Journal of Neurology, Neurosurgery, and Psychiatry 1983;46:669-670

Short report

Ataxic tetraparesis from lacunar infarction in the pons
J VAN GIJN, M VERMEULEN
From the Department of Neurology, University Hospital Rotterdam (Dijkzigt), Rotterdam, The Netherlands

SUMMARY A 45-year-old woman with hypertension suffered four episodes of right hemiparesis
and two attacks of left hemiparesis, within seven months. On examination she showed weakness
and cerebellar ataxia of all four limbs; Computed tomography demonstrated a radiolucent area in
the base of the pons, consistent with lacunar infarction.
An unusual stroke syndrome with hemiparesis and
cerebellar ataxia involving the limbs of the same side
was first described by Fisher and Cole in 1965.'
Pathologic study of three later patients showed in
each case a lacunar infarct in the upper base of the
pons, near the midline and contralateral to the
ataxic hemiparesis.2 After the advent of highresolution computed tomography (Cr), however,
eleven of fourteen consecutively reported patients
with this clinical syndrome had a lesion in the ctralateral internal capsule3-" (one patient had a pontine haemorrhage,3 one patient a tumour in the midbrain,4 and in one case the site of the lesion could
not be determined"). We report a patient in whom
ataxic hemiparesis occurred on both sides, with
separate onset, and in whom Cr showed an infarct
in the pons.

weakness of the left arm and leg, with severe "pins and
needles" in the left hand. The left hemiparesis slowly
regressed, but recurred on March 27.
We first examined her on March 29. The blood pressure
was 200/100 mm Hg. She was mildly dysarthric. The jaw
jerk was brisk, and corneomandibular reflexes could be
elicited on both sides. The muscle tone was increased or,
passive flexion of the knees. The muscle power was
reduced on the left side, especially in the extensors of the
arm and the flexors of the leg. The right arm and leg
showed minimal weakness. All four limbs were ataxic, with
intention tremor and dysmetria, more markedly on the left.
The tendon jerks were symmetrically brisk, with bilateral
patellar clonus. The plantar reflexes were extensor. Sensa-

Cae report
A 45-year-old woman woke in the night of August 24,
1978, with tingling and weakness of the right arm and leg.
The symptoms had disappeared in the morning, but came
back the next day, for an hour, and again four days later,
after which she dragged her right foot for more than two
weeks. She was seen at another hospital; no diagnosis was
made at that stage. A fourth and last attack of right
hemiparesis occurred on December 3; she recoveredincompletely in a few weeks, with persistent tingling in the
right hand. On February 12, 1979, she suffered a sudden
-----------

Address for reprint requests: Dr J van Gijn, Department of
Neurology, University Hospital Rotterdam (Dijkzigt), Dr
Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.

Received 11 February, 1983
Accepted 12 March 1983

ig

Figure CT scan showing left paramedian infarct in the
basis pontis (arrow).

669

670
tion was completely normal. Her gait was broad-based,
with circumduction of the left foot.
Laboratory studies of blood, serum, and cerebrospinal
fluid (including IgG index) gave normal results. CT scanning (EMI 1010) showed a radiolucent area in the base of
the pons on the left of the midline and bordering on the
tegmentum (fig). The region of the internal capsule was
normal on both sides.
After treatment with antihypertensive drugs, no further
episodes of hemiparesis occurred during a follow-up
period of three years. Re-examination in 1982 showed
normal power of individual muscle groups, but a spastic
gait with circumduction of the left leg. Rapid and alternating movements of both hands and feet were impaired,
especially on the left, but without intention tremor or dysmetria. The reflex abnormalities were unchanged. Sensation was still normal, despite persistent tingling of both
hands. A repeat CT scan no longer demonstrated the
lesion in the pons.

Discussion
Two aspects stand out in this case history: the
demonstration of a lacune in the pons by computed
tomography, and the bilateral syndrome of ataxic
hemiparesis, with separate onset on each side. Other
features such as recurrent attacks and sensory symptoms are interesting but not uncommon in ataxic
hemiparesis' and in other lacunar syndromes.'0
Computed tomography has given a new impetus
to the recognition of lacunar infarction.9-1" The
intemal capsule is more often involved than previously suspected, not only in ataxic hemiparesis,-'but also in the dysarthria-dumsy hand syndrome.""3
With capsular infarcts, contralateral cerebellar signs
are difficult to understand, even more than with
lesions of the basis pontis. In some of these cases the
responsible lesion may be in the pons after all, as
lacunar disease can be widespread, whereas the
brainstem is often obscured by artifacts on CT. In
our patient CT showed a small radiolucent area in
the pons. Although the lesion corresponded with the
less affected side, its subsequent decrease in size is
compatible with recent infarction.'4 One other
report also demonstrated a pontine infarct on CT, in
a patient with ataxic hemiparesis as well as trigeminal weakness.'5
The site of the arterial lesion(s) in our patient is
not precisely known. Vertebral angiography was not
performed, as the results would not have altered the
treatment. Occlusion of a single branch of the basilar artery may cause bilateral ischaemia in the base

van Gijn, Vermeulen

of the pons, 16 but alternating hemiparesis has not yet
been reported in such a case. Stenosis or occlusion
of paired branches of the basilar artery may result
from atheroma of the parent vessel, or from intrinsic
atheromatous disease (mirror lesions of this kind are
at least known to occur in anterior perforating
arteries),'7 or finally from a combination of these
two lesions.'6
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