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Neuropsychoanalysis: An Interdisciplinary Journal

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Neuroanatomical Correlates of Dreaming: The

Supramarginal Gyrus Controversy (Dream Work)
a

Calvin Kai-ching Yu
a

Department of Counselling and Psychology, Hong Kong Shue Yan College, 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: The Supramarginal Gyrus
Controversy (Dream Work), Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences,
3:1, 47-59, DOI: 10.1080/15294145.2001.10773336
To link to this article: http://dx.doi.org/10.1080/15294145.2001.10773336

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47

Original Articles

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Neuroanatomical Correlates of Dreaming: The

Supramarginal Gyrus Controversy (Dream
Work)!
Calvin Kai-ching Yu (Hong Kong)

Abstract: This paper aims to resolve the contradictory findings

between PET and human lesion methods concerning the role of
the inferior parietal lobule (supramarginal gyrus) in the functional
architecture of dreaming, and to provide a more comprehensive
neuroscientific justification for its presumed psychoanalytic counterpart, dream work, a mechanism that has long been considered
to be the sine qua non of the Freudian dream model. In contrast
to prevailing belief, the author argues that the classical psychoanalytic notion of this dream mechanism is compatible with, and
also supported by, the most recent neurobiological findings. New
psychoanalytic insights and refinement are also drawn, based on
neuroscientific evidence, which breathe new life into the Freudian
theory of dreaming.

Introduction
This is the first of three articles on the status of Freudian dream theory in the light of recent neuroscientific
findings. This first study concerns the role of the inferior parietal lobule in contemporary neurological models of dreaming and its implications for the Freudian
notion of dream work.
Solms (1995, 1997, 2000), basing his claims on
the clinicoanatomical method, put forth the argument
that in dream formation abstract thoughts and memories are converted into concrete perceptions via the
Acknowledgment: The author dedicates this series of articles to Mark
Solms, from whom (apart from Freud) he has learned most in his life. He
would also like to thank Allen R. Braun, G. William Domhoff, Eric A.
Nofzinger, and Pierre Maquet for the materials they provided. Thanks also
to Hester McIntyre for her indefatigable support.
Calvin Kai-ching Yu, M.Sc., is a Lecturer in Psychology, Department
of Counselling and Psychology, Hong Kong Shue Yan College, Hong
Kong.

path of the inferior parietal lobule, in particular the

supramarginal gyrus (BA40), taking into account its
presumed functions at the highest levels of perceptual
information processing and symbolic operations.
The evidential basis for this claim is Solms' s
(1997) finding that inferior parietal lesions produce a
total cessation of dreaming, whereas unimodal visual
cortical lesions produce modality-specific deficits of
visual dream imagery. According to Solms, the normal
sequence of events in perceptual processing is thus
reversed in dreams following the rule of regression:
"the fabric of the dream-thoughts is resolved into its
raw material" (Freud, 1900, p. 543). Furthermore,
since dorsolateral frontal lesions have no apparent effect on dreaming, Solms (1997) argues that the focal
point of cerebral activity shifts from the dorsolateral
frontal region, the executive end of the motor systems
in waking life, toward the perceptual systems, via the
regressive pathway provided by the inferior parietal
region. This, according to Solms (1997), is exactly
what Freud meant by "topographical regression,"
perhaps the most essential part of the normal process
whereby dreams are formed (the dream work). The
inferior parietal lobule, from this point of view, is
thought to be an indispensable ingredient of the functional architecture of dreaming. Moreover, this attribution of an important functional role to the inferior
parietal lobule applies equally to the "neuropsychological-psychoanalytic" model of Solms (1995, 1999)
and the alternative, "integrated model" of Hobson
(Hobson, Pace-Schott and Stickgold, 2000).1
lThe inferior parietal region appears as "zone 2" in Solms's model,
as depicted by Hobson, and "zone 9" in Hobson's own model (Hobson
et aI., 2000).

Downloaded by [Adelphi University] at 23:21 19 August 2014

48

Some recent PET studies (e.g., Maquet, Peters,

Aerts et aI., 1996; Braun, Balkin, Wesensten, Gwadry
et aI., 1998), however, reveal that the inferior parietal
cortex, including the supramarginal gyrus (BA40), to
which Solms attributes such important functions in
dream formation (and where lesions apparently produce a total loss of dreaming) is significantly deactivated during REM sleep. Furthermore, although Solms
(1999, 2000) has tried to apply neuroscientific findings
to the Freudian dream theory, the picture he describes
is not at all complete. Topographical regression, for
example, is only one of the aspects of dream regression. Dream work, which includes equally basic mechanisms of condensation and displacement, has not
been fully accounted for in Solms's model. Thus,
Braun (2000) argues that the sophisticated process of
dream work requires considerable mobilization of the
brain's reflexive, executive mechanisms. These mechanisms are conventionally linked with the dorsolateral
prefrontal cortex. Yet this region, no less than the inferior parietal lobes, is unequivocally deactivated during
dreaming (Braun, Balkin, Wesensten, Carson et aI.,
1997) and lesions here have no effect on dreams
(Solms, 1997).
The disparity between the clinicoanatomical and
PET methods with respect to the inferior parietal lobes
is striking and has important implications for the scientific viability of psychoanalytic dream theory. The
primary aim of this study is to attempt to clarify the
evidential basis for this disagreement between the two
methods, and to attempt to find a resolution.

