References

Matthias Endres, MD
Klinik und Polikinik für Neurologie, Charité Campus Mitte
Charitéplatz 1
DE–10117 Berlin (Germany)
Tel. +49 30 450 560 257, Fax +49 30 450 560 932
E-Mail matthias.endres@charite.de

Cerebrovasc Dis 2008;25:594–596
DOI: 10.1159/000134376

Isolated Hemiataxia of the Cerebellar Type after a
Small Internal Capsular Infarct
V. Kapina, R. Sztajzel, I. Momjian-Mayor
Department of Neurology, HUG, Geneva University Hospital
and University of Geneva, Geneva, Switzerland

Hemiataxia is classically ascribed to lesions involving the cerebellar system or interrupting the sensory pathways that control
movement. Hemiataxia after supratentorial brain infarction is
not uncommon. It, however, rarely occurs in isolation and most

594

Table 1. Case reports of isolated hemiataxia after a capsular

infarct
Authors

Lesion

Cases

Luijckx et al.
[1], 1993

haemorrhage in the posterior limb
of the internal capsule

1 case

Luijcky et al.
[2], 1994

infarct in the posterior limb
of the internal capsule

2 cases

of the time is accompanied by either pyramidal or sensory defects, or a combination of both. Isolated hemiataxia after supratentorial brain lesion is infrequent. To our knowledge, only 3 cases of internal capsular lesions, of which 2 were ischaemic and 1
haemorrhagic in nature, have been described to date [1, 2] (table 1). The case reported here therefore provides further illustration of hemiataxia of the pure cerebellar type resulting from an
ischaemic lesion restricted to the posterior limb of the internal
capsule.
Case Report
A 65-year-old man with a history of hypercholesterolaemia,
hypertension and smoking suddenly developed clumsiness of the
left arm and unsteadiness of gait, without weakness. Neurological examination performed on admission 24 h after onset of
symptoms showed left hemiataxia consisting of left-sided dysmetria, dysdiadochokinesia and Holmes rebound phenomenon,
hypermetria and intention tremor on finger-to-nose, finger-tofinger and heel-to-shin tests. This incoordination remained unchanged with the eyes open or closed. Ataxia of the arm was severer than that of the leg. Left-sided hypotony and decomposition of movement at tendon reflexes of the left leg were present.
When standing, the patient showed a wide-based unsteady gait
and a slight tendency to fall to the left. There was no weakness or
pyramidal signs, and a normal plantar response. Position and
vibration sense as well as touch, temperature and pain sensation
were preserved. The patient had no signs of brainstem involvement, no pathological nystagmus or saccadic pursuit. There was
no cognitive impairment. Computed tomography of the brain
performed at admission disclosed a small hypodense lesion restricted to the posterior limb of the right internal capsule, compatible with a small deep infarct as well as an older lesion in the
right centrum semiovale. MRI on day 3 confirmed these lesions
with the internal capsular one appearing as new on diffusionweighted MRI sequences and thus responsible for symptoms
(fig. 1a, b).
There was a moderate improvement of the ataxia within the 3
days following the attack.
Discussion
Hemiataxia after supratentorial brain infarction is not uncommon and has been reported by several authors [3–7]. The latter, mainly related to a thalamic or capsular lesion, rarely occurs
in isolation, being currently accompanied by either motor or sensory signs, or both [7–10]. Among hemiataxia secondary to supratentorial brain lesion, both ataxic hemiparesis and thalamic atax-

Stroke Notes

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Fig. 1. a Transverse T2-weighted MRI

