ALLOCENTRIC AND EGOCENTRIC SPATIAL IMPAIRMENTS IN A CASE
OF TOPOGRAPHICAL DISORIENTATION
Thomas Nyffeler, Klemens Gutbrod, Tobias Pflugshaupt, Roman von Wartburg, Christian W. Hess
and René M. Müri
(Perception and Eye Movement Laboratory, Department of Neurology, University Hospital,
University of Berne, Switzerland)

ABSTRACT
We describe a patient with a topographical disorientation after a stroke of the right mediotemporooccipital lobe including
the parahippocampal cortex (PHC). Clinical observations and neuropsychological testing reveal an impairment of allocentric
spatial representations as well as impairments of visuospatial learning and memory. These findings are in accordance with
the well-known function of the PHC in topographical disorientation. As a new finding, results from oculomotor tasks show
additional impairments of the egocentric spatial coordinate frame suggesting that in topographical disorientation due to a
lesion of the right mediotemporooccipital lobe not only allocentric but also egocentric visuospatial functions are disturbed.
Key words: oculomotor, egocentric, allocentric, topographical disorientation, parahippocampal cortex

INTRODUCTION
The ability to follow routes in previously
unfamiliar environments is a complex behaviour. It
depends on many cognitive abilities like attention,
visual perception, and executive functions. Most of
all, however, it depends on the encoding of spatial
information that characterizes the route, i.e. route
knowledge. Processing of topographical information
may be conducted within an egocentric or allocentric
coordinate frame (Aguirre and D’Esposito, 1999;
Barrash et al., 2000). In the former, the location of
an object is processed with reference to the retina,
head, and to the body, in the latter the spatial
relationship between objects of the environment is
processed. It is generally accepted, that egocentric
spatial representations may be formed in the right
posterior parietal cortex (PPC) (Levine et al., 1985;
Bisiach et al., 1993), whereas allocentric spatial
processing depends on the integrity of the right
parahippocampal cortex (PHC) (Epstein and
Kanwisher, 1998; Epstein et al.,1999; Aguirre and
D’Esposito, 1999; Barrash et al., 2000). Humans
with lesions of either the PPC or the PHC may lose
their ability to find their way within environments, a
rare disorder called topographical disorientation
(Levine et al., 1985; Bisiach et al., 1993; Bohbot et
al., 1998; Luzzi et al., 2000; for a review see Aguirre
and D’Esposito,1999).
Patients with lesions of the PPC show deficits in
way finding within previously familiar and novel
environments, and are impaired in tasks needing an
egocentric coordinate system. Hence, topographical
disorientation is seen as a consequence of a spatial
deficit based on egocentric coordinates (Aguirre and
D’Esposito, 1999; Bisiach et al., 1993; Levine et
al., 1985). In contrast, patients with a lesion of the
Cortex, (2005) 41, 133-143

PHC show a topographical impairment that is
confined mainly to novel environments as well as
deficits in visuospatial tasks and spatial memory
needing allocentric coordinates. Neuroimaging
studies emphasize the critical role of the PHC in
allocentric encoding of environments (Maguire et
al., 1996; Aguirre and D’Esposito, 1999). In this
context topographical disorientation is attributed to
a selectively impaired acquisition and storage of
novel topographical knowledge.
However, there is evidence that the PHC not only
subserves
allocentric
visual
processing.
Neurophysiological studies in awake behaving
monkeys describe, amongst other cell types, head
direction and egocentric cells in the PHC (Rolls et
al., 1997). Furthermore, in humans it has been shown
in an oculomotor study that the PHC is involved in
egocentric spatial memorization (Ploner et al., 2000).
In the memory-guided saccade task, subjects have to
memorize the spatial location of a target, and after a
delay, a saccade towards the memorised location has
to be performed. Compared to controls, patients with
a lesion of the PHC showed a significant delaydependent inaccuracy of contralateral memoryguided eye movements.
The aim of the present study was to analyse if in
topographical disorientation due to a lesion of the
PHC not only impairments of the allocentric but also
egocentric coordinate frame could be demonstrated.
We tested a patient with topographical disorientation
due to an ischemic lesion of the right
mediotemporooccipital lobe with impaired
allocentric spatial representations by means of a
comprehensive neuropsychological test battery and
four different oculomotor paradigms. The advantage
of studying eye movements is that the egocentric (i.e.
retinotopic and craniotopic) coordinate frame may