Method

Calvin Kai-ching Yu
Sample 1: Published Cases from the Clinical Literature

The first sample consisted of 61 clinical cases of global

cessation of dreaming reported in the neurological literature (Wilbrand, 1887, 1892; Muller, 1892;
Grunstein, 1924; Lyman, Kwan, and Chao, 1938;
Piehler, 1950; Humphrey and Zangwill, 1951; Gloning
and Sternbach, 1953; Boyle and Nielsen, 1954; Nielsen, 1955; Ettlinger, Warrington, and Zangwill, 1957;
Ritchie, 1959; Michel, Jeannerod, and Devic, 1965;
Farrell, 1969; Benson and Greenberg, 1969; Feldman,
1971; Moss, 1972; Wapner, Judd, and Gardner, 1978;
A. Epstein, 1979; Basso, Bisiach, and Luzzatti, 1980;
Michel and Sieroff, 1981; E. Epstein and Simmons,
1983; Corda, 1985; Schanfald, Pearlman, and
Greenberg, 1985; Pena-Casanova, Roig-Rovira, Bermudez, and Tolosa-Sarro, 1985; Habib and Sirigu,
1987; Farah, Levine, and Calviano, 1988; Neal,
1988).2 These were all patients who experienced
global cessation of dreaming as a consequence of neurological insult, regardless of the lesion site or type
(see Table 1). This sample included 34 males (55.70/0),
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 1
Neuropathology in Sample 1 (N = 61)
Pathology
Cerebrovascular Disease
Tumor
Infection
Trauma
Leukotomy
Toxic Disease
Missing Data
Total

Frequency
34
9
1
5
6
1
5
61

0/0
55.7
14.8
1.6
8.2
9.8
1.6
8.2
100

Subjects

Three different sets of data were analyzed in the current study in order to achieve a more comprehensive
and reliable picture of the part played by the inferior
parietal lobule in dreaming sleep than has hitherto
been available: (1) all previous case reports from the
clinical literature in which precise anatomical data
were provided, prior to Solms's (1997) monograph;
(2) all the available CT and MRI scans of the clinical
cases studied in Solms's monograph; and (3) all the
available PET data in the published literature. The current study involves a detailed reanalysis and comparison of these three sets of data.

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 experienced
global cessation of dreaming as a consequence of neurological insult, regardless of the lesion site or type
(see Table 2). Mean age is 40.8 (s.d. == 17.77, min.
=: 10, max. == 77).
2A complete tabulation of these cases is archived at http://www.neuropsa.com/archive
31 am grateful to Dr. Solms for making this raw data available to me.

Neuroanatomical Correlates of Dreaming

49

Table 2
Neuropathology of Sample 2 (N = 64)
Pathology

Frequency

17

26.6
1.6

Cerebrovascular Disease
Congenital
Malformation
Benign Cyst
Tumor
Trauma
Degenerative Disease
Infection
Total

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Table 3
Methods Used in Sample 3 (N

2
21
19

1
3
64

3.1
32.8
29.7
1.6
4.7
100

Sample 3: Published PET Data

The third sample consisted in PET data drawn from
nine previous studies, involving a total of 118 healthy
subjects (Heiss, Pawlik, Herholz, Wagner, and Wienhard, 1985; Maquet, Dive, Salmon et aI., 1990; Madsen, Holm, Vorstrup et aI., 1991a; Madsen, Schmidt,
Wildschi~dtz et aI., 1991b; Hong, Gillin, Dow, Wu,
and Buchsbaum, 1995; Maquet, Peters, Aerts et aI.,
1996; Nofzinger, Mintun, Wiseman, Kupfer, and
Moore, 1997; Braun, Balkin, Wesensten, Carson et
aI., 1997; Braun, Balkin, Wesensten, Gwadry et aI.,
1998). Ninety-one of these subjects were male
(77.1 %) and 18 were female (15.3%). The sex of 9
subjects was not mentioned in the original studies
(7.6%).
The methods employed across the nine studies,
though similar, were not identical (see Table 3). Hong
et aI.' s study (1995), for example, instead of comparing the cerebral activity in dreaming states against that
of wakefulness, correlated the cerebral metabolic rate
with the number of REMs during "dreaming" sleep.
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 (Madsen et aI., 1991b).

Procedure and Materials

The locations of the lesions in samples 1 and 2 were
coded as precisely as possible, using the cytoarchitectonic maps of Brodmann (1909) and the templates of
Damasio and Damasio (1989), and the original descriptions and illustrations in sample 1 and the original
CT and MRI scans in sample 2. Among the 61 cases
in sample 1, only 8 cases were suitable for such precise
localization, since most of the original descriptions

118 Ss)

PET Study

Measure

REM State
Compared to

No. & Sex of Subjects

Heiss et al.
(1985)
Maquet et al.
(1990)

rCMR Glu

Wakefulness

rCMR Glu

Wakefulness

rCBF

Wakefulness

Experimental: 1 M
Control: 5 M
Experimental: 10 M, 1
F
Control: 9 M
6M&5 F

gCBF
gCMRo 2
rCMR Glu

Wakefulness

8 M &6F

Madsen et al.
(1991a)
Madsen et al.
(1991b)
Hong et al.
(1995)
Maquet et al.
(1996)
Nofzinger et al.
(1997)
Braun et al.
(1997)
Braun et al.
(1998)

rCBF

Correlate with No. of Experimental: 9

REM
Control: 6
Wakefulness & SWS 19 M

rCMR Glu

Wakefulness

6F

rCBF

Wakefulness & SWS

37 M

rCBF

Wakefulness & SWS

10M

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

Flow, Glu = glucose, 02 = oxygen

were either not concrete enough or lacking in illustrations suitable for accurate coding. Likewise, only 35
of the 64 patients in sample 2 could be traced using
this precise method (principally due to current unavailability of the original records).
The PET data (sample 3) was similarly coded,
adopting Damasio and Damasio's (1989) method. The
Brodmann-coded brain lesions of the patients from
the first and second samples and the Brodmann-coded
locations identified by the PET data of REM' 'dreaming" sleep were then analyzed and compared.