ia have been well described. Ataxic hemiparesis was coined by
Fisher [3] and Fisher and Cole [11] and attributed to the infarct
affecting either the internal capsule, the upper basis of the pons
or the corona radiata. Ataxic hemiparesis has also been reported
after a midbrain lesion [12].
While the associated weakness is due to interruption of the
corticospinal fibres, the ataxia has been attributed to damage to
the corticopontine fibres descending into the posterior limb of
the internal capsule as well as to the interruption of the thalamocortical connections which run medially in the posterior limb of
the internal capsule [4, 6].
Thalamic ataxia has been explained by lesions involving the
ventral lateral nucleus of the thalamus, i.e the thalamogeniculate
territory. Interruption of the dentatorubrothalamocortical fibres
appears therefore responsible for the hemiataxia [7, 13]. Thalamic ataxia presents the main clinical characteristics of a cerebellar
type of ataxia. It has been reported in association with either
hemisensory loss (hemiataxia, hypoesthesia), weakness (ataxic
hemiparesis) or both (hypoesthetic ataxic hemiparesis). The sensory loss is caused by damage to the ventral posterolateral and
ventral posteromedial nucleus by interrupting the ascending spinothalamic and medial lemniscus fibres, respectively. When
present, the weakness is usually mild and only transient. The potentially severe weakness observed in ataxic hemiparesis and hypoesthetic ataxic hemiparesis after thalamic stroke appears to result from larger lesions not only restricted to the thalamus, but
also extending to the internal capsule, usually in the setting of a
haemorrhage [13].
Crossed cerebellar diaschisis (CCD, i.e decreased blood flow
and cerebral metabolism in the cerebellar hemisphere contralateral to the side of a supratentorial lesion) [14] is frequently reported after supratentorial infarction in studies with positron emission tomography (PET) and/or single-photon emission computed
tomography (SPECT).
Lesions in the internal capsule and thalamus have been described as a cause of CCD.

Strokes Notes

In both ataxic hemiparesis and thalamic ataxia, the CCD observed by either PET [15–17] or SPECT [18] strongly suggested
that hemiataxia resulted from damage to both cerebellar pathways, not only the corticopontocerebellar as firstly described, but
also the dentatorubrothalamocortical connections.
CCD has also been described in correlation with transient
ischaemic attack in a study where SPECT showed a focal reduction of perfusion during the presence of the clinical symptoms
whereas the control after full clinical recovery was normal. This
study shows that a temporary suppression of regional function is
capable of producing secondary remote effects such as CCD [18].
In our case, the possibility of a concomitant transient ischaemic
attack in the cerebellar hemisphere is highly unlikely since the
ataxia persisted 3 days after the attack.
The patient described in our study is a case of CCD but with a
particular representation.
By contrast, isolated hemiataxia of the cerebellar type after
supratentorial brain lesion appears to be infrequent and has been
only rarely reported [1, 2]. To our knowledge, only 3 cases of isolated hemiataxia after internal capsular lesion have been reported
to date, and they were all by the same group [1, 2]. Two of them
were due to a lacunar infarct restricted to the posterior limb of the
internal capsule on MRI sequences [2] while one was secondary
to a haemorrhage [1].
Classen et al. [19] described a case of visuomotor apraxia after
a lesion in the right dorsal thalamus, the geniculate body and the
adjacent retrothalamic and medial temporal white matter. The
most posterior fibres of the posterior limb of the internal capsule
were interrupted. Glickstein [20] described the participation of
the descending corticopontocerebellar and ascending cerebellothalamocortical projections in the visual guidance of movement.
Hemiataxia in our patient was clinically of the cerebellar type
and cannot be attributed to disturbed proprioception or underlying weakness. There was no deep sensory loss on neurological
testing, eye closure did not worsen the ataxia, optokinetic following was intact and we noted neither weakness nor pyramidal signs

595

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showing a small lesion of high signal intensity in the posterior limb of the right
internal capsule. b Transverse diffusionweighted MRI showing a small recent lesion in the posterior limb of the right internal capsule.

