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Introductory notes to the psychodynamics of a case of

Klüver-Bucy syndrome
a
Jose Fernando Muñoz Zúñiga
a
Neuropsychiatric Unit, National Institute of Neurology and Neurosurgery, Mexico City,
Mexico
Accepted author version posted online: 23 Apr 2015.Published online: 16 Jul 2015.

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To cite this article: Jose Fernando Muñoz Zúñiga (2015) Introductory notes to the psychodynamics of a case of Klüver-Bucy
syndrome, Neuropsychoanalysis: An Interdisciplinary Journal for Psychoanalysis and the Neurosciences, 17:1, 53-62, DOI:
10.1080/15294145.2015.1043745

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 Neuropsychoanalysis, 2015
Vol. 17, No. 1, 53–62, http://dx.doi.org/10.1080/15294145.2015.1043745

Introductory notes to the psychodynamics of a case of Klüver-Bucy syndrome

Jose Fernando Muñoz Zúñiga*

Neuropsychiatric Unit, National Institute of Neurology and Neurosurgery, Mexico City, Mexico
(Received 14 October 2014; accepted 28 March 2015)

Klüver-Bucy syndrome (KBS) is a neuropsychiatric syndrome secondary to damage in anterior temporolimbic

structures. It is composed of severe cognitive, behavioral, and affective symptoms. The case of a young woman who
developed a KBS after a multiphasic acute disseminated encephalomyelitis is examined. The clinical material is taken
from multiple hospitalizations in the Neuropsychiatric Unit of the National Institute of Neurology and Neurosurgery in
Mexico City and from multiple diagnostic interviews with the patient and her family during ambulatory care. A series of
correlations will be made between neuropsychiatric symptoms, neuropsychological data, neuroanatomical lesions as
shown on neuroimaging, and first-person subjective data. This will be done with the purpose of sketching the
psychodynamics of this particular patient while dealing at the same time with relevant issues for the understanding of the
Downloaded by [Jose Fernando Muñoz Zúñiga] at 07:27 25 July 2015

inner world of this type of cases. As the patient did not undergo psychoanalytic therapy, any data emerging from this
single case study should be taken as introductory in nature. This case points out the need of developing new concepts to
describe psychopathological manifestations, as they are understood in metapsychology, when applied to neuropsychia-
tric patients. In this regard, the term “psychodynamic phenocopy” is proposed.
Keywords: Klüver-Bucy; acute disseminated encephalomyelitis; psychodynamic phenocopy

“We may say they are travellers to unimaginable lands -
lands of which otherwise we should have no idea or
conception.” Oliver Sacks, from The Man Who Mistook
His Wife for a Hat
The following paper will deal with the case of a patient
with a devastating neuropsychiatric syndrome called
Klüver-Bucy syndrome (KBS). Specifically, it will attempt
to establish a series of correlations between neuropsychia-
tric symptoms, neuropsychological data, neuroanatomical
lesions as shown on neuroimaging, and first-person
subjective data. This will be done with the purpose of
sketching the psychodynamics of this particular patient
while dealing at the same time with some relevant issues
for the understanding of the inner world of these kinds of
neuropsychiatric cases. A transepistemic approach, as the
nascent field of neuropsychoanalysis intends to be, may be
useful for such a deeper understanding, following Sacks, to
have in sight a “whom” in addition to a “what” (Sacks,
1998).
Methodology and conceptual framework
This is a case analysis of a patient treated in the
Neuropsychiatric Service of the National Institute of
Neurology and Neurosurgery in Mexico City. As the
neurological aspects and neuropsychiatric treatment are
described in detail elsewhere (Muñoz, Ramirez-Bermu-
dez, Flores, & Corona-Vazquez, Forthcoming), the focus
here will be on the narratives of the symptoms suffered
by the patient, the neuroanatomical and neuropsycholo-
gical evidence of the lesions, and the impact they had on
her psychic apparatus, as it is understood in terms of
Freudian metapsychology. This conceptual framework
was chosen much in the spirit of dynamic psychiatry,
where case formulation takes into account theoretical
models that potentially offer greatest heuristic power
(Gabbard, 2005; Perry, Cooper, & Michels, 1987) and
explicitly asserts that therapeutic effectiveness of any
kind of psychiatric treatment is often related to the
understanding of the patient’s dynamics.
The clinical material is taken from a four-year span,
through multiple hospitalizations in the Neuropsychiatric
Unit, as well as multiple diagnostic interviews to the
patient and her family during ambulatory care, focused on
understanding the KBS and its impact on her life. The
patient did not undergo psychoanalytic therapy: first, her
behavioral and affective symptoms severely affected her
capacity to adjust to the frame of any form of psychother-
apy (a cognitive-behavioral intervention took place in the
fourth year of her illness, with poor results). Second, there
was a lack of qualified personnel at the Institute to conduct
a psychodynamically oriented therapy in a patient with
these characteristics. As Kaplan-Solms and Solms showed
in their pioneer work (Kaplan-Solms & Solms, 2000),
psychotherapy for patients with brain lesions represents a
real challenge. Thus, any data emerging from this single
case study should be taken as introductory in nature, as the