Results
This section is divided into three parts corresponding
to the three samples and it clarifies which posterior
cortical structures are actively necessary for dream
formation and which are not. The supramarginal gyrus
is, as mentioned previously, at the heart of the
question.
Neuroanatomical Analysis of Clinical Cases from
the Literature
Posterior cortical lesions were prominent in the 61
cases reported in the clinical literature (38 cases) and

50

Calvin Kai-ching Yu

in the 8 cases from which more precise anatomical

data were available (all 8 cases). The lesions involved
the temporal lobe more than any other (28/61 cases
in the total sample; 6/8 cases in the detailed subsam-

Table 6
Traceable Cytoarchitectonic Data in Sample 1 (N = 8)
Lobe Involved

BA

Laterality & Case No.

Frontal

4
6
9
44
45
46

R58
B58
L58
L58
L58
L58

Parietal

5
7
39
40

L5,
L5,
L5,
L5,

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Table 4
Neuroanatomical Characteristics of the Clinical Cases Reported in the Literature (1) (N = 61)
Lesions Include

Frequency

Frontal Lobe
Parietal Lobe
Temporal Lobe
Occipital Lobe

22
25
28
24

36.1
41.0
45.9
39.3

Temporal

These lesion sites are not exclusive.

pIe; see Table 4). The most common combination of

lesion sites was temporo-occipital (10/61 cases; 7/8
Table 5
Neuroanatomical Characteristics of the Clinical Cases Reported in the Literature (2) (N = 61)
Localization
Frontal
Parietal
Temporal
Occipital
Frontal-Parietal
Frontal-Temporal
Parietal-Temporal
Parietal-Occipital
Temporal-Occipital
Frontal-ParietalTemporal
Left Hemisphere
Pure Centrencephalic
Total

Frequency

10
6
4
6
3
3
5
5
10
3

16.4
9.8
6.6
9.8
4.9
4.9
8.2
8.2
16.4
4.9

3
3
61

4.9
4.9
100

cases; see Table 5). Looking in more detail at the cytoarchitectonic areas involved in the 8 traceable cases
(Table 6), the most common lesion sites were in areas
18 (6 cases), 19 (5 cases), and 37 (5 cases). Area 40
was affected in only two cases (cases 5 [tumor] and
58 [cerebrovascular disease])4. In one of these cases
(Michel et aI., 1965, case with multiple vascular lesions; case 58 in the table archived at http://
www.neuro-psa.com/archive) the lesion was widely
distributed and therefore difficult to interpret in localizationist terms. Significantly, this patient also had pathology in the temporo-occipital area, and in
Brodmann's areas 18 and 19 in particular. The lesion
4These case numbers refer to the table archived at http://www.neuropas.com/archive

Occipital

22
27
28
36
37
23
Insula
17
18
19

Frequency

L58
L45, R58
B58
B58

R30, L58
R46
L37, L45, R46
L37, L45, R46
R30,L37,L45,R46, L47
L45, L58
R30
Rl, R30, L45, L47
Bl,R30,L37,L45,L47,L58
R30,L37,L45,L47,B58

2
3
2

2
2
1

3
3
5
2
1
4

6
5

Case number refers to the table archived at http://www.neuro-psa.com/archive

BA37 = inferior temporal gyrus, BA37 + BA36 = temporo-occipital junction, BA37
+ BA27 = hippocampal-parahippocampal regions, BA37 + BA19 = extrastriate
cortex, BA28 + BA36 = amygdala and hippocampus; R = Right; L = Left; B
= Bilateral.

was therefore circumscribed to area 40 in only one

case (case 5, Lyman et aI.'s 1938 case of parietal
tumor).
Neuroanatomical Analysis of Solms's Original
Records

At first glance, the distribution of the lesions in

Solms's clinical series appears to be quite different
from and even incompatible with that in the previous
literature (Table 7). Posterior lesions predominate
once again. However, in stark contrast to the prevalence of temporo-occipital lesions in the nondreaming
patients from the literature, parietal lesions seem to be
predominant in Solms' s series (27/35 cases == 77.1 %).
This number significantly outweighs the incidence rates of lesions in the other three lobes (X 2 ==
11.64, df == 3, P < 0.01). Consistent with Solms's
(1997) hypothesis but in striking contradiction to the
results drawn from the previous literature (pp. 49-50)
and the PET data (p. 52), this data seem to support
the hypothesis that parietal lesions are a significant
neuroanatomical correlate of cessation of dreaming.