15 Baron JC, Bousser MG, Comar D, Castaigne P: ‘Crossed cerebellar diaschisis’ in human supratentorial brain infarction. Ann Neurol 1980;
8:128.
16 Tanaka M, Kondo S, Hirai S, Ishiguro K, Ishihara T, Morimatsu M:
Crossed cerebellar diaschisis accompanied by hemiataxia: a PET study.
J Neurol Neurosurg Psychiatry 1992;55:121–125.
17 Engelborghs S, Pickut BA, Marien P, Opsomer F, De Deyn PP: Crossed
cerebellar diaschisis and hemiataxia after thalamic hemorrhage. J Neurol 2000;247:476–477.
18 Takasawa M, Hashikawa K, Ohtsuki T, Imaizumi M, Oku N, Kitakawa
K, Hori M, Matsumoto M: Transient crossed cerebellar diaschisis following thalamic hemorrhage. J Neuroimag 2001;11:438–440.
19 Classen J, Kunesch E, Binkofski F, Hilperath F, Schlaug G, Seitz RJ,
Glickstein M, Freund H-J: Subcortical origin of visuomotor apraxia.
Brain 1995;118:1365–1374.
20 Glickstein M: How are visual areas of the brain connected to motor
areas of the sensory guidance of movement? Trends Neurosci 2000;23:
613–617.
21 Carpenter M: Human Neuroanatomy. Baltimore, Williams & Wilkins,
1976.
22 Nieuwenhuys R, Voogd J, van Huijzen C: The human central nervous
system. Berlin, Springer, 1983.
23 Wakana S, Jiang H, Lidia M, et al: Fiber tract-based atlas of human
white matter anatomy. Radiology 2004;230:277.
Viktoria Kapina, MD
Department of Neurology
HUG, University Hospital and Medical School of Geneva
Rue Micheli-du-Crest 24
CH–1211 Geneva 14 (Switzerland)
Tel. +41 79 538 4644, Fax +41 22 751 2301
E-Mail viktoria.kapina@hcuge.ch

References
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Psychiatry 1994;57:742–744.
3 Fisher CM: Ataxic hemiparesis. Arch Neurol 1978;35:126–128.
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7 Melo TP, Bogousslavsky J, Moulin T, Nader J, Regli F: Thalamic ataxia.
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Cerebrovasc Dis 2008;25:596–598
DOI: 10.1159/000134377

Floating Basilar Artery:
An Interesting Clinical Dilemma
Jamie J. Van Gompel b, C.C. Lin a , Irene Meissner a
Departments of a Neurology and b Neurosurgery, Mayo Clinic,
Rochester, Minn., USA

Case Report
Our patient was a 79-year-old right-handed female. She presented with an event of speech and language disturbance, with
right-sided weakness and numbness. Computed Tomography
(CT) was performed in preparation for possible tissue plasminogen activator (tPA) administration but the event resolved completely within an hour. While being interviewed after admission,
the patient had a second spell. She abruptly developed dysarthria, which progressed with right hemiplegia. At 10 min, her
right-side function began to return and the event had resolved
in 30 min. Magnetic resonant angiography (MRA) revealed
minimal backfilling into the basilar artery apex (fig. 1B). Digital
subtraction angiography (DSA) did not visualize the basilar artery (fig. 1A).

Stroke Notes

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suggestive of ataxic hemiparesis. In addition, MRI sequences
clearly showed that the small deep lesion was restricted to the posterior limb of the internal capsule without involvement of the
thalamus. Based on previous observations regarding ataxic hemiparesis and thalamic ataxia together with the 2 previously reported cases of isolated hemiataxia after capsular lacunar infarct, we
strongly believe that in our patient, hemiataxia was more likely
due to a lesion of the cerebellar pathways, either the ascending
dentatorubrothalamocortical tract or the descending corticopontocerebellar pathway at the level of the posterior limb of the internal capsule. Functional MRI, PET or SPECT would have been of
great interest in this patient to demonstrate CCD and thus assess
our hypothesis. Such investigations were, unfortunately, not performed.
To conclude, as previously suggested by Luijckx et al. [1, 2], as
well as discussed in anatomical studies [21–23], the case reported
here provides further clinical evidence of the anatomically segregated passage of the cerebellar fibres through the posterior part
of the posterior limb of the internal capsule. Interruption of the
cerebellar connections in the internal capsule may therefore cause
isolated hemiataxia of the cerebellar type as observed in our patient. The determination of whether the descending or ascending
pathway is severed and responsible for the cerebellar symptoms
appears difficult. However MR diffusion tensor imaging may
provide the answer to this question by studying the development
of a descending or ascending wallerian degeneration in a given
patient with an infarction in the posterior limb of the internal
capsule.