BRAIN INJURY , 2001, VOL. 15, NO . 10, 927 ±

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Case study

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Transient crossed aphasia and persistent
amnesia after right thalamic haemorrhage
SH IN ICH IR O M A ESH IM A { , FU M IN O R I
O ZAK I{ , R Y U JI O K ITA { , H IR O O
YA M AG A { , H ID EO O K AD A{ , K O ZO
K A K ISH ITA { , H IR O SHI M O R IW AK I{
and PETER ROGER‡
{ Department of Neurological Surgery, Hidaka General Hospital, Japan

‡ Brain Damage and Communication Research, University of Sydney and Department
of Linguistics, Macquarie University, Australia
(Received 29 September 2000; accepted 27 April 2001 )
A 45-year-old right-handed woman suffered transient aphasia and persistent amnesia after a right
thalamic haemorrhage. This patient appeared to have crossed aphasia, although it disappeared within
8 weeks. It is noteworthy that the patient had a unilateral right thalamic lesion but exhibited both
verbal and non-verbal memory impairment. Computed tomography and magnetic resonance imaging
revealed cerebral haemorrhage in the right thalamus involving the ventral anterior nucleus, medioventral nucleus, mamillothalamic tract, internal medullary lamina, and mediodorsal nucleus. An amytal
test was performed and suggested that the right hemisphere was dominant for language functions and
the left hemisphere was dominant for visuospatial functions. Single photon emission CT revealed a
low perfusion area only in the right thalamus. These findings suggest that the right hemisphere might
be dominant for both verbal and non-verbal memory function in this patient, although visuospatial
function was lateralized in the left hemisphere.

Introduction
Thalamic haemorrhages account for 25± 35% of intracerebral haemorrhages [1, 2]. It
is well-known that left unilateral thalamic haemorrhage has been associated with
disturbances of language and verbal memory [3]. Aphasia has been reported in
approximately 50% of cases of left thalamic haemorrhage. Kumral et al. [4] reported
a prospective clinical study of 100 patients with thalamic haemorrhage and, out of a
total of 49 left thalamic lesions, found 28 cases of aphasia. In Japan, Kawahara et al.
[1] reported 37 patients with small thalamic haemorrhage and described six cases
with aphasia out of 16 left thalamic lesions. Several previously reported patients with
thalamic haemorrhage were also noted to exhibit an amnestic syndrome. However,
there have been very few reports of amnestic syndrome and/or aphasia caused by
lesions in the right thalamus [5]. Crossed aphasia is a language disturbance in righthanded individuals resulting from lesions in the right hemisphere, and it is estimated
Correspondence to: Shinichiro Maeshima, MD, PhD, Department of Physical Medicine and
Rehabilitation, Wakayama Medical University, 811-1 Kimiidera, Wakayama 641-0012, Japan. email: maeshima@wakayama-med.ac.jp
Brain Injury ISSN 0269± 9052 print/ISSN 1362± 301X online # 2001 Taylor & Francis Ltd
http://www.tandf.co.uk/journals
DOI: 10.1080/02699050110065646

928

S. Maeshima et al.

to occur in 1± 2% of all dextral aphasics [6]. The authors recently had the opportunity to examine a patient who had mild transient aphasia and persistent amnesia
after a discrete right thalamic haemorrhage.