*Email: lucesdeeuforia@hotmail.com

© 2015 International Neuropsychoanalysis Society

 54 J.F. Muñoz Zúñiga
preliminary psychodynamic formulation, if you will, of a
patient with important nondynamic factors. These data,
the author believes, are valuable in its own right, for it is
unusual for Klüver-Bucy patients, due to their often
extensive neurological damage, to share their experience
with this syndrome in any depth. Finally, a series of
hypotheses will be made about this syndrome from the
perspective of the clinico-anatomical method.
Background and neurological data
Patient M. was a 26-year-old married woman who lived
with her husband and her daughter. She graduated as a
physician and did not have any relevant pathological,
psychiatric, or family antecedents. She grew up in a
nuclear family, the eldest of three siblings, after an
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uneventful pregnancy and labor. She had normal psycho-
motor development and had outstanding scholar achieve-
ments since the earliest years of elementary school. She
ended high school with excellent grades and liked to
attend classes, despite having little peer interaction. She
entered medical school, where she had to repeat some
courses, until she graduated in 2010. She had her first
boyfriend at age 12, a neighbor five years older, without
paternal approval. They separated after five years to-
gether, when she was caught by her parents during a
moment of intimacy. Later on she had a two-year
relationship, with frequent arguing over differences with
her boyfriend’s family and infidelity by both parties; she
ended that relationship after discovering him with another
woman. Afterward she met her future husband, whom she
married after two years of courtship. Four years later they
had her only daughter, a desired and accepted child. M.
considered the relationship as warm and fulfilling, despite
some arguing about the amount of time he spent with her
parents-in-law.
She described her relationship with her parents and
siblings as easygoing; during childhood she felt she was
Figure 1. MRI during patient M.’s first hospitalization at the Institute. (a) Right periventricular lesions are seen on T2 sequence. (b)
Right periventricular lesions and left temporal horn lesions on FLAIR sequence. (c) Large mesencephalic lesion on the left side, on
FLAIR sequence.
better understood by her father than her mother. She was
described by her family as an intelligent person, reserved
and shy, an “optimistic nerd” who enjoyed reading and
invested more energy in her studies than in socializing.
In summary, patient M. appeared to be a well-adapted
person, with possible schizoid features, without elements
that suggested a personality disorder, with neurotic and
mature defense mechanisms, who was adjusting herself
to her new role as a mother and a professional doctor.
She attended the National Institute of Neurology and
Neurosurgery, Mexico City, in early 2010. Her illness
began as a systemic viral infection, with subacute progres-
sion to somnolence and eventually catatonia, in presence
of focal neurological signs including ophthalmoplegia, left
ptosis, left facial paralysis, and left-sided hemiparesis.
After ruling out viral encephalitis and other causes, it was
concluded that she fulfilled criteria for acute disseminated
encephalomyelitis (ADEM) based on the multifocal
neurological involvement and asymmetrical, diffuse
lesions in the brain magnetic resonance imaging (MRI;
see Figure 1). ADEM is an inflammatory and demyelinat-
ing disease of autoimmune origin that affects mostly white
matter tracts in the central nervous system (Alper, 2012). It
is usually preceded by a viral infection or a vaccine that
causes a cross-reaction against myelin autoantigens. In
some patients a clear cause cannot be established. Patient
M. received standard neurological treatment with methyl-
prednisolone and prednisone. During her first hospitaliza-
tion she developed a catatonic syndrome, with catalepsy,
mutism, bizarre postures, negativism, and automatic
obedience, probably due to extrapyramidal damage. These
symptoms had rapid resolution with standard neuropsy-
chiatric treatment with lorazepam and amantadine.
While ADEM is usually an entity with good prognosis
(Wingerchuk & Weinshenker, 2013), M. developed a
multiphasic variant. Three months after the initial pre-
sentation, a new MRI showed a decrease on previous
mesencephalic lesions and new, bilateral, periventricular

