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Neuroanatomical Correlates of Dreaming. II: TheVentromesial Frontal Region Controversy (DreamInstigation)Calvin Kai-ching Yua

a Department of Counselling and Psychology, Hong Kong Shue Yan College, 10 Wai TsuiCrescent, Braemar Hill Road, North Point, Hong Kong, e-mail:Published online: 09 Jan 2014.

To cite this article: Calvin Kai-ching Yu (2001) Neuroanatomical Correlates of Dreaming. II: The Ventromesial FrontalRegion Controversy (Dream Instigation), Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and theNeurosciences, 3:2, 193-201, DOI: 10.1080/15294145.2001.10773355

To link to this article: http://dx.doi.org/10.1080/15294145.2001.10773355

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Neuroanatomical Correlates of Dreaming. II:The Ventromesial Frontal Region Controversy(Dream Instigation)

Calvin Kai-ching Yu (Hong Kong)

Abstract: This is the second in a series of three articles consid­ering Freudian dream theory in the light of recent neuroscientificfindings (see Yu, 2001, for the first article). This second articlefocuses on the controversy surrounding the role of the ventrome­sial frontal region in dreaming. Specifically, it aims to identify theprecise structures within this region that appear to instigate thedream process.

Introduction

In replacing Freud's "unscientific" wish-fulfillmenttheory (1900) with a brain-based model, McCarley andHobson (1975; Hobson and McCarley, 1977), follow­ing a hypothetical isomorphism between the neuro­physiological phenomenon of the REM state anddreaming, developed two physiological models ofdreaming sleep, namely the reciprocal-interactionmodel and activation-synthesis model. Both of thesemodels are characterized by the reciprocal on-off ac­tivity of two pontine neuronal populations (cholinergicand aminergic populations). According to the activa­tion-synthesis hypothesis, dreams are actively gener­ated by the brainstem but passively andnonspecifically synthesized by the forebrain, and aretherefore nothing more than "the best possible fit ofintrinsically inchoate data produced by the autoacti­vated brain-mind" (Hobson, 1988, p. 204). In thesemodels, Hobson asserted that dreaming is reducibleto a simple interplay of excitatory (cholinergic) andinhibitory (aminergic) neurones-the product ofpurely endogenous and neurological mechanisms,

Calvin Kai-ching Yu, M.Sc., is a lecturer in Psychology in the Depart­ment of Counselling and Psychology of Hong Kong Shue Yan College,Hong Kong.

which are, so to speak, "motivationally neutral"(Hobson and McCarley, 1977). The credibility of theFreudian theory was severely strained by these mod­els, and the scientific world reverted to the prepsy­choanalytic view that "dreams are forth" (cf. Freud,1900, p. 133).

These authoritative models dominated the mod­ern science of dreams for several decades. However,Solms (1999, 2000a,b) set out a groundbreaking argu­ment to the effect that, although the parts of the brainthat are decisive for REM sleep are in the pons, theparts of the brain that are decisive for dreaming arelocated in the forebrain. Centrally, Solms (1997, 1999,2000a,b) found that bilateral damage to the white mat­ter immediately surrounding the frontal horns of thelateral ventricles (i.e., ventromesial frontal region), alarge fiber pathway which transmits dopamine (DA)from the middle of the brain (the ventral tegmentum)to the higher parts of the brain, renders dreaming im­possible but leaves the REM cycle completely unaf­fected. These surprising findings suggested thatdreaming is generated by a different mechanism fromthe one that generates REM sleep (Solms, 2000b).This conclusion was further substantiated by the phar­macological observation that chemical stimulation ofdopamine pathways (with agents like L-Dopa) leadsto a massive increase in the frequency and vividnessof dreams without having equivalent effects on thefrequency and intensity of REM sleep (Klawans,Moskowitz, Lupton, and Scharf, 1978; Scharf,Moskowitz, Lupton, and Klawans, 1978; Hartmann,Russ, Oldfield, Falke, and Skoff, 1980; Nausieda,Weiner, Kaplan, Weber, and Klawans 1982). Dream­ing can therefore be switched "on" and "off" by aneurochemical pathway which has nothing to do withthe REM oscillator in the pons.

