1571

Case Reports
Magnetic Resonance Imaging of Ataxic
Hemiparesis Localized to the Corona Radiata
David H. Gutmann, MD, PhD, and Steven Scherer, MD, PhD
A 61-year-old woman developed right hemiparesis with homolateral cerebellar-type ataxia.
Computed tomography and magnetic resonance imaging demonstrated left corona radiata
lesions, not present on magnetic resonance imaging 1 year earlier. No brainstem lesions were
identified, suggesting that ataxic hemiparesis can result from lesions in the corona radiata.
{Stroke 1989;20:1571-1573)

A
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taxic hemiparesis syndrome (AHS) was first
described by Fisher and Cole.1 This rare
L. syndrome is manifested by weakness and
ataxia characteristic of cerebellar dyscoordination
(defective postural fixation and limb ataxia) on the
same side of the body. Fisher and Cole1 originally
speculated that the lesion might lie in either the
internal capsule or the corona radiata. Subsequent
pathologic analysis of three cases in 1978 demonstrated small infarcts in the basis pontis at the level
of the junction of the upper one third and the lower
two thirds of the contralateral pons.2 Reports of
additional cases of AHS using computed tomography (CT) have shown lesions in a variety of supratentorial and infratentorial locations, most commonly in the posterior limb of the internal capsule
and corona radiata.3-7 Since these observations
were made by CT alone, which may fail to demonstrate small nonhemorrhagic infarcts, their exact
correlation with AHS has been challenged.8-9 Kistler et al8 described a patient with AHS in whom a
CT scan showed a lesion in the corona radiata only,
while magnetic resonance imaging (MRI) revealed a
pontine lesion that appeared to better explain the
clinical findings. We describe a patient with AHS in
whom premorbid and postictal MRI scans indicated
recent infarction in the corona radiata.
Case Report
A 61-year-old right-handed woman with a history
of hypertension and noninsulin-dependent diabetes
mellitus presented to the Graduate Hospital emergency room after 4 days of right-sided weakness
and clumsiness. Her medical history included glauFrom the Department of Neurology, The University of Pennsylvania, Philadelphia, Pennsylvania.
Address for correspondence: David H. Gutmann, MD, PhD,
Department of Neurology, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104.
Received January 18, 1989; accepted March 13, 1989.

coma, but her visual fields were persistently normal. Vague complaints of dizziness 1 year prior to
admission prompted an MRI scan, which was normal. Four days before admission, the patient developed a staggering gait and clumsiness that progressed over the next 2 days to right-sided weakness,
incoordination, and a vague right-sided numbness.
On the day before admission, she experienced two
episodes of garbled speech lasting several minutes
and characterized by an inability to vocalize words
without an impairment in verbal speech comprehension. She denied diplopia or other visual disturbances, meningismus, nausea, or vomiting.
On admission, examination showed her to be
afebrile; her blood pressure was 138/70 mm Hg and
her pulse was 64/min. The general medical examination was remarkable only for a fourth heart sound
and a crescendo-decrescendo systolic murmur.
There were no carotid bruits, and her neck was
supple. She was alert, with normal cognition and
fluent speech. The cranial nerves were intact. Motor
examination showed 4/5 weakness of the right deltoid, triceps, and dorsal interossei. The sensory
examination revealed that she was intact to cold,
pin, vibration, graphesthesia, and stereognosis.
Defective postural fixation was demonstrated by
marked cerebellar-type ataxia with past-pointing on
finger-to-nose and heel-to-shin testing as well as an
abnormal Holmes rebound response of her right
arm. Limb ataxia was manifested by slow, inaccurate, and dysrhythmic rapid alternating and fine
movements of her right hand. She listed to the right
while standing, and her gait was mildly hemiparetic.
Deep tendon reflexes were brisker on the right side
in both the arm and the leg, and her right plantar
response was equivocal.
On the day of admission, a CT scan revealed a
nonenhancing hypodensity of the left corona radiata
that appeared as two adjacent lesions on an MRI
scan obtained 48 hours later (Figure 1). The MRI

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Stroke Vol 20, No 11, November 1989