Figure 2. Image of new lesions that coincided with the beginning of the KBS on MRI, FLAIR sequence. (a) Generalized cortical
atrophy, with sparing of DLPFC; unimodal cortical areas were spared as well. (b) Bilateral hyperintensities on insulae and deep white
matter hyperintensities on right orbitofrontal cortex. (c) Bilateral hyperintensities on amygdalae and enthorrinal cortex with
attenuation of mesencephalic lesion seen in Figure 1(c).
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white matter lesions, with gadolinium enhancement. New
lesions, which persisted for years, appeared as well on
right orbitofrontal cortex and temporolimbic areas, parti-
cularly on insulae and amygdalae (Figure 2).
Neuropsychiatric and neuroanatomical data
The appearance of these new lesions on the MRI
coincided with the beginning of the KBS, a neuropsychia-
tric syndrome composed of a constellation of affective,
behavioral, and cognitive symptoms (Trimble, Mendez, &
Cummings, 1997), associated with unilateral or bilateral
damage in temporolimbic and paralimbic areas (Mega,
Cummings, Salloway, & Malloy, 1997; Olson, Plotzker,
& Ezzyat, 2007). The syndrome consists of six elements:
(1) visual apperceptive agnosia, an impairment in recog-
nition of objects through visual stimuli; (2) hypermeta-
morphosis, a disturbance in attention and indiscriminate
reaction to environmental stimuli; (3) hyperorality, a
tendency to examine all kind of objects by mouth; (4)
dietary changes, like pica and hyperphagia; (5) hyper-
sexuality, with heightened sex behavior and changes in
the selection of sexual objects; and (6) emotional and
social changes, with placidity, loss of fear, and loss of
aggression. The complete syndrome in humans is uncom-
mon. In addition, it is usually accompanied by extensive
cognitive deficits, like aphasia and dementia (Lilly,
Cummings, Benson, & Frankel, 1983). Etiology varies
widely, with cases secondary to viral encephalitis, neuro-
degenerative disorders, and parasitic disease (Jha & Patel,
2004; Kile, Ellis, Olichney, Farias, & DeCarli, 2009; Lilly
et al., 1983; Marlowe, Mancall, & Thomas, 1975) among
others.
It is not clear which structural and functional damages
are necessary conditions to produce a KBS. It is clear the
syndrome is associated with bilateral anterior temporo-
limbic lesions (Mega et al., 1997), primarily with damage
Neuropsychoanalysis 55
to temporal poles, amygdala (Olson et al., 2007), or
mediodorsal thalamic nucleus (Carroll, Goforth, & Car-
roll, 1999). These closely interacting areas are involved in
emotional processing (Barbas, 2007). They are nodes of
Yakovlev’s circuit, a neuronal circuit also known as lateral
limbic circuit (Trimble et al., 1997) or temporo–amyg-
dala–orbitofrontal network (Catani, Dell'acqua, & Thie-
baut de Schotten, 2013). This circuit links the anterior
temporal lobes and orbitofrontal cortex by a bidirectional
white matter tract called the uncinate fasciculus (Catani
et al., 2013; Martino & De Lucas, 2014; Von Der Heide,
Skipper, Klobusicky, & Olson, 2013). The uncinate
fasciculus has been implicated in functions like semantic
memory retrieval, formation of associations that motivate
behavior by virtue of their affective value, and social-
emotional processing of stimuli with affective valence
(Papagno et al., 2011; Von Der Heide et al., 2013). The
amygdala, another key node in this circuit, has a large
body of evidence supporting its role in fear processing
(Phelps & LeDoux, 2005). In rats, different amygdala
nuclei have been associated with innate processes like
mating, defensive, and maternal behaviors (Sokolowski &
Corbin, 2012). In monkeys with neurosurgical lesions that
develop KBS, bilateral damage has been specifically
associated with hypersexuality (Olson et al., 2007), and
some lesion studies on humans (Baird, Wilson, Bladin,
Saling, & Reutens, 2007; Lilly et al., 1983), but not all
(Corkin, 2013; Feinstein, Adolphs, Damasio, & Tranel,
2011; Tranel, Gullickson, Koch, & Adolphs, 2006), report
KBS after bilateral damage. In a large body of literature,
the amygdala has been associated with the RAGE System,
the LUST System, and through the extended amygdala,
with the CARE System and PANIC/GRIEF System
(Panksepp, 1998; 2011).
At first, Patient M. had widespread damage, typical in
cases of ADEM, affecting basal ganglia, cerebral ped-
uncle, and bilateral deep white matter, among others. Most
 56 J.F. Muñoz Zúñiga
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Figure 3. Wechsler Adult Intelligence Scale (WAIS-III) scores, with a Full-Scale IQ of 90, within average range (average
range = 90–109).
Notes: VIQ, verbal IQ; PIQ, performance IQ, FSIQ, full-scale IQ, VCI, verbal comprehension index; POI, perceptual organization
index. WMI, working memory index, PSI, processing speed index.
of these lesions attenuated and some of them disappeared,
which correlates well with improvement of her multifocal
neurological involvement (multiple cranial nerves affec-
tion, pyramidal syndrome, encephalopathy, and catatonic
syndrome). However, as part of the multiphasic ADEM,
new lesions appeared, mostly in limbic/paralimbic areas
like the amygdalae, orbitofrontal cortex, insular cortex,
and entorrhinal cortex, which marked the beginning of the
KBS. Patient M. developed an almost complete KBS,
with five out of the six classical symptoms (she had no
visual agnosia). Since the amygdalae and the entrance
route of the uncinate fasciculus in the right orbitofrontal
cortex (Brodmann Area 11) were among the compromised
structures, it is highly likely that bilateral damage in
multiple nodes of Yakovlev’s circuit occurred, creating a
disconnection syndrome at a functional level.
Neuropsychological data
A neuropsychological evaluation was performed by the
Behavior and Cognition Department that include the
following battery: the Wechsler Adult Intelligence Scale
(WAIS-III), the Revised Barcelona Test (RBT), the Trail
Making Test, the Stroop Task, and the Beck Depression
Inventory (Golden, 1978; Peña-Casanova, Gramunt-
Frombuena, & Vich-Fullá, 2004). The RBT explores a
wide range of cognitive functions like language, orienta-
tion, attention, reading, writing, praxis, memory, and
abstraction, among others. Verbal IQ, Performance IQ,
and Full-Scale IQ scores obtained in the WAIS-III are
shown in Figure 3.
Distractibility and impulsivity permeated the evalu-
ation, affecting her performance and causing it to be
lower than expected. The patient got distracted by
irrelevant stimuli throughout the whole session, grabbing
objects in her surroundings and requiring frequent
insistence on part of the evaluator to finish the appointed
tasks. The expressive language showed no alterations in
automatic speech, repetition, denomination, and lexical
fluency; there were intrusions of sexual content. Her
receptive language did not show alterations in phone-
matic analysis, audio-verbal retention, or logical gram-
matical structures comprehension. There was no visual
agnosia. There were no alterations on praxis and verbal
memory. Her nonverbal memory was in the lowest range
of the expected performance for her age and education,
with great susceptibility to interference.