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Furthermore, in relation to the Freudian dreamtheory, Solms (1995, 1997, 1999, 2000a) pointed outthat the main function of the dopaminergic (DA) brainpathway, which is so crucial for the generation ofdreams, is to '~instigate goal-seeking behaviors andan organism's appetitive interactions with the world"(Panksepp, 1985, 1998). In other words, the functionof this important brain system is to motivate the sub­ject to seek out and engage with external objects whichcan satisfy its inner biological needs. These are pre­cisely the functions that Freud (1900) attributed to the"libidinal drive"-the primary instigator of dreamsin his theory. Accordingly, damage to this pathwaycauses cessation of dreaming in conjunction with adramatic reduction in motivated behavior (Solms,1997).

This rejuvenation of the drive theory of dreamingwas furthermore supported by findings that surgicaldamage to this pathway (which was the primary targetof the prefrontal leucotomies of the 1950s and 1960s)results in a reduction in psychotic symptoms, togetherwith a cessation of dreaming (Frank, 1946, 1950; Par­tridge, 1950; Schindler, 1953). From his unexpectedfindings, Solms (1999) asserted that contemporaryneuroscientific evidence provided good reason to takeseriously the radical hypothesis, first set out in TheInterpretation of Dreams (1900) 100 years ago, thatdreams are motivated phenomena, driven by wishes.

The Present Controversy

Solms (2000a) argued that the DA pathways and theirfi ber connections within the basal forebrain in the"ventromesial frontal region" (p. 191) are crucial fordreaming as a product of libidinal drive. Yet, in recentcommentaries, Braun (2000) and Hobson (1999) haveboth pointed out that considerable uncertainty remainsas to precisely which part of the basal forebrain Solmsis claiming is crucial for the instigation of dreaming.This controversy concerning the basal forebrain is fur­ther complicated by Solms (2000a) citing activationof "ventromesial" regions of the frontal lobe as evi­dence for an "active censor" (p. 192). Braun (2000)has challenged this claim on the grounds that it isconceptually confused to make one and the same brainstructure the censorship and the wish-fulfilment or"appetitive seeking" system.

Solms seems to equate this region with the ~ 'censor­ing" part of the brain, as well. It seems odd that heplaces the seat of appetitive drives and craving in the

Calvin Kai-Ching Yu

same tissue as the behavioral censor. ... What exactlyis the evidence for this? Moniz's leukotomy patientsare typically described as flat and devoid of appetitiveinterest rather than disinhibited. Were Solms' s (1997)bifrontal patients both adynamic and disinhibited?[Braun, 2000, p. 200].

The primary aim of the current article is to clarify(so far as possible) the precise location of the basalforebrain pathways that instigate dreaming. The puta­tive localization of Freud's "censorship" function isthe subject of the third and last article in this series.

Method

Subjects

Three different sets of data were analyzed in the cur­rent study in order to achieve a more comprehensiveand reliable picture of the anatomical localization ofSolms's "dream instigator": (1) all previous case re­ports from the clinical literature in which precise ana­tomical data was provided, prior to Solms' s (1997)monograph; (2) all the available CT and MRI scansof the clinical cases studied in Solms' s monograph;and (3) all the available PET data in the publishedliterature. The current study involves a detailed reanal­ysis and comparison of these three sets of data.

SamjJle J: Published Cases from the ClinicalLiterature

The first sample consisted in 61 clinical cases of globalcessation of dreaming reported in the neurological lit­erature (Wilbrand, 1887, 1892; MUller, 1892;Grtinstein, 1924; Lyman, Kwan, and Chao, 1938;Piehler, 1950; Humphrey and Zangwill, 1951; Gloningand Sternbach, 1953; Boyle and Nielsen, 1954; Niel­sen, 1955; Ettlinger, Warrington, and Zangwill, 1957;Ritchie, 1959; Michel, Jeannerod, and Devic, 1965;Benson and Greenberg, 1969; Farrell, 1969; Feldman,1971; Moss, 1972; Wapner, Judd, and Gardner, 1978;Epstein, 1979; Basso, Bisiach, and Luzzatti, 1980; Mi­chel and Sieroff, 1981; Epstein and Simmons, 1983;Corda, 1985; Pefia-Casanova, Roig-Rovira, Bermu­dez, and Tolosa-Sarro, 1985; Schanfald, Pearlman,and Greenberg, 1985; Habib and Sirigu, 1987; Farah,Levine, and Calviano, 1988; Neal, 1988).2 These were

:: A complete tabulation of these cases is archived at http://www.neuro-psa.com/archive

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Neuroanatomical Correlates of Dreaming. II 195

