaviors, whichare certainly incompatible with the state of sleep. Con­sequently, in order to protect sleep, these drives (expe­rienced as "wishes") cannot be satisfied in the realworld and they must be dealt with in some other way.For this reason, according to Freud, the sleeper imag­ines such wishes as being fulfilled in an hallucinatoryfashion, and in this way temporarily fends off the de­mands of the underlying, ascendant drives. That, in anutshell, according to Freud, is the core mechanismof the dream process; that is why our sleeping thoughtsare punctuated every night by the vivid, hallucinatoryexperiences that we call dreams. So, according toFreud, the crucial factor that distinguishes thinkingduring sleep from dreaming proper is the interventionofdisinhibited appetitive drives during sleep. If it werenot for this disinhibition of the drives, the ongoingthought processes that occur during sleep would notbe transformed into hallucinations. Thus, on Freud'sview, dreaming only becomes possible once appetitiveinterest (a highly excited state of an instinctual kind)attaches to and intervenes in our ordinary nocturnalthought processes.

Freud used the analogy of the relationship be­tween an entrepreneur and a capitalist to illustrate thiscentral aspect of his theory. He said that the ordinarymental processes that occur throughout sleep (memo­ries, volitions, perceptions, etc.) are only the "entre­preneurs" of dreams-they trigger the process whicheventually leads to a dream-but that the dream itselfonly occurs if and when the mental processes initiatedby the entrepreneur attract the interest of a "capital­ist" (the libidinal drives). Without capital the entre­preneur's idea will not be transformed into a reality(hallucination). This analogy usefully captures thecentral problem that Hobson has posed for us.

At first sight one might be inclined to argue, inthe light of this analogy, that Hobson's activa­tion-synthesis theory of dreaming is not fundamen-

Mark Solms

tally incompatible with Freud's entrepreneur­capitalist theory. A good few decades ago Foulkes(1962) demonstrated empirically-by awakening ex­perimental subjects at various points during the sleepcycle (not only during REM sleep)-that there is in­deed ongoing mental activity throughout sleep, just asFreud claimed. This mental activity is not dreaming,it is "thinking" (or something like thinking). Then,every 90 minutes or so, a radical change occurs inthe form of this mental activity. It becomes bizarre,affectively charged, hallucinatory, and delusional; thisis the dream proper-a very different type of mentalactivity. This type of mental activity is highly corre­lated with the physiological state known as REM.

As Hobson and others have demonstrated more­or-less conclusively, this state is caused by pontinebrainstem release (aminergic demodulation) of cholin­ergic activation. On this theory, it is cholinergic acti­vation of the forebrain during sleep that is unique todreaming. It is the cholinergic activation of REM sleepthat transforms ordinary thinking into the unique men­tal process that is the dream proper. Might not cholin­ergic activation, therefore, be the "capitalist" (thelibidinal drives) of Freud's theory?

One can see why, at first sight, psychoanalystsmight wish to equate libidinal drive with cholinergicREM activation. Through this simple equation, thewhole of Freudian dream theory would be brought intoline with the findings of contemporary dream research.But there are many problems with this equation. Forexample, why does the "capitalist" appear on thescene every 90 minutes or so with such monotonousregularity? Why should it appear automatically, byway of a simple brainstem switch which is activatedso predictably, no matter what the sleeper has beenthinking about, in fact, regardless of any mental state,wishful or otherwise?

These disparities could still perhaps be reconciledwith the Freudian theory. It is possible, for example,that libidinal drives do simply become active every 90minutes or so during sleep, due perhaps to an auto­matic disinhibitory process, or some other intrinsicrhythm of instinctual control (cf. Wassermann, 1978).But this kind of ad hoc theorizing ultimately strikes arock: if we are going to respect the scientific facts, wehave to admit that there is nothing about the choliner­gic systems of the brain that would justify the hypothe­sis that they are the physiological correlate of whatFreud called the t t libidinal drives." Acetylcholinesimply is not the command neurotransmitter of appeti­tive interest; and none of the cholinergic pathwaysleading from the brainstem to the forebrain has ever

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been shown to mediate this function. Cholinergic acti­vation is therefore not a viable candidate for the roleof the "capitalist" in Freud's dream theory. Instead,as Hobson has pointed out, cortical acetylcholineseems to participate primarily in selective attentionalprocessing. (It contributes to many different complexfunctions, of course, but one of the fundamental physi­ological effects of cortical acetylcholine seems to bean improvement in discriminative mental processes.)I do not see how we can validly construe this focusingfunction as the neural equivalent of an instinctual urge.Some might still want to dispute that, but I cannotagree with them and I do not think they will succeed.

If it is at all legitimate to seek a single neuro­transmitter system which might be the neurophysio­logical correlate of what Freud called libidinal drive,then it would probably have to be part of the mesocor­tical-mesolimbic dopamine systems of the brain-the"curiosity-interest-expectancy" circuit of Panksepp(1985), about which I will have a lot more to say later.If contemporary Freudians are seeking a commandneurotransmitter system which might be equated withtheir "capitalist," it would have to be this one, ratherthan the cholinergic systems identified by Hobson.

Here, then, is the nub of the problem we are dis­cussing. This is the main point of divergence betweenHobson's viewpoint-and the whole paradigm ofwork that has developed around his discoveries andtheories-and the older, Freudian viewpoint. In Hob­son's view, what distinguishes dreaming proper fromthe ongoing, banal mental processes that occur duringordinary (non-REM) sleep is not an appetitiveurge-not a libidinal drive or a "wish"-but rather a"motivationally neutral" upsurge in cholinergic acti­vation (McCarley and Hobson, 1977, p. 1219). Andthis upsurge, as Hobson has so elegantly shown, re­sults from the simple, mechanical release of brainstem(and possibly basal forebrain) cholinergic nuclei fromthe modulatory constraints imposed on them duringnon-REM sleep by a network of reciprocally inter­acting brainstem serotonergic and noradrenergicnuclei.

