Journal of Neurology, Neurosurgery, and Psychiatry 1983 ;46:561-563

Short report

Hemiataxia and crural hemiparesis following
capsular infarct
E DE RENZI,* P NICHELLI,* G CRISIt
From Clinica Neurologica* and Istituto di Radiologiat Universita di Modena, Modena, Italy

SUMMARY Two patients presenting with hemiataxia and hemiparesis on the same side are
described. Both had cr scan evidence of an infarct located in the posterior limb of the con-

tralateral internal capsule.
The association of cerebellar ataxia and pyramidal
signs involving the limbs of the same side was first
described by Fisher and Cole' in 1965, who tentatively located the lesion in the posterior limb of the
internal capsule. Subsequently ataxic hemiparesis
has been reported in six patients with lesion in the
basis pontis contralateral to the involved limb,25 in
a patient with a ventrolateral midbrain lesion6 and in
three patients showing CT scan evidence of an
infarct of the posterior limb of the internal capsule.7-9 We report two more cases of ataxia and
homolateral crural paresis. In both patients a lesion
located in the posterior limb of the internal capsule
was identified on the CT scan.

but both upper and lower right extremities were still dysmetric and the right lower limb was still moderately weak
particularly in the hamstrings and peroneal muscles. Four
and a half months after the onset of disease, ataxia persisted with only minimal improvement, while weakness of
the left hamstrings had almost completely recovered.
CT scan one day after admission revealed a small
decreased density area in the left posterior limb of the
internal capsule with possible involvement of the adjacent
thalamus. One month after the onset of illness CT scan
(Fig la) showed a clear-cut hypodensity area in the two
middle quarters of the posterior limb of the left internal
capsule. The lesion extended upward from a midthalamic
to a high thalamic level, but spared the corona radiata and
that most superior part of internal capsule which is
immediately adjacent to corona radiata.

Case I
A 45-year-old man was admitted to the wards after the
sudden onset of a right hemiparesis. On neurological
examination he was alert and oriented. Speech and cranial
nerves were normal. There was slight right-sided weakness
of the peroneal muscles with minimal weakness of the
extensor muscles of the right arm. Tendon reflexes on the
right were slightly brisker than those on the left and the
right plantar response was extensor. On standing with the
feet together the patient fell to the right. There was a
severe dysmetria on both finger-to-nose and heel-to-knee
tests. Rapid alternating movements were slow and clumsy
on the right side. Sensory functions and visual fields were
normal. Weakness and ataxia increased in a step-wise fashion in the next two days. Weakness was greater in the
proximal muscles of the upper limb and in the distal muscles of the lower limb. At the end of the fourth week of
illness the right arm had completely recovered its strength,

Case 2
A 55-year-old man, with a long history of hypertension
and diabetes, suddenly noticed dragging of his left leg and
loss of motor power and tingling of his left arm. On admission the patient was alert and fully oriented. Visual fields
were intact. There was moderate left central facial weakness and a gross left hemiparesis which in the upper limb,
mainly affected the proximal muscles. Tendon reflexes
were slightly brisker on the left side. The left plantar
response was extensor. Light touch and joint position sense
were slightly impaired on the left. At that time tests of
coordination could not be carried out, because of the
severe motor weakness. Computed tomography revealed a
low density area occupying a great part of the posterior
limb of the internal capsule with involvement of the most
lateral part of the thalamus. The corona radiata also was
involved (Fig lb). The patient's paralysis began to improve
after two weeks, and after a month the muscle power of
arm and forearm flexors and extensors had recovered to
the point of permitting finger-to-nose and finger-to-finger
testing. The latter manoeuvre was carried out holding the
examiner's thumb at the same horizontal level as the
patient's hand, so that no movement of the shoulder muscles, which were still weak, was required. These tests dis-

Address for reprint requests: Dr Ennio De Renzi, Clinica

Neurologica Via del Pozzo 71, 41100 Modena, Italy.
Received 21 October 1982 and in revised form 9 January 1983.
Accepted 1 February 1983

561

de Renzi, Nichelli, Crisi

562

Fig 1 (a) Case 1:2nd CTscan (one month after onset of disease) shows a lesion in the posterior limb of
the left internal capsule, (b) Case 2. CT scan (8 days after onset ofdisease) shows a low density area in the
posterior limb of the right internal capsule encroaching upon the thalamus.

closed a gross wavering ataxia, which did not change with
the eyes closed and could not be explained by weakness.
There was also exaggerated rebound on the same side and,
when sitting on the bed with his feet dangling, the patient
slowly toppled to the left. Heel-to-knee test could not be
performed owing to the weakness of the left limb.

Discussion
Both patients had a lesion in the superior portion of
the internal capsule, which encroached upon the lateral thalamus, marginally in case 1, more extensively
in case 2. The location of the infarcts corresponds to
that shown by CT scan in analogous cases, of which
three were reported in detail7-9 and three were mentioned in a recent paper'0 devoted to lacunar
infarcts. Also the finding that paresis was more
marked on the lower limb appears to be typical of
this kind of capsular infarcts.
As suggested by Fisher and Cole,' the mechanism
whereby hemiataxia follows a capsular lesion is
probably the interruption of the cortico-pontinecerebellar connections. Their origin and course has
recently been the subject of a number of studies.
These have shown that neither Arnold's bundle, nor
Turk's bundle, which are reported by many anatomical textbooks'l-'' to be the main constituents of
these pathways, are implicated in the transmission of
information from the cerebral cortex to the cerebel-

lum, since both tracts terminate above the pontine
level.'4-'6 By studying areas of degeneration in the
pontine nuclei of monkeys which had undergone
cortical excisions, Brodal'7 was able to demonstrate
that cortico-pontine fibres originate predominantly
from area 4, areas 3, 1 and 2, area 5 and parts of the
visual cortex representing the peripheral visual field.
The contribution from area 6 and 7 is less substantial, and only a minor contingent of fibres comes
from the prefontal and temporal cortex. Part of the
cortico-pontine connections are collaterals of
pyramidal fibres, while the majority have an independent origin in approximately the same areas giving rise to the cortico-spinal pathway. It is, therefore, suggested that they do not run separately, but
adjacent to, or even intermingled with the pyramidal
tract in the caudal sector of the posterior limb of the
internal capsule, a hypothesis already advanced in
the monkey.'4
In addition to the involvement of cortico-pontine
fibres, the capsular lesion may produce cerebellar
symptoms by encroaching upon the ventro-lateralis
(VLo) nucleus of the thalamus or its efferents to the
motor cortex, which run in the medial part of the
posterior limb of internal capsule.'8 This nucleus
receives fibres from the contralateral dentate nucleus and is connected with the motor cortex, thus
entering as a component of the afferent limb of the
cortico-cerebellar loop. Its damage has been

Hemiataxia and crural hemiparesis following capsular infarct

reported to produce cerebellar symptoms, mainly in
the form of intention tremor,19 although a more destructive injury of this nucleus and of the neighbouring ventralis anterior nucleus abolishes the tremor,
as shown by stereotaxic surgery findings.20
It may prove to be extremely difficult to estimate
the extent to which the cerebellar symptomatology
consequent to capsular infarcts is contingent upon
damage of cortico-pontine or thalamo-cortical connections. At any rate its occurrence is likely to be a
common event, which is usually obscured by the
concomitant hemiparesis and can only be detected
when the latter abates. Even so, there is the risk that
hemiataxia is overlooked by the examiner, who may
feel hesitant to diagnose it in the presence of motor
weakness. The CT scan detection of a posterior capsular infarct should alert neurologists to carefully
test cerebellar functions.

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