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be examined in a detailed way. The same oculomotor
paradigms were chosen that are generally used to
examine the egocentric reference frame controlled
by the PPC (Pierrot-Deseilligny et al., 1991; Heide
et al., 1995). First, the retinotopic coordinate frame,
where a saccade is planned and executed on the basis
of retinal information was analysed with the
aforementioned paradigm of memory-guided
saccades and the gap and overlap task.
In the gap task, the lateral visual target appears
200 ms after the central fixation point is switched
off, whereas in the overlap task the central fixation
point remains switched on during lateral target
presentation. In patients with lesions of the
egocentric coordinate frame due to a lesion of the
PPC the amplitude of such reflexive visually-guided
saccades is decreased. Furthermore, the latency i.e.
the triggering of these saccades is delayed (PierrotDeseilligny et al., 1991). Second, the craniotopic
coordinate frame, where saccadic programming is
based on craniotopic information, was analysed with
the double-step task. In the double-step task, subjects
have to make two successive saccades in response to
two successively flashed targets located in both
hemifields. Since the targets are very rapidly flashed
within the latency of the first saccade, the amplitude
of the second saccade cannot be calculated in
retinotopic coordinates. In patients with lesions of
the craniotopic coordinate frame due to a lesion of
the PPC the second saccade is inaccurate when the
first saccade is directed into the lesional hemifield
(Heide et al., 1995).
CASE REPORT
M.E., a 67 year-old right-handed man was
on holiday when suddenly he developed acute

a

visual blurring, gait disturbances, and difficulty
in orienting himself in the holiday apartment
adjoining his wife’s bedroom with his own. The next
day he was referred to the neurological department
for evaluation. The neurological examination
revealed a left incomplete homonymous hemianopia
and a slight left-sided hemiparesis. MRI showed
a right posterior cerebral artery stroke with
destruction of the parahippocampal gyrus, fusiform
gyrus, lingual gyrus, and mediotemporooccipital
gyrus.
CLINICAL OBSERVATIONS
As long as M.E. was an inpatient, he remained
incapable of orienting himself. In the room
he shared with five other patients, he had
great difficulty finding his own bed, his wardrobe,
and the toilets. He tried to manage these problems
by relying on landmarks, names, and numbers.
For example, he reported that he only could
recognize his bed by reading his name on it (name
and date of birth of the patients are noted on the
bed frame) and by his own alarm clock on the
bedside table. When asked to draw a map of the
hospital room from memory he completely failed
(Figure 1).
When walking in the ward alone he tried to cope
by verbalizing the way: “When I go downstairs, I
know that I have to turn right when I see the painting
of the boy eating an apple…I always count the doors,
the third is the one of the resident..”.. However,
according to his wife he had no special problems
orientating himself in well-known environments
such as his apartment, where he had been living for
30 years. Moreover, he could draw a correct map of
this apartment (Figure 2).

b

Fig. 1 – Drawings of the hospital room. a) The patient was asked to draw a map of the hospital room from memory. Although all
elements (bed, table) are drawn, he completely failed to arrange them in an accurate manner. Furthermore, when asked to draw also the
alignment of the walls and the balcony he was not able to. b) The same task is perfectly performed by a patient at the same age with a
polyneuropathy who slept in the same room. (Translation: Tisch = table, Bett = bed, Balkon = balcony, Eingang = entrance, Terrasse =
terrace, Waschen = lavatory, WC = toilet).

Topographical disorientation

a

135

b

c
Fig. 2 – Drawings of the patient’s apartment. a) The patient was asked to draw a map of his apartment from memory where he had
been living for 30 years. The floor plan is correctly drawn when comparing it with the drawing of his wife b) and illustrates the
preserved topographical orientation in familiar buildings. Translations and a simplified plan of the apartment is shown in c).

One year after the ischemic stroke, the patient
still had major problems orientating himself in novel
environments. When he came to our hospital, he told
us that he would have practically no problems when
leaving his apartment and walking through the
streets to the bus station which was about 500 metres
away. However it was much more difficult for him
to find his way from the bus station to the hospital.
Also, when walking home after a meal out with
friends from a restaurant he had never visited before,
he got lost and had to ask the way.
NEUROPSYCHOLOGICAL ASSESSMENT
Scores with percentiles of neuropsychological
tests are presented in Table I.