That is the essence of Hobson's post-Freudianmodel. On the basis of this model, Hobson has drawnvarious conclusions about the psychology of dreams,including the claim that the reciprocal interactions be­tween cholinergic and aminergic brainstem nuclei ex­plain not only the causation of dreams, but also theirformal characteristics. In Freud's model, the causationand hallucinatory-delusional quality of dreaming wasexplained by the libidinal wish-fulfillment hypothesis.However, various subsidiary hypotheses were required

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to explain other cardinal features of dreams, such asthe hypothesis of "censorship," which was invokedto explain some of the bizarre content of dreams, thefact that some dreams are unpleasurable and unsatis­fying experiences, and the fact that we forget dreamsso readily. On Hobson's theory, all of these character­istic features of dream psychology can be explainedwith reference to a simple oscillatory switch in a tinypart of the brainstem (Hobson, 1992). Therefore, ac­cording to Hobson, all of the complicated mentalmechanisms that Freud proposed can be removed likea scruffy beard with Ockham's razor.

The problems with Hobson's theory start here.The unique state of mind that we call dreaming, withall those special mental features that Hobson reducesisomorphically to the neurochemistry of the REMstate, does not occur during REM sleep alone. Pre­cisely the same state of mind occurs at other points inthe sleep cycle, which have different neurochemicalproperties. In fact, a full 20 percent of all dreams occurduring non-REM sleep.l This is a conservative esti­mate (see Cavellero, Cicogna, Natale, Occhonero, andZito, 1992). I am referring here to REMlike dreaming;not thoughtlike dreaming or thinking. Hobson himselfhas conceded that these non-REM dreams' 'are indis­tinguishable by any criterion from REM dreams"(Hobson, 1988, p. 143). But I think he does not makeenough of this fact. I think that it really poses a funda­mental problem for his theory.

Let me spell out its implications as I see them.If, as Hobson suggests, the whole of dream psychol­ogy can be accounted for by the physiology of REMsleep-by cholinergic activation coupled with aminer­gic demodulation-then why does exactly the samemental state occur in the absence of that mechanism?If the REM state has a unique neurochemical basis,which is absent by definition during the non-REMstate, then the existence and formal characteristics ofnon-REM dreams cannot be accounted for by theunique physiology of the REM state (Vogel, 1978).This implies either that REM dreams and these non­REM dreams are governed by two entirely differentphysiological mechanisms (which seems highly un­likely in view of the equivalence of their formal char­acteristics), or alternatively, dreams in general arecaused and regulated by something other than the sim-

1 Hobson (1988, pp. 142-143) concedes that 5 to 10 percent of non­REM dreams are indistinguishable by any criterion from REM dreams.This constitutes approximately 20 percent of all dream reports if the num­ber of reports are weighted for sleep-stage duration; 5 to 10 percent of non­REM sleep (which occupies 75 percent of total sleep time) is equivalent toroughly 15 to 30 percent of total sleep.

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pie oscillatory mechanism that governs the REM/non­REM dichotomy. The fact that dreams occur duringnon-REM sleep leaves open the possibility that cholin­ergic activation may interact with the mechanism thatis the "capitalist" of the dream process, but REMsleep itself cannot be that "capitalist." In short,dreaming must be governed by something other thanthe brainstem mechanisms that govern REM sleep.

The new research that I want to mention has, Ibelieve, identified this other mechanism, which is thetrue instigator of dreams. Before I describe this othermechanism, however, I want briefly to review somefurther data, derived from earlier research, which un~

derscore the dissociation I am drawing here betweendreaming and REM sleep. Then I will describe thebrain mechanism which I believe underlies dreamingand show how it differs from the mechanism of REMsleep. Finally, I will suggest how these two mecha­nisms might interact with each other, and explain thehigh correlation that certainly exists between dream­ing and REM sleep. In the process, I hope to showthat there is a complex relationship between the men­tal things called dreams which 'Freud studied (andwhich other psychoanalysts study today), and thebrainstem things that Hobson and his colleagues havetraditionally studied.

I am going to argue, and present evidence for theview, that even at the level of brain mechanisms, weare in fact dealing with two entirely different things.There is the brainstem mechanism of REM sleep andthere is the forebrain mechanism of dreaming. Thesetwo things are frequently activated in tandem, or atleast they are highly correlated. But they are dissocia­ble under certain conditions, and this makes it impos­sible for them to be one and the same thing. Dreamingcan occur without REM and REM can occur withoutdreaming. This proves that cholinergic activation (themechanism of REM sleep) is neither necessary norsufficient for dreaming. Once we have established this,we need to identify what the brain state could be thatis responsible for dreaming. We need to identify theanatomical and chemical properties of the dream pro­cess, and distinguish them from the above-describedmechanisms of the REM process. Then, finally, weneed to understand why these two mechanisms are sofrequently activated together.

The first point that I have to convince the readerof is that there are indeed two separate brain mecha­nisms for dreaming and REM sleep. This obviouslyhas fundamental implications for the sort of criticismthat Hobson has directed at Freud's theory.

Mark Solms

As I said earlier, during non-REM sleep, in theabsence of the unique state of cholinergic activationthat characterizes REM, the subject is usually in a stateof thoughtlike mentation. If one awakens a sleepingsubject during non-REM sleep, one has a 50 percentchance of obtaining a subjective report of what he orshe was thinking about preconsciously. These are notdreams. However, as already mentioned, sometimes(in 5-10% of non-REM awakenings) one obtainsdream reports which are indistinguishable by any cri­terion from REM dream reports. As I have said al­ready, although Hobson concedes this point, this iswhere the main problem with his theory lies. How canthe same mental state occur regardless of the presenceor absence of the cholinergic mechanism that is sup­posed to generate it?

