Acta Neurochir (Wien) (2004) 146: 1267–1270
DOI 10.1007/s00701-004-0373-6

Case Report
Human Kluver-Bucy syndrome following acute subdural haematoma
Y. Yoneoka1;2 , N. Takeda1;2 , A. Inoue1 , Y. Ibuchi1 , T. Kumagai1 , T. Sugai1 ,
K.-I. Takeda1 , and K. Ueda1
1
2

Department of Neurosurgery, Yamagata Prefecture Central Hospital, Yamagata, Japan
Department of Emergency Medicine, Yamagata Prefecture Central Hospital, Yamagata, Japan

Published online September 13, 2004
# Springer-Verlag 2004

Summary
We present a rare case of complete human Kluver-Bucy syndrome
(KBS) following recovery from transtentorial herniation caused by acute
subdural haematoma (ASDH). A 17-year-old right-handed high school
boy got into stupor within five minutes after 3-rounds of sparing at
boxing. Emergency computed tomographic (CT) scan showed right
cerebral hemispheric ASDH, which was evacuated following intentional
decompressive craniectomy. After recovery of consciousness, he developed emotional changes (placidity with loss of normal fear and anger),
psychic blindness, aberrant sexual behaviour, excessive oral tendencies,
increased appetite, and hypermetamorphosis in order of mention, which
were observed with waxing and waning from 17th to 28th hospital day.
Peri-operative CT scaning and magnetic resonance imaging showed
lesions of the right temporal lobe and right-dominant orbitofrontal
regions including bilateral rectal and medial orbital gyri, and the intact
left temporal lobe. Two pathogeneses can be thought of and the whole
picture of KBS following ASDH can arise even though one (left in this
case) temporal lobe is preserved, 1) in which associated orbitofrontal
lesions of the frontal lobes may correlate with occurrence of KBS, or 2)
cerebral blood hypoperfusion of both temporal lobes due to increased
intracranial pressure and=or compression of both posterior cerebral
arteries at the edge of the tentorium cerebelli occurs.
Keywords: Kluver-Bucy syndrome; acute subdural hematoma;
temporal lobe; orbitofrontal region; posterior cerebral artery.

Introduction
Since Kluver and Bucy first described the syndrome
including tendencies to examine all objects orally, loss
of anger and fear responses, increased sexual activity
and ‘‘psychic blindness’’ following bilateral temporal
lobectomy in rhesus monkeys [14, 15], the clinical
presentation and anatomical correlation with a human
Kluver-Bucy syndrome (KBS) has been discussed [3, 4,
7, 10, 11, 13, 16, 18, 20, 21, 24]. Among them, unilateral

temporal lobe lesions [4, 11, 22] have been noted to
produce the KBS although KBS has been classically
associated with bitemporal lesions. Interestingly, all
the three cases of unitemporal-lesion-induced KBS
affected the left temporal lobe [4, 11, 22]. We report
an extremely rare case of complete human KBS following recovery from right-sided transtentorial herniation
caused by acute subdural haematoma (ASDH). Our case
presented with emotional changes (placidity with loss of
normal fear and anger), psychic blindness, aberrant
sexual behaviour, excessive oral tendencies, increased
appetite, and hypermetamorphosis (in order of mention)
without aphasia, anmesia, finger agnosia, or right-left
disorientation, which were self-limited and observed
with waxing and waning after regression of cerebral
oedema in the right temporal and right-dominant orbitofrontal regions. In this article, we discuss the pathogenesis of transient human KBS following right-sided
ASDH.
Case report
A 17-year-old right-handed high school boy lapsed into stupor within
five minutes after 3-rounds of sparing at boxing. He had a past oneweek hospitalization history of minor traumatic subarachnoid haemorrhage without cerebral contusion complicated only by headache after a
boxing competition four months prior to admission, which was selflimited and never affected his good level of academic achievement nor
his popularity as a boxer in high school. On arrival (Day0), he was
in coma with decerebrate rigidity and a dilated right pupil, indicating right-sided uncal herniation. An emergency computed tomographic
(CT) scan showed right cerebral hemispheric ASDH with midline shift
to the left, which was successfully evacuated after intentional decom-