Executive functions associated with dorsolateral pre-
frontal cortex (DLPFC) like programming, sequencing,
and working memory were preserved, with performance
within average range. Nevertheless, it was evident for the
evaluating team that the patient had a cognitive/behavioral
dissociation that spread to her daily life. The cognitive or
“cold” executive functions were relatively preserved,
while those aspects involved in decision-making about
events with emotionally relevant consequences were
altered. These affective or “hot” aspects of executive
functions have been associated with orbitofrontal cortex;
traditional neuropsychological tests are more sensitive to
DLPFC damage (Kerr & Zelazo, 2004; Lovstad et al.,
2012). Consequently, the patient showed poor real-life
decision-making and altered self-regulatory behavior.
Finally, the Beck Depression Inventory indicated a severe
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depression, with a score of 34, on account of hope-
lessness, suicidal thoughts, and guilty feelings, among
others, as elaborated upon below.
First-person data and family experience
During the second self-limited and transient demyelinat-
ing phase, patient M. began to approach both family and
strangers, invading their personal space, and asking them
private, socially inappropriate questions, mostly about
their sex life and the aspect of their genitals. She would
touch the private parts of both men and women alike,
including her parents. On several occasions she ran away
from home looking forward to have sexual intercourse
with strangers or recently met people. Through social
networks she would offer to have sex with strangers. Her
discourse, permeated with sexual references, was
described by her family as “impudent” and “straightfor-
ward.” For instance, on one occasion she confessed to her
husband of other sexual partners she had during their
marriage. M. did not seem to notice the anger and sadness
expressed by her husband. Later on, when her mother
arrived home and found her son-in-law upset, M. said to
him with childlike prosody “You forgive me, don’t you?”
During the first year of illness this lack of emotional
insight, along with her hypersexuality, proved to be too
disruptive for his husband, who left her at the end of
the year.
M. also set up courses of action that put her in constant
risk. Sometimes she would give childish rationalizations
for these actions, on other occasions she seemed per-
plexed by the motivations behind those actions. To give an
example, while being an inpatient, she tried to have sexual
intercourse with another patient, who, she found out, had
an infectious lesion on his genitalia. After being caught by
the staff, she explained that she had wanted to have sex,
although she understood that the lesion suggested a
Neuropsychoanalysis 57
sexually transmitted disease; in addition, she found this
revolting, but alas, she could not stop her behavior.
As part of her hyperorality, she would introduce all
kinds of objects in her mouth; when asked for the reasons
to do this, she would say she wanted to know how they
tasted. As an inpatient she sneaked in to different rooms
and stole food from other patients; on some occasions she
looked for food in the trash. She kept food in her mouth
for hours, causing her to lose all of her teeth. She exhibited
changes in dietary habits, with preference for foods high
in sugar content. One time, while changing diapers for her
daughter, she presented coprophagia.
Most of the time her attention got focused on new,
often irrelevant environmental stimuli and she would
grab objects and belongings in her surroundings. Her
social behavior changed: she became puerile, constantly
demanding attention from her parents, getting easily
frustrated but never aggressive. She neglected her own
personal grooming as well as her maternal duties, despite
saying otherwise.
After the first year of illness, her hypersexual beha-
viors decreased mildly. Her lack of emotional insight over
her symptoms and its potential impact on others (i.e.
anosodiaphoria) diminished as well. As this happened,
she began to experience the social implications of her
behavioral symptoms, prompting depressive ruminations,
and suicidal thoughts. Eventually, she made several
suicidal attempts, in addition to impulsive suicidal
gestures, that led to a diagnosis of a depressive disorder.
M. used to mention how guilty she felt about telling her
husband about prior infidelities. Moreover, as time went
by and she realized her symptoms prevented her from
practicing her career, let alone postgraduate studies, she
felt life had left her behind.
In addition to M.’s distress, these symptoms produced
caregiver burnout in her parents, who complained about
her placidity and the fact that M. seemed unable to learn
from experience. It did not matter whether they argued
with her, grounded her or gave her final warnings.
Eventually, it became clear that these symptoms were
permanent; their daughter now tragically changed.
Case analysis: the first-person/third-person
continuum
From a clinical point of view, M. developed a full-blown
KBS. As seen in multiple MRI and her neuropsychologi-
cal profile, the ADEM spared most of her unimodal and
transmodal cortical areas, leaving mostly untouched
mnesic, gnosic, praxic, and some of the executive
functions, specifically those cognitive or “cold” functions
associated with the DLPFC. This state of affairs left M.
with very severe affective and behavioral disturbances,
poor behavioral inhibition, and the cognitive substrate to
 58 J.F. Muñoz Zúñiga
act out her altered drives in a pathological fashion. I will
elaborate on this below.
What is known about the neuroanatomy of the KBS
fits well with the semiological purity of the symptoms