Even more important than the fact that 5 to 10percent of non-REM reports are indistinguishablefrom REM reports is the fact that these reports arenot randomly distributed through the non-REMphases. There is a clustering of these reports at specificpoints in the non-REM cycle. The best example ofthis clustering occurs during descending stage I sleep(sleep onset): at sleep onset, a full 70 percent ofawak­enings elicit hallucinatory dream reports. The onlysignificant difference between these dream reports andREM reports is that the sleep onset reports are shorter(Foulkes and Vogel, 1965). In other respects (if thefactor of length is included) they are statistically indis­tinguishable from REM mentation, and they cannotbe described as anything other than "dreams." Thetemporal location of this cluster of non-REM dreamsis especially telling. It lays to rest any lingering suspi­cion that non-REM dream reports are merely misre­membered REM dreams (i.e., that the sleeper believesthat he or she has just been dreaming, but actuallythey were dreaming a good twenty minutes ago duringthe previous REM stage). Sleep onset dream reportsare elicited before any REM episodes have occurred.So these dreams may safely be attributed to a mecha­nism other than the aminergically demodulated, cho­linergic mechanism that Hobson postulated.

The same thing as occurs at sleep onset occurs,to a lesser extent, at the other end of the sleep cycle.Toward the end of a night's sleep, as the sleeper isstarting to stir (during the so-called rising morningphase of the diurnal rhythm), progressively more andlonger dream reports are obtained during awakeningsfrom the non-REM sleep stages. This is called the"late morning effect" (Kondo, Antrobus, and Fein,1989). As with sleep onset, so with the rising morningphase of the diurnal rhythm: non-REM dreams exist,

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and they are attributable to mechanisms other than thecholinergic mechanism that Hobson claimed causesdreaming during REM sleep.

There is something else about the temporal clus­tering of both REM and non-REM dreams that I wantto mention in passing. Please notice when these clus­ters occur: they occur just as one is falling asleep, atsleep onset; then they occur in the highly excited stateof "paradoxical sleep" (as REM sleep used to becalled); then they occur again with increasing fre­quency as sleep starts to give way to renewed wake­fulness. This pattern suggests that there might be somesort of relationship between dreaming and arousalstates in general. So this might be the specific physio­logical correlate of dreams; perhaps dreams are pro­voked not only by REM arousal,2 but by any persistentarousal state which occurs during sleep. This wouldappear to account for all the facts I have reviewedso far.

As it happens, Hobson himself has already sug­gested something like this to account for the (acknowl­edged) fact that some dreams occur during non-REMsleep. His latest revision of his activation-synthesismodel (the AIM model) incorporates just such an ex­planation. It is unnecessary for me to recount the de­tails of the AIM model; Hobson has summarized ithimself. But I do want to indicate a problem with it.The revised model still assumes that all dreams(whether REM or non-REM) can be explained interms of the dynamics of reciprocally interactingbrainstem aminergic and cholinergic systems. If thisassumption is correct, the existence of non-REMdreams does nothing to diminish the challenge thatHobson's original model posed to psychoanalyticdream theory. If dreams (whether REM or non-REM)are still reducible to cholinergic-aminergic brainstemneurodynamics, then they still have nothing to do withmotivated mental states, which are principally medi­ated by forebrain mechanisms (localized mainly to thelimbic system and frontal lobes).

The problem with Hobson's revised model (orany other model which reduces the causation ofdreams to brainstem mechanisms) is this. There is apathological state known as complex partial epilepsy,in which seizures of a particular kind occur which are

2 There is interesting data to show that the cholinergic activationwhich is characteristic of REM does indeed arouse the sleeper. If choliner­gic agonists are introduced during non-REM sleep, they trigger REM sleep.If cholinergic agonists are introduced during REM sleep, they provokewaking. If cholinergic agonists are administered prior to sleep onset, theyinduce insomnia (Sitaram, Wyatt, Dawson, and Gillin, 1976; Sitaram,Moore, and Gillin, 1978).

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by definition focal forebrain events. These seizurestypically manifest in the form of what Hughlings Jack­son called "dreamy states." They almost always arisefrom limbic and frontal lobe structures-and theynever spread to the brainstem structures which Hobsonclaims are the primary instigators of dreams. If theydid spread to those structures they would be neithercomplex nor partial seizures; they would be somethingcompletely different. This type of seizure commonlyoccurs during sleep, and to be more specific, it typi­cally occurs during non-REM sleep (Janz, 1974; Kella­way and Frost, 1983). This type of seizure isassociated with a distinctive dream phenomenon: re­curring stereotyped anxiety dreams (Epstein, 1964). Itwas demonstrated long ago, conclusively, that theserecurring anxiety dreams are seizure equivalents-thatthey are merely complex partial seizures occurringwhile the patient is asleep (Penfield, 1938; Penfieldand Erickson, 1941; Penfield and Rasmussen, 1955).Penfield was actually able to trigger these seizures,these dreams, experimentally by stimulating the af­fected area of the temporal lobe. So these dreams, atleast, which typically occur outside of REM sleep, areinstigated by a mechanism which is completely unre­lated to the oscillatory brainstem mechanism that Hob­son described. These dreams are without a shadow ofdoubt caused by a (highly specific) forebrain mech­anism.

The first major problem with Hobson's activationsynthesis model is that many dreams occur outside ofREM sleep. The second is that some non-REM dreamsare certainly caused by forebrain mechanisms. Thisleads to the first of the six questions that I would liketo ask Professor Hobson: How does he account fornon-REM dreaming in general and for the recurringnightmares that are associated with complex partialseizure disorders in particular?

Now I want to introduce a third line of evidence,one that begins to suggest that in fact all dreams mightbe generated by forebrain mechanisms. For obviousreasons, the research program that Hobson has fol­lowed for the past thirty years was conducted not withhuman subjects but rather with lower mammals-prin­cipally the domestic cat. The REM state in humanswas discovered more than forty years ago, and onceit was established that an identical physiological stateoccurs in almost all mammals, it seemed reasonableto study the neuroanatomy and neurophysiology of theREM state in animals, on the assumption that thiswould teach us something about the anatomy andphysiology of its equivalent in humans. Although thisgeneralization seemed reasonable enough with respect

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to REM sleep, it rested on somewhat shakier founda­tions when it came to the correlation between REMsleep and dreaming.

