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Memory impairment following right cerebellar
infarction: a case study
ab

a

a

Fumiko Kusunoki Nakamoto , Michiko Tsutsumiuchi , Meiko Hashimoto Maeda , Yoshikazu
a

Uesaka & Katsuhiko Takeda

c

a

Department of Neurology, Toranomon Hospital, Tokyo, Japan

b

Department of Neurology, University of Tokyo, Graduate School of Medicine, Tokyo, Japan

c

Department of Neurology, International University of Health and Welfare Mita Hospital,
Tokyo, Japan
Published online: 28 Oct 2014.

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To cite this article: Fumiko Kusunoki Nakamoto, Michiko Tsutsumiuchi, Meiko Hashimoto Maeda, Yoshikazu Uesaka &
Katsuhiko Takeda (2015) Memory impairment following right cerebellar infarction: a case study, Neurocase: The Neural Basis
of Cognition, 21:5, 660-664, DOI: 10.1080/13554794.2014.969277
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Neurocase, 2015
Vol. 21, No. 5, 660–664, http://dx.doi.org/10.1080/13554794.2014.969277

Memory impairment following right cerebellar infarction: a case study
Fumiko Kusunoki Nakamotoa,b, Michiko Tsutsumiuchia, Meiko Hashimoto Maedaa, Yoshikazu Uesakaa*
and Katsuhiko Takedac
a

Department of Neurology, Toranomon Hospital, Tokyo, Japan; bDepartment of Neurology, University of Tokyo, Graduate School of
Medicine, Tokyo, Japan; cDepartment of Neurology, International University of Health and Welfare Mita Hospital, Tokyo, Japan

Downloaded by [New York University] at 05:02 25 July 2015

(Received 25 April 2014; accepted 16 September 2014)
We reported a patient with a right cerebellar infarction who showed anterograde amnesia. Cognitive dysfunction caused by
cerebellar lesions was called cerebellar cognitive affective syndrome, and deactivation of the contralateral prefrontal cortex
function due to disconnections of cerebello-cerebral fiber tracts have been hypothesized as mechanism underlying the
syndrome. The episodic memory impairment, however, could not be supported by the same mechanism because the
prefrontal lesions cannot cause amnesia syndrome. The feature of the impairment of our patient was similar to that of
diencephalic amnesia, and a single photon emission computed tomography study showed a relative hypoperfusion in the
right cerebellar hemisphere and left anterior thalamus. We considered that the memory deficit was caused by the dysfunction
of the thalamus, which is a relay center of the cerebello-cerebral connectivity network.
Keywords: cerebellar cognitive affective syndrome; cerebellar stroke; cerebellum; episodic memory; amnesia

Over the last few decades, neuroimaging studies and neuropsychological investigations have clarified the role of
the cerebellum in higher-order cognitive functions.
Schmahmann and Sherman evaluated patients with different cerebellar lesions, observing cognitive dysfunction and
named this clinical entity “cerebellar cognitive affective
syndrome (CCAS)” (Schmahmann & Sherman, 1998).
This syndrome consists of executive, visuospatial, linguistic, and emotional deficits.
Disconnections of cerebello-cerebral fiber tracts have
been hypothesized as the mechanism underlying the
syndrome (O’Halloran, Kinsella, & Storey, 2012). Some
functional magnetic resonance imaging (MRI) studies
revealed the cerebello-cortical pathway with multiple
fiber tracts that terminate within the regions of the contralateral prefrontal cortex (O’Halloran et al., 2012).
According to previous reports, cognitive impairments
caused by a cerebellar lesion have been often explained
by the functional suppression of the contralateral frontal
lobe (Baillieux et al., 2006; Cooper et al., 2012; Lagarde,
Hantkie, Hajjioui, & Yelnik, 2009; Mariën et al., 2008,
1996; Neau, Arroyo-Anllo, Bonnaud, Ingrand, & Gil,
2000; Peterburs, Bellebaum, Koch, Schwarz, & Daum,
2010; Suenaga et al., 2008).
We herein report of a patient with CCAS whose deteriorations of executive function and language function
were supported by a mechanism described in previous
reports (O’Halloran et al., 2012); however, the episodic
memory impairment could not be supported by the same