Y. Yoneoka et al.: Kluver-Bucy syndrome following acute subdural haematoma
pressive craniectomy. Micro-operative observation to investigate the
origin of the subdural bleeding confirmed rupture of the right olfactory
bulb and its vasculature. Further cerebral contusion was not observed.
Bleeding from the frontal base was controlled by bipolar coagulation
and gentle pressure. Postoperative examinations showed mild left-sided
hemiparesis (until discharge), stupor (for seven days), and conjugate
deviation of eyes to the right (for eight days). Postoperative CT scans
showed transient oedema of the right temporal and basal frontal lobes
(bilateral rectal and medial orbital gyri) until 11th postoperative day
(POD11) but the intact left temporal lobe remained intact. Following
recovery of consciousness, he developed emotional changes (placidity
with loss of normal fear and anger), psychic blindness (loss of recognition of people, even his parents, e.g. calling his mother ‘‘fairy’’),
aberrant sexual behaviour (mainly abnormal sexual desire and verbalization), excessive oral tendencies (a strong tendency to examine all
objects orally, putting objects in mouth, licking, biting, chewing, touching with lips), increased appetite (to spend the whole time blind eating),
and hypermetamorphosis (strong tendency to react to every visual
stimulus, to touch everything in sight, and to attend to every visual
stimulus with grasping, hugging movements) in that order, which
showed some overlapping and were observed with waxing and waning
from POD16 to POD27. Orientation and memory function were preserved during the affected period. Examinations detected no aphasia,
anmesia, acalculia, finger agnosia, or right-left confusion, indicating
intact left temporoparietal lobes. He could sing as well as he sang
before admission. Electroencephalogram (EEG) failed to detect seizure
activity. He left our hospital on foot with mild clumsiness of the right
extremities and returned to the high school he went to before admission. Follow-up magnetic resonance (MR) imaging on POD89 revealed
mainly the right atrophic anterior temporal lobe, damage of the basal
frontal lobes (bilaterally rectal and medial orbital gyri), and the intact
left temporal lobe. He led a meaningful school life and proceeded to a
local college 14 months after discharge inspite of a worse school record
than he had prior to the present episode.

Discussion
To the best of our knowledge, this is the first report
of transient complete human Kluver-Bucy syndrome
(KBS) following a unilateral acute subdural haematoma:
an extra-neuro-axial lesion. A combination of at least 3
or more of the symptoms and signs is typically suggestive of the Kluver-Bucy Syndrome [12]. Our patient
presented the six major components of KBS as exposed
by Rossitch [21]: (1) Placidity, (2) Psychic blindness,
(3) Hypersexuality, (4) Increased oral activity, (5)
Increased appetite, (6) Hypermetamorphosis. Amnesia
or aphasia, however, was not observed in our case. In
humans, KBS is generally incomplete [6, 19, 23, 24].
Complete KBS as found in this case is less frequent
[4, 11, 18, 20].

