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Neuropsychoanalysis: An Interdisciplinary Journal for

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Neuroanatomical Correlates of Dreaming, III: The

Frontal-Lobe Controversy (Dream Censorship)
a

Calvin Kai-ching Yu
a

Department of Counselling and Psychology, Hong Kong Shue Yan College, Hong Kong.
Published online: 09 Jan 2014.

To cite this article: Calvin Kai-ching Yu (2003) Neuroanatomical Correlates of Dreaming, III: The Frontal-Lobe Controversy
(Dream Censorship), Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences, 5:2,
159-169, DOI: 10.1080/15294145.2003.10773422
To link to this article: http://dx.doi.org/10.1080/15294145.2003.10773422

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Neuro-Psychoanalysis, 2003, 5 (2)

159

Neuroanatomical Correlates of Dreaming, III:

The Frontal-Lobe Controversy (Dream Censorship)

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Calvin Kai-ching Yu (Hong Kong)

This paper aims to resolve the contradictory findings between PET and human lesion methods with regard to the role of the
frontal convexity in the functional architecture of dreaming, and to consider the neuroscientific justification for its presumed
psychoanalytic counterpartthe dream censoran ultimate parameter that is believed to be behind the scene in charge of
the entire manifestation of dreaming in the Freudian model. In contrast to prevailing beliefs, the author asserts that the
latest neurophysiological findings are not necessarily incompatible with the classical psychoanalytic notion of dream
censorship, provided that misunderstanding and confusion surrounding the psychoanalytic concepts and localization
matters are cleared. The paper concludes with a proposed neurodynamic model of dreaming (the neuro-structural model)
on the basis of the reconcilement between classical Freudian dream theory and the contemporary neurophysiological
findings enumerated in this series of papers.

This is the third and closing paper of a trio of papers

that attempt to subject Freudian dream theory to
neuroscientific investigation (see Yu, 2001a, 2001b,
for the first two papers). The specific purpose of this
final study is to explore the remaining crucial component of Freudian dream theory (as discussed by
Hobson and Braun) that has not been adequately
scrutinizednamely, censorship. In view of considerable misunderstanding surrounding this extraordinarily controversial issue, the concept of the
disguise-censorship principle is at the outset briefly
restated.
Attributed by Freud in 1900, dream distortion or
dream work is said to be the coupled effect of two
powerful mechanisms: censorship and regression. The first mechanism, indeed, coincides with
the fundamental demarcation between the psychic
structure of adults and that of children. Called the
superego by day and censor at night, it develops in
the oedipal phase (around 3 years of age) (Freud,
1923). This censor or superego, which is recognized
as conscience and moral judgment, becomes
weaker during sleep and dreaming, when, even
though it is not at its full strength, it nevertheless
remains operative. Seizing the chance of favorable
circumstances, the ego chooses a disguised way
of finding satisfaction in order to circumvent the
vigilance of this censor.
Though censorship plays a crucial role in dream
formation, dream distortion is by no means attribut-

able to censorship alone. Regression, for example,

subserves the distortion of dreams independently of
the effect of the censorship. Along with the restoration of the power of the id, which takes advantage of
the weakened censor, sleepers withdraw their interest or libido from the whole external world and
temporarily regress to their earliest condition, a
revival of their childhood and infancy, restoring the
primitive narcissism of the instinctual impulses that
dominated at that time (temporal or developmental
regression) (Freud, 1900, 1914). At the same time,
direct motor discharge is suppressed and motor impulses regress to perceptual systems in the form of
hallucinatory wish-fulfillment (topographical regression) (Freud, 1917/1915) (see Yu, 2001a for
details). Abandoning reality and rationality, disregarding external constraints, the childish and narcissistic pleasure principle once again dominates the
ego and tempts it to seek immediate satisfaction.
Factors such as these, in conjunction with the residual power of censorship, lead to the bizarreness
of dreams, according to Freudian theory.
Argued by Solms in his neuropsychological-psychoanalytic model, the imagined dream scene is
uncritically accepted and the dreamer mistakes the
internally generated scene for a real perception owing to the relative inactivation during sleep of crucial parts of the reflective systems in the frontal
parts of the limbic system (i.e. ventromesial frontal
region). Accordingly, appetitive subcortical im-

Calvin Kai-ching Yu: Department of Counselling and Psychology, Hong Kong Shue Yan College, Hong Kong.
Correspondence: Calvin Kai-ching Yu, Department of Counselling and Psychology, Hong Kong Shue Yan College, 10 Wai Tsui Crescent,
Braemar Hill Road, North Point, Hong Kong (email: calyu2000@hotmail.com).