*Corresponding author. Email: yoshi-uesaka@umin.ac.jp
© 2014 Taylor & Francis

mechanism. Thus, we consider other possible causes of
memory dysfunction.
Case report
Following 12 days of continuous headaches, a 42-year-old
right-handed man with 16th grade education presented at
our emergency room with acute onset of disturbance of
consciousness. The patient was a government worker and
did not have any history of serious illness. His neurologic
examination revealed mild drowsiness, dysarthria, and
minor motor dysfunctions such as mild cerebellar ataxia
and dysmetria. Following 24 hr of admission, disturbance
of consciousness, dysarthria, and motor features almost
disappeared.
Cranial MRI showed no structural damage at the supratentorial level including the thalamus, but revealed acute
cerebellar infarction involving the vermis and superior part
of the right cerebellar hemisphere (Figure 1(a–c)). Cerebral
angiography showed a dissection of bilateral vertebral
arteries and the basilar artery. A quantified N-isopropyl-p
[123I] iodoamphetamine single photon emission computed
tomography (IMP SPECT) of the brain, performed 3 weeks
after the onset of consciousness disturbance revealed a
hypoperfusion in the right hemicerebellum and the left
frontotemporal region including the left ventrolateral prefrontal cortex and a slightly decreased perfusion in the left
anterior thalamus (Figure 1(d–f)). The results of electroencephalography, performed 3 weeks after the onset were

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661

Figure 1. Brain MRI axial diffusion weighted imaging showing hyperintense signals in the anterior lobe of the superior right cerebellar
hemisphere (right superior cerebellar artery). No structural damage was observed at the supratentorial level (a–c). Quantified IMP single
photon emission CT (IMP SPECT) performed 22 days after the onset of consciousness disturbance showed hypoperfusion not only in the
vermis and hemisphere where the infarction was found but also in the left inferior frontal area and anterior thalamus (d–f). [To view this
figure in color, please see the online version of this journal.]

found to be within normal limits, suggesting that he had no
disturbance of general brain function.
In his daily life, although he had a high educational
level, the patient tended to ask the same questions several
times and tended to forget the nursing care he had already
received. To evaluate his cognitive dysfunction, neuropsychological evaluation was started 13 days after the onset.
His performance on Cognistat (The Neurobehavioral
Cognitive Status Examination) was markedly deficient on
the subtest of memory (Table 1). The Wechsler Memory
Scale-Revise revealed a discrepancy of 51 index points
between visual memory (index = 113) and verbal memory
(index = 62). The index of delayed recall was 64, which

Table 1.

showed the episodic memory impairment. His scores revealed
that his memory function was impaired for his age, and he had
a deficit of verbal memory rather than visuospatial memory.
In the Rey auditory verbal learning test (revised
Japanese version), his delayed recall score (3/15) was
low, whereas his score in the recognition part was normal.
These findings suggest that encoding of novel aspects of
information into episodic memory was intact whereas
memory retrieval was affected. While he was recalling
the words, confabulation occurred.
The patient had a low score in the Rule Shift Card
Test included in the Behavioral Assessment of the
Dysexecutive Syndrome (BADS). In the modified Stroop

Cognistat profile.
Language

Reasoning

Subtest of Cognistat (test range)

Loc

Ori
(0–12)

Atten
(0–12)

Comp
(0–12)

Rep
(0–12)

Nam
(0–12)

Const
(0–12)

Mem
(0–12)

Calc
(0–12)

Sim
(0–12)

Judg
(0–12)

1 week after stroke
8 weeks after stroke

Alrt
Alrt

10
10

10
10

10
10

11
11

9
10

11
11

6
9

10
10

9
10

10
10

Notes: Loc = level of consciousness; Ori = Orientation subtest; Atten = Attention subtest; Comp = Comprehension subtest; Rep = Repetition subtest;
Nam = Naming subtest; Const = Construction subtest; Mem = Memory subtest; Calc = Calculations subtest; Sim = Similarities subtest; Judg = Judgment
subtest; Alrt = Alert.

