is an English translation of an introductory essay written for a
centenary reprint of the 1st edition of Freud’s Traumdeutung (Fischer Verlag, Frankfurt am Main) due November 1999.
The paper provides a basis for the further ideas which will be
presented at the Scientific Meeting of The British
psychoAnalytical Society on 17th November, 1999.
after Freud’s death, the study of dreaming from the perspective
of neuroscience began in earnest. Initially, these studies yielded
results which were hard to reconcile with the psychological
conclusions set out in this book [Traumdeutung (see
footnote)]. The first major breakthrough came in 1953, when
Aserinsky and Kleitman discovered a physiological state which
occurs periodically (in 90 minute cycles) throughout sleep, and
occupies approximately 25% of our sleeping hours. This state is
characterised, amongst other things, by heightened brain
activation, bursts of rapid eye movement (REM), increased
breathing and heart rate, genital engorgement and paralysis of
bodily movement. It consists, in short, in a paradoxical
physiological condition in which one is simultaneously highly
aroused and yet fast asleep. Not surprisingly, Aserinsky and
Kleitman suspected that this REM state (as it came to be known)
was the external manifestation of the subjective dream state. That
suspicion was soon confirmed experimentally, by Aserinsky and
Kleitman (1955) and Dement and Kleitman (1957a, 1957b). It is now
generally accepted that if someone is awakened from REM sleep and
asked whether or not they have been dreaming, they will report
that they were dreaming in as many as 95% of such awakenings.
Non-REM sleep, by contrast, yields dream reports at a rate of only
5-10% of awakenings.
discoveries generated great excitement in the neuroscientific
field: for the first time it appeared to have in its grasp an
objective, physical manifestation of dreaming, the most subjective
of all mental states. All that remained to be done, it seemed, was
to lay bare the brain mechanisms that produced this physiological
state; then we would have discovered nothing less than how the
brain produces dreams. Since the REM state can be demonstrated in
almost all mammals, this research could also be conducted in
subhuman species (which has important methodological implications,
for brain mechanisms can be manipulated in animal experiments in
ways that they cannot in human research).
A sequence of
studies followed, in quick succession, in which different parts of
the brain were systematically removed (in cats) in order to
isolate the precise structures that produced REM sleep. On this
basis, Jouvet was able to report in 1962 that REM (and therefore
dreaming) was produced by a small region of cells in a part of the
brain stem known as the ‘pons’. This part of the nervous
system is situated at a level only slightly above the spinal cord,
near the nape of the neck. The higher levels of the brain, such as
the cerebral hemispheres themselves which fill out the great
hollow of the human skull, did not appear to play any causal role
whatever in the generation of dreaming. REM sleep occurs with
monotonous regularity, throughout sleep, so long as the pons is
intact, even if the great cerebral hemispheres are removed
research into the mechanism of REM sleep continued along these
lines, using a wide variety of methods and, by 1975, a detailed
picture of the anatomy and physiology of ‘dreaming sleep’ had
emerged. This picture, which is embodied in the reciprocal
interaction and activation-synthesis models of McCarley
and Hobson (1975, 1977), has dominated the field ever since: or,
at least, as we shall see, until very recently. These
authoritative models proposed that REM sleep and dreaming were
literally ‘switched on’ by a small group of cells situated
deep within the pons, which excrete a chemical called ‘acetylcholine’.
This chemical activates the higher parts of the brain, which are
thereby prompted to generate (meaningless) conscious images. These
meaningless images are nothing more than the higher brain making
‘the best of a bad job… from the noisy signals sent up from
the brain stem’ (Hobson & McCarley, 1977, p1347). After a
few minutes of REM activity, the cholinergic activation arising
from the brainstem is counteracted by another group of cells, also
situated in the pons, which excrete two other chemicals:
noradrenaline and serotonin. These chemicals ‘switch off’ the
cholinergic activation (and thereby, according to the theory, the
conscious experience of dreaming).
