Letter to the Editor
Received: November 15, 2006
Accepted: March 17, 2007
Published online: October 11, 2008

Eur Neurol 2008;59:79–82
DOI: 10.1159/000109572

Topographic Disorientation and
Amnesia due to Cerebral Hemorrhage
in the Left Retrosplenial Region
Aiko Osawa a Shinichiro Maeshima b Katsuzo Kunishio a
a

Department of Rehabilitation Medicine, Kawasaki Medical School Kawasaki Hospital, Okayama, b Department of
Rehabilitation Medicine, Saitama International Medical Center, Saitama Medical University, Saitama, Japan

Dear Sir,
Since the report by Valenstein et al. [1],
it has been known that a lesion in the dominant retrosplenial region produces amnesia. On the other hand, a lesion in the same
location in the nondominant hemisphere
produces topographical disorientation [2].
Specifically, connections between the in-

ferior parietal lobe and the limbic system
are impaired, leading to heading disorientation – a disorder in which patients are
unable to remember the direction in which
to go, although they are still able to recognize familiar buildings and homes [3]. In
this study, we report a case of a patient

who, due to intracerebral hemorrhage in
the left retrosplenial region, was unable to
learn new buildings and routes (anterograde disorientation), in addition to having heading disorientation in familiar surroundings.

Cold store
Parking
HOME

McDonald‘s

Store
Bus terminal

River

Library

River

Library

HOME

To McDonald‘s

High school

Footpath
Supermarket
Skating rink

a

b

Fig. 1. A map of the neighborhood of the patient. a The patient’s drawing. b His son’s drawing. Although the
patient could recall some names of surrounding buildings, it was impossible for him to note their positions.

© 2007 S. Karger AG, Basel
0014–3022/08/0592–0079$24.50/0
Fax +41 61 306 12 34
E-Mail karger@karger.ch
www.karger.com

Accessible online at:
www.karger.com/ene

Dr. Aiko Osawa
Department of Rehabilitation Medicine
Kawasaki Medical School Kawasaki Hospital
2-1-80 Nakasange, Okayama 700-8505 (Japan)
Tel./Fax +86 225 2111, E-Mail maeshima@saitama-med.ac.jp

Table 1. Neuropsychological assessments

Period of assessments

2006.4
(2 weeks)

Wechsler Adult Intelligence Scale-revised
Verbal IQ
88
Performance IQ
76
Full scale IQ
82
Mini-Mental State Examination (/30)
12
Raven’s Colored Progressive
Matrices (/36)
6
Wechsler Memory Scale-revised
Verbal memory
59
Visual memory
<50
Common sense memory
<50
Attention/concentration
<50
Delayed recall
<50
Rivermead Behavioral Memory Test
Total profile (/24)
2
Screening (/12)
1
Auditory Verbal Learning Test (/15)
Immediate recall
2-4-3-4-3
Recognition
3
Delayed recall
0
Frontal Assessment Battery
8
Behavioral assessment of the executive dysfunction system
Total profile
20: average
Word Fluency Test (/min)
Category (animal + fruit + vehicle)
5-3-2
Letter (‘shi’ + ‘i’ + ‘re’)
4-0-2
Digit Span
Forward
5
Backward
3

Case Report
A 56-year-old, right-handed man was
admitted to our hospital on March 30,
2006, with sudden onset of headache and
a narrowing visual field. His son noticed
that he had begun to lose his way even in
familiar surroundings, and became forgetful of recent events several days before.
On admission, he was alert and cooperative. He showed right hemianopsia but no
sensorimotor loss. Neuropsychological
examination showed recent memory loss
and topographical disorientation. He was
aware of his memory disturbance, but expressed no serious concern. His autobiographical memory for the events that had
occurred up to the cerebral attack was excellent. For example, he could remember
the previous day’s news. Thus, he did not
exhibit retrograde amnesia. Retrograde
episodic memory concerning both personal and public remote events was nearly