displayed by patient M. Thus, although initially her
ADEM produced diffuse neurological damage, from the
second demyelinating phase onwards, there was a pre-
dominance of affective and behavioral symptoms that
point out to bilateral damage in multiple nodes of
Yakovlev’s circuit. Serial MRIs showed an almost com-
plete resolution of the original lesions and a cortical-
subcortical generalized atrophy. In spite of this, the patient
did not have other features like aphasia, dementia, or a
typical orbitofrontal syndrome. Four years later she still
does not meet the clinical criteria for these features.
It seems plausible that the limbic/paralimbic damage
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may have caused a double hit to the hierarchical organ-
ization of neural networks responsible for emotional
processing, as described by Feinberg (Feinberg, 2009)
and applied by Panksepp and Solms (Panksepp, 2011;
Panksepp & Solms, 2012). Such a model of nested
hierarchies, with constitutive elements at lower levels
contributing to the emergence of higher ones, allows
neuronal contextualization of primary affects through
bottom-up differentiation. This makes possible, through
the course of development, for top-down constraint to
occur, with higher-order reflexive thinking, at epigeneti-
cally emergent levels, eventually regulating emotional
processing. In view of the lesions sustained by the patient
on different levels of neural circuits associated with
different aspects of emotion expression and regulation, it
is possible that the two kind of processes, bottom-up
differentiation and top-down constraint, were altered,
resulting in unmanageable appetitive behaviors, insuffi-
ciently modulated by her prefrontal cortex.
In this regard, it seems relevant that Freud always gave
a privileged place in his model of the psychic apparatus to
libidinal drives; endogenous sources of excitation that
imposed a demand upon the mind, that of finding ways to
reduce stimuli to the lowest possible level (Freud, 1905),
through objects in the external world (Ellman, 2010;
Freud, 1915). Deep-rooted in the system unconscious, and
later on in the id, drives emerge from the inner body and
walk with us until the day we cease to exist. Freud made a
distinction between the biological origins of instinctual
needs, for which he reserved the German word of
“Instinkts,” and the way these were represented and
elaborated in the mind as drives, for which he used the
German word of “Triebe” (Solms, 2013b).
Patient M. seemed to live under ruthless control of her
instincts and their corresponding libidinal drives, experi-
encing instinctual needs as raw affects that had to be
satisfied in peremptory and socially inappropriate ways.
Although she was often – as part of social-emotional
disturbances in KBS – in a state of placidity, with lack of
response to stimuli with negative emotional salience, she
seemed constantly overwhelmed by raw affects, so one
could find her maintaining food in her mouth, while
grabbing objects in her surroundings and approaching the
medical staff as well as other patients, with inadequate
questions about their sex life and proposals of intimacy;
all this in less than a minute, in a sort of libidinal
cacophony.
This may be explained by the aforementioned double-
hit model over the hierarchical organization of neural
networks involved in emotional processing. Inputs arising
from these networks would suffer insufficient neuronal
contextualization, reaching superior levels in raw, poorly
differentiated, states. We never experience during devel-
opment a stage where poorly differentiated drives assault
us in such a way; we do not find these kinds of drives in
the unconscious derivatives of neurotic patients either nor
psychotic, for that matter. I would argue that this was no
return of the repressed, but something more archaic in
nature. Owing to the absence of psychic elaboration upon
the demands imposed by the instincts, these presented
themselves with inclement pressure for discharge, refus-
ing to become compromise formations, exceeding the
metabolic capacities of her psychic apparatus, immune to
any logical link to her biography.
From a structural point of view, these disturbances
suggested id intrusions of primitive presymbolic contents
belonging to the unrepressed unconscious. But also her
ego, the executive agency of the mind, was compromised.
M. had preservation of some ego functions. In particular,
the autonomous ego functions, as described by ego
psychology, including language, perception, memory,
and motor functions (Ellman, 2010; Gabbard, 2005).
However, although these cognitive functions were highly
preserved, her judgment was severely debilitated.
Although M. never had frank psychotic symptoms, like
delusions and hallucinations, by virtue of her incapacity to
modulate and inhibit libidinal discharges, and her inability
to work through her emotions by reflective thinking, she
could not anticipate or weigh adequately the conse-
quences of her actions.
Solms (Kaplan-Solms & Solms, 2000) has correlated
the so-called autonomous ego functions with unimodal
cortices, associative heteromodal cortices, and their
thalamic connections. These would function as transmo-
dal gateways allowing integration and stabilization of data
beyond their simple perceptual attributes, in order to guide
behavior (Solms, 2013a). According to this formulation,
other functions of the ego in its “dynamic manifestation”
(Kaplan-Solms & Solms, 2000) are linked to prefrontal
areas. In his neuroanatomical model of the psychic
apparatus, these areas are interpolated both between
perceptual-mnestic posterior systems and motor areas,
and between motor areas and subcortical/cortical net-
works related to arousal, interoception, and primary