Thus all the
complex mental processes that Freud elucidated in this book were
swept aside and replaced by a simple oscillatory mechanism by
means of which consciousness is automatically switched on and off
at approximately 90 minute intervals throughout sleep by
reciprocally interacting chemicals which are excreted in an
elementary part of the brain that has nothing to do with complex
mental functions. Thus, even the most basic claims of Freud’s
theory no longer seemed tenable:
motivating force of dreaming is not psychological but
physiological since the time of occurrence and duration of
dreaming sleep are quite constant suggesting a pre-programmed,
neurally determined genesis. In fact, the neural mechanisms
involved can now be precisely specified. If we assume that the
physiological substrate of consciousness is in the forebrain,
these facts [i.e. that REM is automatically generated by brainstem
mechanisms] completely eliminate any possible contribution of
ideas (or their neural substrate) to the primary driving force of
the dream process (Hobson & McCarley, 1977, p1346, 1338).
On this basis, it
seemed justifiable to conclude that the causal mechanisms
underlying dreaming were ‘motivationally neutral’ (McCarley
& Hobson, 1977, p1219) and that dream imagery was nothing more
than ‘the best possible fit of intrinsically inchoate data
produced by the auto-activated brain-mind’ (Hobson, 1988, p204).
The credibility of Freud’s theory was, in short, severely
strained by the first wave of data about dreaming that was
obtained from ‘anatomical preparations’ (Freud, 1900a, p536):
and the neuroscientific world (indeed the scientific world as a
whole) reverted to the pre-psychoanalytic view that ‘dreams are
froth’ (Freud, 1900a, p133).
the observations just reviewed, which provided an increasingly
precise and detailed picture of the neurology of REM sleep, a
second body of evidence gradually began to accumulate, which led
some neuroscientists to recognise that perhaps REM sleep was
not the physiological equivalent of dreaming after all (Solms,
The notion that
dreaming is merely ‘an epiphenomenon of REM sleep’ (Hobson et
al, 1998, pR12) rested almost exclusively on the observation that
arousal from the REM state yielded dream reports on 70-95% of
awakenings, whereas non-REM awakenings yielded such reports in
only 5-10% of attempts. Considering the vagaries of subjective
memory (and especially memory for dreams), this is as close to a
perfect correlation as one could reasonably expect. However, the
sharp division between REM (‘dreaming’) sleep and non-REM
(‘non-dreaming’) sleep began to fray when it was discovered
that reports of complex mentation could, in fact, be elicited in
as many as 50% of awakenings from non-REM sleep. This became
apparent when Foulkes awakened subjects from non-REM sleep and
asked them, ‘What was passing through your mind?’ rather than,
‘Have you been dreaming?’ (Foulkes, 1962). The resultant
non-REM dream reports were more ‘thought-like’ (less vivid)
than the REM dream reports but this distinction held only for the
statistical average. The fact remained that at least 5-10% of
non-REM dream reports were ‘indistinguishable by any criterion
from those obtained from post-REM awakenings’ (Hobson, 1988,
p143). These findings ‘do not support a dichotomic distinction
between REM and NREM mentation, rather they suggest the hypothesis
of the existence of continuous dream processing characterised by a
variability within and between sleep stages’ (Cavallero et al,
The non-REM dream
reports could not be explained away as misremembered REM dreams,
for it soon became apparent that dream reports could regularly be
obtained even before the dreamer had entered the first REM phase.
In fact, we now know that dream reports are obtainable from as
many as 50-70% of awakenings during the sleep onset phase, that
is, in the first few minutes after falling asleep (Foulkes &
Vogel, 1965; Foulkes et al, 1966; Vogel et al, 1972). This is a
far higher rate than at any other point during the non-REM cycle,
and almost as high as the REM rate. Similarly, it was recently
discovered that non-REM dreams appear with increasing length and
frequency towards the end of sleep, during the rising morning
phase of the diurnal rhythm (Kondo et al, 1989). In other words,
non-REM dreams do not appear randomly during the sleep cycle;
dreaming is generated during non-REM sleep by specific non-REM
The only reliable
difference between REM dream reports, sleep-onset reports, and
certain other classes of non-REM dream report is that the REM
reports are longer. In all other respects, the non-REM and REM
dreams appear to be identical. This demonstrates conclusively that
fully-fledged dreams can occur independently of the unique
physiological state of REM sleep. Therefore, whatever the
explanation may be for the strong correlation that exists between
dreaming and REM sleep, it is no longer accepted that dreaming is
caused exclusively by the REM state.