It is true that the high correlation between REMsleep and dreaming is firmly established in humans,but it is impossible to determine whether or not thiscorrelation holds good for cats; indeed it is impossibleto know whether cats ever dream (during REM sleepor at any other time). Thus, when Hobson and hiscolleagues performed ablation, stimulation, and re­cording experiments on cats in order to determine theireffects on REM sleep, the simultaneous effects ofthese experiments on the cats' dreams remained quiteunknown. This applied even at the most basic level ofcorrelation. For example, when Jones (1979) demon­strated that ablation of a large portion of the paramed­ian pons completely obliterates REM sleep in cats, hehad no way of knowing whether or not these REM­deprived cats still dreamed. In this way, Hobson andhis animal-research colleagues have had to carry overa large unknown factor into all their theoretical formu­lations about dreams, and their inferences about theneuropsychological mechanisms of dreaming in hu­mans could not be directly tested.

For more than one hundred years, the standardempirical method of establishing mind-brain correla­tions in humans has been the clinico-anatomicalmethod. By this method it is very easy to test hypothe­ses about the neural correlates of mental functions ofthe kind that Hobson has advanced with respect todreaming and the brainstem. If one believes that aparticular mental function is intrinsically related to thephysiological activity of a particular part of the brain,then this predicts what should happen to that mentalfunction when that part of the brain is damaged. Forexample, Broca justified his belief that the productionof speech was a function of the third frontal convolu­tion of the left cerebral hemisphere by demonstratingempirically that damage to that part of the brain re­sulted in a loss of expressive speech. Thus, if Hobsonis justified in his belief that the generation of dreamsis a function of the paramedian pontine tegmentum,then it should be possible for him to demonstrate thatdamage to that part of the brain results in a loss, notonly of REM sleep, but also of dreaming.

Nature has provided science with human subjectswith discrete lesions in this part of the brain.3 Twenty­six such patients, human cases, have been reported

3 Contrary to Hobson's statement, which in general is true, some ofthese patients are conscious and alert enough to be able to state whetherthey dream or not.

Mark Solms

in the neurological literature; twenty-six patients withpontine brainstem lesions, who no longer had REMsleep (Adey, Bors, and Porter, 1968; Chase, Moretti,and Prensky, 1968; Feldman, 1971; Markand and Dy­ken, 1976; Cummings and Greenberg, 1977; Osorioand Daroff, 1980; Lavie, Pratt, Scharf, Peled, andBrown, 1984). In only one of these twenty-six caseswas it demonstrated that there was a cessation ofdreaming (Feldman, 1971); in all other cases the corre­lation between loss of REM and loss of dreaming waseither absent or it was not even considered by the au­thors.

The one positive case suffered a traumatic occlu­sion of the basilar artery. Since this case report waspublished in 1971, before the advent (or at least, be­fore the widespread use of) CT imagery, we do notknow the precise extent of the lesion that producedthe combined loss of REM sleep and dreaming in thatcase. A diagnosis of massive pontine damage wasmade on purely clinical grounds. Although the evi­dence for that diagnosis was good, there is little in thepublished report to reassure the clinical neuroscientistthat this patient did not also sustain damage to theforebrain. Certainly, given what we know about thepathological anatomy of basilar artery infarctions, itis in fact highly likely that this patient did also haveabnormalities in the region of the posterior cerebralcirculation-that is to say, forebrain damage. So, forscientific purposes, we can more-or-less exclude eventhe one case among the twenty-six human brainstempatients where it was demonstrated that loss of REMsleep was accompanied by loss of dreaming.

It is true that the neuropsychological investiga­tion of patients with pontine lesions presents difficul­ties. These patients are few and far between, they arevery ill, consciousness is often clouded, and so on. Ireadily accept that this is an area that needs furtherinvestigation. Nevertheless, it is very striking indeed,considering the huge amount of scientific interest thathas been devoted to REM sleep precisely because ofits correlation with dreaming, that this standard re­quirement of neuropsychological correlation has neverbeen met-that it has never been demonstrated thatbrainstem lesions cause cessation of dreaming. Thefailure to meet this rudimentary clinico-anatomicalstandard greatly undermines any theory which wouldreduce the neuropsychology of dreams to brainstemneurophysiology.

But in clinico-anatomical research, negative evi­dence (absence of a correlation) is seldom as tellingas positive evidence (presence of a correlation). Thefollowing line of evidence is therefore still more un-

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dermining of Hobson's brainstem conception ofdreaming.

It has been demonstrated that certain brain le­sions, highly focal brain lesions, do cause cessationof dreaming, but these brain lesions are in an entirelydifferent part of the brain from the brainstem locationof the mechanism which regulates the sleep cycle. Thelesions in question are localized in two parts of thehigher brain. Patients with damage in either of theseareas experience a total cessation of dreaming, andtheir retrospective reports in this regard are confirmedby REM sleep awakening (Solms, 1995, 1997). Thesepatients simply do not dream anymore. The REM cy­cle is unaffected in these cases; they still have normalREM episodes, despite their complete inability todream. This confirms the dissociation between dream­ing and REM sleep.

Such cases have been reported in their hundreds.Only one case with a dubious focal pontine brainstemlesion has been reported with cessation of dreaming inassociation with cessation of REM sleep. By contrast,literally hundreds of cases with unequivocal focalforebrain lesions have been reported with cessation ofdreaming in association with completely normal REMsleep. This leads to the second question I want to poseto Professor Hobson: How does he account for thedemonstrable dissociation that exists between REMand dreaming, using the standard clinico-anatomicalparadigm of brain-behavior correlation?

