Retrosplenial Amnesia without Topographic Disorientation
Caused by a Lesion in the Nondominant Hemisphere
Shinichiro Maeshima, MD, PhD,* Aiko Osawa, MD, PhD,* Fumitaka Yamane, MD, PhD,†
Tomoyuki Yoshihara, MD, PhD,† Ryuzaburo Kanazawa, MD, PhD,†
and Shoichiro Ishihara, MD, PhD†

We report the case of a 68-year-old right-handed man who was admitted to our
hospital because of sudden onset of headache. On admission, he presented with
left homonymous hemianopsia, disorientation, and recent memory disturbance;
however, he had normal remote memory and digit span. He was able to recall the
room layout of his house and describe the route from the nearest station to his
home on a map. However, at the hospital, he sometimes lost his way because of
amnesia. Computed tomography (CT) and magnetic resonance imaging revealed
a subcortical hematoma in the right occipital forceps and the parietal lobe, involving
the cingulate isthmus. Single-photon emission CT imaging showed reduced perfusion not only in the retrosplenial region but also in the right thalamus. These findings suggested that the retrosplenial amnesia might have been caused by the
interruption of hippocampal input into the anterior thalamus. Key Words:
Memory impairment—amnesia—cerebral hemorrhage—thalamus—retrosplenial
region.
Ó 2014 by National Stroke Association

Introduction
Lesions of the limbic system, particularly the hippocampus or anterior thalamus, are well known to cause
memory impairment. Retrosplenial cortex also plays an
important role in the human memory by connecting the
hippocampus with other structures involved with memory, including the anterior thalami, septal nuclei, and
mammillary bodies.1 Amnesia, resulting from lesions involving the retrosplenial region, has been attributed to the
damage of this vital link. Valenstein et al1 reported a case
From the *Department of Rehabilitation Medicine, Saitama Medical
University International Medical Center, Hidaka, Saitama, Japan; and
†Department of Endovascular Neurosurgery, Saitama Medical University International Medical Center, Hidaka, Saitama, Japan.
Received January 3, 2013; revision received March 11, 2013;
accepted March 19, 2013.
Address correspondence to Shinichiro Maeshima, MD, PhD,
Department of Rehabilitation Medicine II, School of Medicine, Fujita
Health University, 424-1 Oodori-cho, Tsu, Mie 514-1295, Japan.
E-mail: maeshima@fujita-hu.ac.jp.
1052-3057/$ - see front matter
Ó 2014 by National Stroke Association
http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2013.03.026

of retrograde and anterograde amnesia after hemorrhage
because of an arteriovenous malformation situated close
to the retrosplenium of the corpus callosum. They termed
this amnesia ‘‘retrosplenial amnesia.’’ Lesions in the left
hemisphere are common; however, lesions in the right
hemisphere are rare.2,3 A lesion in the same location
in the right hemisphere as that in the left hemisphere
produces topographical disorientation.4,5 We report
a case of amnesia without topographical disorientation
because of intracerebral hemorrhage in the right
retrosplenial region.

Case Report
A 68-year-old man with an educational history of
9 years was admitted to our hospital. He was completely
right handed with a laterality quotient of 1100 when formally assessed by the Edinburgh Handedness Inventory,6
and all members of his immediate family are right
handed. He presented with a 3-day history of headache
and had developed untidy behavior and memory disturbance over a couple of days. He had no neurological deficits except left hemianopsia and amnesia.

Journal of Stroke and Cerebrovascular Diseases, Vol. 23, No. 3 (March), 2014: pp 441-445

441

S. MAESHIMA ET AL.

442

Table 1. Results of neuropsychological tests

Mini-mental state examination (/30)
Digit span (forward/backward)
Auditory verbal learning test (/15)
Immediate
Recognition
Delayed
Raven’s progressive matrices (/36)
Frontal Assessment Battery (/18)
Trail-Making Test
A
B
Wechsler Adult Intelligence Scale, Third
Edition
Verbal IQ
Performance IQ
Full IQ
Verbal comprehension
Visual perception
Working memory
Process speed
Wechsler Memory Scale-Revised
Verbal memory
Visual memory
General memory
Concentration/attention
Delayed recall
The Rivermead Behavioral Memory
Test
Screening score (/12)
Profile score (/24)
Behavioral Assessment of Dysexecutive
Syndrome
Age matched score (classification)

3d

6 wk

Cutoff score

21
4/3

22
4/3

23/24

1, 5, 7, 8, 7
12
0
17
11

4, 5, 6, 5, 6
13
4
23
16

2’15"
Not done

221"
3’23"

24/25
12/13

—*
72
57
62
76
54
65
66

80
72
74
82
75
76
75

70
55
61
72
59

87
88
86
78
71

4
9
44

5
15
69

Impaired

Impaired

—*

5/6
15/16

Abbreviation: IQ, intelligence quotient.
*The median of Wechsler Scale is centered at 100, with an SD of 15.