isomorphism between REM sleep and dreaming was further undermined
by the emergence, very recently, of new and unexpected evidence
regarding the brain mechanisms of dreaming. As already noted, the
hypothesis that dreaming is merely an epiphenomenon of REM sleep
rested on the high correlation between REM awakening and dream
reports. But this does not necessarily imply that REM and dreaming
share a unitary brain mechanism. In the light of the discovery
that dreams regularly occur independently of REM sleep, it is
certainly possible that the REM state and dreaming are controlled
by independent brain mechanisms. The two mechanisms could well be
situated in different parts of the brain, with the REM mechanism
frequently triggering the dream mechanism. A two-stage causation
of REM dreaming implies that the dream mechanism could also be
stimulated into action by triggers other than the REM mechanism,
which would explain why dreaming so frequently occurs outside of
that two separate mechanisms - one for REM and one for dreaming -
exist in the brain, can easily be tested by a standard
neurological research method known as clinico-anatomical
correlation. This is the classical method for testing such
hypotheses: the parts of the brain that obliterate REM sleep are
removed and the investigator observes whether or not dreaming
still occurs; then the parts of the brain that obliterate dreaming
are removed and the investigator observes whether or not REM still
occurs. If the two effects dissociate, then they are caused by
different brain mechanisms. If they are affected simultaneously by
damage to a single brain structure, then they are served by a
It is known that
destruction of parts of the pons (and nowhere else) leads to a
cessation of REM sleep in lower mammals (Jones, 1979), but such
experiments cannot, of course, be performed on humans: the only
species which is in a position to tell us whether or not
destruction of those parts of the brain leads simultaneously to a
cessation of dreaming. Fortunately (for science), the relevant
brain structures are occasionally destroyed in human cases by
naturally occurring damage, due to spontaneous illness or
traumatic injury to the brain. Twenty-six such cases have been
reported in the neurological literature, with damage to the pons,
which resulted in a total or near-total loss of REM sleep1.
Surprisingly, the elimination of REM in these cases was
accompanied by reported loss of dreaming in only one of the 26
patients (Feldman, 1971). In the other 25 cases, the investigators
either could not establish this correlation or they did not
consider it. By contrast, in all the other cases ever published in
the neuroscientific literature in which damage to the brain did
result in a reported loss of dreaming (a total of 110 patients), a
completely different part of the brain was damaged and the pons
was spared completely2.
Moreover, it has been proven that REM sleep is completely
preserved in these cases, despite their loss of dreaming3.
This dissociation between cessation of REM and cessation of
dreaming seriously undermines the doctrine that the REM state is
the physiological equivalent of the dream state.
The parts of the
brain that are crucial for dreaming and those that are crucial for
REM sleep are widely separated, both anatomically and
functionally. The parts of the brain that are crucial for REM are
in the pons, which is located in the brainstem, near the nape of
the neck. The parts of the brain that are crucial for dreaming, by
contrast, are situated exclusively in the higher parts of the
brain, in two specific locations within the cerebral hemispheres
The first of these
locations is in the deep matter of the frontal lobes of the
brain, just above the eyes (Solms, 1997). This part of the frontal
lobes contains a large fibre-pathway, which transmits a chemical
called ‘dopamine’ from the middle of the brain to the higher
parts of the brain. Damage to this pathway renders dreaming
impossible but it leaves the REM cycle completely unaffected (Jus
et al, 1973). This suggests that dreaming is generated by a
different mechanism than the one that generates REM sleep: a
conclusion which is strongly supported by the observation that
chemical stimulation of this dopamine pathway (with drugs like
L-DOPA) leads to a massive increase in the frequency and vividness
of dreams without it having any effect on the frequency and
intensity of REM sleep (Klawans et al, 1978; Scharf et al, 1978;
Hartmann et al, 1980; Nausieda et al, 1982). Likewise, excessively
frequent and vivid dreaming which is caused by dopamine stimulants
can be stopped by drugs (like anti-psychotics) which block the
transmission of dopamine in this pathway (Sacks, 1985, 1990,
1991). In short, dreaming can be switched ‘on’ and ‘off’
by a neurochemical pathway which has nothing to do with the REM
oscillator in the pons. What, then, is the function of this higher
brain pathway which is so crucial for the generation of dreams?