160

pulses are perhaps censored by the anterior limbic

system and then safely back-projected to posterior
cortical representational mechanisms. As shown by
Solms (1997), damage to these reflective systems
results in an exotic state of almost constant dreaming during sleep and an inability to distinguish
between thoughts and real events during waking
life (Gallassi, Morreale, Montagna, Gambetti, &
Lugaresi, 1992; Lugaresi et al., 1986; Morris, Bowers, Chatterjee, & Heilman, 1992; Sacks, 1995;
Whitty & Lewin, 1957).

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The present controversy and remaining

uncertainty
Although Solms (1999, 2000) has tried to find
neuroscientific evidence for the dream-censorship,
the picture is not at all complete [e.g. the brainbased version of censorship cannot be fully accounted for by a reality-monitoring mechanism
(uncritical acceptance of the hallucination as real
perception), and its parallel operation, temporal regression, remains unexplored] and is ferociously
criticized by Braun (1999) and Hobson (1999;
Hobson & Pace-Schott, 1999).
Solms (1999) cites activation of ventromesial
regions of the frontal lobe as evidence for an active
censor. He, however, simultaneously argues that
the dopamine (DA) pathways and their fiber connections within the basal forebrain in the ventromesial frontal region are crucial for dreaming as a
product of libidinal drive. It is conceptually confusing to make the two hypothetically opposite functions one and the same brain structure.
Still, Solmss evidence of censorship appears to
be very inconsistent. If reality testing is equivalent
to censorship (Solms, 1995), based on the findings
of inactivation during sleep of crucial parts of the
reflective systems in the frontal parts of the limbic
brain (Solms, 1999, p. 33), then how can Solms
also attribute the censorship part of the brain to
the fact that the ventromesial frontal cortex is
highly activated during REM sleep (Solms, 2000,
p. 192)? Solmss censorship part of the brain seems
very precarious: in certain circumstances, it deactivates, yet in others, it activates.
By and large, the recent arguments raised by both
Hobson (2000) and Braun (2000) represent a fundamental request for neuroscientific evidence of
dream-censorship. Its twin controversy concerning
dream distortion and topographical regression has
been discussed in detail in Yu (2001a), the first of
this trio of papers. The primary question that the
current paper intends to deal with is whether a
plausible neuroanatomical correlate can be identi-

Calvin Kai-ching Yu

fied for the dream-censor. Its parallel mechanism

temporal regressionis also addressed. Finally, an
epitomized model is devised on the basis of the
converging findings of the three studies in this
series.

Method
Three different sets of data were included in the
current study, to achieve a more comprehensive and
reliable picture of the neuroanatomical localization
of the dream-censor as well as its role in dreaming
sleep: (1) all previous case reports from the clinical
literature (N = 61); (2) all the available CT and MRI
scans of the cases studied in Solmss 1997 monograph (N = 64); and (3) all the available PET data in
the published literature (N = 118). The first two
samples comprised patients who experienced global
cessation of dreaming as a consequence of neurological insult, regardless of the lesion site or type.
Furthermore, 10 additional cases of patients (4 males
and 6 females) who experienced increased reality or
frequency of dreaming along with fantasyreality
confusion after neurological insults, also from
Solmss original records, were included. Sufficiently detailed data for precise localization purposes was available in 8 of the 61 cases in Sample 1,
and in 35 of the 64 patients and all 10 additional
cases in Sample 2. The current study involves a
detailed analysis and comparison among the three
sets of data (see Yu, 2001a, 2001b, for details).