He was alert and cooperative to a series of neuropsychological examinations, although he was in an amnesic
state, with disorientation and recent memory loss.
Retrograde episodic memory concerning both personal
and public remote events was nearly intact, but he had
anterograde amnesia. For instance, he had no memory
of whether he had received his meals and repeatedly
asked for them. He even kept forgetting the most recent
conversations. He did not show confabulation.
His speech was fluent and not aphasic. Objective naming,
letter reading, verbal comprehension, and dictation
were normal. He showed constructional apraxia, but
ideomotor or ideational apraxia and unilateral spatial
neglect were not noted. He had no signs of callosal disconnection such as apraxia or tactile anomia in his left
hand. He could recall the room layout of his house and
describe the route from the nearest station to his home
on a map. However, he sometimes lost his way at the

hospital because of amnesia without topographic disorientation.
Table 1 shows the results of neuropsychological tests
in this patient. On the Wechsler Adult Intelligence Scale,
Third Edition, his verbal intelligence quotient (IQ) was
72; performance IQ, 57; and full IQ, 62. His verbal memory
was 70 and visual memory was 55 on the revised Wechsler
Memory Scale. The score on the Frontal Assessment Battery
was 11/18, and the word fluency test where the patient
was required to produce exemplars from given categories
resulted in scores of 9, 3, and 5 for the categories ‘‘animal,’’
‘‘fruit,’’ and ‘‘vehicle,’’ respectively, and where he was
required to produce words that begin with given letters
resulted in scores of 2, 5, and 3 for the letters ‘‘shi,’’ ‘‘i,’’
and ‘‘re,’’ respectively. The level of executive functioning
was classified as ‘‘impaired’’ on the basis of the scores of
Behavioral Assessment of the Dysexecutive Function, that
is, overall profile, 5, and age-corrected score, 44 (impaired).

RETROSPLENIAL AMNESIA

443

from the hospital 10 days after the onset. He was able
to accurately recognize familiar buildings and find his
way. The amnesia gradually improved, but memory
impairments were detected at 6 weeks after the onset by
using neuropsychological tests. Single-photon emission
CT performed 45 days after onset showed an improvement of cerebral blood flow in the right thalamus
(Fig 2, B).

Discussion

Figure 1. CT scan on admission (upper) and magnetic resonance imaging
tomography 6 days after the admission (lower). A subcortical hematoma was
evident between the right forceps occipitalis and the parietal lobe, involving
the right cingulate isthmus. A high-density area in CT scan was evident in
right globus pallidus without pathologic calcification. Abbreviations: CT,
computed tomography; FLAIR, Fluid attenuated inversion recovery; L,
left; MRI, magnetic resonance imaging; R, right; T1WI, T1 weighted images;
T2WI, T2 weighted images.

Neuroradiological Findings
Computed tomography (CT) and magnetic resonance
imaging (MRI) revealed a subcortical hematoma
(2 3 2.5 3 2 cm) between the right forceps occipitalis
and the parietal lobe, involving the right cingulate isthmus (Fig 1). Single-photon emission CT imaging using
Technetium-99m–labeled ethyl cysteinate dimer performed 3 days from the onset of stroke revealed reduced
perfusion not only in the retrosplenial region but also in
the right thalamus (Fig 2, A).

Clinical Course
The patient was treated medically and visual field defect resolved within several days. He was discharged

The sequential memory of our patient was intact, and
he could recall prehospital events very well, indicating
the absence of retrograde amnesia. However, he could
not learn the disease name, patient room number, and
the primary physician’s name, suggesting mainly anterograde amnesia.
Damage to the retrosplenial region has been reported to
be sufficient to induce anterograde amnesia.1-3,7-10 Several
etiologies of the tumor, infarction, and hemorrhage have
been reported in patients with retrosplenial amnesia,
but lesions in the right hemisphere are less common.
Regarding dysmnesia, the lesions in the left hemisphere are known to mainly impair verbal memory and
those in the right hemisphere mainly impair visual spatial
memory.11 In our case, although the lesions were in the
right hemisphere, both visual and verbal memories
were impaired (visual . verbal). These findings suggested that the laterality of memory was not as distinct
as that of language or visuospatial cognition, which was
not limited to retrosplenial amnesia. In fact, some cases
have been reported in which both the verbal and visual
memories were impaired by the lesions in the right hemisphere.11 Some experimental studies have also shown that
anterograde disorientation can be caused by lesions on either side.12 Thus, in our case, it seemed that the memory
function was not completely lateralized congenitally, and
the lesions in the right hemisphere caused damage to both
verbal and visuospatial memory.
The isthmus of the cingulate gyrus connects the visual
cortex in the occipital lobe with such limbic structures as
the hippocampus, anterior cingulate gyrus, and anterior
thalamus.13,14 Lesions in the retrosplenial cortex may
disrupt the connections between the anterior thalamus
and hippocampus and thus cause memory disturbance.
In the present case, amnesia improved only slightly with
an increase in cerebral blood flow in the right thalamus.
We suspected that the retrosplenial amnesia was caused
by the interruption of hippocampal input into the
anterior thalamus. Because the retrosplenial cortex itself
is vital for memory, the remote effect might alter the
impact of anterior thalamic lesions. These findings
provide novel insights into the functional pathology of
diencephalic amnesia and might be useful to determine
the causes of posterior cingulate hypoactivity and show
how distal changes in plasticity could contribute to