Its main function is to ‘instigate goal-seeking behaviors and an
organism’s appetitive interactions with the world’ (Panksepp,
1985, p273); that is, to motivate the subject to seek out and
engage with external objects which can satisfy its inner
biological needs. These are precisely the functions that Freud
attributed to the ‘libidinal drive’ - the primary instigator
of dreams - in his (1900a) theory. Accordingly, it is of
considerable interest to note that damage to this pathway causes
cessation of dreaming in conjunction with a massive reduction in
motivated behaviour (Solms, 1997). In view of the close
association between dreams and certain forms of insanity, it is
also interesting to note that surgical damage to this pathway
(which was the primary target of the prefrontal leucotomies of the
1950s and 60s) leads to a reduction in some symptoms of psychotic
illness, together with a cessation of dreaming (Frank, 1946, 1950;
Partridge, 1953; Schindler, 1953). Whatever it is that prevented
leucotomised patients from maintaining their psychiatric symptoms
also prevented them from generating dreams.
In short, the
current neuroscientific evidence gives us every reason to take
seriously the radical hypothesis - first set out in this book 100
years ago - to the effect that dreams are motivated phenomena,
driven by our wishes. Although it is true that the (cholinergic)
mechanism which generates the REM state is ‘motivationally
neutral’, this cannot be said of the (dopaminergic) mechanism
which generates the dream state. In fact, the latter mechanism is
the appetitive (i.e. libidinal) ‘command system’ of the brain
(Panksepp, 1985, 1998).
As stated, it now
appears that REM only causes dreaming via the intermediary of this
motivational mechanism. Moreover, REM is just one of the many
different triggers which are capable of activating this mechanism.
A variety of other triggers, which act independently of REM, have
exactly the same effect. Sleep-onset dreams and late morning
dreams are two examples of this kind. Dreams induced by L-DOPA
(and various stimulant drugs) are further examples. Of special
interest in this regard is the fact that recurring, stereotyped
nightmares can be induced by seizures which occur during sleep4.
We know from the work of Penfield5
exactly where in the brain these seizures begin, namely, in the
temporal limbic system. This system, which subserves emotional and
memory functions, is situated in the higher forebrain, and is
richly interconnected with the frontal lobe dopamine pathway
discussed above. Moreover, we know that such seizures usually
occur during non-REM sleep (Janz, 1974; Kellaway & Frost,
1983). The fact that nightmares can be ‘switched on’ by
mechanisms in the higher parts of the brain which have nothing to
do with the pons and nothing to do with REM sleep is further
evidence that dreaming and REM are generated by separate and
independent brain mechanisms.
It is surely no
accident that what all of these different mechanisms capable of
triggering dreams have in common is the fact that they create a
state of arousal during sleep. This lends support to another of
the cardinal hypotheses that Freud put forward in this book,
namely the hypothesis that dreams are a response to something
which disturbs sleep6.
But it appears that the arousal stimuli enumerated above only
trigger dreaming if and when they activate the final common
motivational pathway within the frontal lobes of the brain, for it
is only when this pathway is removed (rather than the arousal
triggers themselves, including REM) that dreaming becomes
impossible. This relationship between the various arousal triggers
and the dream-onset mechanism itself is reminiscent of Freud’s
famous analogy: dreaming only occurs if the stimulus which acts as
the ‘entrepreneur’ of the dream attracts the support of a
‘capitalist’, an unconscious libidinal urge, which alone has
the power to generate dreaming (1900a, p561).
major inferences from psychological evidence regarding both the
causes and the function of dreaming are at least compatible with,
and even indirectly supported by, current neuroscientific
knowledge. Does the same apply to the mechanism of dreaming?