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Case report
O.N. is a 45-year-old right-handed factory worker with 12 years of school education. She had a history of mild hypertension for 2 years, but no prior history of
neurological problems. Her parents, brothers and sisters are all right-handed. She
experienced a sudden onset of disorientation with respect to time, day and place on
13 October 1998, and was admitted to the hospital on the following day. Initially,
she was alert and co-operative. Neurological examination revealed no motor or
sensory disturbance.
Her spontaneous speech was fluent. She had no difficulty initiating speech,
articulated normally, and did not have logorrhea. Echolalia was not observed and
phonological structure was clear. Confrontation naming was moderately impaired,
with considerable paraphasia. Repetition was excellent. Reading aloud was good.
Writing was impaired, and considerable paragraphia was seen. On the Western
aphasia battery (W AB) 5 days after admission, her scores were fluency 15, auditory
comprehension 5.8, repetition 10, naming 5.8, reading 3.2, and writing 3.6 (table 1).
In addition, she demonstrated constructional apraxia, but not oral, ideomotor, or
ideational apraxia. There were no signs of motor impersistence or unilateral spatial
neglect. On the Wechsler Adult Intelligence Scale-Revised (WAIS-R), her performance intelligence quotient (IQ) was 59. Verbal IQ was unmeasurable because
of the aphasia.
Brain CT scan on admission showed an area of high density consistent with
haemorrhage in the right thalamus (figure 1(a)). Magnetic resonance imaging (MRI)
5 days after admission revealed cerebral haemorrhage in the right thalamus, involving the anteromedial aspect (figure 1(b)).
Cerebral angiography was performed via transfemoral catheterization of the
internal carotid artery 6 days after admission, and did not show any abnormal
findings. Informed consent was obtained to perform the Amytal test (W ada test)
via the left and right internal carotid artery (ICA) to determine hemispheric
language dominance. The patient was instructed to raise both arms, and a dose of
100 mg sodium amobarbital in a 10% saline solution was hand-injected. The drug
effect was confirmed by the presence of hemiplegia. Before the injection, the
patient was able to repeat a short sentence of 5± 6 words and read a few words
aloud. For 6 minutes following the injection to the right ICA, she could not
Table 1.

Results of the Western aphasia battery (WAB)

Fluency
Auditory comprehension
Repetition
Naming
Writing

5 days

8 weeks

15
5.8
10
5.8
3.6

20
10
10
10
9.8

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(a )

(b)

(c)

Figure 1. (a) Brain CT scan on admission showed an area of high density consistent with haemorrhage in the right thalamus. (b) Magnetic resonance imaging (MRI) 5 days after admission
revealed cerebral haemorrhage in the right thalamus, involving the anteromedial aspect. (c)
Single photon emission CT 10 days after admission revealed an area of low perfusion limited
to then right thalamus.

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S. Maeshima et al.

repeat or read any words. After a certain interval her repetition ability recovered.
The amytal test was then repeated, this time via the left ICA. For 5 minutes
following the injection into the left ICA, the patient exhibited unilateral spatial
neglect on the right. These results suggested that the right hemisphere was dominant for language functions and the left hemisphere was dominant for visuospatial
functions.
Single photon emission CT 10 days after admission revealed an area of low
perfusion limited to the right thalamus (figure 1(c)).
O.N.’s aphasia gradually lessened, her scores of WAB 8 weeks after the onset
(table 1) becoming normal (fluency 20, auditory comprehension 10, repetition 10,
naming 10, reading 10, and writing 9.8). On the revised Wechsler Adult
Intelligence Scale (W AIS-R), her verbal intelligence quotient (IQ) was 84 and
her performance IQ was 79, with an overall IQ of 81. The score on Raven’s
coloured progressive matrices was 27/36. Despite these preserved functions, her
memory was clearly disturbed. Although she did not show confabulation, she
remained disoriented with respect to day and place. On the Wechsler memory
scale, all tasks were impaired except for digit span, and the memory quotient was
89. Both verbal and non-verbal memory were compromised. The Benton visual
recognition test showed an immediate recall score of 3/10; delayed recall, 1/10; and
copying, 10/10. On the auditory verbal learning test, immediate recall was 4, 5, 6,
5, 4/15, delayed recall was 1/15, and recognition was 10/15.
Twenty weeks after the onset, retrograde episodic memory concerning both
personal and public remote events was nearly intact, although the patient had a
profound anterograde amnesia.

Discussion
Although this patient experienced thalamic aphasia immediately after her stroke, the
aphasia resolved over a subsequent 8-week period. She was left with an isolated
disturbance of memory; in the absence of any dementia, aphasia or disturbance of
consciousness, her condition was classified as one of amnesia.
If the dominant hemisphere is affected, aphasia may be seen following a
thalamic haemorrhage [7], and contralateral neglect has been reported following
non-dominant thalamic haemorrhage [8]. It appeared that this case was one of
`crossed aphasia’, occurring as it did following a right hemisphere lesion in a
right-handed person. The diagnosis of crossed aphasia requires definite documentation of a language disorder in a patient who is not only strongly right-handed but
who also has no family history of left-handedness and has definite evidence of a
lesion in the right hemisphere on CT scan, MRI, or autopsy [9, 10]. This patient
met these criteria. In addition, one was able to confirm, using the amytal test, that an
opposite pattern of dominance was present in this patient, with language being
localized to the right hemisphere and visuospatial functions to the left. Some authors
have pointed out that patients with crossed aphasia provide insights into different
patterns of cerebral localization [6], and it is well-known that crossed aphasics are
more likely to exhibit a more bilateral representation of language functions. For this
reason, together with the fact that the thalamic lesion was relatively small, a good
recovery of language was anticipated in this particular patient. With thalamic lesions,
amnesia tends to persist, even in cases where the associated aphasia resolves or
improves to a considerable degree (as exemplified by the case considered in this