process emotions. As described above, M. had right
orbitofrontal cortex damage, in the entrance route of the
uncinate fasciculus. This component may have contrib-
uted to top-down constraint alterations, preeminently
contributing to her anosodiaphoria (Howorth & Saper,
2003; Mendez & Shapira, 2005, 2011) and her inability to
regulate her emotions and inhibit the consummation of
appetitive urges – that is, to delay the libidinal discharge
according to the demands made by the external world. In
his famous passage in The Ego and the Id (Freud, 1923),
Freud said:
The functional importance of the ego is manifested in
the fact that normally control over the approaches to
motility devolves upon it. Thus in its relation to the id it
is like a man on horseback, who has to hold in check the
superior strength of the horse; with this difference, that
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the rider tries to do so with his own strength while the
ego uses borrowed forces … often a rider, if he is not to
be parted from his horse, is obliged to guide it where it
wants to go; so in the same way the ego is in the habit of
transforming the id’s will into action as if it were its
own. (p. 25)
The overall picture was as if M. had lost the reins of her
id, which became a runaway horse; and witnessed, as a
defenseless rider, the drives accessing the motor pole.
Figure 4 shows the relationship with key points of the
anatomical damage, following Freud’s analogy.
In his model, Solms correlated the superego with
ventromedial prefrontal areas, which hold regulatory
functions over emotional processing areas, as a stimulus
barrier protecting the ego from the incessant demands of
instinctual life (Kaplan-Solms & Solms, 2000). Perhaps
not surprisingly, for patient M. there was greater com-
promise in the introjected social norms, the aspect of the
Figure 4. The double-hit model. Bottom-up (thicker arrow, number 2) and top-down disturbances (interrupted arrow, number 1) in
hierarchical emotional processing possibly due to bilateral damage to Yakovlev’s circuit, in right orbitofrontal cortex/uncinate
fasciculus and amygdalae. Like a defenseless rider M. seemed to have lost the reins (impaired ego/superego regulation of drives), over
her id, which became a runaway horse (increased/undifferentiated id intrusions).
Neuropsychoanalysis 59
superego implicated in behavior inhibition. It is note-
worthy that the sexual symptoms of her KBS included the
indiscriminate touching of women’s breasts, including her
mother, and frequent touching of men’s genitals, includ-
ing her father, in conjunction with repetitive questioning
about her parents’ sexual behavior. That is to say that the
very origin, allegedly, of the superego, the fundamental
prohibition of incest, was compromised.
The ego ideal was, nevertheless, relatively intact, as
evidenced by her depressive thoughts about guilt and
hopelessness. In this regard it is notable that her lack of
emotional insight seemed to fluctuate constantly. It seems
as if sometimes she could take distance from her abnormal
drives and reflect upon them; and on other occasions she
would be taken captive, in endless cycles of acting-out, as
though a volatilization of inner ego boundaries, with the id
contents invading the ego (Ellman, 2010; Gabbard, 2005),
had taken place. In those moments the feeling her
behavior elicited was one of anguish, prompting the
spectator to wonder, not as a theoretical, but as a very
real issue how much incursion of the drives could the ego
tolerate before it started to become undifferentiated from
the id itself. A fragment of a prototypical interview with
M., about her daughter, whom her cares she continued to
neglect, might illustrate the point:
Psychiatrist: so how do you feel about your daugh-
ter now?
M.: I’m not being a good mother.
(She turns serious; she seems really focused on my
question).
I want to be a good mother, for her. She needs me.
(She looks right back, and for the first time I feel she is
here with me, that I have bumped into something; an
aspect of her former self, remains of what once was).
 60 J.F. Muñoz Zúñiga
P: Have you been able to take care of her?
M.: I like to hold her and hug her; she’s the reason that
keeps me going.
(She gets up off the couch and starts wandering through
the room, I feel her attention is gone; her face changes
and seems childish again, filled with hollow excitement.
She scans several objects with her sight and the presence
I felt a moment ago is gone.)
P: You are saying she protects you against depressive
feelings.
(I try to get back to the subject, but she seems fascinated
with the texture of my tie; she gets close and reaches to
touch it).
M.: Uh huh. What is this made of?
P: I think it’s silk.
(Now she wants to touch my shirt; I grab her hand and
step back a little to regain my personal space. She takes
my hand, says she likes the way it smells and in a quick