neuroscientific understanding of the mechanism of dreaming
revolves centrally around the concept of regression. The
prevailing view is that imagery of all kinds (including dream
imagery) is generated by ‘projecting information backward in the
system’ (Kosslyn, 1994, p75). Accordingly, dreaming is
conceptualised as ‘internally generated images which are fed
backwards into the cortex as if they were coming from the
outside’ (Zeki, 1993, p326). This conception of dream imagery is
based on wide-ranging neurophysiological and neuropsychological
research into numerous aspects of visual processing. However the
regressive nature of dream processing has recently been
demonstrated directly in clinical neurological cases (Solms,
In order to
illustrate this point, it is necessary to remind the reader that
loss of dreaming due to neurological damage is associated with
damage in two brain locations. The first of these is the
fibre pathway of the frontal lobes that we have considered
already. The second location is a portion of the grey cortex at
the back of the brain (just behind and above the ears) called the
occipito-temporo-parietal junction. This part of the brain
performs the highest levels of processing of perceptual
information and it is essential for:
conversion of concrete perception into abstract thinking, which
always proceeds in the form of internal schemes, and for the
memorizing of organized experience or, in other words, not only
for the perception of information but also for its storage'. (Luria,
The fact that
dreaming ceases completely with damage to this part of the brain
suggests that these functions (the conversion of concrete
perceptions into abstract thoughts and memories), like the
motivational functions performed by the frontal lobe pathway
discussed previously, are fundamental to the whole process of
dreaming. However, if the theory that dream imagery is generated
by a process which reverses the normal sequence of events in
perceptual processing is correct, then we may expect that in
dreams abstract thoughts and memories are converted into concrete
perceptions. This is exactly what Freud had in mind when he wrote
that, ‘in regression, the fabric of the dream-thoughts is
resolved into its raw material’ (1900a, p543). This inference is
supported empirically by the observation that dreaming as a whole
stops completely with damage at the highest level of the
perceptual systems (in the region of the occipito-temporo-junction),
whereas only specific aspects of dream imagery are affected by
damage at lower levels of the visual system, closer to the
perceptual periphery (in the region of the occipital lobe)7.
This implies that the contribution of the higher levels precedes
that of the lower levels. When there is damage at the higher
levels, dreaming is blocked completely, whereas damage at the
lower levels merely subtracts something from the terminal stage of
the dream process. This is the opposite of what happens in waking
perception, which is obliterated entirely by damage at the lowest
levels of the system. In other words, dreaming reverses the normal
sequence of perceptual events.
neuroscientific evidence, therefore, is compatible with Freud’s
conception of where and how the dream process is initiated (for
example, by an arousing stimulus which activates the emotional and
motivational systems), and of where and how it terminates (such as
by abstract thinking in the memory systems, which is projected
backwards in the form of concrete images onto the perceptual
In fact, it is now
possible to actually see where this neural activity is
distributed in the dreaming brain. Modern neuroradiological
methods produce pictures of the pattern of metabolic activity in
the living brain while it is actually performing a particular
function, and in the case of dreaming these images clearly show
how the brain’s energic ‘cathexis’ (as Freud called it) is
concentrated within the anatomical areas discussed above: namely,
the (frontal and limbic) parts of the brain concerned with
arousal, emotion, memory and motivation, on the one hand, and the
parts (at the back of the brain) concerned with abstract thinking
and visual perception, on the other8.
pictures also reveal something about what happens in between the
initial and terminal ends of the dream process. The most striking
feature of the dreaming brain in this respect is the fact that a
region of the brain known as the dorsolateral frontal convexity is
completely inactive during dreams. This is striking, because this
part of the brain, which is inactive during dreams, is one of the
most active of all brain areas during waking mental activity. If
one compares the pictures of the waking brain with those of the
dreaming brain, one literally sees the truth of Fechner’s (1889)
assertion to the effect that ‘the scene of action of dreams is
different from that of waking ideational life’ (cf. Freud,
1900a, p536). Whereas in waking ideational life, the ‘scene of
action’ is concentrated in the dorsolateral region at the front
of the brain - ‘the upper end of the motor system - the gateway
from thought to action’ (Solms, 1997, p223) - in dreams it is
concentrated in the occipito-temporo-parietal region at the back
of the brain, on the memory and perceptual systems. In short, in
dreams, the ‘scene’ shifts from the motor end of the apparatus
to the perceptual end9.
This reflects the
fact that whereas in waking life the normal course of mental
events is directed toward action, in dreams this path is
unavailable. The ‘gateway’ to the motor systems (the
dorsolateral frontal convexity of the brain) is blocked in dreams
(Braun et al, 1997, 1998; Solms, 1997), as are the motor output
channels (the alpha motor neurons of the spinal cord, Pompeiano,
1979). Thus both the intention to act and the ability to act are
blocked during sleep, and it seems reasonable to infer (as did
Freud) that this block is the immediate cause of the dream process
assuming a regressive path, away from the motor systems of the
brain, toward the perceptual systems (Solms, 1997).