Neuroanatomical Correlates of Dreaming

51

Table 7
Traceable Gross Lesion Data in Sample 2 (N = 35)
Frequency

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Localization
Frontal
Parietal
Temporal
Occipital
Frontal-Parietal
Frontal-Temporal
Parietal-Temporal
Parietal-Occipital
Temporo-Occipital
Frontal-Parietal-Temporal
Frontal-Parietal-Occipital
Parietal-Temporal-Occipital
Total

4
3
1
0
8
0
7
2
3
5
1
1
35

11.4
8.6
2.9
0
22.9
0
20.0
5.7
8.6
14.3
2.9
2.9
100

Seventeen cytoarchitectonic regions of interest

with reference to Solms's series are listed in Table 8.
Table 8
Traceable Cytoarchitectonic Data in Sample 2 (N = 35)
Lobe

Substructures Left Right Bilateral Total

Frontal

BA8
BA9
BAIO
BAil
BA45
BA46
BA47

1
3
2
1
3
2
2

2
6
3
3
6
3
1

Parietal

BA39
BA40

3
8

6
12

Temporal

BA20
BA21
BA22
BA37

4
7
10
6

4
6
II
8

Occipital

BA17
BA18
BA19

3
3
5

Subcortical

Thalamus

3
9
5
4
10
6
3

8.6
25.7
14.3
11.4
28.6
17.1
8.6

10
21

28.6
60

0
0
0
0

8
13
21
14

22.9
37.1
60
40

0
1
3

0
0
0

3
4
8

8.6
11.4
22.9

10

28.6

0
0
0
0
I
1
0

These 17 regions are not all the Brodmann areas damaged in the nondreaming patients, but all are related
to the controversy at issue here. Consonant with the
impressive incidence of the parietal lesions noted
above, the supramarginal gyrus (BA40) is also the
most frequent cytoarchitectonic site of lesion (60%).
However, the same rate of occurrence was found in
the superior temporal gyrus (BA22). An area that appeared significant in our analysis of the cases in the
previous literature (pp. 49-50) also demonstrated rela-

tively high frequencies in Solms' s series (40%),

namely, the temporo-occipital junction (BA37). The
same cannot be said for areas 18 and 19 (frequency
== 11.4 and 22.9% respectively).
Although BA40 lesions were common in comparison with the other regions of interest in this series,
cessation of dreaming in the cases with BA40 lesions
is nevertheless not necessarily the result of BA40 lesion alone. Rather, it may be the consequence of neuropathology concurrently affecting other crucial
components of the functional architecture of dreaming
in the same patients. In this regard, areas 22 and 37
appear to be of particular interest. If nondreaming patients with BA40 lesions also sustained injury to BA22
or BA37, the role of BA40 in the neural network of
dreaming is more questionable.
A significant positive correlation between BA40
and BA22, which is located immediately inferior to
BA40, was found (Pearson's X2 == 5.73, df == 1, P <
0.05; <I> == 0.40, P < 0.05). More than half of the
Table 9
Other Lesion Sites Found in BA40 Patients in Sample 2 (N =
21)

Regions

Frequency

BA22
BA37
Thalamus
BA19
BA18

16
10
8
5
2

76.19
47.62
38.1
23.8
9.5

BA40 patients sustained lesions to BA22 (Table 9).

Although there is no significant association between
lesions in BA40 and BA37 (Pearson's X2 == 1.27, df
== 1, P > 0.1), a considerable number of patients sustained both lesions, that is, half of the patients who
had BA40 lesions also sustained BA37 lesions. The
same applies to the thalamus, which may be important
in this connection due to its function of relaying information to various cortical areas. Further, despite the
small number of cases with occipital pathology in this
sample, 23.8% of BA40 patients had lesions in BA19.
Only three of the 21 cases with BA40 lesions
(14.3% of cases with BA40 lesions) were entirely free
of lesions in BA37 and 22 or the thalamus. In other
words, 85.7% of the cases with BA40 lesions also sustained injuries to these three other cytoarchitectonic
regions of interest. The three exceptional cases with
BA40 lesions but intact BA37, BA22, 19 and 18 and
thalamus (cases 17 [Solms's case 143 with right parietal infarct], 29 [Solms's case 244 with left parietal

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52
tumor]5 and 41 [Solms's case 327 with right parietal
hemorrhage]) sustained relatively circumscribed parietallesions.)6 Nonetheless, it should also be noted that
while two nondreamers sustained injury to BA40
alone, there are also 3 patients in Solms's series whose
cessation of dreaming was evidently caused by the
pure temporo-occipital lesions, which completely
spared the parietal lobes (case 7 [arachnoid cyst], 61
[meningioma], and 63 [intracerebral hemorrhage and
shrapnel trauma]).
In summary, although BA40 lesions are relatively prevalent in Solms's series, and although there
are two nondreamers whose lesions were entirely circumscribed to BA40, dream cessation in 90.5% of
Solms's patients with BA40 lesions could also be attributed to concomitant lesions in regions of the temporo-occipital junction and thalamus.
Neuroanatomical Analysis of the PET Data