Sample 2: Solms's Original CT and MRI Records

Sixty-four clinical cases first reported in Solms's(1997) monograph constitute the second sample, com­prising 36 (56.3%) male and 28 (43.8%) female pa­tients.3 These, too, were all patients who experiencedglobal cessation of dreaming as a consequence of neu­rological insult, regardless of the lesion site or type(see Table 2). Mean age is 40.84 (s.d. == 17.77, min.== 10, max. == 77).

all patients who experienced global cessation ofdreaming as a consequence of neurological insult, re­gardless of the lesion site or type (see Table 1). Thissample included 34 males (55.7%), 20 females(32.8%), and 7 cases in which the sex was not speci­fied (11.5%). The average age was 47 years (s.d.14.13, min. == 18, max. == 74).

TABLE 1Neuropathology in Sample 1 (N = 61)

Frequency

r = regional, g = global, CMR = Cerebral Metabolic Rate, CBF = Cerebral Blood

Flow, Glu = glucose. 02 = oxygen

PET Study Measure REM State No. & SexCompared to of Subjects

Heiss et al. rCMR Glu Wakefulness Experimental: I M(1985) Control: 5 MMaquet et al. rCMR Glu Wakefulness Experimental: 10 M, IF(1990)

Control: 9 MMadsen. gCBF Wakefulness 8 M & 6 FSchmidt, et al. gCMR02(1991)

Madsen, Holm, rCBF Wakefulness 6 M & 5 Fet al.(1991)

Hong et al. rCMR Glu Correlate with No. of Experimental: 9

(1995) REM Control: 6

Maquet, Peters, rCBF Wakefulness & SWS 19 M

et al.(1996)

Nofzinger et al. rCMR Glu Wakefulness 6F(1997)

Braun, Balkin, rCBF Wakefulness & SWS 37 M

Wesensten, &

Carson(1997)

Braun, Balkin, rCBF Wakefulness & SWS 10M

Wesensten,

Gwadry, et al.(1998)

not identical (see Table 3). Two methods of measure­ment, cerebral blood flow (CBF) and cerebral meta­bolic rate (CMR), were used in these PET studies.Only in one study were both techniques employed.

hard, 1985; Maquet, Dive, Salmon et aI., 1990; Mad­sen, Schmidt, Wildschi~dtz et aI., 1991; Madsen,Holm, Vorstrup et aI., 1991; Hong, Gillin, Dow, Wu,and Buchsbaum, 1995; Maquet, Peters, Aerts et aI.,1996; Braun, Balkin, Wesensten, Carson et aI., 1997;Nofzinger, Mintun, Wiseman, Kupfer, and Moore,1997; Braun, Balkin, Wesensten, Gwadry et aI., 1998).Ninety-one of these subjects were male (77.1 %) and18 were female (15.3%). The sex of9 subjects was notmentioned in the original studies (7.6%). The methodsemployed across the nine studies, though similar, were

TABLE 3Methods Used in Sample 3 (N = 118 Ss)

%

0/0

26.61.63.1

32.829.7

1.64.7100

55.714.8

1.68.29.8

1.68.2100

34

915615

61

1712

211913

64

Frequency

TABLE 2Neuropathology of Sample 2 (N = 64)

Pathology

Pathology

Cerebrovascular DiseaseTumorInfectionTrauma

LeucotomyToxic DiseaseMissing DataTotal

Cerebrovascular DiseaseCongenital Malformation

Benign CystTumorTrauma

Degenerative DiseaseInfectionTotal

Sample 3: Published PET Data Procedure and Materials

The third sample consisted of PET data drawn fromnine previous studies, involving a total of 118 healthysubjects (Heiss, Pawlik, Herholz, Wagner, and Wien-

3 I am grateful to Dr. Solms for making this raw data available to me.

The locations of the lesions in samples 1 and 2 werecoded as precisely as possible, using the cytoarchitec­tonic maps of Brodmann (1909) and the templates ofDamasio and Damasio (1989), and the original de­scriptions and illustrations in sample 1 and the original

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196 Calvin Kai-Ching Yu

*These categories are not exclusive.

Neuroanatomical Analysis of Solms's OriginalRecords

Subcortical lesion data extracted from the 35 traceablecases from Solms's series are provided in Table 4.