Results
On the basis of the three samples, this section is
divided into three parts, which aim at clarifying
precisely which frontal structures are implicated in
the functional mechanism of dreaming and which
are not. Somewhere within this broad area is, as
addressed previously, the potential neural substrate
for the dream-censor.
Neuroanatomical analysis of clinical cases
from the literature

In the 8 precise cases, no lesions circumscribed to

major prefrontal regions (BA8, BA10, BA11,
BA,47) were detected except BA9 and BA46, which
were found in Case 581 (Michel, Jeannerod, &
Devic, 1965, a diffused case with multiple vascular
lesions), the only patient who had prefrontal lesions

1
The case numbers refer to the table archived at www.neuropsa.com/yu.

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Neuroanatomical Correlates of Dreaming, III: The Frontal-Lobe Controversy

(BA9, BA44, BA45, BA46). However, the cessation

effect in this case was almost certainly caused not
by the prefrontal lesion but, instead, by the compromised temporo-occipital region (see Yu, 2001a). If
this case is excluded, no prefrontal damage could be
clearly and precisely identified in this nondreaming
sample.
With regard to the 10 cases with pure frontal
lesions in the whole sample, 8 of them had lesions in
the deep mesial frontal region, which spared the
prefrontal convexity. The precise localization of the
neuropathological changes in the other 2 cases
(Cases 48 and 49: Corda, 1985) cannot be determined due to ambiguous descriptions in the original
reports. In other words, only in these 2 of the 61
clinical cases (3.28%) could the neurological symptom of dream cessation be inferred as a consequence
of a lesion that might have involved the frontal
cortical convexity. With reference to both the whole
sample of the 61 clinical case reports and the subsample of the precise cases, the prefrontal cortex
does not appear to have strong associations with
cessation of dreaming.
Neuroanatomical analysis
of Solmss original records

Frontal-lesion data extracted from the 35 traceable cases from Sample 2 are presented in Table 1.
In contrast to the remarkably high frequency of the
ventromesial frontal lesions (i.e., the frontal white
matter F09 and the head of the caudate nucleus),
relatively few patients in this sample had lesions in
the prefrontal convexity (i.e., BA8, BA9, BA10,
BA11, BA45, BA46, BA47). This distribution resembles the results drawn from the clinical literature.

161

With respect to lesions of the prefrontal convexity, there are two main regions of interest, namely,
the dorsolateral prefrontal cortex (made up by BA46
and BA9) and the lateral orbital cortex (constituted
by BA11 and BA10). Their incidence rates are
relatively low, and all patients with BA46, BA9,
BA11, or BA10 lesions also sustained neuropathology to the two robust neuroanatomical correlates of
dream cessationnamely, BA37 (Yu, 2001a) and
the head of the caudate nucleus and the frontal white
matter F09 (Yu, 2001b). In other words, the symptom of dream cessation in these rare cases is not
necessarily ascribed to the prefrontal lesions, but,
rather, should be more convincingly recognized as
the consequence of the lesions of BA37 or the
mesial frontal region.
In a similar vein, nondreaming patients had a
relatively high incidence rate of BA45 lesions
(28.6%) compared with the other prefrontal regions.
Predictably, all these cases also showed lesions to
the head of the caudate nucleus or BA37, except
Case 13 (which had lesions in the frontal white
matter F09) (see Table 2). The prefrontal lesion
does not, therefore, appear to be a significant cause
of dream cessation, in view of the notably low
incidence of this neuropathology in the nondreaming patients.
On the other hand, among the 10 dreaming patients with increased reality of dreaming and varying degrees of confusion between dreams and
reality after insults (i.e., the cases with opposite
symptoms), 6 of them (Cases 106, 136, 147, 194,
281, and 357: the numbers refer to the original case
numbers in Solmss monograph) in stark contrast
had sustained lesions in various prefrontal regions
(e.g., orbital prefrontal lesions, BA11 and BA10,
were found in 4 cases). Without exception, these 6

Table 1
Frontal Lesions in Sample 2
Region

Substructures

Frequency

Frontal (convexity)

BA8
BA9
BA10
BA11
BA45
BA46
BA47

3
9
5
4
10
6
3

8.6*
25.7
14.3
11.4
28.6
17.1
8.6

Frontal (ventromesial)

frontal white matter (F09)

head of caudate nucleus

16
16

45.7
45.7

*These categories are not exclusive.

Sample: N = 35.

