Original Paper
Received: August 8, 2009
Accepted: November 5, 2009
Published online: January 16, 2010

Eur Neurol 2010;63:87–93
DOI: 10.1159/000276398

Heading Disorientation: A New Test and a
Possible Underlying Mechanism
Ritsuo Hashimoto a Yasufumi Tanaka b Imaharu Nakano c
a

Department of Neurology, International University of Health and Welfare Hospital, Nasushiobara, b Shion Clinic,
and c Division of Neurology, Department of Medicine, Jichi Medical University, Shimotsuke, Japan

Key Words
Topographical disorientation ⴢ Heading disorientation ⴢ
Egocentric reference frame ⴢ Directional signal ⴢ
Retrosplenial cortex

Abstract
Background/Aims: Heading disorientation (HD) is a type of
pure topographical disorientation. Reported cases showing
HD have been very few so far, and its underlying mechanism
remains unclear. The aim of this study is to find the anatomic substrates of HD and to demonstrate a possible underlying mechanism for the symptom. Methods: We investigated
3 patients with HD by a new test, the card-placing test (CPT).
Part A of the test assesses the ability of a subject to retain
information on spatial locations of cards placed on the floor
around the subject. Part B examines the subject’s ability to
integrate information on the spatial locations of similarly arranged cards and that on changes of the body directions.
Results: The patients had a lesion that commonly involved
the right retrosplenial cortex and showed good record results for part A but very poor ones for part B. Conclusions:
The results of the CPT suggest that HD patients cannot integrate information on the spatial locations of objects derived
from an egocentric reference frame with that on changes of
the body directions. The retrosplenial cortex may be the
place where these different types of information necessary
for navigation converge.
Copyright © 2010 S. Karger AG, Basel

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Introduction

Topographical disorientation is defined as the loss of
the ability to find one’s way within one’s locomotor environment. This symptom is often observed in patients
with diffuse brain damage (e.g. dementia and acute confusional state). There are certain individuals, however,
who show topographical disorientation after focal brain
damage. By reviewing such cases comprehensively,
Aguirre and D’Esposito [1] recently proposed that there
are at least four varieties of topographical disorientation:
egocentric disorientation, landmark agnosia, anterograde disorientation, and heading disorientation (HD).
Patients with egocentric disorientation, although they
have intact visual recognition ability, exhibit severe deficits as to the relative locations of objects with respect to
the self [2–5]. Their performance is often impaired in a
wide range of visuospatial tasks such as mental rotation
and spatial tapping tasks. Thus, their disability includes
not only the representation of a large-scale environment
but also wide varieties of cognition that need spatial representational function. Such patients usually have a lesion in the right or bilateral posterior parietal region(s)
[2–5].
In contrast to egocentric disorientation, patients with
landmark agnosia retain the ability to identify and to represent the locations of objects, but are defective in recognizing salient or prominent environmental features for
Ritsuo Hashimoto, MD
Department of Neurology, International University of Health and Welfare Hospital
537-3 Iguchi, Nasushiobara (Japan)
Tel. +81 287 39 3060, Fax +81 287 39 3001
E-Mail ritsuo @ iuhw.ac.jp

a

R

b

L

Fig. 1. Fluid attenuated inversion recovery
(FLAIR) MRI scan of case 1 (a, axial; b,
sagittal views). High signal intensity can
be seen in the right retrosplenial area that
extends into the right splenium and forceps major of the corpus callosum.

the purposes of orientation [6–9]. They usually have a lesion that involves the right or bilateral lingual gyrus, this
being very close to the anatomical substrates of patients
with visual agnosia whose visual recognition deficits are
not confined to landmarks [6–9].
In anterograde disorientation, only impairment in a
novel environment is seen, the ability to navigate in familiar places being good. The lesion site responsible for
this is presumed to be the parahippocampal gyrus, which
is supposed to have some computational function necessary for the acquisition of novel topographical knowledge
[10].
HD is different from the above-mentioned three varieties in that HD patients can represent the relative locations of objects and they are able to easily recognize landmarks, but suffer from topographical impairment not
only in a novel but also in a familiar environment. It is
implied that the primary deficit in HD is an inability to
derive directional information from landmarks to reach
a destination [1, 11].
HD is thus a very unique and intriguing symptom,
however the number of reported cases has been limited
so far and a specific test for HD has not been developed
yet. Therefore, the underlying mechanism of HD remains
unclear. Here, we report 3 HD patients examined by using a new clinical test that we had developed, and discuss
a possible underlying mechanism of HD.
Case Reports
Patient 1
On August 12, 2001, a 67-year-old right-handed salesman with
9 years of education, who had been under treatment for diabetes
mellitus and hypertension for 10 years, was driving a car on his