TABLE 4Subcortical lesions in Sample 2 (N = 35)

Lesions of the frontal white matter (especially the crit­ical area F09 in Damasio and Damasio' s [1989] classi­fication; see Figure 1) and the head of the caudatenucleus (including the ventral striatum) were the mostcommon among all subcortical regions-with each be­ing manifest in almost half of the patients (45.7% foreach). These lesion sites were also the second mostfrequent sites among all regions associated with cessa­tion of dreaming present in this sample (both corticaland subcortical, anterior and posterior), even higherthan BA37 (40%), whose importance for dreamingwas demonstrated in the first article in this series (Yu,2001). The two critical subcortical sites are the mostventromesial regions of the frontal lobe surroundingthe frontal horn, and are located in the middle of themesolimbic DA pathways, superior to the amygdaloidcomplex and inferior to the cingulate gyrus and theremainder of the frontal lobe.

There is a significant positive correlation be­tween the lesions of frontal white matter F09 and thelesions of head of caudate nucleus (Pearson's X2 ==6.30, df == 1, p < 0.01; <p == 0.42, p < 0.01). Aconsiderable number of cases (11/35; 31.43%) hadboth lesions simultaneously, and patients with head ofcaudate nucleus lesions tended to have lesions in F09and vice versa. F09 and the head of caudate nucleusare both situated at the tip of the frontal horn andwithout doubt fall squarely within the DA pathwaysof the ventromesial frontal region. Indeed, a high pro­portion of the DA fibers coursing through F09 termi-

Substructures Frequency %

Frontal White Matter 8 22.9*(FOI)

Frontal White Matter 16 45.7(F09)Head of Caudate Nucleus 16 45.7Putamen 10 28.6External Capsule 8 22.9Anterior Internal Capsule 8 22.9Hypothalamus I 2.9Amygdala 4 11.4

Hippocampus 6 17.1

Thalamus 10 28.6

Frontal

Lobe

Subcortical

On the basis of the three samples, this section is di­vided into three parts, which attempt to clarify pre­cisely which frontal structures may reasonably beimplicated in the instigation of dreams.

CT and MRI scans in sample 2. None of the 61 casesin sample 1 provided sufficiently detailed anatomicaldata for the precise localization of subcortical regionsof interest.

Sufficiently detailed data for precise localizationpurposes were available in only 35 of the 64 patientsin sample 2 (principally due to current unavailabilityof the original records).

The PET data (sample 3) were similarly coded,adopting Damasio and Damasio's (1989) method. TheBrodmann-coded brain lesions of the patients fromthe first and second samples and the Brodmann-codedlocations identified by the PET data of REM "dream­ing" sleep were then analyzed and compared.

Results

Neuroanatomical Analysis of Clinical Cases fromthe Literature

Among the 61 nondreaming cases from the literaturereports, 10 patients (16.4%) showed pure frontal lobedamage; 7 of them were bilateral. These 7 cases allhad deep bifrontallesions (mesial aspect) in the regionof the mesolimbic DA pathways and their projections(see below). It was unclear whether these structureswere affected in the remaining three cases. Case 39(Epstein and Simmons, 1983), who had a lesion cir­cumscribed to the left frontal lobe superior to the tem­poral lobe, which is anatomically very close to thebasal forebrain and temporal limbic zones (BA38 and36)-and situated between them-probably did havedamage to the mesolimbic DA pathways. The preciselocalization of the neuropathological changes in theother two cases (no. 48 and 49 reported by Corda[1985]) cannot be determined due to ambiguous de­scriptions in the original reports. Therefore 80%, atleast, of the pure frontal cases' lesions fell within thecritical ventromesial frontal region. Within the frontalcontext, therefore, only lesions confined to the ven­tromesial frontal system, roughly halfway along themesolimbic DA pathways connecting frontal and tem­poral regions, appeared to produce cessation ofdreaming.

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Neuroanatomical Correlates of Dreaming. II

Figure 1. The Critical Area F09. (indicated in black) (after Damasioand Damasio, 1989)

nate on the nucleus accumbens in the ventral striatumin the region of the head of the caudate.

Associations between BA37 and (Head of CaudateNucleus +F09)

If the ventromesial frontal system (in particular, thehead of the caudate nucleus and the frontal white mat­ter F09) and BA37 (as discussed in Yu, 2001) aretwo significant neurological substrates of dreaming,lesions to which would lead to dream cessation, thequestion that arises is whether patients who had le­sions in one of these two primary regions also sus­tained injury to another critical area. Morespecifically, if a significant number of patients suf­fered lesions in both BA37 and F09/head of caudate,it is difficult to determine whether the dream cessationeffect should be attributed to one of these zones orboth.