The bulk of the data from different laboratories shows

a significant decrease in activity of the supramarginal
gyrus (BA40) during REM "dreaming" sleep. The
same seems to apply to the remainder of the inferior
parietal lobule: the angular gyrus (BA39) (see Table
10). Increased activity in these areas is documented
by Madsen's group, but this was not statistically significant. The single subject from Heiss's laboratory
who experienced an extended nightmare (frightening
dream with intimidating human figures moving around
and toward him) also showed activation in this area;
but Heiss's case also displayed considerably higher
metabolic rates throughout the brain and thus seems
to be a potentially biased case. It should also be noted
once again that Hong's data are based on a different
method of measurement. Nonetheless, in Maquet's
study, right anterior BA40 did seem to be activated
during "dreaming" sleep.
On a statistical level, across the 9 PET studies,
the number of subjects with decreased CMR or CBF
in BA40 is far greater than the number of subjects
with increased activity in this area (including cases
with nonsignificant increases and Heiss's potentially
biased case). The only exception to this rule is right
5This patient had a metastatic carcinoma in the deep parietal-occipital
area. The lesion included BA19, which is situated directly adjacent to
BA37. Furthermore, the left temporal horn was distorted to the point of
being invisible on CT scan, due to the space-displacing effect of the mass
lesion. The lesion therefore probably included the tempore-occipital junction and thus BA37 was almost certainly disconnected.
6These case numbers refer to the table archived at http://www.neuropsa.com/archive

Calvin Kai-ching Yu

Table 10
Activation and Deactivation of BA40 & BA39 in REM Sleep
PET Study

Heiss et al.
(1985)
Maquet et al.
(1990)
Madsen et al.
(199la)
Madsen et al.
(199lb)
Hong et al.
(1995)
Maquet et al.
(1996)
Nofzinger et al.
(1997)
Braun et al.
(1997)
Braun et al.
(1998)

LA
BA40

LP
BA40

RA
BA40

RP
BA40

BA39

I (NS)

I (NS)

I (NS)

I (NS)

(NS)

(NS)

(NS)

(NS)

(NS)

LABA40: left anterior supramarginal gyrus, LPBA40: left posterior supramarginal

gyrus, RABA40: right anterior supramarginal gyrus, RPBA40: right posterior supramarginal gyrus, BA39: angular gyrus. I: increase, D: decrease, NS: nonsignificant,
Empty cells: no change or no mention in original study.

anterior BA40 (binomial test, p > 0.5).7 However, deactivation of right anterior BA40 is still more prevalent than activation during dreaming sleep if the
nonsignificant cases are excluded from the sample (binomial test, p == 0.05). The PET data therefore suggest
that the inferior parietal lobule does not playa significant part in dreaming.
In contrast to the general deactivation of BA40
and BA39, the PET data consensually indicate significant activation in almost all regions surrounding
BA40 and BA39 (Table 11). This applies especially
to temporo-occipital regions BA22, 37, and 19. None
of the studies showed significant or nonsignificant deactivation in these three Brodmann areas.

Discussion
Neuroanatomical Correlates of the Dream Work

On the grounds of the overlapping results presented

above, this section will endeavor to resolve the controversies posed by Hobson (2000) and Braun's (2000)
commentaries, and simultaneously explore their impli7Left anterior BA40 (binomial test, p < 0.001), left posterior BA40
(binomial test, p < 0.001), right posterior BA40 (binomial test, p < 0.001).

Neuroanatomical Correlates of Dreaming

53

Table 11
Activation of Regions Surrounding BA40 in REM Sleep
PET Study

BAS

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Heiss et al.
(1985)
Maquet et al.
(1990)
Madsen et al.
(1991a)
Madsen et al.
(1991b)
Hong et al.
(1995)
Maquet et al. D
(1996)

BA7

BA22 BA37 BA19 BA23 BA31 Insula

I (NS) I (L)

I (L)

I (NS)

I (Post)I

D
PosCing

N ofzinger et al.
(1997)
Braun et al.
(1977)

I (R)

I (R)

I (L)

D
PosCing

I (Ant)
D (post)

Braun et al.
(1998)
BAS (supplementary sensory area), 7 (high-order somatosensory system): superior
parietal cortex (precuneus), superior to BA40; BA22: superior temporal cortex, inferior to BA40; BA37: inferior temporal lobule, inferior and posterior to BA40; BA19:
extrastriate cortex, caudal to BA40; BA23, 31: medial parietal-limbic regions (posterior cingulate), behind BA40; Insula: medial tempo-parietal cortex, behind BA40. I:
increase, 0: decrease, NS: nonsignificant, Empty cells: no change or no mention in
original study, R: significant on right side only, L: significant on left side only, Ant:
anterior, Post: posterior.

cations for the Freudian dream theory in the context

of neuroscience. It should be made clear at the outset
that the discrepancy between the distribution of the
first two samples (i.e., the preponderance of temporooccipital lesions in the previous literature as opposed
to parietal lesions in Solms's cases) might be due to
the fact that Solms's cases were an unselected continuous clinical series, whereas the cases in the literature
were selected for publication by virtue of the fact that
they presented with interesting visual disorders (rather
than cessation of dreaming). This is likely to have
resulted in a disproportionately high incidence of temporo-occipital lesions in the latter group.
The PET findings, too, may be potentially biased
(and the role of BA40 in dreaming may accordingly
be rejuvenated) in view of the increasingly apparent
fact that REM sleep is not equal to dreaming sleep
(Solms, 2000). The fact that the inferior parietal lobule
is not consistently activated in REM sleep does not
exclude the possibility that it is consistently activated
in the dreaming portion of both REM and NREM
sleep. A critical test of this possibility must await the
findings of fMRI studies (which permit more precise