88

Eur Neurol 2010;63:87–93

usual way back to home. When he stopped at a crossroad, he suddenly became embarrassed. In the front, he saw buildings and
trees that were familiar to him. He was aware that he was near his
house, but was unable to determine which direction he should
drive. After having made many wrong turns along the way, he
managed to finally arrive at his house; it had taken him 2 h from
a place where he usually only needed 5 min by car. Nine days
later, he was referred to our hospital.
On admission, he was alert, cooperative, and neurologically
normal including the visual field and visual acuity. He did not
show any visual agnosias such as object agnosia or prosopagnosia.
The line bisection and line cancellation tasks revealed no hemispatial neglect. His language function was intact. He could repeat
6 digits forward and 5 digits backward. He could tap 6 points forward and 5 backward. His episodic memory function seemed to
be intact, because he could remember events that had occurred
before, during, and after the onset of his topographical disorientation. During his 1-month stay at our hospital, he frequently lost
his way to his room. He said that he had difficulty in remembering the positional relationship of the nurse station, toilets, laboratories and his room. Indeed, even when he could recognize that
he was near his room by identifying the nurse station, he could
not determine which direction he should go to return back to his
room. Although he could say the names of stores or offices near
his house, he was unable to draw a map of the vicinity of his house.
On the Wechsler Adult Intelligence Scale-Revised (WAIS-R), his
verbal IQ was 100, performance IQ was 91, and total IQ was 97.
His verbal memory quotient on the Wechsler Memory Scale-Revised (WMS-R, Japanese version) was 110 and that of visual memory was 63.
MRI performed 2 days after his admission revealed an ischemic cerebral lesion at the right retrosplenial area that extended
into the right splenium and forceps major of the corpus callosum
(fig. 1). His topographical disorientation gradually ameliorated
and had almost disappeared 6 months after the onset of his
stroke.
Patient 2
This 72-year-old right-handed man with 9 years of education
had a history of cardiac arrhythmia. On May 13, 2004, when he
was riding a bicycle, he suddenly lost his way back home. He rec-

Hashimoto /Tanaka /Nakano

b

a

R

L

Fig. 2. FLAIR MRI scan of case 2 (a, axial;
b, sagittal views). High signal intensity can

be seen in the right medial occipital lobe
that extends into the right retrosplenial
area. Low signal intensity that suggests an
old infarction can also be seen in the right
frontal lobe.

ognized that he was in front of a store near to his house, but was
unable to recall the direction his house was in. He needed 30 min
to get back home from a place where he usually needed 5 min by
bicycle. He remembered that he made many mistakes when turning and finally arrived at his house only by spotting familiar landmarks. Two days later, he was referred to our hospital.
On admission, he was alert and cooperative. He had atrial fibrillation but no signs of heart failure. He had left homonymous
hemianopsia, but did not show obvious left hemispatial neglect,
judging from the line bisection and line cancellation tasks. He did
not show any visual agnosias such as object agnosia or prosopagnosia. His language function was intact. He could repeat 5 digits
forward and 4 backward. His episodic memory function was
thought to be preserved because he could relate things that he had
experienced before, during, and after the onset of his topographical disorientation. During his stay at our hospital for 1 month, he
had a great trouble in remembering the location of his room and
often got lost, even when returning from the toilet that was only
10 m away from his room. On the WAIS-R, his verbal IQ was 82,
performance IQ was 79, and total IQ was 79. In the Rey-Osterrieth
Complex Figure Test (ROCFT), his score for copying was 36/36,
with 12/36 for immediate recall and 6/36 for delayed recall (30
min after the copying).
MRI on the admission day revealed a fresh infarction in the
medial aspect of the right occipital lobe that extended into the
right retrosplenial area, and an old infarction in the right frontal
lobe (fig. 2). His topographical disorientation gradually improved,
but he still had some trouble even 6 months after the stroke.
Patient 3
This 67-year-old right-handed man with 9 years of education
had undergone an operation, partial resectioning of the left lung,
because of lung cancer on April 2, 2005. Two days after the operation, he suddenly became unable to return to his room from a
toilet that was about 20 m away. During the following several
days, he was often found wandering about the surgical ward looking for his room. Two weeks after the operation, he was referred
to the hospital’s neurology department.
On the initial neurological examination, he was alert and cooperative. General neurological examination showed that he was