162

Calvin Kai-ching Yu

Table 2
Head of Caudate Nucleus or BA37 Lesions of BA45
Patients
Head
of Caudate

Lesion

BA37 Yes
BA37 No
Total

Head
of Caudate

Yes

No

1
6

2
1

7 (70%)

3 (30%)

Total
3 (30%)
7 (70%)
10 (100%)

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Sample: N = 10.

patients were all assessed by Solms as global fantasyreality confusion (or global dreamreality confusion), while, for the 4 other cases whose focal
lesions clearly did not involve any frontal regions,
there was no indication in 3 of them (Cases 239,
356, and 98) of actual fantasyreality breakdown,
nor of dreamlike thinking extending into waking
life. The one case left (Case 354), according to
Solms, suffered circumscribed fantasyreality
confusion, which was, indeed, if studied more cautiously, quite different from the actual fantasyreality confusion. This patient was capable of noting
that the entire episode had been a dream, though at
first he mistook it as real. Put briefly, lesions in the
prefrontal convexity did not bring about cessation
of dreaming, but, on the contrary, could only result
in dramatizing or intensifying the phenomenon
of dreaming in both qualitative and quantitative
aspects.

Neuroanatomical analysis of PET data

In accordance with highly consistent PET data,

the activity of almost the entire prefrontal convexity
including both the dorsolateral and lateral orbital
aspects is attenuated during the dreaming state,
in contrast to the significant increase in cerebral
activation within the medial frontal region, which
includes the anterior limbic system and basal forebrain (see Table 3). The only slightly controversial
region is BA46. From a statistical point of view,
however, the PET sample shows that the number of
subjects with BA46 deactivation is significantly
greater than the number of activation cases (binomial test, p < .001). The single subject from Heisss
laboratory who experienced an extended nightmare
displayed unselectively higher metabolic rates
throughout the brain and thus seems to be a potentially biased case (see Yu, 2001a).

Discussion
Neuroanatomical correlates
of the dream-censor
In resolving the controversies and uncertainties surrounding dream-censorship on the grounds of the
converging results presented above, the precise
neuroanatomical localization of the dream-censor
will be first clarified in accordance with the functional and developmental point of view, and after
that the discussion moves on to the implications of
the current neuroscientific findings for the notion of

Table 3
Relative Activity of Prefrontal Cortex in Dreaming State
PET Study

BA8

BA9

BA10

BA11

BA46

BA47

Medial

Heiss et al., 1985

Maquet et al., 1990

I (n.s.)

Madsen et al., 1991a

Madsen et al., 1991b
Hong et al., 1995
Maquet et al., 1996

I (R)
D

D (La)

Nofzinger et al., 1997

I (BA24, BA32, WM)

D

I (BA24)
I (BA24, BA25, BA32)

Braun et al., 1997

D (La) I (M)

D (La)

I (BA10, BA32)

Braun et al., 1998

D (La)

Note: I = increase; D = decrease; n.s. = nonsignificant; empty cells = no mention in the study; R = significant only on right side; M =
increase in medial aspect only; La = significant in lateral aspect only; WM = white matter.

Neuroanatomical Correlates of Dreaming, III: The Frontal-Lobe Controversy

censorship as well as for the Freudian model of

dreaming.

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Functions of the prefrontal cortex

and censor
A major organizing principle of prefrontal functions
has long been that of a duality between the dorsolateral (BA46 and BA9) and orbital (BA11 and BA10)
cortices. The interpretation often given to this division is that the orbital prefrontal cortex plays a role
in inhibiting or overcoming incorrect or pre-potent
response tendencies, whereas the dorsolateral convexity, exemplified by the salient delayed-response
deficits, is pivotal to the memorial programming of
appropriate motor sequences (Goldman-Rakic,
1998). In Freuds terms, these are secondary processes, the substitution of the reality principle for
the pleasure principle, and a herald to the censorship.
Following the initial descriptions in the last century of the mental sequelae of frontal damage, it
became apparent that changes in mood, disposition,
and personality are the most evident (Parker &
Crawford, 1992). As Hcaen (1964) demonstrated
in a sample of 131 cases of frontal tumor, 51 (39%)
could be classified as personality-changed, and the
most common symptoms were euphoria and irritability. Kretschmer (1956) divided prefrontal patients into two syndrome groups: a disinhibited
group, associated with orbital lesions, in which an
impulsive, emotionally labile, euphoric, and sometimes jocular disposition was combined with poor
judgment and distractibility; and an apathetic
group, associated with dorsolateral lesions, in
whom incidental angry or aggressive eruptions
could occur, but where psychomotor retardation and
indifference were usual. The disinhibited group, as
highlighted by Parker and Crawford (1992), corresponded to pseudopsychopathic descriptions. In a
study by Eslinger and Damasio (1985), a patient
who had a restricted frontal-lobe resection to treat
an orbital meningioma developed severe social-conduct disturbances. Damage to the orbitofrontal cortex also results in disturbances in emotional and
social behavior (Butter, Snyder, & McDonald,
1970; Myers, Swett, and Miller, 1973) as well as in
learning and reversing stimulusreinforcement associations (Iversen & Mishkin, 1970; Jones &
Mishkin, 1972).
Converging evidence has led to the notion that
the ability to judge the appropriateness of ones own
behaviors (Mesulam, 1985, 1986) and to suppress
inappropriate pre-potent response tendencies is an
intrinsic property of the prefrontal cortex as a whole
(Robert, Robbins, & Weiskrantz, 1998). These