movement she leans to smell the back of my hand).
Downloaded by [Jose Fernando Muñoz Zúñiga] at 07:27 25 July 2015
Her mind seemed to function in ways that draw her close
to the primary process thinking. Her drives did not take
account of time or contradictions; they demanded satis-
faction in the present at all costs. Likewise, the object
paled in comparison to the necessity of discharge; it was
unimportant with whom or under what circumstances the
drives achieved their goal. Nevertheless, unlike the
patients studied by Solms, with greater ventromesial
frontal damage (Kaplan-Solms & Solms, 2000), M. was
not disorientated, did not confuse internal and external
reality, and did not have confabulations or psychotic
symptoms like delusions or hallucinations. When con-
fronted, she could reflect about her situation with logical
thoughts. Owing to her medical background, in time she
understood, at least on a cognitive level, what it meant to
have been diagnosed with KBS. This, however, would
not, or could not, translate into behavioral change.
Thus, when her case formulation led to an attempt to
classify her level of functioning according to a model that
follows the concept of a psychotic part of personality
(Bléandonu, 1999), personality organization (Kernberg,
1975; Trimboli, Marshall, & Keenan, 2013), and the
concept of levels of functioning (Cancrini, 2007), a
conundrum unfolded. Although these conceptual frame-
works were not developed for neuropsychiatric patients,
the issue remains that a greater understanding of their
inner world will have to apprehend their level of mental
functioning, taking into account nondynamic factors as
well. If one were to apply these models, it would put
patient M. somewhere between the low-level borderline
and psychotic functioning. This, in view of her use of
lower level defense mechanisms, her volatile inner ego
boundaries, impaired superego functioning and ego lab-
ility with insufficient control over the drives, among
others. Nonetheless, if one were to pursue this line of
thought one should refer to a “borderline-like” function-
ing or “psychotic-like” functioning to avoid conceptual
confusion; since these phenomena appeared after a
specific neurological insult (i.e. the ADEM) and its
sequelae (i.e. the KBS). Diagnostic conundrums are no
strangers to the field of neuropsychiatry; quite often we
find clinical phenomena in which traditional psycho-
pathological conceptions are distorted by the conse-
quences of the neurobiological insult, leading to
secondary symptoms that sometimes appear as faint
shadows of their psychiatric counterparts, and other times
are almost indistinguishable from primary psychiatric
symptoms. Berrios has referred to these phenomena as
“behavioral phenocopies” or “behavioral copies” (Ber-
rios, 2007). In a similar vein, the term “psychodynamic
phenocopies” is proposed for psychopathological mani-
festations, as they are defined and understood in metap-
sychology, when applied to these kinds of patients.
Final remarks
We cannot conclude anything definitive from a single
clinical case; it should, however, provide insights into
clinical phenomena. Following the principles of dynamic
localization (Luria, 1973), we believe this analysis
accounts for the psychodynamic features of this syn-
drome as it presented in our patient; other subtypes of
the KBS may occur depending on the particular com-
promised networks or nodes in Yakovlev’s circuit (i.e.
the specific factors pointed out by Luria). In turn,
patients with other subtypes may demonstrate different
repercussions on their psychic apparatus. This introduct-
ory formulation may give a better understanding of how
a patient with KBS experiences her symptoms, at the
same time it may help the medical staff to understand the
powerful manifestations of countertransference these
symptoms generate. As some of them have diminished
over time, perhaps someday patient M. could receive a
psychodynamically oriented therapy; that is, after all, the
only way to test and modify the current model. More-
over, case series of patients with KBS due to different
etiologies are needed, both to establish better neural
correlates for each symptom and to pinpoint sufficient
and necessary conditions for the disturbances presumed,
based on observed behavior, in the psychic apparatus of
patients like M. Furthermore, exhaustive MRI imaging
should be done in the future in patients with KBS
due to a disconnection syndrome; probably including
refined versions of tractography by diffusion tensor
imaging, to assess white matter fiber integrity, such
as the uncinate fasciculus (Thiebaut de Schotten,
Dell'Acqua, Valabregue, & Catani, 2012). In the mean-
time it is proposed that:
(1) Yakovlev’s circuit seems to play a key role in
orbitofrontal top-down constraint over temporal
limbic and paralimbic areas involved in neuronal
contextualization of primary process emotions.