Heading Disorientation

intact including the visual acuity and visual field. His language
function was normal. He showed no visual agnosias. The line bisection and line cancellation tasks demonstrated that he had no
spatial neglect. On the Mini-Mental Status Examination (MMSE,
Japanese version), his score was 26/30. In the Auditory Verbal
Learning Test (Japanese version), his performance was presumed
to be normal because he could say 11 out of 15 words on the fifth
recall and remembered 8 of them after a 30-min delay. His episodic memory function appeared to be preserved because he
could say why and when he had received the operation and could
relate episodes when he got lost in the surgical ward. In the
ROCFT, his scores for copying, immediate recall and delayed recall (30 min after the copying), were 34/36, 7.5/36 and 4/36, respectively.
MRI on his reference to the neurological department revealed
a fresh infarction in the medial aspect of the right occipital lobe
that extended into the right retrosplenial area (fig. 3).
Card-Placing Test
We investigated these 3 patients using a new test, which we
named the card-placing test (CPT). The CPT examines the ability to represent spatial locations of objects placed on the floor
around a subject. The CPT consists of two parts – part A and B.
In part A, a subject stands in the center square of nine, 3 ! 3 each
35 ! 35 cm drawn on the floor. The subject is instructed to remember locations of three cards with different signs (circle, triangle and cross), each randomly placed in one of the eight squares
surrounding the subject. After 10 s, the examiner takes away all
the cards, hands them to the subject, and orders the subject to put
them back in their original positions. In part B, the subject has to
remember the locations of the same three cards placed on the
floor as in part A. Immediately after the three cards have been
removed, the subject is rotated to the right or to the left by 90 or
180°, as determined in advance (fig. 4), and then asked to restore
the three cards to the same locations as before. For each of part A
and part B of the CPT, a subject undergoes 10 consecutive trials.
The subject gets 1 point each time he puts one card in the right
place and thus the full scores for each of part A and part B are 30
points.

Eur Neurol 2010;63:87–93

89

b

a

L

R

Fig. 3. FLAIR MRI scan of case 3 (a, axial;
b, sagittal views). High signal intensity can

be seen in the right medial occipital lobe
that extends into the retrosplenial area.

1

2

3

4

5

6

7

8

9

10

Fig. 4. Card-placing test (CPT). In part A of the CPT, a subject

stands in the center square of nine, 3 ! 3 squares, drawn on the
floor. The subject is instructed to remember the spatial locations
of three different cards (circle, triangle and cross), each of which
is randomly placed in one of the eight squares surrounding the
subject. After 10 s, all the cards are taken away and the subject is
requested to restore them to their original positions. The figure
shows the positions of the three cards that we used. In part B, the
subject also has to remember the locations of the three cards. The
positions of the cards are the same as in part A. Immediately after
the cards have been removed, the subject is rotated to the right or

90

Eur Neurol 2010;63:87–93

to the left by 90 or 180°, and then asked to replace the cards. For
both part A and part B of the CPT, the subject undergoes 10 consecutive trials. The rotations in trials 1–10 of part B are as follows:
trial 1, 90° to the right; trial 2, 90° to the left; trial 3, 180° to the
right; trial 4, 180° to the left; trial 5, 90° to the right; trial 6, 90° to
the left; trial 7, 180° to the right; trial 8, 180° to the left; trial 9, 90°
to the right, and trial 10, 90° to the left. The numbers indicate the
trial numbers. A subject gets 1 point if the location of a card that
the subject has replaced is correct, the full score of each of part A
and part B of the CPT being 30 points.