What, then, are these forebrain lesion sites thatare associated with loss of dreaming (as opposed toloss of REM sleep); and what do they tell us about thebrain mechanisms of dreaming (as opposed to those ofREM sleep)? There are, as already mentioned, two ofthem. First, lesions of either hemisphere in the regionof the parieto-temporo-occipital (PTO) junction(where the parietal, temporal, and occipital lobes con­verge) lead to a cessation of dreaming during the acutephase of the underlying neurological illness (dreamingusually recovers within one year). Why should lesionsin this highly evolved part of the human forebrain leadto an acute cessation of dreaming? Due to the highnumber of available cases, it is possible to answerthis question by multivariate analysis of the cognitivedeficits that coincide with the loss of dreaming in thesepatients. The results suggest that the loss of dreamingin these cases is due to an abnormality of spatial cogni­tion, or to be more precise, of what cognitive psychol­ogists call the "visual cache" of working memory.These patients are defective with respect to visuospa­tial working memory and related functions, and theyare therefore unable to construct (or maintain) in con-

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sciousness a stable "mental space." Since dreams arefundamentally grounded in such a space, it is perhapsnot surprising that these patients are unable to dream.

I am sure that Hobson would agree that the factthat these patients do not dream does not representcompelling evidence against his theory that dreamsare generated by pontine brainstem mechanisms. Nomatter where the process of generating dreams maybegin, at some point it would have to engage thesehigher spatial mechanisms in order to produce a com­plex hallucinatory experience grounded in the con­scious "mental space" of working memory. The factthat dreaming ceases following PTO junction lesions,therefore, does not mean that dreams are actually gen­erated in the PTO junction; the process could merelyculminate there. So the involvement of this part of thebrain in the dream process is, so to speak, merely thetip of the neuropsychological iceberg.

However, here it is necessary to digress for amoment, in order to make the point that although eventhe activation-synthesis model would have predictedthat the neocortical structures subserving visuospatialworking memory must somewhere be involved in thedream process, it would not have predicted the speci-ficity of the involvement of these structures that hasactually been observed (Solms, 1997; Braun et aI.,1998). In the activation-synthesis model, pontinebrainstem aminergic mechanisms demodulate as­cending brainstem cholinergic mechanisms, resultingin widespread cortical activation (this is the' 'activa­tion" aspect of activation-synthesis). The activatedforebrain then "synthesizes" the meaningless brain­stem stimulation, thereby producing the conscious ex­perience of the dream itself. The dream itself, then,according to the activation-synthesis model, is ulti­mately an attempt by the cortex to synthesize all ofthe meaningless images that are generated by a diffuseautoactivatory process.

In the light of this model, it is important to notethat only a very specific part of the great expanseof imagery-producing perceptual and motor cortex isimplicated in the dreaming process by the clinico-ana­tomical evidence. It is only with lesions in the fewsquare centimeters that constitute the region of thePTO junction that dreaming stops completely. Lesionsanywhere else in the whole of the vast expanse of thecerebral cortex do not have this effect.4

4 Recent PET findings reported by Braun et aI., (1997, 1998) suggestthat the critical lesion site for cessation of dreaming might, in fact, be theinsula (which lies immediately beneath the PTa junction) or the posterioraspect of the superior temporal gyrus (which is immediately adjacent tothe PTa junction), rather than the PTa junction itself. Nevertheless, thespecificity of the structures identified by Braun support the point beingmade here.

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Moreover, it can be demonstrated that the imag­ery generated in some of these other parts of the cortexis positively preserved in dreams, despite massivedamage to the structures concerned. What this sug­gests is that dreaming is not merely a synthetic mani­festation of diffuse cortical arousal; rather, it appearsthat highly complex representational and rerepresen­tational mechanisms are actively involved in the cog­nitive construction of dream images. For example,lesions in the somatosensory and motor cor­tex-which produce dense hemiplegia in wakinglife-are not accompanied by hemiplegic imagery indreams. Hemiplegic patients experience intact somato­sensorimotor functions in their dreams. There is a verypoignant description of this in an early report by Mach(1906), where he tells how he dreamed of himselfplaying the piano and thinking he was normal again,only to wake up and find that his hemiplegia wasstill there.

If the simple, isomorphic relationship that Hob­son postulated really existed between the excitation ofmotor cortical elements and the dream experience,then one would not expect this kind of dissociation tooccur between lesions of the cortical motor systemand motor imagery in dreaming. The same applies tothe other unimodal cortical structures. For example,lesions in the visual cortex which produce hemianopiain waking life are not accompanied by hemianopia indreams. These patients, despite losing half their visualfield in waking perception, experience normal visionin their dreams. This demonstrates that the perceptualand motor images we experience in our dreams arenot simple, isomorphic products of nonspecific activa­tion of perceptual and motor cortex during sleep;highly complex, heteromodal representational mecha­nisms appear to be involved in the active constructionof the manifest dream.

Now we can return to the main theme. I saidthat cessation of dreaming was associated with twoforebrain lesion sites. The first of these was the regionof the PTO junction. The second lesion site is thewhite matter of the ventromesial quadrant of the fron­tal lobes (the fibers immediately surrounding and infe­rior to the frontal horns of the lateral ventricles).Bilateral lesions in this highly specific area lead to acessation of dreaming-permanent, global cessationof dreaming. Again, despite the demonstrable absenceof dreams in these cases, REM sleep is completely pre­served.

What is the function of this second part of thebrain which is so crucial for dreaming? This is pre­cisely the part of the brain that the psychosurgeons

Mark Solms

targeted in the modified prefrontal leucotomy proce­dure that was so extensively performed in the fifties,sixties, and early seventies for the treatment of severemental illness (Bradley, Dax, and Walsh, 1958). Thisprocedure produced large numbers of patients withbilateral lesions in the part of the brain just mentioned.In my own clinico-anatomical study (1997) I collectedonly nine nondreaming cases with lesions in this area(which is seldom damaged bilaterally through naturalcauses). However, I was very struck by the similarityof this lesion site to the site of the old prefrontalleuco­tomies; so I went back to the psychosurgical literatureand, 10 and behold, completely unnoticed by all of us,there they were reported in the hundreds-very largeseries of prefrontalleucotomy cases, with a 70 percentincidence of loss of dreaming following the procedure(Frank, 1946, 1950; Partridge, 1950; Piehler, 1950;Schindler, 1953; Jus et aI., 1973). And again, REMsleep was preserved, despite the loss of dreaming (Juset aI., 1973).