(2) Disconnection of Yakovlev’s circuit in the
KBS appears to affect in radical ways the
psychic apparatus agencies described in Freud-
ian metapsychology.
(3) At least in some cases, the psychodynamic
impact of neurological damage in KBS may
modify qualitatively and quantitatively the mani-
festation of instincts found in the id; and it may
affect ego functions concerning the regulation
and control of the drives, with internalized
prohibitions succumbing to id intrusions.
(4) At least in some cases, the neuroanatomical
lesions in KBS bring the psychic apparatus
closer to primitive levels of functioning, remin-
iscent of both low-level borderline functioning
and psychotic functioning.
Downloaded by [Jose Fernando Muñoz Zúñiga] at 07:27 25 July 2015
(5) The term “psychodynamic phenocopy” is pro-
posed to avoid conceptual confusion when
neurological insult and its sequelae cause
changes in the psychic apparatus of neuropsy-
chiatric patients, particularly when these
changes resemble specific phenomena
described or treated psychoanalytically in
patients without focal neurological damage.
Neuropsychiatric illness frequently reminds us of the
delicate constitution of the emergent self. Random events
may change it in unpredictable and, too often, tragic ways.
The symptoms experienced by patient M. have subsided
to a small degree over the years, but she remains
dependent on her family for care. Pursuing a deeper
understanding of the afflictions that undermine neuropsy-
chiatric patients might give them or their families better,
more useful narratives. At the minimum, this understand-
ing may help patients and their families live with the
changes wrought by the brain injury. At best, it may also
provide us with useful knowledge to more effectively treat
future patients with these types of syndromes. In addition,
it gives us a glimpse of the workings of the mind, through
the reverse engineering of their inner world.
Acknowledgement
To patient M. for her collaboration, to Dr Jesus Ramirez-
Bermudez and Dr Ana Ruth Díaz for their support.
Disclosure statement
No potential conflict of interest was reported by the author.
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