197

The problem is resolved by the finding that BA37lesions have negative associations with both head ofcaudate nucleus lesions (Pearson's X2 == 5.55, df == 1,p < 0.05; cP == -0.40, p < 0.05) and F09 lesions(Pearson's X2 == 2.76, df == 1, p == 0.096; cP == -0.28,

TABLE 5Overlapping lesions of BA37 and Frontal White Matter F09

(N=35)

Lesion FWM F09 FWM F09

Yes No TotalBA37 Yes 4 10 14 (40%)BA37 No 12 9 21 (600/0)

Total 16 (45.7%) 19 (54.3%) 35 (100%)

p == 0.096) (Table 5). Though the negative associationis not significant in the latter instance, the number ofpatients who had either BA37 or F09 lesions is fargreater (5.5 times more) than the number of patientswho sustained both lesions simultaneously. In otherwords, patients who h~ve lesions to BA37 tend to bespared from ventromesial frontal pathology and viceversa. It therefore appears that dream cessation effectscaused by lesions in these regions are independent ofeach other.

Neuroanatomical Analysis of the PET Data

According to recent PET data, although prefrontal de­activation is typical in REM sleep, this deactivationdoes not occur in the various substructures of the ven­tromesial frontal region during dreaming sleep. Onthe contrary, all basal forebrain substructures listed inTable 6 show significant increases in activity duringdreaming. It therefore appears likely that all of thesestructures participate in the functional architecture ofdreaming.

Nonetheless, certain variations between the lev­els of increase among these substructures do exist (seethe rankings in parentheses). For instance, with refer­ence to Braun, Balkin, Wesensten, Carson, et aI's.(1997) data, the anterior hypothalamus preoptic area(AH-POA) has the most robust increase in cerebralblood flow (CBF) compared to the other substructureswithin the basal forebrain. Its activity is also the sec­ond highest of all forebrain structures, relative to CBFin non-REM sleep. Within the basal forebrain, the nexthighest CBF increase is in the caudate nucleus, fol­lowed by the putamen. These results seem to be highlyconsistent with those drawn from sample 2.

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198 Calvin Kai-Ching Yu

TABLE 6Relative Activity of Ventromesial Forebrain Structures in Dreaming State

PET STUDY Left Amygdala Right Amygdala Hypothalamus Caudal Orbital Caudate Putamen VetralRegion Nucleus Striatum

Heiss et al. (1985) I I IMaquet et al. (1990) TL TL I (NS)Madsen, Schmidt, et al. (1991)Madsen, Holm, et al. (1991)Hong et al. (1995) TLMaquet et al. (1996) INofzinger et al. (1997) I I (R) I I (L.A. Inf) IBraun et al. (1997) I (6) I (6) I (A) (1) I (4) I (2) I (3) I (5)Braun et al. (1998) I I I (A) I I I I

Note. Besides amygdala, hypothalamus, caudal orbital region, caudate nucleus, putamen and ventral striatum (including nucleus accumbens), basal forebrain can also beextended to include the following neural structures: olfactory tubercle, septum, diagonal band nuclei, bed nucleus of stria terminalis, substantia innominata, olfactory cortex,and hippocampus formation. I: increase, D: decrease, NS: nonsignificant, Empty cells: no change or no mention in the study, TL: technical limitations in study, L.A. Inf: leftanterior inferior, R: right, A: anterior.

Discussion

Within the frontal region, two distinct branches of theDA systems ascending into the striatum are recog­nized: the nigrostriatal system, which ascends fromthe substantia nigra to the dorsal striatum (the caudate­putamen complex), and the mesolimbic-mesocorticalpathways, which ascend from the ventral tegmentalarea (VTA) to the ventral striatum (beneath the headof the caudate nucleus) and the amygdaloid body, aswell as to the frontal convexity. It is generally recog­nized that the ventral striatal system is one of the ave­nues through which affective processes are blendedwith basic motor tendencies (Panksepp, 1998).