163

functions are at least partly equivalent to the censorship and are subsumed under the rubric of the
superego in the Freudian paradigm.
The orbitofrontal cortex projects extensively
ramifying pathways to the aggressive instinctual
infrastructure in the temporal pole and amygdala, to
the subcortical drive centers in the hypothalamus,
and to the DA neurons in reward centers in the
ventral tegmental area (Nauta, 1964; Schore, 1994,
1996). As Zborszky, Cullinan, and Braun delineated (1991), basal forebrain cholinergic neurons
(note that according to Hobson, 1999, dreams are
activated by cholinergic activity) that receive
orbitofrontal input project to the limbic cortical
areas operating as a gateway between corticolimbic
interactions in waking states. Rolls (1984, 1994)
and Rolls and Johnstone (1992) outline a theory of
striatal function according to which all areas of the
cerebral cortex gain access to the striatum and compete within the striatum and the rest of the basal
ganglia system for behavioral output depending on
how strongly each part of the cerebral cortex is
calling for output, and the striatum maps (as a result
of previous habit or stimulus-response learning)
each particular type of input to the striatum to the
appropriate behavioral output. Over and above the
prefrontal convexity, the basal forebrain acetylcholine (ACh) projection system therefore also plays a
role in the functional networks of the censorship.
Solmss proposition may therefore not be totally
wrong, though it appears conceptually fuzzy to attribute both libidinal drive centers and the censorship to the ventromesial prefrontal region, given the
evidence that the ACh neurons in the basal forebrain
do engage in inhibitory activity, but in a comparatively passive way, effected by the afferents projecting from the orbitofrontal cortex. For the sake of
theoretical clarity, perhaps a more clear-cut demarcation can be drawn by localizing the censor in the
prefrontal convexity.
In any case, the censorship is an extraordinarily
intricate and sophisticated mental process in both a
psychoanalytic and a neurodynamic sense. Not infrequently, when combining with other ego functions, it constitutes what Freud (1940 [1938])
called an ego-organization. It should not be oversimplified and therefore overlocalized to any single
anatomical microstructure but, rather, ought to be
understood in terms of a neural orchestra. The
dream-censor literally functions as an inhibitory
agency, but the term inhibition is far too condensed to capture the complete meaning of the
Freudian censorship. Conscious or unconscious
self-control, primitive inherited affect regulation
(largely determined by genetic factors but still under the impact of social exchange), adaptation via
reinforcement and punishment, social judgment,