This begins to suggest what the functional contri­bution of this part of the brain, so crucial for dreaming,might be. At the same time as these patients lost what­ever it was that generated their psychiatric symptoms,they also lost the ability to dream. A common sideeffect of prefrontalleucotomy was adynamia-loss ofspontaneous interactive interest in the world. Thispoints to the fact that this part of the brain is cruciallyinvolved in motivation. In fact, there is a major moti­vational system in this sector of the frontal lobes, thecore of which is a pathway that connects dopaminergicnuclei in the upper ventral tegmental area, via the lat­eral hypothalamus, with the amygdala, septal area andnucleus accumbens, anterior cingulate gyrus, and ven­tromesial frontal cortex. This system, which is richlyinterconnected with the limbic temporal lobe struc­tures that were discussed earlier, forms part of themesocortical-mesolimbic dopamine system. The spe­cific portion of this system which seems to be crucialfor dreaming has been described as the' 'curiosity-in­terest--expectancy" system (Panksepp, 1985) or the"seeking" system (Panksepp, 1998) or the "wanting"system (Berridge, 1999). This system is engaged withall appetitive behaviors; it drives our interactive inter­est in the world. It is especially active in states ofcraving (such as occur in addiction). The fact that le­sions along this pathway cause a cessation of dream­ing is very interesting in light of the Freudian dreamtheory, for it suggests that dreams are indeed-no lessthan the excited cravings of the drug addict-moti­vated mental states.

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I have already mentioned that the psychosurgicalprocedure of prefrontal leucotomy targeted this sys­tem. On this basis, it has long been suggested thatthe therapeutic benefit of prefrontal leucotomy wasattributable to the amotivational state that such lesionsproduce (Panksepp, 1985); these patients simply lostinterest in the world, and all the excitement that fueledtheir psychiatric symptoms was lost along with it. Thelink between cessation of dreaming and improvementof positive psychotic symptoms will therefore also beof interest to psychoanalysts, in view of the theoreticalparallels that Freud always drew between dreams andmental illness.

Modern psychopharmacological treatments ofschizophrenia target the "curiosity-interest-expec­tancy" system, too, no less than the old psychosurgicalapproaches did. Antipsychotic medications are dopa­mine blockers, and they are thought to act on preciselythe pathway that was described above (Role and Kelly,1991). This coincidence has even lead some authorsto suggest that antipsychotic medications are merely"chemical leucotomies" (Breggin, 1980). This viewwould certainly be consistent with the view that theprimary therapeutic effect of these medications is areduction of interactive interest in the world (Lehmannand Hanrahan, 1954). One might therefore expect thatdrugs which excite the dopaminergic motivational sys­tems of the brain would artificially stimulate psychoticsymptoms and dreaming. This is precisely what drugswhich have an excitatory action on this system do:L-dopa, cocaine, and amphetamine intoxication, forexample, all induce psychotic symptoms, together withexcessively vivid dreaming and nightmares. Again, theincreased frequency and vivacity of dreaming is notassociated with similarly increased REM frequencyand density (Hartmann, Russ, Oldfield, Falke, andSkoff, 1980). This putative causal link between dopa­minergic activity and dreaming is further supported bythe fact that excessive dreaming (and other psychoticsymptoms) can be successfully treated by the adminis­tration of dopamine blockers.

What all of this provides, I think, is a firm baseof evidence for the conclusion that this pathway, thedopaminergic pathway in the ventromesial frontal re­gion (this motivational system of the brain, the appeti­tive interest command system) is involved causally inthe instigation of dreams and dreamlike mentation. Sohere we have a specific relationship between dreamingand a brain mechanism which coincides quite closelywith the fundamental hypothesis of Freud's dream the­ory: namely that dreaming is generated under the di­rect influence of a highly motivated, wishful state of

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mind. More about that later. For now, I would like toask Professor Hobson my third question: What doeshe make of the causal relationship that appears toexist between mesocortical-mesolimbic dopaminergicstimulation and dreaming and dreamlike mentation?

This leads to another digression. There is some­thing that always puzzled me about the cholinergichypothesis of dreaming. As I have said already, I donot dispute the mass of evidence that Hobson has pre­sented in support of his cholinergic hypothesis of REMactivation, but there is something that does not add upabout the cholinergic hypothesis of dream activation.I mentioned earlier that increased cortical acetylcho­line in waking mental life produces an increasedfocus­ing of mental powers. One of the reasons why peoplelike to smoke, for example, is because smoking im­proves concentration and sharpens selective atten­tion-an effect which is mediated by acetylcholine vianicotinic receptors. But according to Hobson's hy­pothesis, excitation of cholinergic neurons should in­duce dreamlike mentation in waking cognition. Itcertainly does not do that; if anything it does the veryopposite. It is drugs with the opposite action---anticho­linergic agents-which induce dreamlike states inwaking life. That is what has puzzled me: I can't un­derstand why forebrain cholinergic activation duringsleep leads to dreaming whereas in waking life it hasthe opposite effect. This, then, is my fourth question:I would be interested to know how Hobson accountsfor this disparity between the effects on waking andsleeping mentation of cholinergic activation.

What I make of it is that either pontine choliner­gic activation (or aminergic deactivation) has an inhib­itory effect on forebrain cholinergic activity (which iscertainly not what Hobson has hypothesized, but seebelow) or some intermediate link between the cholin­ergic activation and the mental effect isneeded-something that intervenes between the cho­linergic activation and the REM dream state. This in­termediate mechanism would account for the mentalcharacteristics of the REM state, since they cannot beaccounted for by cholinergic activation itself. I amproposing that this intermediate link is provided by thedopaminergic mechanism described above.