The converging results discussed above verify aparticular contribution to the organization of the func­tional system of dreaming made by DA systems in thebasal forebrain. Based on the findings of the clinicalliterature and the PET data, however, it seems ratherdifficult to single out one or two locations along thesetwo avenues, let alone to specify exactly which path­way may function as the instigator of dreaming. Allprimary components of the mesolimbic (e.g., amygda­loid body, ventral striatum) and the dorsal dopaminer­gic system (e.g., caudate, putamen, anterior cingulategyrus) show significant involvement. Notwithstandingthis, in view of the discrepancies between the activa­tion levels of the various components as revealed bythe PET data and the relative incidence rates of theircorresponding lesions with reference to the secondsample, it can be suggested that the part played by thehead of the caudate nucleus (i.e., ventral striatum) inthe ventral branch is particularly prominent. A caveat,however, is required: The localization of a lesion isnot to be confused with the localization of a function.

"Human mental processes are complex functionalsystems and they are not 'localised' in narrow, circum­scribed areas of the brain, but take place through theparticipation of groups of concertedly working brainstructures" (Luria, 1973, p. 43). It is prudent to con­clude, therefore, that our findings suggest that thewhole mesolimbic DA system, including the hypothal­amus, the amygdaloid body, and the ventral striatum,contribute to the neural infrastructure for the instiga­tion of dreaming, though within this system lesions inthe ventral striatum region near the head of the caudatenucleus appear to be the strongest neuroanatomicalcorrelate of dream cessation.

Ventral Striatum

The mesolimbic DA circuit, terminating on the ventralstriatum in the region of the head of caudate identifiedabove, is termed the SEEKING system by Panksepp(1998), and is thought to "drive and energize manymental complexities that humans experience as persis­tent feelings of interest, curiosity, sensation seeking"(p. 145).

The caudate nucleus, from the strict anatomicalpoint of view, is divided into three portions: the head,located within the frontal lobe; the body, located deepin the parietal lobe; and the tail, which goes into thetemporal lobe. The nucleus accumbens is situated im­mediately beneath the head of the caudate nucleus,just anterior to the ventral part of the putamen, in theventral striatum, which is below the ventral part of theputamen. Therefore, the nucleus accumbens is locatedwithin the frontal lobe, more precisely, in the ventro­medial prefrontal region, attached to the inferior cau-

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Neuroanatomical Correlates of Dreaming. II

dal part of the frontal horn of the lateral ventricle andsurrounded by the white matter (F09) enclosing thefrontal horn of the lateral ventricle.

According to Panksepp (1998), the nucleus ac­cumbens, together with other subcortical structureslike the cerebral peduncles, globus pallidus, and sub­stantia nigra, is at the center of the' 'instinctual motorbrain." Many psychobehavioral routines, including allthe basic instinctual functions and satisfactions, aregoverned by interactions with the basal ganglia, espe­cially ventral striatal areas such as the nucleus accum­bens, as well as ventromedial zones of the caudatenucleus of the dorsal striatum. As already mentioned,this nucleus is also one of the most important constit­uents of the motivational SEEKING system. It is per­haps analogous to the "great reservoir of libido"(Freud, 1923, p. 369).

Hypothalamus

Although very few patients sustained damage to thehypothalamus in the current study (probably due toits protected anatomical position), its role cannot beignored in the functional architecture of dreaming inthat, with reference to the PET data, the hypothalamus,and especially the preoptic area (AH-POA), has themost robust increase in cerebral activity within theDA systems and also the second highest in the wholeforebrain. Interestingly, the hypothalamus, togetherwith the neural substrate of negative emotions, theamygdala, plays a paramount role in sexual arousalcircuits, named the "LUST system" by Panksepp(1998). These systems operate by sensitizing varioussensory input channels that promote copulatory re­flexes on the one hand, emotions, drive (i.e., nucleusaccumbens), and hormonal inputs on the other.

Conclusion

It is unconvincing and inappropriate to overlocalizethe libidinal drive systems in any single microstructureof the brain, taking into account the widely acceptedneuroscientific principle that all complicated mentalfunctions arise from the conjoint action of a numberof subsystems. However, when considering that thereason for such precise localization of the dream insti­gator is that Solms ascribed both censorship and drive(two contrasting incompatible functions of dreaming)to one highly organized and inextricably intertwinedsystem of the brain, controversy is bound to ensue. If

199

however the instinctual functions alone are localizedin the ventromesial dopaminergic system, and the cen­sorship function can be attributed to a different set ofstructures in this broad region, as will be elaboratedin the next article in this series, progress will havebeen made.

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Calvin Kai-Ching YuDepartment of Counselling and PsychologyHong Kong Shue Yan College10 Wai Tsui CrescentBraemar Hill RoadNorth PointHong Konge-mail: calyu@hongkong.com

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