80

intact, although the patient had an anterograde amnesia; he did not show confabulation. He scored 12/30 in the Mini-Mental
State Examination, with declining performance in orientation, attention and calculation, and reproduction. On the Auditory
Verbal Learning Test, immediate recall (2,
4, 3, 5, 3/15), delayed recall (0/15), and recognition (8/15) were all decreased. On the
Wechsler Memory Scale, revised, verbal
memory quotient was 59, while the other
quotient was under 50. The results of these
tests showed that he had severe anterograde amnesia. The Wechsler Adult Intelligence Scale-Revised scores were: verbal
intelligence quotient (IQ) = 88, performance IQ = 76, and full scale IQ = 82 (table 1). He did not show aphasia, unilateral
spatial neglect, constructional apraxia, or
agraphia, tactile objective anomia, ideomotor or ideational apraxia in the bilateral
hand. He was able to recognize familiar

Eur Neurol 2008;59:79–82

2006.5
(6 weeks)
99
96
98
24
23
67
79
66
73
<50
8
3
4-6-7-5-5
7
0
14

11-7-8
4-4-2
5
4

buildings with accuracy, and was also able
to identify them on a map. However, the
patient could not describe the route from
the nearest bus stop to his home very well,
nor could he draw a map (fig. 1). He was
able to recall the room layout in his house,
but made mistakes in recalling the physical relationship between the rooms, the
corridors, and the entrance. When he actually tried to walk, the patient was able to
recognize landmarks, but often got lost
and did not know which way to go. The
patient could not learn the previously unknown hospital ward or the layout of the
hospital, and often got lost finding the toilet located several meters from his room.
Neuroradiological Examination
A cranial CT performed on the day of
onset showed a hematoma in the retrosplenial region, diagnosed as subcortical hemorrhage. Magnetic resonance imaging 3

Osawa/Maeshima/Kunishio

Fig. 2. a Magnetic resonance imaging 3 days after onset showed hyperintense areas

between the left forceps occipitalis and the parietal lobe, involving the left cingulate isthmus. b SPECT 10 days after onset revealed a decrease in blood flow in the
left retrosplenial region.

days after onset showed hyperintense areas between the left forceps occipitalis and
the parietal lobe, involving the left cingulate isthmus (fig. 2a). Single photon-emission computed tomography (SPECT) 10
days after onset revealed a decrease in
blood flow in the left retrosplenial region
(fig. 2b).

Topographic Disorientation and
Retrosplenial Amnesia

Discussion
This case demonstrates lesions confined to the left retrosplenial region, with
amnestic syndrome and topographical
disorientation. There have been several articles on retrosplenial amnesia since the
first by Valenstein et al. [1], and this condition is regarded as due to damage to a part

of the Papez circuit. A lesion in the left
hemisphere is common, but a right hemisphere lesion has also been reported, although it is rare [4]. Regarding dysmnesia,
lesions in the left hemisphere impair verbal memory, and those in the right hemisphere impair visual memory. In this case,
however, although the lesions were in the

Eur Neurol 2008;59:79–82

81

left hemisphere, both memories were impaired. Laterality of memory is not as distinct as that of language or visuospatial
cognition, and is not limited to retrosplenial amnesia. In fact, there have been some
cases in which both verbal and visual
memories were impaired by lesions in the
right hemisphere. Experiments in monkeys have also shown that anterograde disorientation can be caused by lesions on either side [5]. Thus, in our case, it seems
that memory function was not fully lateralized congenitally, and the lesions in the
right hemisphere caused damage to both
verbal memory and visual memory, including topographical memory.
Topographical disorientation was divided into four categories of the syndrome:
landmark agnosia, egocentric disorientation, heading disorientation and anterograde disorientation [6]. Landmark agnosia is characterized by an inability to use
salient environmental features for orientation [7]. This is caused by damage to the
right ventral occipitotemporal cortex (fusiform, lingual, and parahippocampal
gyri) [8]. Egocentric disorientation describes people who are unable to represent
the location of objects with respect to self,
even though they are able to identify prominent environmental objects [9]. Lesions of
the right posterior parietal cortex are generally responsible for this deficit [10].
Heading disorientation leads to an inability to remember the direction in which to
go with respect to the external environment [2, 3]. These patients have lesions in
the retrosplenial cortex (posterior cingulate). Patients with anterograde disorientation who have preserved way-finding in
environments that were known prior to
the onset of their impairment but who are
unable to create new representations of
surrounding information are classified in
this category. In these patients, the impairment is caused by a right parahippocampal
lesion [8, 11, 12].