444

S. MAESHIMA ET AL.

Figure 2. SPECT imaging performed 3 days
from stroke onset at around the revealed reduced
perfusion not only in the retrosplenial region but
also in the right thalamus (upper). SPECT performed 45 days after onset showed an improvement of cerebral blood flow in the right thalamus
(lower). Abbreviations: L, left; R, right; SPECT,
single-photon emission computed tomography.
(Color version of figure is available online.)

diaschisis.15 Therefore, the clinical course of retrosplenial
amnesia might have a good prognosis.
Topographical disorientations are usually caused by
the lesions in the retrosplenial region.5 Our patient could
not remember the name of the previously unknown hospital ward or the layout of the hospital and often could
not find the toilet located several meters away from his
room. However, he could accurately recognize familiar
buildings and identify them on the map. Furthermore,
he could describe the route from the nearest station to
his home and could draw the map. The anterograde
amnesia might have been caused by the retrosplenial
lesion. We, therefore, suspected that his impaired
ability to remember unfamiliar landscape was because
of anterograde amnesia and not because of topographic
disorder.

References
1. Valenstein E, Bower D, Verfaellie M, et al. Retrosplenial
amnesia. Brain 1987;110:1631-1646.

2. Yasuda Y, Watanabe T, Tanaka H, et al. Amnesia following infarction in the right retrosplenial region. Clin Neurol Neurosurg 1997;99:102-105.
3. Masuo O, Maeshima S, Kubo K, et al. A case of amnestic
syndrome caused by a subcortical haematoma in the right
occipital lobe. Brain Inj 1999;13:213-216.
4. Cammalleri R, Gangitano M, D’Amelio M, et al. Transient
topographical amnesia and cingulate cortex damage:
a case report. Neuropsychologia 1996;34:321-326.
5. Takahashi N, Kawamura M, Shiota J, et al. Pure topographic disorientation due to right retrosplenial lesion.
Neurology 1997;49:464-469.
6. Oldfield RC. The assessment and analysis of handedness:
the Edinburgh inventory. Neuropsychologia 1971;9:97-113.
7. Rudge P, Warrington EK. Selective impairment of memory and visual perception in splenial tumours. Brain
1991;114:349-360.
8. Maguire EA. The retrosplenial contribution to human
navigation: a review of lesion and neuroimaging findings. Scand J Psychol 2001;42:225-238.
9. Maeshima S, Ozaki F, Masuo O, et al. Memory impairment and spatial disorientation following a left retrosplenial lesion. J Clin Neurosci 2001;8:450-451.
10. Osawa A, Maeshima S, Kubo K, et al. Neuropsychological deficits associated with a tumour in the posterior

RETROSPLENIAL AMNESIA
corpus callosum: a report of two cases. Brain Inj 2006;
20:673-676.
11. Aggleton JP. Understanding retrosplenial amnesia: insights from animal studies. Neuropsychologia 2010;
48:2328-2338.
12. Olton DS. Strategies for the development of animal
models of human memory impairments. Ann N Y Acad
Sci 1985;444:113-121.
13. Garden DL, Massey PV, Caruana DA, et al. Anterior thalamic lesions stop synaptic plasticity in retrosplenial cor-

445
tex slices: expanding the pathology of diencephalic
amnesia. Brain 2009;132:1847-1857.
14. Rosene DL, van Hoesen GW. Hippocampal efferents
reach widespread areas of cerebral cortex and
amygdala in the rhesus monkey. Science 1977;198:
315-317.
15. Irle E, Markowitsch HJ. Connections of the hippocampal formation, mammillary bodies, anterior thalamus and cingulate cortex. Exp Brain Res 1982;
47:79-94.