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164

logical reasoning, self-monitoring, and moral schemata acquired through internalization and socializationthe amalgam of all of these is what
Freud called the censorship. Solmss censor,
Damasios somatic marker, Rollss basal ganglia gateway, and Allan Schores affect regulatory circuits bear their different names with
discrete emphases, covering the overlapping and
cognate neuroanatomical geographythat is, the
orbitofrontal system, or, more precisely, the caudal
orbital (ventromedial frontal) region. They all aver
that this region of the brain functions distinctly for
behavioral and sometimes affective inhibition
more correctly, unconscious and primitive inhibitionnot necessarily sustained by moral and
logical scaffoldings, but, instead, under the predisposition of genetic programming and alterations,
modulated and maintained via social affective interactions and stimulus-response learning (Rolls,
1975, 1986a, 1986b, 1990, 1992, 1994, 1995, 1998;
Schore, 1994, 1996, 1997). It is presymbolic and is
well-developed before full language competency
(around 2 to 3 years of age) (Schore, 1994, 1996).
This very primitive inhibitory function, which can
transpire unconsciously (Rolls, 1998), is undoubtedly merely a very small but pivotal portion of the
censor. To put it in Freuds terms, it can be conceived of as the sine qua non or the core of the
censorship because it develops before 3 years of
age, preceding the development of conscience and
logical reasoning. In line with the solid research
findings discussed above, the censorship proper
comprises both this core and derivatives of it,
which lie on the lateral orbital and dorsolateral
regions of the prefrontal convexity. These are neural substrates for sophisticated moral and logical
reasoning and working memory (Luria, 1973;
Roberts, Robbins, & Weiskrantz, 1998), which
clearly encompass essential attributes of Freuds
censor.
Apparently, the deactivation of the prefrontal
convexity during dreaming sleep, as demonstrated
by the consensual findings, resembles the conditions of prefrontal lesionsthat is, disinhibited,
euphoric, and even narcissistic ruthlessness, due to
loosening governance over the id energies by the
self-monitoring agency, and, along with the loss of
the function of reality-testing and the withdrawal of
cathexes from external reality, a temporary pseudopsychopathic type of psychic life is the result. This
effect becomes even more dramatic and obvious in
patients with the very symptom of fantasyreality
breakdown due to prefrontal lesions.
Frank (1950) observed that patients with ablated
orbital cortices showed a reduction in the complexity of dreams and their dream content reflected, like
the dreams of children, direct wish-fulfillment.

Calvin Kai-ching Yu

Development of the prefrontal cortex and

censor
The dream-censor or superego, which begins to
develop in the oedipal phase, is the product of
socialization, learning, and cultural orientation
rather than being an instinctual or inborn function.
As underlined by Schore (1994, 1996, 1997), the
interval between ages 1012 and 1718 months is
indeed a critical period for the final maturation of
the orbital prefrontal system, including, of course,
the ventromesial frontal region, whose offset is
thereafter supervened by the onset of a critical period for the maturation of the dorsolateral prefrontal
association cortex (Schore, 1994, 1997). The experience-dependent growth of descending fibers to the
locus coeruleus from this later-maturing prefrontal
cortex occurs at the end of the second and into the
third year, thereby allowing for an arousal-regulating function of this cortical structure.
Consistently, Chuganis research (1998) showed
that glucose utilization in the frontal cortex increases between ages 6 and 12 months, and the
overall level of glucose use in the developing brain
increases until the age of 4 years, plateaus through
about age 10 years, and decreases gradually to adult
levels between the ages of 16 and 18 years. Crosssectional studies examining brain development in
children and adolescents demonstrated increasing
white-matter volume and decreasing gray-matter
volume in later childhood and early adolescence
(Jernigan & Tallal, 1990; Reiss, Abrams, Singer,
Ross, & Denckla, 1996; Pfefferbaum et al., 1994).
These findings were further confirmed in Giedd et
al.s (1999) study, which found that white-matter
volume increases linearly between ages 4 to 20
years and that the time course is similar for different
cortical regions, whereas, in contrast, cortical graymatter changes are quadratic rather than linear,
showing a preadolescent increase followed by a
postadolescent decrease. The time course of graymatter increases and decreases are different across
different cortical regions. Specifically, gray matter
reaches maximum volume at approximately age 12
years in the frontal lobes, and after this age graymatter volumes decrease.
According to Luria (1973), as the prefrontal cortex develops, a childs behavior begins to become
subordinated to logical reasoning, complex programs, and assessment and correction of errors.
Similar phenomenon of brain-dependent functional
development was revealed by Caseys fMRI study
(1999), in which the brain circuitry underlying inhibitory mental processes is the same in children
(ages 712 years) and adults (ages 2124) during
the performance of a task requiring behavioral inhibitionthat is, prefrontal activation. However, this