Finally, due to
relative inactivation during sleep of crucial parts of the
reflective systems in the frontal parts of the limbic brain, the
imagined dream scene is uncritically accepted and the dreamer
mistakes the internally generated scene for a real perception.
Damage to these reflective systems (which evidently are not
entirely inactive during sleep) results in a curious state of
almost constant dreaming during sleep and an inability to
distinguish between thoughts and real events during waking life10.
This provides further evidence of a continuous thought process
occurring during sleep, which is converted into dreaming under
various physiological conditions, of which REM sleep is just one
The picture of the
dreaming brain which emerges from recent neuroscientific research
may therefore be summarised as follows: the process of dreaming is
initiated by an arousal stimulus. If this stimulus is sufficiently
intense or persistent to activate the motivational mechanisms of
the brain (or if it attracts the interest of these mechanisms for
some other reason), the dream process proper begins. The
functioning of the motivational systems of the brain is normally
channelled toward goal-directed action but access to the motor
systems is blocked during sleep. The purposive action which would
be the normal outcome of motivated interest is thereby rendered
impossible during sleep. As a result (and quite possibly in order
to protect sleep), the process of activation assumes a regressive
course. This appears to involve a two-stage process. First, the
higher parts of the perceptual systems (which serve memory and
abstract thinking) are activated; then the lower parts (which
serve concrete imagery) are activated. As a result of this
regressive process, the dreamer does not actually engage in
motivated activity during sleep, but rather imagines himself to be
doing so. Due to inactivation during sleep of the reflective
systems in the frontal part of the limbic brain, the imagined
scene is uncritically accepted, and the dreamer mistakes it for a
There is a great
deal about the dreaming brain that we still do not understand. It
is also evident that we have not yet discovered the neurological
correlates of some crucial components of the ‘dream-work’ as
Freud understood it. The function of ‘censorship’ is the most
glaring example of this kind. However, we are beginning to
understand something about the neurological correlates of that
function, and we know at least that the structures which are most
likely to be implicated (Solms, 1998) are indeed highly active
during dreaming sleep (Braun et al, 1997, 1998).
Hopefully it is
apparent to the reader from this brief overview that the picture
of the dreaming brain which has begun to emerge from the most
recent neuroscientific researches is broadly compatible with the
psychological theory that Freud advanced. In fact, aspects of
Freud’s account of the dreaming mind are so consistent with the
currently available neuroscientific data that I personally think
we would be well advised to use Freud’s model as a guide for the
next phase of our neuroscientific investigations. Unlike the
research effort of the past few decades, the next stage in our
search for the brain mechanisms of dreaming (if it is to succeed)
must take as its starting point the new perspective we have gained
on the role of REM sleep. REM sleep, which has hitherto diverted
our attention away from the neuropsychological mechanisms of
dreaming, should simply be added to the various ‘somatic
sources’ of dreams that Freud discussed in chapters 1 and 5 of
his book (1900a). The major focus of our future research efforts
should then be directed toward elucidating the brain correlates of
the mechanisms that Freud discussed in his 6th and 7th chapters:
the mechanisms of the dream-work proper:
We shall feel no
surprise at the over-estimation of the part played in forming
dreams by stimuli which do not arise from mental life. Not only
are they easy to discover and even open to experimental
confirmation; but the somatic view of the origin of dreams is
completely in line with the prevailing trend of thought in
psychiatry to-day. It is true that the dominance of the brain over
the organism is asserted with apparent confidence. Nevertheless,
anything that might indicate that mental life is in any way
independent of demonstrable organic changes or that its
manifestations are in any way spontaneous alarms the modern
psychiatrist, as though a recognition of such things would
inevitably bring back the days of the Philosophy of Nature, and
the metaphysical view of the nature of mind. The suspicions of the
psychiatrists have put the mind, as it were, under tutelage, and
they now insist that none of its impulses shall be allowed to
suggest that it has any means of its own. This behaviour of theirs
only shows how little trust they really have in the validity of a
causal connection between the somatic and the mental. Even when
investigation shows the primary exciting cause of a phenomenon is
psychical, deeper research will one day trace the path further and
discover an organic basis for the mental event. But if at the
moment we cannot see beyond the mental, that is no reason for
denying its existence (Freud 1900a, p41-2).