temporal resolution than PET studies). Such studies

are currently still in the planning stages. In the present
state of our knowledge, however, the discrepancy between Solms's findings and the available functional
imaging findings are best interpreted as follows. It is
understandable that Solms (1997) privileged the finding in his own unselected continuous clinical series
of a high correlation between inferior parietal lobule
lesions and cessation of dreaming over the previous
literature (cases selectively published for unusual visual disorders), which demonstrated the preponderance of occipito-temporal lesions. However, in light
of the subsequent functional imaging (PET) findings,
unless and until fMRI findings reveal a high correlation between inferior parietal activation and dreaming
sleep, it is more reasonable to reinterpret Solms's
findings in light of the consistent finding in the previ0us literature and the PET literature to the effect that
temporo-occipital structures and not the inferior parietal lobule are implicated in dreaming (or at least
REM) sleep. This brings new significance to the fact
that areas immediately surrounding BA40 and 39 (i.e.
areas BA22, 19 and 37) were contiguously lesioned in
most of Solms's cases. These areas are also implicated
in both the previous clinical literature and the existing
functional imaging studies. In other words it now appears more likely that it was the contiguous occipitotemporal component of the lesions in Solms's cases
that was responsible for the cessation of dreaming.

Pathways of Topographical Regression

Solms (1995, 1999,2000) found a bridge between motivational systems (i.e., the limbic core) and the perceptual hallucinatory apparatus (i.e., the visual cortex)
in the inferior parietal lobule (supramarginal gyrus,
BA40). He linked this with the Freudian theory of
dream formation and topographical regression. The
role of the inferior parietal lobule, however, was
shown to be questionable in the present study where
overlapping results did not provide compelling evidence for its active involvement in dreaming.
The supramarginal gyrus is part of the association
cortex of the posterior cerebrum (BAS, 7, 40, 39, 21
and 37), a "zone of overlapping" within the cortical
end of the various perceptual analyzers that enables
the different modalities to wor k in concert (Luria,
1973). This work of the associative zones of the posterior cortical regions is essential, not only for the successful integration of information reaching man
through his visual system, but also for the transition

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54

from direct, visually represented synthesis to the level

of symbolic processes. BA40 performs critical functions in associating and organizing cross-modal perceptions and visuospatial activities and, in the left
hemisphere, in operations with word meanings, with
complex grammatical and logical structures, with systems of numbers and mathematical relationships.
A theoretical question arises as to whether such
functions are necessary for dream formation. The answer is: almost certainly not. First, visuospatial cognition is indispensable for dreaming not simply because
the visual content of dreams necessarily comprises
concrete space with coordinates that presumably require a minimal level of objective frames of reference,
but rather because they involve objects in the psychoanalytic sense. Second, as regards the "logicogrammatical" functions of the left inferior parietal lobule,
the basic quality of dreaming is not logicogrammatical, but rather elusive and paralogical. This, however,
leads to two further problems.
First, does the inferior parietal lobule never take
part in dream formation? The probable answer to this
question (which can only properly be answered by
further research) is that it most likely depends on the
kind of dreaming (i.e., the nature of the representations) an.d the quality of the dreams in question. Relatively complex dreams made up of sophisticated
spatial and verbal elements, which surely obligate the
functions of spatial orientation and grammatical organization, may recruit the involvement of this important
transmodal cortex. In such dreams significant variances in content and representation are found among
different populations (Foulkes, 1982, 1999; Domhoff,
2000). Children's dreams, for example, the most primal and simple ones, tend to be more visually based
than adults' dreams, as verbal linguistic skills and thus
complicated verbal linguistic elements do not play a
role until dreaming is fully developed around ages 11
to 13 (Foulkes, 1982, 1999). Also, it is an undeniable
fact (as shown in the Results section of this study) that
some patients do lose the capacity to dream after pure
parietal insults, and, therefore, attention may need to
be given to a certain level of individual difference or
dreaming style.
So, if it is accepted that the inferior parietal lobule
is not normally essential to connect the motivational
systems and the visual cortex in the way that Solms
(1997) hypothesized, how might the dream work of
regression be performed? The findings of this study
suggest another pathway for the formation of dreaming in typical cases, namely, the inferior mesial temporal lobe (BA37), which has been identified by this

