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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
159
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.
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).
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Calvin Kai-ching Yu
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
1
The case numbers refer to the table archived at www.neuropsa.com/yu.
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)
16
16
45.7
45.7
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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%)
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.
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
I (n.s.)
I (R)
D
D (La)
I (BA24)
I (BA24, BA25, BA32)
D (La) I (M)
D (La)
I (BA10, BA32)
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.
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,
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
165
166
Calvin Kai-ching Yu
1 Withdrawal of libido
4 Kindom of illogic
7 Epicenter of censorship
2 Developmental regression
3 Weakened censorship
6 Eros
Figure 1.
9 Topographical regression
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-
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