82

Regarding sequential memory, our patient was able to recall prehospital events
very well, showing no retrograde amnesia,
but could not learn the name of his disease,
his room number, and the name of his own
primary physician, showing mainly anterograde amnesia. These symptoms seem
to be consistent with those of retrosplenial
amnesia.
As shown by the above-indicated symptoms, the patient seems to have had both
heading disorientation and anterograde
disorientation. Regarding the location of
the lesions, it has been reported that heading disorientation is associated with the
cortex of the retrosplenial region (the posterior cingulate cortex) [3], and anterograde disorientation is associated with the
parahippocampal gyrus. Either topographical disorientation is usually caused
by lesions in the right hemisphere, while
that caused by a lesion in the left hemisphere has rarely been reported [13, 14]. In
a case reported by Obi et al. [13], lesions
were in the left hemisphere, and the presence of transient right neglect was observed, suggesting that lateralization of
visuospatial cognition may have been
involved. In our case, the patient was righthanded, so lateralization is unlikely to
have been affected. SPECT only revealed a
decrease in blood flow in the left retrosplenial region, which coincided with the location of the lesions; findings suggestive of
decreased function on the other side were
not observed. Previous studies, in which
the involvement of the parahippocampal
gyrus in anterograde disorientation was
examined in animal experiments, have reported that laterality is not associated with
anterograde disorientation. Our report is
the first to examine cerebral blood flow in
relation to disorientation, and this case
seems to be very important in examining
the effects of damage to the posterior cingulate cortex and the parahippocampal
gyrus on topographical disorientation.

Eur Neurol 2008;59:79–82

References
1 Valenstein E, Bower D, Veraellie M, Heilman
KM, Day A, Watson RT: Retrosplenial amnesia. Brain 1987;110:1631–1646.
2 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;34:321–326.
3 Takahashi N, Kawamura M, Shiota J, Kasahata N, Hirayama K: Pure topographical disorientation due to right retrosplenial lesion.
Neurology 1997;49:464–469.
4 Masuo O, Maeshima S, Kubo K, Terada T,
Nakai K, Itakuta T, Komai N: A case of amnestic syndrome caused by a subcortical haematoma in the right occipital lobe. Brain Injury 1999;13:213–216.
5 Olton DS: Spatial memory. Sci Am 1977;236:
82–99.
6 Aguirre GK, D’Esposite M: Topographical
disorientation: a synthesis and taxonomy.
Brain 1999;122:1613–1628.
7 Hecaen H, Tzortzis C, Rondot P: Loss of topographical memory with learning deficits.
Cortex 1980;16:525–542.
8 Aguirre GK, Dettre JA, Alsop DC, D’Esposito
M: The parahippocampus subserves topographical learning in man. Cereb Cortex
1996;6:823–829.
9 Stark M, Coslett HB, Saffran EM: Impairment of an egocentric map of locations: implications for perception and action. Cogn
Neuropsychol 1996;13:481–523.
10 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.
11 Epstein R, DeYoe EA, Press DZ: Neuropsychological evidence for a topographical
learning mechanism in parahippocampal
cortex. Cogn Neuropsychol 2001; 18: 481–
508.
12 Habib M, Sirigu A: Pure topographical disorientation: a definition and anatomical basis. Cortex 1987;23:73–85.
13 Obi T, Bando M, Takeda K, Sakuta M: A case
of topographic disturbance following a left
medial parieto-occipital lobe infarction.
Clin Neurol (Tokyo) 1992;32:426–429.
14 Maeshima S, Ozaki F, Masuo O, Yamaga H,
Okita R, Moriwaki H: Memory impairment
and spatial disorientation following a left
retrosplenial lesion. J Clin Neurosci 2000; 8:
450–451.

Osawa/Maeshima/Kunishio