Calvin Kai-ching Yu
research as one of the most crucial structures in
dream formation.
The anatomical situation of BA37 equips it with
compact neuroanatomical and functional associations
with the occipital cortex (BA19 and 18) on the one
hand, and the paralimbic and limbic structures (BA23,
27, 28, and 36) on the other. Hippocampal and parahippocampal regions (BA37, 36, and 27) are centers
which participate centrally in the encoding and retrieval of memory. The amygdala in anterior BA28
and 36, which serves as a neural substrate of emotional
behaviors and motivation, is intimately connected
with the hippocampus, hypothalamus, cingulate gyrus,
and basal forebrain. The functions subsumed by all
these structures embody basic characteristics of, and
probably necessary preconditions for, dreaming.
Ample evidence supports the suggestion that the
inferotemporal cortex is a "bridge" between the visual cortex and the limbic system, which has intense
afferent and efferent connections with both regions
(e.g., amygdala, hypothalamus, entorhinal area, and
fusiform gyrus) (Whitlok and Nauta, 1956; Akert,
Gruesen, Woolsey, and Meyer, 1961; Prelevic, McIntyre-Burnham, and Gloor, 1976; Turner, Mishkin, and
Knapp, 1980; Creutzfeldt, 1995). Moreover, specific
thalamic afferents to the inferotemporal cortex arrive
via Arnold's bundle from the nucleus inferior of the
pulvinar (thalamus), which in turn receives its afferents from the tectum and the pretectum, as well as
from BA17 and 18. A similar situation also applies to
its connection with the amygdala. Conversely, descending efferents from the temporal cortex project to
the optic tectum, the putamen, and the claustrum (in
external capsule), in addition to the corticofugal reciprocal connections with the pulvinar (Whitlok and
Nauta, 1956).
These connections, furthermore, are consistent
with Braun, Balkin, Wesensten, Gwadrey et al.'s
(1998) finding that the extrastriate activity of BA37
and BA19 is associated with concomitant activation
of the limbic and paralimbic regions. Therefore, lesions here would imply that the intercurrent activity
of this way station is blocked. It is therefore highly
plausible that BA37 constitutes the inferomesio-temporo-Limbic-occipital pathway for topographical regression, and thus for the formation of dreaming, by
connecting motivational and perceptuo-hallucinatory
systems. This pathway is more primitive than the relatively sophisticated pathway constituted by the supramarginal gyrus, but no less capable of performing the
requisite functions.

Neuroanatomical Correlates of Dreaming

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Representation
Interestingly, though unsurprisingly, according to
Frackowiak, Friston, Frith, Dolan, and Mazziotta
(1997), the ability to represent things in mind even in
the absence of direct perception of such things (e.g.,
imaging, active memory) is contributed by a neural
network including the posterior brain. However, the
location of the coactivated posterior brain regions in
question is dependent upon the nature of the representation. As Frackowiak et al. (1997) underscored, research findings consistently indicate relative
functional specialization in the parietal cortex for spatial representations and the inferior temporal cortex
for object representations. The activation of the inferotemporal cortex also provides relatively coarse and
imprecise representations of visual objects. Inferotemporal representation is therefore mainly driven by
"complexity rather than specificity" (Creutzfeldt,
1995, p. 418). More importantly, the inferotemporal
cortex plays a role in categorization, specifically in
the classification of visual stimuli into certain behaviorally meaningful categories, and therefore, forges
connections between visual experience, complex or
sequential behavioral patterns, and temporal emotional
experience (Weiskrantz, 1974; Creutzfeldt, 1995).
In analogy to the parietal association cortex, where
the relationship between visual and somatosensory
signals to the body and the extracorporal space of
action is represented, one could say that in the temporal neocortex the reference of auditory, visual, and
visceral signals to a more subjective' 'space" ofexperience, emotion, and attention is represented, relating
them to behavior as it is controlled by limbic and
hypothalamic mechanisms [Creutzfeldt, 1995, p. 419;
emphasis added].

These bidirectional anatomical pathways seem to signify the qualitative aspect of what most dreams are;
in other words most dreams are complex but vague
rather than specific, object rather than space dominated, oriented in subjective space rather than in objective space, visceral and emotional instead of
external and rational. All these factors cover the essential attributes of dreaming, and seem to resonate with
the Freudian (1914) assertion that the absolute narcissism of the state of sleep implies a withdrawal of cathexis from the external world of real objects back
into the subjective space of the self. "We know that
dreams are completely egoistic and that the person
who plays the chief part in their scenes is always to

55

be recognized as the dreamer" (Freud, 1917, p. 223).

Perhaps, in agreement with the current neuroscientific
findings, this statement can be fine-tuned; dreams are
representations of emotionally charged "object-relationships" in an egoistic context, in which objective
reality and external constraints are relatively disregarded.

Primary Process: Temporal Regression,

Condensation, and Displacement
Intriguingly, it is well known that abnormal excitation
of the temporal lobe alone during an epileptic attack
or exploratory electrical stimulation during surgery
can lead to hallucinations or dreamlike states, termed
"experiential hallucinations" and' 'interpretative illusions" by Penfield (1958). "Stimulation of the cerebral cortex produces perceptual illusions only in the
temporal regions and perhaps extending somewhat
into occipital cortex" (Penfield and Rasmussen, 1955,
p. 173).
As reviewed and delineated by Luria (1973), various kinds of visual-verbal and even spatial hallucinations involve temporo-occipital stimulation, especially
of the inferior regions; for instance, BA18 for elementary visual hallucination, BA19 and 37 for complex
visual hallucination, BA37 for complex spatial displacement, BA22, 41, and 42 for acoustico-verbal hallucination, and BA20 for lingual hallucination. Luria
(1973) described all these hallucinations as reflecting
the subject's previous experience.
The experiential hallucinations comprise elements of
the individual's previous experience drawn together.
They can appear to him so unfamiliar that he describes them as dreams, but after careful analysis
these hallucinations can be broken up into shorter or
longer sequences of earlier experiences. The patient
relives an episode from the past, although he is aware
of the fact of being in the present. All the elements
of the earlier state of consciousness appear to be there
again; light impression, sounds, explanations and
emotions 8 In the case of an illusion of interpretation, there is sudden false explanation or a changed
explanation of the meaning of a current experience.
Things which one has just heard or seen appear suddenly familiar (deja vu == already seen, deja vecu ==
already experienced) or they may, in contrast, appear
strange or nonsensical. They appear to be larger or
8Note the multimodal character of these experiences (vide infra).