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662

F.K. Nakamoto et al.

test, he was unable to disregard the verbal content. These
results suggest that his executive function involving
divided and switching attention was disturbed.
His total Wechslar intelligence quotient (IQ) was 79.
This result was caused by decreased verbal IQ and deterioration of executive function caused by diaschisis in the left
frontal cortex. Although he did not show aphasia in the
Western aphasia battery (WAB), he showed mild impairment
of language function, such as impairment of comprehension
of the meaning of written sentences, impairment of speech
production, and reduced phonemic fluency. These findings
suggest decreased verbal IQ that was not due to aphasia.
A repeat neuropsychological evaluation 4–6 weeks after
his stroke showed slight improvement. Table 2 shows a
summary of his cognitive assessments at 2–3 weeks, 4–
6 weeks, and 4 months after the stroke. Follow-up investigations using Cognistat 8 weeks postonset revealed an
improvement of the memory profile (Table 1).
Discussion
The patient developed episodic memory deficit and deteriorations of executive function and language function.
The deteriorations of executive function and language
function in CCAS were noted in previous reports, in
which the mechanism underlying the syndrome was deactivation of the contralateral prefrontal cortex function due
to the loss of excitatory impulses through cerebellar cortical pathways.
The episodic memory impairment, however, could not
be supported by this mechanism because the prefrontal
lesions cannot cause an amnestic syndrome. Although
the lesions can affect the memory process and cause
secondary long-term memory deficits, such as source
memory impairment, false memory, and prospective memory impairment, the memory deficits of our patient differed
from those findings. Therefore, we needed to evaluate the
mechanism underlying the condition, and we considered
some possible causes of memory dysfunction.
First, we considered that the decreased blood flow in
the left anterior thalamus caused the amnesia in our
patient, because his brain SPECT showed decreased perfusion in this region. The feedback or efferent loop originates from the deep nuclei of the cerebellum, which
project to the nuclei of the thalamus. In turn, the nuclei
of the thalamus project to the motor and premotor cortices
and also to nonmotor areas including the prefrontal cortex
(Marien, Engelborghs, Fabbro, & De Deyn, 2001; Smet,
Paquier, Verhoeven, & Mariën, 2013). Several clinical
reports suggest evidences for cerebello-thalamo-cortical
pathways. Kim et al. reported amnesia syndrome following left anterior thalamic infarction, and the brain SPECT
image revealed decreased uptake in the ipsilateral frontotemporoparietal cortex and contralateral cerebellum that
caused by disconnection of the cerebello-thalamo-cortical

pathways (Kim, Hong, & Roh, 1994). The phenomenon of
cerebello-cerebral diaschisis was also shown in patients of
posterior fossa syndrome, and the 99mTc-Ethyl cysteinate
dimer SPECT results showed decreased perfusion in the
thalamus as well as an area of hypoperfusion in the vermis
(Baillieux et al., 2006; Mariën et al., 2013). It is considered that disconnection of cerebello-thalamic tracts causes
functional suppression of the left anterior thalamus.
Besides, several reports suggest that a thalamic lesion
can cause episodic memory impairment (Kim et al.,
1994). Diencephalic amnesia is characterized by the clinical features of normal intelligence and immediate memory, anterograde and retrograde amnesia, disorientation,
anosodiaphoria, and confabulation. Our patient did not
show significant retrograde amnesia and encoding and
storage deficits; however, the feature of confabulation
was similar to that of diencephalic amnesia. It is considered that the memory deficit of our patient was caused by
the dysfunction of the thalamus, which is a relay center of
the cerebello-cerebral connectivity network.
Second, we considered that the cerebellum itself has a
role in episodic memory. Both neuroimaging and neuropsychological lesion studies suggest that the cerebellum
contributes to verbal working memory processes. Some
neuropsychological and neuroimaging studies have shown
indirect supports for the assumption that the cerebellum
contributes to episodic memory process because of involvement of verbal working memory processes (Davachi,
Maril, & Wagner, 2001; Ranganath, Cohen, &
Brozinsky, 2005). These concepts are supported by imaging studies that demonstrate an overlap between brain
regions involved both in working memory processing and
in long-term memory encoding (Fliessbach, Trautner,
Quesada, Elger, & Weber, 2007). Impaired working memory of our patient was, however, not severe, and we speculate that decline in working memory may not be involved
in his episodic memory disturbance. On the other hand,
using functional MRI, some studies suggested that the
cerebellum supports episodic memory formation and
retrieval, which was not explained by involvement of
verbal working memory (Fliessbach, Weis, Klaver, Elger,
& Weber, 2006; Weis, Klaver, Reul, Elger, & Fernández,
2004). It is speculated that activations of the cerebellar
hemispheres during episodic memory retrieval is due to
the induction of imagined manipulations by concrete
words such as tools because the cerebellum is known to
be involved in motor imagery (Fliessbach et al., 2006).
These studies suggest that the cerebellum has a role in
episodic memory.
On comparing the performance after cognitive rehabilitation with the performance immediately after stroke, an
improvement of verbal IQ was shown while the scores of
performance IQ, processing speed, verbal memory, and
delayed recall were almost unchanged or showed partial
recovery. The observation suggested that it is difficult to