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Amnesia after right thalamic haemorrhage

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paper). The discrepancies in the characteristics of thalamic aphasia and thalamic
amnesia suggest that neither is solely of neuropsychological origin. The important
role of the ventrolateral nucleus (VL) in thalamic aphasia and amnesia has been
extensively discussed [11]. Ojemann et al. [12] found that electrical stimulation of
the VL facilitated recording of verbal information caused deterioration of retrieval of
verbal memories, and disturbed object naming. Thalamic aphasia is often accompanied by amnesia [13, 14], suggesting that the VL may be involved in both aphasia
and amnesia. In the case of O.N., one possible reason for the recovery of the aphasia
and persistence of amnesia may be that the VL was not affected by the haemorrhage
itself, but rather by surrounding oedema, which gradually resolved in the weeks
following the stroke.
A reduction in cerebral blood flow and metabolism in the hemisphere contralateral to cerebral stroke was described by Lenzi et al. [15]. In addition, a correlation
between neuropsychological impairment after a unilateral thalamic lesion and
cortical hypometabolism was reported by Baron et al. [16]. This exemplifies the
concept of `diaschisis’, a term used to describe the phenomenon in which damage to
one part of the brain causes a disruption of function in another part (which may
be remote in location but is connected to the damaged area) through loss of
excitatory input (see Feeney and Baron [17] for a complete discussion of diaschisis).
In some cases, thalamic aphasia may be correlated with cortical hypometabolism
rather than with the extent of the lesion itself. Further analysis of the relationships
between the anatomical structures affected, the neuropsychological impairments
observed, and the degree of impairment of cortical metabolism is necessary to
elucidate the mechanism of aphasia and amnesia following thalamic haemorrhage.
The mechanisms underlying neuropsychological recovery in patients such as the
one described in this case report have also been the subject of study. Baron et al. [18]
were able to show that cortical hypometabolism associated with thalamic lesions
improved gradually, suggesting that synaptic activity in the thalamo-cortical system
was being re-established, and/or that a reorganization of post-neuronal circuitry was
taking place. Yamaguchi et al. [19], who studied changes in cortical metabolism
following callosotomy in baboons, also reported a gradual recovery in cortical
metabolic activity. They suggested that the contralateral cerebral cortex could
play a role in this recovery, proposing that synaptic activity within the deafferented
cortex may be slowly restored through reinnervation by collaterals of intact callosal
neurons, reorganization of neuronal circuitry, or post-synaptic hypersensitivity.
As Feeney and Baron [17] point out, a more complete understanding of the
mechanisms which underlie spontaneous recovery following stroke may have
important therapeutic implications.
Amnesia affecting both verbal and non-verbal memory following a right
thalamic lesion is an extremely rare clinical finding; it is generally accepted that
there is dominance of the left hemisphere in verbal memory, and the right hemisphere in non-verbal memory. Speedie and Heilman [20] described amnesia for
visuo-spatial material following right thalamic infarction and a case in which a lesion
in the left dorsomedial nucleus of the thalamus was associated with verbal memory
disturbance [21] However, one case which shares some similarities with this was
described by Tsoi et al. [22] Their patient (who suffered a haemorrhage largely
confined to the right medial thalamus) exhibited persistent anterograde amnesia
and memory impairment for both verbal and visual material. The authors noted,
however, that the CT scan revealed the possible involvement (to a lesser degree) of

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S. Maeshima et al.

the medial aspect of the left thalamus, which may have contributed to the verbal
memory disturbances. Another possibility is that functional asymmetry is less
well-defined at the thalamic level [22]. This latter explanation would appear
more likely to apply to this patient, whose CT findings were limited to the right
thalamus. Furthermore, given the `opposite’ pattern of dominance established in this
patient through the amytal test, a pattern of lateralization which was less asymmetrical than usual could reasonably be expected, at both the cortical and thalamic
levels.

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