56

Calvin Kai-ching Yu

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smaller, to come closer or go further away [Penfield,

1958, pp. 23-24; emphasis added].

A few words seem to paraphrase and reiterate

what Freud set forth about dream work and temporal
regression. The experiential hallucinations caused by
excitations of the temporal cortex appear to be unfamiliar, strange, and senseless, but after analysis "can
be broken up into shorter or longer sequences of earlier
experiences." This is similar to what Freud referred
to as "condensation." In Freudian theory, any event
of incoherent, accentuated, or diminished intensity occurring in dreams is ascribed to the effect of displacement (transvaluation). This too, it seems, can be
triggered by the stimulation of the temporal cortex:
Things suddenly become familiar or, by contrast, appear strange or senseless; they appear to be "larger or
smaller, to come closer or go further away." In this
sense, Penfield's "experiential hallucinations" and
"illusion of perception and interpretation," which
makes things strange and incomprehensible, or dramatically change their original appearances, are homologous to Freud's dream distortion.
It is worth noting that these hallucinations provoked by the temporal lobe excitations, according to
Penfield (and highly congruent with Freud's theory),
are recollections of the unconscious past, which allow
reliving of previous experience that is not normally
accessible to consciousness when awake. To put it in
Freud's words, "the unconscious material forces its
way into the ego" (Freud, 1940, p. 47).
In such repetitions of previous experience perceptions
are largely auditory, or visual, or both. Time seems
to unroll at its normal tempo. The return of the content of consciousness thus evoked, is quite at random,
except that there is some evidence of cortical conditioning. The evolving detail is far greater than in
memories which can be summoned voluntarily. This
demonstrates the existence of a functional system devoted to subconscious recall ofpast experiences [Penfield and Perot, 1963, p. 692; emphasis added].
Memory is far more comprehensive in dreams than
in waking life [Freud, 1940, p. 166].

Multiple Pathways to Regression

BA22, albeit an auditory association area, may provide a potent contribution along the path of the dream
formation by transforming abstract thoughts into the
concrete acoustic or visual content of dreams (e.g.

,'dream thoughts" might, perhaps, first pass through

BA22 before being processed by BA37 and eventually
arriving at BAI9).
Two patients reported by Solms (1997) sustained
lesions to BA37 but instead of a total loss of dreaming,
they reported a cessation of visual dream imagery and
continued to dream with other channels. The incidence
of this kind of disorder is extremely low (1.1 %) and
per contra a considerable number of negative cases
with the same lesions experienced a global cessation
of dreaming. Also, BA37 in these two cases was not
completely destroyed; rather the lesions involved
merely a relatively small portion, that is to say, the
ventromesial aspects of BA37. The lateral aspects of
BA37 were almost completely spared in these cases.
Perhaps the degree to which auditory material predominates in dreams or individual dreamers is determined by the extent to which this channel is relied
upon in any given case.
Other Controversial Issues

Braun (2000) argues that the dream work requires

considerable mobilization of the reflective and other
executive functions of the dorsolateral frontal convexity, which is unequivocally deactivated during dreaming (Braun, et aI., 1997; Solms, 1997). I take an
opposite point of view (Yu, 2000): The pervasive deactivation of all association cortex apart from BA37
(which strongly implies a dissociation of cerebral activity and thereby explains the bewildering effect of
most information processing during dreaming), underscores what Freud put forward as regards the dream
wor k. The dream work and dream distortion may,
accordingly, not only be facilitated by the deactivation
of dorsolateral prefrontal cortex and other association
areas (including BA40) but also positively caused by
the activation of BA37 and related occipito-temporal
structures.
Partly contradicting another controversial argument posed by Hobson (2000), these neuroscientific
findings seem to justify the Freudian view of the distinction between the manifest and latent content of
dreams. Although dream distortion seems not to be
directly related to (or a direct product of) censorship,
so long as dream distortion exists, there is necessarily
a demarcation between the manifest and latent content. Hobson contradicts himself by insisting on the
proposition that there is no real difference between
the manifest content and latent dream thoughts, and
therefore that dreams are transparent and can be read

Neuroanatomical Correlates of Dreaming

directly, while simultaneously recognizing the existence of dream distortion, including the mechanisms
of condensation, displacement, and "symbol formation" (Hobson, 1988; Hobson, Pace-Schott, and
Stickgold, 2000). How can he read a dream directly
without any reconstruction if he acknowledges that
the original content or meaning has been distorted?

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Conclusion
In a nutshell, the combined findings from PET and
clinicoanatomical methods, analyzed in this study,
suggest that the inferomesial temporal cortex is a significant pathway for transforming motivated thoughts
into perceptual hallucinatory satisfactions, regressing
topographically from executive discharge to its perceptual counterpart. Therefore, the inferior parietal
pathway, albeit probably involved in certain kinds of
dreams, is nevertheless not a necessary anatomical
substrate for dream formation. Indeed, the duality (or
multiplicity) of pathways of dream formation and topographical regression not only reflect the diversity of
the quality of dreams, but may also explain why most
nondreamers with focal posterior cortical lesions recover after a certain period (Solms, 1997).
The second article in this series 9 will consider the
precise location of the ventromesial forebrain pathways which appear to instigate dreaming.

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Department of Counselling and Psychology
Hong Kong Shue Yan College
Braemar Hill Road
North Point
Hong Kong
e-mail: calyu@hongkong.com