The main finding was a profound deficit in
non-verbal, visuospatial learning, and memory.
Although his immediate visual memory span was
normal (low average) he showed severe deficits in
non-verbal and visuospatial learning and recall of
non-verbal designs (Rey Visual Design Learning)
as well as a visuospatial trail (Ruff-Light Trail
Learning Test). Normal values for performance
were found in intelligence, orientation, language,
arithmetic skills, praxis, executive functions, verbal
learning and memory, and attention. There were no
signs of agnosia or neglect. Basic as well as higher
processes of visuoperceptual, visuospatial, and
visuoconstructive abilities were average to above
average. Due to the left incomplete hemianopia
speed of visual information processing was mildly
impaired.

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TABLE I

Scores of neurophsychological tests
Task / Reference

Score

Percentile

Intelligence
• Vocabulary Intelligence Test (Lehrl et al., 1991); IQ

94

36

Orientation
• Orientation questionnaire (von Cramon and Säring, 1982)
Person (max. 5)
Place (max. 5
Situation (max. 5)
Time (max. 5)

4
4
5
5

✔*
✔
✔
✔

Language
• Token Test of the Aachen Aphasia Test (Huber et al., 1983); Errors (max. 50)
• Naming of the Aachen Aphasia Test (Huber et al., 1983); (max. 120)

3
113

95
97

Arithmetic Skills
• Simple Calculations (Errors; max. 25)
• Arithmetic of the Wechsler Adult Intelligence Scale-R (Tewes, 1991)

2
11

✔

Praxis
• Ideomotor (Errors; max. 5)
• Limb Kinetic (Errors; max. 3)
• Buccofacial (Errors; max. 3)

0
0
0

✔
✔
✔

28
32

76
76

25
0

24
100

5
13

30
46

6

24

48
9
10

50
24
18

20
25

18
82

6

14

21
3
10
6

3
<1
<1
2

71
82
9
7

<1
<1
<1
<1

Executive Functions
• Word Fluency (Aschenbrenner et al., 2000); Correct
• Design Fluency (Haid et al., 2004); Correct
• Stroop Test (Spreen and Strauss, 1991)
Part C: Seconds
Errors
• Wisconsin Card Sorting Test (Heaton, 1981)
Categories achieved
Perseverative errors
Verbal Learning and Memory
• Digit Span Forward (Härting et al., 2000)
• Auditory-Verbal Learning Test (Helmstaedter et al., 2001)
Learning total
Delayed recall
Recognition
• Logical Memory of the Wechsler Memory Scale-R (Härting et al., 2000)
Immediate recall
Delayed recall
Non-verbal Learning and Memory
• Visual Memory Span Forward (Härting et al., 2000)
• Rey Visual Design Learning Test (Rey, 1964)
Learning total
Delayed recall
Recognition
• Rey-Osterrieth Complex Figure Test: Delayed Recall (Meyers and Meyers, 1995)
• Ruff-Light Trail Learning Test (Ruff and Allen, 1999)
Total correct (Trials 2-10)
Total step errors (Trials 2-10)
Delayed correct
Delayed errors

25

Visuoperceptual, Visuospatial, and Visuocunstructive Abilities; Agnosia
• Brimingham Object Recognition Battery (Riddoch and Humphreys, 1993)
Length match task (version B)
Size match task (version B)
Orientation match task (version B)
Position of gap match task (version B)
Overlapping figures (letters, shapes, drawings); in seconds ; (all within normal limits of healthy
controls)
Minimal feature view task
Foreshortened view task
Object decision (version A; hard)
Item match task
• Rey-Osterrieth Complex Figure Test: Copy (Meyers and Meyers, 1995)
• Block Design of the Wechsler Adult Intelligence Scale-R (Tewes, 1991)

26/30
29/30
23/30
39/40

31
74
26
83

24/25
22/25
30/32
32/32
32
20

61
55
96
85
> 16
38

Neglect
• Star cancellation (Wilson et al., 1987)

54/54

✔

Attention
• Concentration Endurance d2 Test, (Brickenkamp, 1981; Spreen and Strauss, 1991)
Total
Error Percentage
• Trail Making Test A (extended Version; Oswald and Roth, 1978); sec.

378
11
110

54
30
10

* = no deficit

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137

Fig. 3 – MRI scan showing axial cuts of the patient one year after the ischemic stroke. Areas of high signal are noticeable in the
distribution of the right posterior cerebral artery involving the parahippocampal gyrus, fusiform gyrus, lingual gyrus and medial
occipitotemporal gyrus.