Hashimoto /Tanaka /Nakano

Table 1. CPT scores of controls and patients

Our 3 patients demonstrated marked topographical
disorientation characterized by the following common
features: (i) inability to derive directional information
from salient landmarks in spite of their ability to recognize them; (ii) topographical disorientation in a novel as
well as a familiar environment; (iii) a mild to moderate
visual memory disorder; (iv) absence of prominent visuospatial disorientation, as proved by preserved tapping
span, no signs of hemispatial neglect and intact constructional abilities, and (v) fairly well-preserved general intellectual functions. These clinical characteristics are quite
similar to those in previous case reports [11–17], and according to Aguirre and D’Esposito [1] this type of topographical disorientation is a type of pure topographical
disorientation, namely HD.
With respect to the responsible lesion for the development of HD, our 3 cases each had a localized lesion affecting a specific cortical area in common: case 1 had an
infarct in the right retrosplenial area that extended into

the right splenium and forceps major of the corpus callosum; case 2 had an old infarction in the right dorsolateral frontal lobe and exhibited his HD when he developed
a fresh infarction in the right medial occipital lobe involving the right retrosplenial area, and case 3 also had a
single ischemic lesion confined to the right retrosplenial
area and medial aspect of the right occipital lobe. Damage
to the left retrosplenial has been reported to be associated
not with HD but with episodic memory deficits [18–21].
Thus, the findings in our cases combined with recent reviews [1, 22] strongly indicate that the right retrosplenial
region is the critical site for HD. The differences of symptoms between the right and left retrosplenial lesions
would be one of the examples of asymmetric organization of higher cerebral functions in humans; in this case,
the left retrosplenial area is more associated with aspects
of episodic memory, whereas the right one is preferentially concerned with spatial navigation.
What, then, is the mechanism underlying heading disorientation? In normal circumstances, it is considered
that the identification of landmarks, information on their
spatial locations, heading orientation, and learning and
updating information in response to new environment
are integrated and used altogether for navigation. Because previous cases with HD and our 3 cases showed
mild to moderate anterograde visual memory disturbance, the deficits may contribute their topographical
disorientation especially in a setting of new environment.
A case reported by Suzuki et al. [15], however, did not
demonstrate visual memory disturbance at all and the
patients with HD including ours showed disorientation
not only in a new but also in a well-known familiar environment [1, 11–17, 22]. Thus, anterograde visual memory
disturbance alone cannot explain their disorientation.
Given that patients with HD retain the abilities to recognize landmarks and to map the spatial locations of immediate objects, they should be specifically defective in
integrating head directional signals. This is further supported by the results of the CPT in our 3 patients.
To accomplish part A of the test, the subjects are likely to have to use an egocentric reference frame. The normal scores for part A in our 3 patients suggest that they
were able to use an egocentric reference frame to represent the spatial locations of objects surrounding them. In
contrast, all 3 patients had great difficulty in performing
part B. Although the score of 1 patient (case 3) was borderline, those of the other 2 (cases 1 and 2) were well below the controls’. Moreover, all of them appeared to be
truly perplexed when they were engaged in performing
part B: an observation that was not seen in control sub-

Heading Disorientation

Eur Neurol 2010;63:87–93

Controls (n = 9)
Case 1
Case 2
Case 3

Age
(mean 8 SD)

CPT part A
(mean 8 SD)
full scores; 30

CPT part B
(mean 8 SD)
full scores; 30

65.484.8
67
72
67

27.683.0
28
26
26

25.084.3
4
12
17

CPT Scores of Control Subjects
We carried out the CPT in 9 healthy right-handed volunteers
(5 women and 4 men) who had never experienced a brain disease
such as cerebrovascular disease, head trauma or epilepsy. Their
ages ranged from 60 to 72 (65.4 8 4.8 [mean 8 SD]). They were
independent in daily life and did not complain of topographical
disorientation. All of them scored over 27/30 (29.1 8 1.1 [mean
8 SD]) in the MMSE (Japanese version). As for the CPT, all of
them scored over 21/30 (27.6 8 3.0 [mean 8 SD]) in part A and
over 17/30 (25.0 8 4.3 [mean 8 SD]) in part B.
CPT Scores of the Three Patients
We examined all the 3 patients within 2 weeks after their
stroke, when they showed marked topographical disorientation.
The respective scores of cases 1, 2, and 3 in part A were 28/30,
26/30, and 26/30, and those in part B were 4/30, 12/30, and 17/30
(table 1).