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Neuroanatomical Correlates of Dreaming, III: The Frontal-Lobe Controversy

study also found that the volume of the activation

was greater for children than for adults, especially
in the dorsolateral prefrontal cortex. This suggests
that children may have to activate and thus utilize
more of the dorsolateral prefrontal area to perform
the task, whereas adults greater efficiency (i.e., less
activation volume) corresponds to the greater neural-selectivity characteristic of the more mature prefrontal brain.
Apparently, the development of the prefrontal
regions is far more complicated than what earlier
studies showed. It is not easy to specify the chronological agenda of the frontal development, and the
concept of maturation seems to be relative rather
than definitive. Nevertheless, the accumulating consistent evidence indicates that the frontal cortices
the most superior and anterior part of the
brainand therefore their functions as well would
be expected to develop last. So does the superego in
the structural evolution.
On the one hand, the parallel neuropsychological
evolution of the prefrontal cortex and the dreamcensor provides compelling evidence for a deep
homology between them. On the other hand, the
pervasive deactivation of the prefrontal cortex, as
opposed to the activation of the mesolimbic DA
system during dreaming, as indicated by the current
findings, underpins the intrapsychic theory that
through dreaming, mental activity regresses developmentally from the experience-dependent adult
cortex back to the subcortical regions that dominate in infancy and childhood; mature logical reasoning and modes of thinking are temporarily
abandoned in the service of childish ones (e.g.,
irrational, illogical, unbridled, id-determined, and
pleasure-oriented).

Incessant combat between the censor

and the id
Braun (1999) and Hobson (1999; Hobson & PaceSchott, 1999) argue that there is no distinction between manifest dream-material and latent
dream-thoughts, inasmuch as the hypothetical censorship (the dorsolateral prefrontal cortex) has been
shown to be a fallacy vis--vis its deactivation.
. . . if there is any single region of the brain felt to be
essential for self-monitoring, abstraction and symbolic encoding, it would be the dorsolateral prefrontal cortexa region in which activity plummets
at sleep onset and in which functional inactivity is
destined to persist throughout the entire sleep cycle.
[Braun, 1999, p. 199]
. . . areas of the dorsolateral and orbital prefrontal
cortex that one would think might play such a role
via their mediation of behavioural inhibition . . . are

165

deactivated in both REM and NREM sleep, not

activated as Solms would have to predict. [Hobson
& Pace-Schott, 1999, p. 211]

It is wrong, however, first, to assume that the

neural infrastructure of the censorship should be
more activated during sleep than during waking,
and, second, to suppose any equivalence between
deactivation and the absolute tranquility of any part
of the brain. Concerning the first theoretical error
committed by Hobson and Braun, the opposite is, in
fact, the case:
. . . we have every reason to suppose that in sleep
the censorship between the Pcs. and the Ucs. is
greatly reduced, so that communication between the
two systems is made easier. [Freud, 1917/1915, p.
225]
In the state of sleep this probably occurs owing to a
relaxation of the censorship; when this happens it
becomes possible for what has hitherto been repressed to make a path for itself to consciousness.
[Freud, 1901, p. 676]

With regard to the second error, as evidenced by the

PET data, though the prefrontal cortex is largely
deactivated, its activity is nevertheless still presentin other words, it remains operative.
. . . however, the censorship is never completely
eliminated but merely reduced. [Freud, 1901, p.
676]
. . . the censorship between the Ucs. and the Pcs.
must remain, even if not at its full strength. [Freud,
1917/1915, p. 225]

What appeared so incompatible in the Freudian

supposition of censorship to Braun and Hobson,
after theoretical clarification, is congruous with the
theoretical picture in every way and in fact breathes
new life into Freuds concept of censorship in
dreaming. On the grounds of the PET findings,
Braun et al. (1997) hypothesized that REM episodes
occurring later in the sleep period would be characterized by increasing coherence of prefrontal,
dorsomedial thalamic, and striatal activity, which
could in turn correlate with the time-of-nightdependent changes in the length and complexity of
REM sleep dream reports (Cipolli & Poli, 1992;
Snyder, 1970). The level of activation or deactivation of the prefrontal cortex therefore changes
across different REM episodes within one sleep
epoch and, in fact, graduallyinstead of instantaneouslyrecovers its normal activity from its lowest
point in the first REM episode, via progressive
activation in the intermediate REM episodes, to its
full convalescence in postsleep waking. By implication, not only is this vigilant agency never totally
quiescent during all REM episodes, but it also
gradually recuperates from deep relaxation and becomes highly alert toward the end of sleep.