That dopaminergic mechanism does not have anexclusive relationship with REM; it can eq\lally betriggered by other arousal stimuli. REM is just one ofthe many things that is apt to arouse the interest ofthe dopaminergic appetitive systems; other thingswhich have the same effect are the various sourcesof non-REM arousal discussed above: the relativelyaroused state of sleep onset, the relative arousal of

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late-morning sleep, the various stimulant drugs, andthe complex partial seizures.

My proposal, therefore, is this: dreaming can oc­cur as a result of anything that arouses the sleeper,but only if the arousal stimulus in question attractsappetitive interest. In other words, anything that ex­cites the motivational systems of the forebrain andthereby initiates a goal-directed intention-which isby definition incompatible with the state ofsleep----eanstimulate the dream process proper. The final commonpath leading from all these various different types ofarousal (sleep onset, stimulant drugs, REM, seizures,late-morning effect, etc.) to dreaming is the dopamin­ergic "curiosity-interest-expectancy" system in theventromesial quadrant of the frontal lobes. The finalcommon path from all of these things to dreaming isthe excitement ofappetitive interest. If appetitive inter­est is stimulated, then dreaming can occur; if it is notthen dreaming does not occur. That is why dreamscannot occur (despite the persistence of normal REM)when this pathway is bilaterally damaged.

This is my main point. Before I close, however,there are two other questions I want to ask ProfessorHobson. He spoke about censorship and he spokeabout the function of dreams. I will quickly addresseach of these issues in turn.

First, if I may transgress for a moment the restric­tions I imposed earlier on my own discussion ofFreudian dream theory, I would like to correct Hob­son's reading of that theory on one small point. InFreud's dream theory, the bizarreness of the dream isnot attributable to censorship alone; in fact, it is attrib­uted to two different factors which act in combination.The first factor is what Freud (1900) described as thedecathexis (i.e., deactivation) during sleep of the mo­tor and perceptual systems of the ego-the withdrawalof the ego from reality into the narcissistic state ofsleep. This represents a massive weakening of the ego(the executive system of the mind), resulting in a re­gression to primary-process activity, which is whatdominates in sleep (and especially in dreaming): thedisplacements, condensations, regression, and so on,which are so characteristic of dreams. These are posi­tive symptoms of a relative shift in the dynamics ofthe mind, a weakening of the ego in favor of the ideThe withdrawal from contact with reality is a with­drawal from the fundamental principle that determinesthe ego's domination of waking mental life-the real­ity principle. Taking account of reality is what the egois for. Once that function is relinquished, there is arelease from inhibition of the other great principle ofmental life-the pleasure principle-and the feeble

Mark Solms

ego is thenceforth dominated by the wishful type ofthinking that governs the id: "I want it, I want it now,therefore I have it now." This type of thinking, whichdoes not recognize the constraints of reality, accountsfor a good deal of what might be called the bizarreness(the irrationality and so on) of dreaming-and it doesso quite independently of the censorship.

The hypothesis of censorship states that some­thing more happens, in addition to the irrationality thatflows naturally from the type of thinking that is re­leased from the constraints of the reality principle.Some of the wishes that are activated and hallucinator­ily gratified in dreams under the influence of the plea­sure principle cause great anxiety to the ego (theenfeebled sleeping ego). That is why the ego censorsthose wishes. Censorship is a very crude, rough-and­ready way of rendering the wishful hallucinations gen­erated under the influence of the id tolerable to thesleeping ego. It simply chops them up and changesthem about in order to make them more acceptable toitself. This too, like the dream as a whole, ultimatelyserves the purpose of sleep protection: that isFreud's theory.

So in Freud's theory, censorship does not accountfor the whole of the bizarreness of dreams. Much ofit is accounted for simply by the withdrawal of theego from reality; and this, I think, would seem to bethe equivalent of what Hobson described-his hypo­thetical demodulation by aminergic systems, i.e., thedepletion of cortical serotonin and noradrenaline, andthe resultant inactivation of the dorsolateral prefrontallobes (the executive' 'scene of action" of normal wak­ing cognition) and other higher cortical structures. Thepattern of deactivation that is observed during sleep,and accentuated during REM sleep (Braun et aI., 1997,1998) would be more compatible with what is de­scribed in Freud's theory as the withdrawal of cathexisfrom the reality-oriented perceptual and executive sys­tems, than with the withdrawal of censorship.

We do not yet know what the specific neural cor­relates are of the mental functions that Freud de­scribed as censorship, but on the basis of our own,initial clinico-anatomical observations (Solms, 1998),we have at least been able to determine that ventrome­sial frontal cortex (the very cortex that the "curio­sity--expectancy-interest" system projects onto) iscrucial for the maintenance of that function. The integ­rity of ventromesial frontal cortex, more than anyother region of the brain, seems to be necessary forthe function of executive inhibition, in other words,for the broader function of which censorship is a spe­cial variety.

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For this reason, it is important to note that thePET studies which Hobson used to support his argu­ment that the "censoring" part of the brain is inactiveduring sleep, actually report that ventromesial frontalcortex is highly activated during REM sleep. So I thinkthat it is plausible to say that the available PET evi­dence is at least compatible with the Freudian "cen­sorship" hypothesis, although I readily accept that itdoes not by any means prove that hypothesis. Furtherinvestigations-focused more specifically on this neu­ropsychological question-are obviously required.But at this stage I would be interested to know whatHobson's interpretation is of the ventromesial frontalcortical activation that Braun and others have ob­served during REM sleep. That is my fifth question.

As for the function of dreaming, I'll just say this.It may be true that the function of dreaming is memoryconsolidation. It may be that this is the function ofdreaming, but it may also be true that it is not; and itmay equally be that the function of dreaming is justwhat Freud said it was-the protection of sleep. Theimportant point at this stage, I think, is that we needto differentiate between the function of REM sleepand the function of dreaming. They are not the samething. The REM state triggers the dream state, butdreaming can also be triggered by many other things.So understanding the function of REM sleep is some­thing separate from understanding the function ofdreaming. The time has now come for us to study thefunction of dreaming directly. We have not done thisin the past, and as a result, the effects of dream depri­vation have always been conflated with the effects ofREM deprivation and those of sleep deprivation.