OCULOMOTOR ASSESSMENT
The extent of the brain lesion at the time of
examination is shown in Figure 3.
Ophthalmological assessment revealed a left
incomplete homonymous hemianopia sparing 20°
of central vision (Figure 4).
Four oculomotor paradigms were tested (Figure
5): 1) the gap task, 2) the overlap task, 3)
the double-step task, and 4) the paradigm of
memory-guided saccades with two different delays
(figure 5).
During the experiment the patient was seated in
total darkness 114 cm from a light emitting diodes
(LED) target screen. Visual targets were bright
LED. The head was fixed to avoid head
movements. Eye movements were measured with
an infrared corneal reflection device (Iris Skalar)
(gap task, overlap task, double step task) with a
spatial resolution of 0.1° and sample rate of 1000
Hz. Memory-guided saccades were acquired by
means of dc-electro-oculography (bitemporal
electrodes, sampling frequency 1000 Hz,
bandwidth 0 – 100 Hz). Before each data
acquisition, the eye movement recording device
was calibrated. The signals were stored on the

computer for off-line analysis. The trials were
presented in blocks of three or five, and the patient
was always informed beforehand which condition
will be tested. Pauses were made between the
blocks.
The patient was examined in five sessions each
lasting about 45 min. Due to the incomplete
hemianopia, all visual targets were presented
within 16 degrees eccentricity.
GAP AND OVERLAP TASK
In the gap task, the patient started to look at a
central fixation point. After a random duration of
between 1,5 and 2,5 sec the central fixation point
was switched off and after another 200 msec, a
horizontal, lateral target with a distance of 12°
occurred (with unpredictable direction). The patient
had then to perform a saccade to the lateral target.
For each direction 40 trials were acquired. Median
saccadic gain (saccade amplitude/target amplitude)
and latency for each direction were calculated. The
overlap task differed from the gap task by the fact
that the central fixation point was switched
continuously on.

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Fig. 4 – Goldmann perimetry is shown revealing a left incomplete homonymous hemianopia sparing central vision with 20°.

DOUBLE-STEP TASK
In the double-step task, the patient was
instructed to make two successive saccades in
response to two successively, flashed lateral
targets. After the central fixation point was
switched off a first lateral peripheral target
appeared during 140 msec to the left or right of
the center (ranging from 8 to 16 degrees),
immediately followed by a second target presented
for 100 msec in the opposite hemifield (ranging
from 8 to 16 degrees). Thus, both targets

disappeared prior to the onset of the first saccade.
The patient was always informed beforehand
whether the first target would appear in either the
left or the right hemifield. For each direction 40
trials were acquired. Data analysis was performed
as described in a previous paper (Van Donkelaar
and Müri, 2002). Using this paradigm it is
possible to separate retinotopic and craniotopic
coding of the saccade. Whereas the first saccade is
done on the basis of retinal information, the
second saccade relies on a craniotopic coordinate
frame: as the retinal coordinates of the second

Topographical disorientation

139

a

c

b

d

Fig. 5 – Oculomotor paradigms. a) gap task, in which the lateral target appears after the central fixation point is switched off 200
ms before; b) overlap task, in which the central fixation point remains switched on while the lateral target occurs; c) double-step task,
in which the subject has to make two successive saccades in response to two successively flashed lateral targets; d) memory-guided
saccade paradigm, in which a peripheral flashed target has to be memorized. After the go signal a memory-guided saccade has to be
performed to the remembered position of the peripheral flashed target.
F = Fixation point (central), T = target (lateral).

target have changed after the first saccade, the
brain must use a signal of eye displacement to
update the retinal representation (Guthrie et al.,
1983; Goldberg and Bruce, 1990; Duhamel et al.,
1992; Hallett and Lightstone, 1976). Furthermore,
the second saccade can compensate the error of
the first saccade. However, if there is a failure of
craniotopic coding no compensation occurs. To
study these properties, linear regression was
performed to analyse the relationship between the
first saccade gain and the second saccade gain
(Van Donkelaar and Müri, 2002).
PARADIGM OF MEMORY-GUIDED SACCADES
The patient was instructed to memorise the
location of a horizontally flashed lateral target
(with a non-predictive amplitude ranging from 8 to
16 degrees) while fixating a central point. The
target was always flashed for 80 msec. After the
memorisation delay (3 or 30 sec) the central
fixation point was switched off, which was the gosignal for the patient to perform a saccade towards
the memorised target. After another 2 sec, the
target was shown again and the subject had to
make a corrective saccade if necessary. For each
delay condition and each direction 20 trials were
performed, and the patient was always informed
beforehand which condition would be tested.
Percentage of error in amplitude (PEA) for each
condition and direction was calculated. PEA was
calculated according to the formula:

saccade amplitude – target amplitude
× 100
target amplitude
The statistical analysis was based on MannWhitney U Test, comparing leftward versus
rightward saccades.
RESULTS