Discussion

91

jects. The only difference between part A and part B is
the subjects’ rotation in part B just before they replace the
cards. The most plausible explanation for their poor
achievement in part B is that the patients were unable to
use the information on changes in their body direction.
In other words, they were defective in the processing of
directional signals of the self, or unable to integrate information on the registered external spatial locations of
objects with that on their body direction.
There are lines of evidence that the retrosplenial cortex is concerned with spatial navigation. For example, excision of the retrosplenial cortex of rats can impair spatial
navigation [23, 24]. Recent neuroimaging studies in humans using PET or fMRI also revealed that the retrosplenial area was activated when subjects were involved in a
large-scale navigation task, although the activation was
usually bilateral [25–27]. Moreover, it is noteworthy that
in rats, head direction cells – cells that are excited when
rats are maintaining a certain heading or orientation
within an environment – are found in the retrosplenial
cortex in addition to several neural structures such as the
anterior dorsal nucleus of the thalamus, lateral dorsal
thalamus, lateral mammillary nuclei, striatum, and postsubiculum [28, 29]. These neural substrates may constitute a functional circuit dealing with directional signals
of the self [28].

Several experiments in monkeys have shown that the
retrosplenial cortex is reciprocally connected with the
parahippocampal cortical areas, presubiculum, entorhinal cortex, mid-dorsolateral prefrontal cortex, superior
temporal sulcus, and posterior parietal cortex [30–32].
Therefore, the retrosplenial cortex seems to be a pivotal
constituent of both the medial temporal lobe memory
system and head directional system as well as interacting
with the lateral parietofrontal large-scale network, which
contributes to the processing of information on the egocentric visuospatial locations of objects.
In conclusion, our 3 cases suggest that the right retrosplenial lesions were responsible for their HD. The CPT
implied that HD patients cannot integrate information
well on object locations in the space derived from an egocentric reference frame and that on changes in body direction. The right retrosplenial cortex may be a place
where these different types of information necessary for
navigation converge. The CPT is a very useful clinical
tool for evaluating patients with HD.

Acknowledgements
We thank Drs. Hiroyuki Kato, Tomoko Ogawa, and Ryohei
Hishida for their help in examining the patients. We also thank
Ms. Noriyo Komori and Ms. Tomomi Miyazaki for their neuropsychological assessment of the patients.

References
1 Aguirre GK, D’Esposito M: Topographical
disorientation: a synthesis and taxonomy.
Brain 1999;122:1613–1628.
2 Kase CS, Troncoso JF, Court JE, Tapia JF,
Mohr JP: Global spatial disorientation. Clinico-pathologic correlations. J Neurol Sci
1977;34:267–278.
3 Levine DN, Warach J, Farah MJ: Two visual
systems in mental imagery: dissociation of
‘what’ and ‘where’ in imagery disorders due
to bilateral posterior cerebral lesions. Neurology 1985; 35:1010–1018.
4 Stark M, Coslett HB, Saffran EM: Impairment of an egocentric map of locations: implications for perception and action. Cogn
Neuropsychol 1996;13:481–523.
5 Wilson BA, Berry E, Gracey F, Harrison C,
Stow I, Macniven J, Weatherley J, Young AW:
Egocentric disorientation following bilateral
parietal lobe damage. Cortex 2005; 41: 547–
554.
6 Hécaen H, Tzortzis C, Rondot P: Loss of topographic memory with learning deficits.
Cortex 1980;16:525–542.

92

7 McCarthy RA, Evans JJ, Hodges JR: Topographical amnesia: spatial memory disorder,
perceptual dysfunction, or category specific
semantic memory impairment? J Neurol
Neurosurg Psychiatry 1996;60:318–325.
8 Landis T, Cummings JL, Benson DF, Palmer
EP: Loss of topographic familiarity. An environmental agnosia. Arch Neurol 1986; 43:
132–136.
9 Takahashi N, Kawamura M, Hirayama K,
Tagawa K: Non-verbal facial and topographic visual object agnosia – a problem of familiarity in prosopagnosia and topographic disorientation (in Japanese). No To Shinkei
1989;41:703–710.
10 Habib M, Sirigu A: Pure topographical disorientation: a definition and anatomical basis. Cortex 1987;23:73–85.
11 Takahashi N, Kawamura M, Shiota J, Kasahata N, Hirayama K: Pure topographical disorientation due to right retrosplenial lesion.
Neurology 1997;49:464–469.
12 Bottini G, Cappa S, Geminiani G, Sterzi R:
Topographic disorientation – a case report.
Neuropsychologia 1990; 28:309–312.