1269

Several reports about KBS without bitemporal lesions
are available [2, 11, 17, 20, 22]. These have not completely ruled out the possibility of transient or permanent
bitemporal dysfunction caused by haemodynamic [17],
epileptic [2, 11], traumatic [22] events.
Formisano et al. describes Kluver-Bucy syndrome as
a syndrome associated with favourable prognosis in the
outcome of traumatic disturbances of consciousness in
survivors of head trauma [8]. The dynamics in the development of a KBS show a delineation between a prestage, full-stage, and remission stage [10]. These stages
only occur in posttraumatic cases and have not been seen
in KBS of other etiology [1]. In our case, as described in
the literature [1, 8, 10], KBS was observed with waxing
and waning after remission of oedema of the right temporal and bifrontobasal regions (bilateral rectal and medial orbital gyri), which culminated in full recovery.
KBS has first been described as a result of total
bilateral temporal lobectomy in rhesus monkeys [15].
On the other hand, KBS has already been reported in
the literature as atypical post-traumatic remission phase
[9]. This syndrome, consisting in the increase of oral
automatisms and of sexual drive, has been interpreted
as a disconnection syndrome with loss of inhibitory
cortical control over the limbic system [10]. The orbitofrontal and caudal medial (limbic) prefrontal cortices receive major projections from the amygdala,
associated with emotional memory, and from medial
temporal and thalamic structures associated with longterm memory [5].
Thus, as demonstrated by CT scans, the chief cause
of the presented self-limited KBS was responsible
for, albeit hypothetically, oedema-induced transient
dysfunction of the right temporal and the basal frontal
lobes (bilateral rectal and medial orbital gyri which are
supposed to conduct inhibitory cortical control over the
limbic system). This is applicable as a pathogenesis of
KBS to the one case with putaminal hemorrhage [20].
As an alternative pathogenesis of KBS following
recovery from transtentorial herniation, cerebral blood
hypoperfusion of both temporal lobes due to increased
intracranial pressure and=or compression of both posterior cerebral arteries at the edge of the tentorium cerebelli

1
Fig. 1. (A, B, and C) Preoperative CT scan images on admission (Day0) show right hemispheric acute subdural haematoma with midline shift to the
left. (D, E, and F) Post-decompression CT scan images on postoperative day (POD) 11 demonstrate oedema of the right temporal and basal frontal
lobes (bilateral rectal and medial orbital gyri) and reveal the intact left temporal lobe. (G, H, and I) Post-decompression CT scan images on POD29
show regression of the oedema. (J, K, and L) Fluid attenuation inversion recovery images on POD89 reveal damaged scars in the basal frontal lobes
and the right temporal lobe with the dilated temporal horn indicating atrophy

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Y. Yoneoka et al.: Kluver-Bucy syndrome following acute subdural haematoma

can be implicated. So, KBS described in this report can be
compatible with reversible ischemic neurological deficits
due to ASDH. This hypothesis, however, has a little difficulty explaining the rarity of KBS following transtentorial herniation; Neurosurgeons encounter transtentorial
herniation occasionally but KBS scarcely. Disturbance of
consciousness during the recovery phase may mask KBS
following transtentorial herniation in many cases.
KBS remains a fascinating syndrome whose exact
neuro-anatomical basis is unclear. The presented transient KBS caused by oedema of the right temporal lobe
and bilateral rectal and medial orbital gyri bilaterally
following right ASDH, sparing the left temporal lobe,
provides new and interesting insights into the potential
pathophysiology of KBS. The self-limited etiology of
our case provides not only a hypothetical pathogenesis
of KBS but also an important framework for deciphering
its infrequency and the mechanisms of both post-traumatic and non-traumatic cases.
Acknowledgement
We deeply appreciate Susumu SATOH, M.D., ex-director of our
medical center, for his critical review of our manuscript.

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Comment
This interesting case report describes a 17-year old patient who went
through a transient complete Kluver-Bucy syndrome caused by an acute
subdural haematoma following a sports accident. This case presentation
provides some interesting and rare observations because a complete
Kluver-Bucy syndrome is rarely encountered in the neurosurgical treatment of acute subdural haematomas. Furthermore, the authors demonstrate that the whole clinical picture of KBS was transiently expressed
although the left temporal lobe was not significantly effected by the
trauma as shown on the CT and MRI scans. This provides new and
interesting insights into the potential pathophysiology of KBS and is
therefore of considerable interest for the neurosurgical community.
G. Nikkhah
Correspondence: Yuichiro Yoneoka, Department of Neurosurgery,
Yamagata Prefecture Central Hospital, 1800 Aoyagi, Yamagata,
990-2292, Japan. e-mail: yone@bri.niigata-u.ac.jp