Gap task
There was no statistically significant difference
in the latencies between leftward and rightward
saccades (median latency for leftward saccades:
161 msec, interquartile range (IQR) 70; median
latency for rightward saccades: 147 msec, IQR 30).
The gain of leftward saccades was significantly
decreased (hypometric saccades) compared to
rightward saccades (median gain for rightward
saccades 0.9, IQR 17; median gain for leftward
saccades 0.83; IQR 0.24; p = 0.004).
Overlap task
The median latency was symmetric for both
leftward and rightward saccades (median latency
for leftward saccades: 317 msec, IQR 149; median
latency for rightward saccades: 329 msec, IQR
130). The gain for leftward saccades was
significantly decreased (hypometric saccades)
compared to rightward saccades (median gain for
rightward saccades 0.93, IQR 11; median gain for
leftward saccades 0.8, IQR 0.16 (p = 0.001).

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Thomas Nyffeler and Others

a

b

Fig.6 – The correlation between the first saccade gain and the second saccade gain in the double-step task.

Double-step task
The results from the analysis of the relationship
between the first saccade gain and the second
saccade gain are shown in Figure 6.
When the first saccade is made to the left the
error of the first saccade can be compensated by
the second saccade (Figure 6a) (Regression
analysis: Beta 0.544; p < 0.001) i.e. a craniotopic
coordinate frame was used to calculate the second
saccade. However, when the first saccade is made
to the right the error of the first saccade was not
compensated suggesting a failure of the craniotopic
updating process for the calculation of the second
saccade (figure 6b) (Regression analysis: Beta
0.242; p > 0.1).
The gain of the second leftward saccades in the
double-step paradigm furthermore shows a
significant correlation with the gain of leftward
saccades in the gap (Pearson correlation coefficient
0. 717; p < 0.001) and overlap paradigm (Pearson
correlation coefficient 0. 845; p < 0.001).
Paradigm of memory-guided saccades
The median latencies were symmetric in both
short and long delay paradigms (Short delay
paradigm: median latency for leftward saccades
248 msec, IQR 85; median latency for rightward
saccades 265 msec, IQR 110. Long delay
paradigm: median latency for leftward saccades
354 msec, IQR 105; median latency for rightward
saccades 354 msec, ICR 108).
For the short delay paradigm there was no
difference between leftward and rightward saccades
in the PEA (PEA for leftward saccades 3, IQR

0.16; PEA for rightward saccades 5, IQR 0.13). In
the long delay paradigm, the PEA was significantly
increased for leftward saccades (PEA 38, IQR
0.24) relative to rightward saccades (PEA 19 ; IQR
0.27, p < 0.05). This is shown in Figure 7.
DISCUSSION
We describe a patient who showed a severe and
long lasting deficit in orientating himself in novel
environments after an ischemic stroke of the right
mediotemporooccipital lobe including the PHC.
Clinical observations and neuropsychological
testing revealed an impairment of allocentric spatial
representations mainly confined to novel
environments and a profound deficit in non-verbal,
visuospatial learning and memory. These findings
are in accordance with results from previous case
reports and emphasize the importance of an
impaired allocentric coordinate frame in the
pathogenesis of topographical disorientation which
may arise after a lesion of the PHC (Maguire et al.,
1996; Luzzi et al., 2000; Aguirre and D’Esposito,
1999). The salient finding of this case report is that
results from oculomotor testing provide evidence
for an additional impairment of the egocentric
coordinate frame, independently of the control of
the PPC.
First, in the gap and overlap task reflexive
visually guided saccades were hypometric when
directed into the lesional hemifield. It is known
from previous studies that patients with complete,
dense hemianopia due to an occipital lesion may
undershoot visual targets presented in the lesional
hemifield (Meienberg et al., 1981). As hypometric

Topographical disorientation

141

Fig 7 – The PEA of memory-guided saccades with 3 and 30 sec delay.