1 Adey et al, 1968; Chase et al, 1968; Cummings
& Greenberg, 1977; Feldman, 1971; Lavie et al, 1984; Markand
& Dyken, 1976; Osorio & Daroff, 1980 (for
bibliographic details see Solms, 1997).
2 Basso, Bisiach & Luzzatti, 1980;
Boyle & Nielsen, 1954; Epstein, 1979; Epstein & Simmons,
1983; Ettlinger, Warrington & Zangwill, 1957; Farah, Levine
1988; Farrell, 1969; Gloning & Sternbach, 1953; Griinstein,
1924; Habib & Sirigu, 1987; Humphrey & Zangwill, 1951;
Lyman, Kwan & Chao, 1938; Michel & Sieroff, 1981;
Moss, 1972; Mòller, 1892; Neal, 1988; Nielsen, 1955; Pefia-Casanova
et al, 1985; Piehler, 1950; Ritchie, 1959; Solms, 1997; Wapner,
Judd & Gardner, 1978; Wilbrand,
1887, 1892 (for bibliographic details see Solms, 1997).
3 Benson & Greenberg, 1969; Brown,
1972; Cathala et al, 1983; Efron, 1968; Jus et al, 1973; Kerr,
Foulkes & Jurkovic, 1978; Michel & Sieroff, 1981; Murri et
al, 1985 (for
bibliographic details see Solms, 1997).
4 De Sanctis, 1896; Thomayer, 1897;
Clarke, 1915; Kardiner, 1932; Naville & Brantmay, 1935; Rodin
et al, 1955; Ostow, 1954; Epstein & Ervin, 1956; Snyder, 1958;
Epstein, 1964; Epstein & Hill, 1966; Epstein, 1967; Boller et
al, 1975; Epstein, 1979; Epstein & Freeman, 1981; Solms, 1997
(for bibliographic details see Solms, 1997).
5 Penfield was able to artificially
generate the recurring nightmare scenes by directly stimulating
the seizure focus in the temporal lobe (Penfield, 1938; Penfield
Erickson, 1941; Penfield & Rasmussen, 1955).
6 Solms (1995, 1997) provides limited
empirical evidence to support the hypothesis that dreams protect
sleep: patients who lose the ability to dream due to brain damage
report more disturbed sleep than brain damaged patients with
7 Charcot, 1883; Adler, 1944, 1950; Brain,
1950, 1954; Macrae & Trolle, 1956; Tzavaras, 1967; Kerr et al,
1978; Botez et al, 1985; Sacks & Wassermann, 1987; Solms,
1997 (for bibliographic details see Solms, 1997).
8 Braun et al, 1997, 1998; Franck et al,
1987; Franzini, 1992; Heiss et al, 1985; Hong et al, 1995; Madsen,
1993; Madsen & Vorstrup, 1991; Madsen et al, 1991a, 1991b;
Maquet et al, 1990, 1996 (for bibliographic details see Braun et
9 It is of utmost interest to note that
the major inhibitory systems of the forebrain are concentrated at
its motor end, as they were in Freud’s (1900a) diagrammatic
representation of the mental apparatus.
10 Whitty & Lewin, 1957; Lugaresi et
al, 1986; Gallassi et al, 1992; Morris et al, 1992; Sacks, 1995;
Solms, 1997 (for bibliographic details see Solms, 1997).
Aserinsky, E. & Kleitman, N. (1953). Regularly occurring
periods of eye motility and concurrent phenomena during sleep.
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Mark Solms is a psychoanalyst and an Honorary
Lecturer in Neurosurgery at the St. Bartholomew's and Royal London
School of Medicine. His publications include A
moment of Transition: Two Neuroscientific Articles by Sigmund
Freud (Karnac 1990) and The Neuropsychology of Dreams: A Clinico-Anatomical
Erlbaum Associates, 1997).
Freud, S. (1893) 'Some Points for a Comparative
Study of Organic and Hysterical Motor Paralyses'. Standard
Edition, 1: 160-172.
Solms,M. (1995) 'Is the Brain more Real than the Mind?'.
Psychoanalytic Psychotherapy, 9: 107-120.
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