FIGURE 1. Magnetic resonance images of patient with ataxic hemiparesis 1 year after normal scan. Two small lesions
are demonstrated in left corona radiata in axial plane (A). Coronal view (B) better delineates extent of these lesions. Both
images are T2-weighted (resonance time, 2400 msec; echo time, 80 msec) produced on 1.5-T General Electric Signa unit
(Milwaukee, Wisconsin) with spin-echo multisection imaging sequences.
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scan also showed a small lesion at the tip of the left
occipital lobe but no lesions in the brainstem.
Complete blood count was normal, erythrocyte
sedimentation rate was 18 mm/hr, and antinuclear
antibody titer was <\'-2. The rapid plasma reagin
test was positive at a titer of 1^8, and the fluorescent Treponema antibody test was positive. Cerebrospinal fluid examination revealed three leukocytes, a protein concentration of 52 mg/dl, a glucose
concentration of 114 mg/dl, and a nonreactive
VDRL. An echocardiogram was unremarkable,
while carotid Doppler ultrasound studies revealed a
50% stenosis in the left internal carotid artery. Over
the next 5 days, there was partial resolution of her
right hemiparesis and ataxia.
Discussion
Since Fisher's pathologic study,2 there have been
numerous descriptions of AHS in patients whose
CT scans demonstrated lesions in only the internal
capsule or corona radiata.3-5 However, the possibility of a concomitant pontine lesion could not be
excluded on the basis of these CT findings. Rothrock et al9 reviewed a series of cases of lacunar
strokes evaluated by MRI and reported one case of
AHS with two normal MRI scans that failed to
identify any lesions. Recently, Helwig et al10 reported
three cases of AHS studied by MRI. Lesions were
identified in the posterior limb of the internal cap-

sule, the midpons, and the red nucleus. None of
these lesions were apparent on CT scans.
In our patient, who presented with a right hemiparesis and homolateral cerebellar-type ataxia, the
initial CT scan demonstrated only a single left
corona radiata lesion. It was suspected, based on
the report of Kistler et al,8 that MRI would demonstrate a pontine lesion that was undetected on CT
scan. Despite this, MRI failed to demonstrate any
brainstem pathology and confirmed the presence of
the left corona radiata lesion. These results provide
strong support for the notion of Fisher and Cole1 (as
well as the findings of others) who described an
association between corona radiata lesions and AHS.
The significance of our patient's left occipital lesion
is unknown; Goldman perimeter examinations of
her visual fields have persistently been normal.
Lesions responsible for AHS have also been
reported in the rostral mesencephalon and thalamus.6-7'9 The "cerebellar" qualities of the limb
ataxia and postural fixation do not imply localization to the cerebellum, but rather imply that pathways affected in AHS are relatively preserved in
pure hemiparesis. To produce homolateral ataxia
and hemiparesis, it has been suggested that lesions
must interrupt the fibers connecting the ventrolateral nucleus of the thalamus with the precentral
cortex as they pass through the corona radiata and
internal capsule. Alternatively, a lesion could pro-

Gutmann and Scherer Ataxic Hemiparesis
duce AHS by disrupting the corticopontine fibers
descending from the precentral cortex through the
posterior capsular area to make connections in the
basis pontis.5
Acknowledgments

We thank Drs. Donald Silberberg and Michael
Kushner for their critical review of this manuscript.
References
1. Fisher CM, Cole M: Homolateral ataxia and crural paresis:
A vascular syndrome. J Neurol Neurosurg Psychiatry 1965;
28:48-55
2. Fisher CM: Ataxic hemiparesis: A pathologic study. Arch
Neurol 1978;35:126-128
3. Sage JI, Lepore FE: Ataxic hemiparesis from lesions of the
corona radiata. Arch Neurol 1983;40:449-450
4. Sanguineti I, Tredici G, Beghi E, Aiello U, Bogliun G,
DiLelio A, Tagliabue M: Ataxic hemiparesis syndrome:

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Clinical and CT study of 20 new cases and a review of the
literature. Italj Neurol Sci 1986;7:51-59
5. Iragui VJ, McCutchen CB: Capsular ataxic hemiparesis.
Arch Neurol 1982;39:528-529
6. Bendheim PE, Berg BO: Ataxic hemiparesis from a midbrain
lesion. Ann Neurol 1981;9:405-407
7. Murthy JMK: Ataxic hemiparesis—Ventrolateral nucleus of
the thalamus: Yet another site of lesion (letter). Stroke 1988;
19:122
8. Kistler JP, Buonanno FS, DeWitt LD, Davis KR, Brady TJ,
Fisher CM: Vertebral-basilar posterior cerebral territory
stroke—Delineation by proton nuclear resonance imaging.
Stroke 1984;15:417-426
9. Rothrock JF, Lyden PD, Hesselink JR, Brown JJ, Healy
ME: Brain magnetic resonance imaging in the evaluation of
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10. Helwig S, Larsson H, Henricksen O, Sorensen PS: Ataxic
hemiparesis: Three different locations of lesions studied by
MRI. Neurology 1988;38:1322-1324
KEY WORDS • ataxia • magnetic resonance imaging

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