Neurocase
Table 2.

663

Neuropsychological test results in the present case.

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2–3 weeks after stroke 4–6 weeks after stroke 4 months after stroke
Measures
General cognition ability and memory
HDS-R (/30)
MMSE (/30)
Frontal Assessment Battery (/18)
WAIS-III
Total IQ
Verbal IQ
Performance IQ
Verbal comprehension
Sensory integration
Working memory
Processing speed
Wechsler Memory Scale-R
Verbal memory
Visual memory
General memory
Attention/concentration
Delayed recall
RBMT (/24)
Standard profile
Scleening
Learning and retrieval
Rey Auditory Verbal Learning Test
Immediate recall 1st (/15)
2nd (/15)
3rd (/15)
4th (/15)
5th (/15)
Recognition (/44)
Delayed recall (/15)
Rey–Osterrieth Figure (/36)
Copy
Delayed recall
Attention
Trail making Test A (execution time)
Trail making Test B (execution time)
BADS
Rule Shift Card (/4)
Action Program (/4)
Key Search (/4)
Temporal Judgement (/4)
Zoo Map (/4)
Modified Six Elements (/4)
Overall profile (/24)
Standardized score
Age-corrected score
Stroop
Part I (execution time)
Part III (execution time)
Language function
WAB (AQ%)

27
30

30
15

79
77
85
78
99
85
78

93
101
83
105
95
98
78

62
113
73
103
64

82
115
90
101
82

16
8

19
8

5
9
8
6
4
42
3

4
8
10
10
9
41
7

7
8
9
12
13
44
10

35
18.5
106 s
105 s

94 s
105 s

1
3
4
2
4
3
17
95
93
25 s
29 s
99.8

Note: HDS-R, Hasegawa’s Dementia Scale Revised; MMSE, Mini-Mental State Examination; WAIS-III, Wechsler Adult
Intelligence Scale-Third Edition; AQ, Aphasia quotient.

improve executive dysfunction and memory impairment,
while language impairment tends to improve earlier than
these functions. In this patient, the language impairment is
caused by the deactivation of the contralateral cortex

function due to disconnections of cerebello-cerebral fiber
tracts, and the language impairment showed improvement
following functional recovery after cerebellar damage. On
the other hand, memory impairment was caused by

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F.K. Nakamoto et al.

disconnection of neural circuits through the anterior thalamus, and it could not be improved immediately after recovery of cerebellar function. Although the executive
dysfunction is also caused by the deactivation of the left
frontal cortex function due to diaschisis of the cerebellar
lesion, improvement of executive dysfunction was delayed.
We speculated that the cause of the delay of improvement
of executive dysfunction is the delay of improvement of
memory function because executive function was associated
strongly with memory function rather than with language
function which showed significant improvement.
In summary, with a lesion in the right cerebellum, the
patient showed episodic memory impairment, and we
observed diaschisis in the anterior thalamus on brain
SPECT. This finding suggests that memory disturbance
in the right cerebellum caused by a lesion is a type of
disconnection syndrome interrupting the cerebellar modulation of neural circuits linked to the anterior thalamus.

Disclosure statement
No potential conflict of interest was reported by the authors.

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