I'll give an example of the sort of research I havein mind. We know that cortical lesions in the PTOjunction of either hemisphere lead to a cessation ofdreaming with preservation of REM sleep. Likewise,bilateral ventromesial frontal white matter lesions areassociated with cessation of dreaming and preservedREM sleep. So if we want to understand somethingabout the function of dreaming, as opposed to thefunction of REM sleep, we should focus our effortson a study of these two groups of patients. Here wehave the possibility of performing a critical test of anyhypothesis concerning the function of dreaming-thesleep protection hypothesis included.

If dreams protect sleep then the sleep of patientswho are unable to dream due to brain lesions (but whonevertheless have intact REM sleep) should be moredisturbed; they should have more frequent awakeningsand they should have quantitatively less sleep thanneurological patients who are able to dream. That

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would be a simple, controlled study of one of the cen­tral hypotheses of the whole Freudian dream theory.This is the sort of experiment that really needs to bedone, as I think Hobson was suggesting, if we wantto take psychoanalysis forward into the twenty-firstcentury. And here is an opportunity to do so. I hopeI have made myself clear. The important point is thathypotheses like this can now be tested (neuropsycho­logically) and I do not believe they have been ade­quately tested before. So this is my final question toProfessor Hobson: Does he not agree, in view of theconflation in the past of the REM state with dreaming,that the sleep protection theory of dreaming has notyet been adequately tested?

I want to conclude by describing an alternativeto Hobson's model of how the dreaming brain works.It is this: there is an ongoing thought process in sleep.During this process, something happens which arousesthe sleeper. This might be due to the thought processitself, or it might be due to an external stimulus, or itmight be due to REM, or to something else. This acti­vates the sleeping brain and threatens to awaken thesleeper. Then, if and only if the arousal stimulus at­tracts appetitive interest-if it excites the dopaminer­gic "seeking" system of the ventromesialforebrain-then the dream proper begins. Appetitiveinterest normally instigates goal-directed activitywhich terminates in a motivated act. But this outcomeis incompatible with the maintenance of sleep. This,perhaps, is why the executive systems of thebrain-together with spinal motor systems-are deac­tivated during sleep. As a result of these systems beingunavailable for action, the emotion and memory sys­tems (which have been activated by the appetitive in­terest) prime the perceptual systems to the point ofhallucination. Instead of motor action, a regressivehallucinatory process occurs; and that is the basis ofthe dreamwork proper. From the ventromesial frontalmotivational systems there is a regressive activationof, first of all, the emotional and episodic memorysystems of the mesial temporal lobe, then, second, theassociative semantic processing and spatial represen­tational systems of the PTO junction; and then, finally,backwards from there onto unimodal visual systemsin the ventral occipitotemporal region (which repre­sents the conscious visual experience of the manifestdream). This hallucinatory experience is mistaken fora real event, due to the inactivation of dorsolateralfrontal reflexive systems, but not only because of that.

This leads to a last point, which I have touchedon once already. Another reason why the hallucinatoryexperience of the dream is uncritically accepted as a

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real event is perhaps because the basal forebrain nu­clei are actively inhibited during dreaming sleep. Isuspect that this could be the specific effect of as­cending pontine cholinergic activation during REM: itinhibits the cholinergic basal forebrain. I have beenled to this suspicion by a curious finding. Lesions ofthe basal forebrain-affecting, for example, the nu­cleus basalis of Meynert, the septal nuclei, and so on(caused, for example, by aneurysmal rupture of theanterior communicating artery)-provoke dreamlikestates in which the patient is unable to distinguishthoughts from reality (Solms, 1997). In many respects,these states are highly reminiscent of the effects ofanticholinergic medication. So lesions in the (cholin­ergic) basal forebrain nuclei, anticholinergic medica­tion, and REM sleep all have the same consequence:inability to distinguish between fantasy and reality(once more, the very opposite of what one would ex­pect on the basis of the activation-synthesis model).That is why I believe that inhibition of the cholinergicbasal forebrain during REM sleep may be another rea­son why the sleeping ego mistakes dreams for realevents.

So that is what I think happens in the dreamingbrain, based on the evidence that has emerged overthe last few years about the forebrain ~echanisms ofdreaming. And these are some of the main reasonswhy I cannot accept Hobson's critique of the Freudiandream theory. I think Freud's understanding of themental processes underlying the manifest dream areas viable today as they ever were-perhaps even moreviable, scientifically, than they were before. I think weare on the threshold of an exciting new era in dreamscience, in which the neuropsychological mechanismsof dreaming are finally going to be laid bare, and I forone will not be at all surprised if we find that Freud'sunderstanding of those mechanisms was basically onthe right track all along.

I will close by restating my six questions to Pro­fessor Hobson:

1. How does he account for non-REM dreaming ingeneral and for the recurring anxiety dreams thatare associated with complex partial seizure disor­ders in particular?

2. How does he account for the demonstrable dissoci­ation that exists between the REM state and dream­ing, using the standard clinico-anatomicalparadigm of brain-behavior correlation?

3. What does he make of the causal relationship thatappears to exist between mesocortical-mesolimbicdopaminergic stimulation and dreaming anddreamlike mentation?

Mark Solms

4. I would be interested to know how he accountsfor the disparity between the effects of cholinergicactivation on waking and sleeping mentation.

5. I would like to know what his interpretation is ofthe ventromesial frontal cortical activation thatBraun and others have observed during REM sleep.

6. Does he not agree, in view of the conflation in thepast of the REM state and dreaming, that the sleepprotection theory of dreaming has not yet been ade­quately tested?

I would like to thank Professor Hobson most sin­cerely for his willingness to participate in this dia­logue.

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Mark SolmsAcademic Department of NeurosurgeryRoyal London HospitalLondon E1 1BB, United Kingdome-mail: mlsolms@mds.qmw.ac.uk

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