166

Calvin Kai-ching Yu

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1 Withdrawal of libido

4 Kindom of illogic

7 Epicenter of censorship

2 Developmental regression

3 Weakened censorship

5 Condensation and displacement

6 Eros

8 Suppression of motor discharge

Figure 1.

9 Topographical regression

A Neuro-Structural Model of Dreaming.

While the most robust activity in the nucleus

accumbens (mesial frontal region) was detected in
REM sleep, where the most precipitous decreases
were found in the prefrontal cortex, the most silent
moment of the nucleus accumbens (except in slowwave sleep) appears in presleep wakefulness, where
the prefrontal cortex is most activated. These striking oscillatory neurodynamics between the prefrontal and subcortical activities seem to define the
nature of sleep per se and therefore, perhaps, the
psychodynamics between the superego and the id.
When the state of sleep is over, the censorship
quickly recovers its full strength; and it can now
wipe out all that was won from it during the period
of its weakness. [Freud, 1901, p. 677]

Conclusion:
A neurostructural model of dreaming
amenable to further scientific validation
After we have completed our psycho-analytic work
we shall have to find a point of contact with biol-

ogy; and we may rightly feel glad if that contact is

already assured at one important point or another.
[Freud, 1913, pp. 181-182]

Here, then, is the story of dreaming suggested by the

findings of this and the other two research papers
(Yu, 2001a, 2001b) in the series. Striate cortexthe
primary visual cortex, which mediates interactions
with the external world in the daytime, being the
primary window (named the attention window
and visual buffer by Kosslyn & Koenig, 1995),
connecting as it does the external and visceral milieu
and being a channel for directing peoples interest to
external objectsshuts down at night. This reflects
the withdrawal of interest, libido, and object-cathexes from external realitythat is, the revival of
narcissism (Figure 1, Panel 1). The prefrontal cortexthe mature experience-dependent cortex,
which grows in parallel with psychological and
cognitive evolutionis characterized by its immaturity and incapacity to function during infancy; however, in contrast, when developed, it dominates the
psychological and cognitive functions of adulthood
and equips people with adultlike thoughts. Side by

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Neuroanatomical Correlates of Dreaming, III: The Frontal-Lobe Controversy

side with the withdrawal of libido, the deactivation

of this rational and logical system therefore paves
the way for a return to early infancya developmental regressionand simultaneously its concomitance, the pleasure principle, which has ever
dominated in infancy and childhood, once again
surpasses the reality principle (Panel 2). One of the
prefrontal systemsthe orbitofrontal cortexlies
anatomically and psychologically between the neocortex (the system Conscious) and the subcortical
regions (the system Unconscious); this system functions as the lord of the ego and inhibition and
therefore censorship. It becomes weaker during
sleep and dreaming, when, even though it is not at its
full strength, it nevertheless remains operative
(Panel 3). Seizing the chance of favorable circumstances, with a disguised way of expression furnished by the disintegration of the whole cortical
system as a result of the widespread deactivation
over the associative regions on the one hand (Panel
4), and by the condensation and displacement fabricated actively by the inferotemporal cortex on the
other (Panel 5), the ego is freed from ethical bonds. It
finds itself at one with the demands of sexual and
primitive desire via the mesolimbic dopaminergic
and LUST (Panksepp, 1998) systems, Eros (Panel
6), even those that have long been prohibited by the
orbital and dorsolateral prefrontal cortices, the experience-dependent growth regions that are subject to
parental, societal, and moral influences and to social
conditioning throughout their maturation (Panel 7).
In this vein, control over the unconscious id is
loosened. Along with the restoration of the power of
the id, which takes advantage of the weakened censorship, the decision-making systems behind each
movement executed during the daynamely, the
dorsolateral prefrontal cortexare, conversely, deactivated and direct motor discharge is suppressed
(Panel 8). In order to protect sleep from disturbing
stimuli, the instinctual impulses, therefore, via the
inferomesial temporal-limbic pathway (Panel 9),
topographically regress to the visual perceptual systemsthe extrastriate visual corticesin the form
of hallucinatory wish-fulfillment.
The deficiencies in our description would probably
vanish if we were already in a position to replace
the psychological terms by physiological or chemical ones. [Freud, 1920, p. 60]

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