saccades were nearly always followed by further
small saccades producing a staircase pattern, it was
suggested that patients might use a compensatory
strategy to find and fixate objects in the blind
hemifield. Our results rather suggest an impairment
of the egocentric coordinate frame than an
employment of a compensatory strategy since in
our patient left hemianopia was incomplete sparing
central vision with 20 degrees, and all visual
targets (bright LED’s) were presented within 16
degrees. Theoretically, it may be assumed that a
large lesion of the mediotemporooccipital lobe may
result in retrograde effects on the posterior parietal
cortex and therefore affecting the egocentric
coordinate frame, as intense anatomical
connections between those areas have been
described (Seltzer and Pandya, 1984; Ding et al.,
2000). However, in patients with posterior parietal
lesions the latency of contralateral reflexive
visually guided saccades are typically prolonged
(Pierrot-Deseilligny et al., 1991), whereas in our
patient the latencies were symmetrical and within
normal range. Further evidence for an impairment
of the egocentric coordinate frame comes from the
double-step task. In this paradigm, where the
subject has to make two successive saccades in
response to two successively flashed lateral targets,
the egocentric spatial representations may be tested
accurately (Van Donkelaar and Müri, 2002). In our
patient craniotopic updating of the second saccade
(i.e. an egocentric spatial representation) was

impaired when the first saccade had been directed
into the right, nonlesional hemifield. To our
knowledge this has not been described before. The
results clearly differ from those which are found in
patients with an impaired egocentric coordinate
frame due to right posterior parietal lesions (Heide
et al., 1995). In the latter, a failure of craniotopic
updating of the second saccade occurs when the
first saccade is directed into the lesional hemifield.
More evidence for an impaired egocentric
coordinate frame, independent of the control of the
PPC, comes from the memory-guided saccade task.
In the short delay paradigm the accuracy of
memory-guided eye movements was symmetrical.
In patients with a lesion of the PPC the accuracy
of contralateral memory-guided saccades would be
decreased (Pierrot-Deseilligny et al., 2002). In the
long delay paradigm however, the accuracy of
memory-guided eye movements contralateral to the
lesion side was significantly impaired. This result
is in line with previous studies and suggests that
the mediotemporal lobe contributes to egocentric
spatial memory at delays longer than 20 seconds
(Ploner et al., 1998, 1999, 2000).
In summary the results of our oculomotor study
suggest that a lesion of the mediotemporooccipital
lobe itself may affect specifically the egocentric
coordinate frame. This assumption is corroborated
by the significant correlation between the gain of
leftward saccades in the gap and overlap paradigm
and the gain of the second leftward saccade in the

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Thomas Nyffeler and Others

double step paradigm. The part of the egocentric
coordinate frame, which is controlled by the PPC,
however, seems to be intact.
Our
findings
are
supported
by
electrophysiological studies in monkeys. Neurons
in the mediotemporal cortex have been described
which display an activity related to the egocentric
spatial position of stimuli, some responding during
sample presentation and some in the delay period
(Cahusac et al., 1989; Rolls et al., 1989;
Feigenbaum and Rolls, 1991). Furthermore, some
neurons have been described in the hippocampal
and inferotemporal cortex, which respond due to
eye position (Nowicka and Ringo, 2000).
The extent to which the egocentric impairments
of our patient may contribute to topographical
disorientation remains speculative. The reduced
amplitude of left-sided reflexive visually guided
saccades and the impaired updating of left visual
space across saccades in the double-step task seems
not to be of much relevance, as both in the clinical
and neuropsychological assessment a general
visuospatial deficit was absent. However,
theoretically it may be conceivable that an
encoding deficit of left-sided objects, as it was
found in the memory-guided saccade paradigm
with long delays, may contribute to impaired route
knowledge in our patient. Finally, one might also
speculate that impaired functions of egocentric
orientation in the mediotemporal lobe may
contribute to topographical disorientation by
preventing the building up of allocentric spatial
representations.
In
conclusion,
additionally
to
the
neuropsychological tests our oculomotor studies
give new insight into the mechanism of
topographical disorientation due to a lesion of the
right mediotemporooccipital lobe suggesting that
not only the allocentric but also egocentric
coordinate frame is disturbed.
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e-mail: thomas.nyffeler@insel.ch

(Received 28 April 2003; reviewed 27 June 2003; revised 31 July 2003; accepted 15 August 2003; Action Editor Jason
Mattingley)