Eur Neurol 2010;63:87–93

13 Obi T, Bando M, Takeda K, Sakuta M: A case
of topographical disturbance following left
medial parieto-occipital lobe infarction (in
Japanese). Rinsho Shinkeigaku 1992; 32:
426–429.
14 Cammalleri R, Gangitano M, D’Amelio M,
Raieli V, Raimondo D, Camarda R: Transient
topographical amnesia and cingulated cortex damage: a case report. Neuropsychologia
1996;42:321–326.
15 Suzuki K, Yamadori A, Hayakawa Y, Fujii T:
Pure topographical disorientation related to
dysfunction of the viewpoint dependent visual system. Cortex 1998;34:589–599.
16 Katayama K, Takahashi N, Ogawara K, Hattori T: Pure topographical disorientation due
to right posterior cingulated lesion. Cortex
1999;35:279–282.
17 Alsaadi T, Binder JR, Lazar RM, Doorani T,
Mohr JP: Pure topographical disorientation:
a distinctive syndrome with varied lesion location. Neurology 2000;54:1864–1866.

Hashimoto /Tanaka /Nakano

18 Valenstein E, Bowers D, Verfaellie M, Heilman KM, Day A, Watson RT: Retrosplenial
amnesia. Brain 1987;110:1631–1646.
19 Takayama Y, Kamo H, Ohkawa Y, Akiguchi
I, Kimura J: A case of retrosplenial amnesia
(in Japanese). Rinsho Shinkeigaku 1991; 31:
331–333.
20 Katai S, Maruyama T, Hashimoto T, Yanagisawa N: A case of cerebral infarction presenting as retrosplenial amnesia (in Japanese).
Rinsho Shinkeigaku 1992;32:1281–1287.
21 Gainotti G, Aimonti S, Di Betta AM, Silveri
MC: Retrograde amnesia in a patient with
retrosplenial tumour. Neurocase 1998; 4:
519–526.
22 Maguire EA: The retrosplenial contribution
to human navigation: a review of lesion and
neuroimaging findings. Scand J Psychol
2001;42:225–238.

Heading Disorientation

23 Sutherland RJ, Whishaw IQ, Kolb B: Contributions of the cingulate cortex to two forms
of spatial learning and memory. J Neurosci
1988;8:1863–1872.
24 Cooper BG, Mizumori SJY: Retrosplenial
cortex inactivation selectively impairs navigation in darkness. Neuroreport 1999; 10:
625–630.
25 Aguirre GK, D’Esposito M: Environmental
knowledge is subserved by separable dorsal/
ventral neural areas. J Neurosci 1997; 17:
2512–2517.
26 Ghaem O, Mellet E, Crivello F, Tzourio N,
Mazoyer B, Bethoz A, Denis M: Mental navigation along memorized routes activates the
hippocampus, precuneus, and insula. Neuroreport 1997; 8:739–744.
27 Maguire EA, Burgress N, Donnet JG, Frakowiak RSJ, Frith CD, O’Keefe J: Knowing
where, and getting there: a human navigation network. Science 1998;280:921–924.
28 Taube JS: Head direction cells and the neurophysiological basis of a sense of direction.
Prog Neurobiol 1998; 55:225–256.

29 Chen LL, Lin LH, Green EJ, Barnes CA, MacNaughton BL: Head-direction cells in the rat
posterior cortex. I. Anatomical distribution
and behavioral modulation. Exp Brain Res
1994;101:8–23.
30 Kobayashi Y, Amaral D: Macaque monkey
retrosplenial cortex. I. Three-dimensional
and cytoarchitectonic organization. J Comp
Neurol 2000;426:339–365.
31 Suzuki WA, Amaral D: Perirhinal and parahippocampal cortices of the macaque monkey: cortical afferents. J Comp Neurol 1994;
350:497–533.
32 Morris R, Pandya D, Petrides M: Fiber system linking the mid-dorsolateral frontal
cortex with the retrosplenial/presubicular
region in the rhesus monkey. J Comp Neurol
1999;407:183–192.

Eur Neurol 2010;63:87–93

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