tion. In most cases, transient ischemie
attacks, including transient monocu¬
lar blindness, or cerebrovascular acci¬
dents result.8·9 Occasionally, an oculosympathetic palsy associated with an
ipsilateral headache is the only clini¬
cal manifestation.10
In the cavernous sinus, the sixth
nerve lies adherent to the sheath of
the carotid artery on its medial side
and to the sinus wall on its lateral
side." The dorsal meningeal artery
arising from the meningohypophyseal
trunk sends a branch to the sixth
nerve. An expansion of the wall of the
intracavernous carotid could there¬
fore produce sixth-nerve dysfunction,
either by direct compression or by
interruption of its blood supply. Abad
et al7 demonstrated a traumatic intra¬
cavernous saccular aneurysm in this
location in a patient with a sixthnerve palsy and Horner's syndrome.
Other cranial-nerve palsies are
rarely associated with carotid artery
dissections. Paralysis of the tongue
secondary to compression of the hypo¬
glossal nerve at the base of the skull
has been noted on occasion.8 Our
patient complained of an unpleasant
taste that persisted for days. Dysgeu-

sia has been noted previously and
presumed to result from involvement
of the chorda tympani.8 We suggest
that a more likely cause is compres¬
sion of the glossopharyngeal nerve in
the neck as it passes forward between
the internal jugular vein and internal
carotid artery. Lane et al12 docu¬
mented by angiogram an aneurysm of
the internal carotid artery at the base
of the skull that produced palsies of
both hypoglossal and glossopharyn¬
geal nerves without perversion of taste.
An isolated cranial-nerve palsy may
be the only neurologic sign of an inter¬
nal carotid artery dissection. Dys¬
function of the cranial nerves travel¬
ing through the neck at the skull base
is most common. The sixth cranial
nerve can also be affected, because of
its anatomic relationship to the intra¬
cavernous carotid artery. Associated
hemicranial headache and signs of
Horner's syndrome may provide addi¬
tional diagnostic clues.

2. Rucker CW: The causes of paralysis of the
third, fourth and sixth cranial nerves. Am J
Ophthalmol 1966;61:1293-1298.
3. Rush JA, Younge BR: Paralysis of cranial
nerves III, IV, and VI: Cause and prognosis in
1,000 cases. Arch Ophthalmol 1981;99:76-79.
4. Madsen PH: Carotid-cavernous fistulae: A

study of 18 cases. Ada Ophthalmol 1970;48:731-

751.
5. Newton TH, Hoyt WF: Durai arteriovenous
shunts in the region of the cavernous sinus.

Neuroradiology 1970;1:71-81.
6. Trobe JD, Glaser JS, Post JD: Meningiomas

and aneurysms of the cavernous sinus. Arch

Ophthalmol 1979;96:457-467.

7. Abad JM, Alvarez F, Blazquez MG: An
unrecognized neurological syndrome: Sixthnerve palsy and Horner's syndrome due to trau¬
matic intracavernous carotid aneurysm. Surg

Neurol 1981;16:140-144.
8. Fisher CM, Ojemann RG, Roberson GH:
Spontaneous dissection of cervico-cerebral arter¬
ies. Can J Neurol Sci 1978;5:9-19.
9. Ehrenfeld WK, Wylie EJ: Spontaneous dis¬
section of the internal carotid artery. Arch Surg

1976;111:1294-1301.
10. Mokri B, Sundt TM, Houser OW: Spontane¬
ous internal carotid dissection, hemicrania, and
Horner's syndrome. Arch Neurol 1979;36:677-

680.

Anatomy of the
microsurgical study. J Neuro¬

11. Harris FS, Rhoton AL:
cavernous sinus: A

surg 1976;45:169-180.

References
1. Shrader EC, Schlezinger NS: Neuro-ophthalmologic evaluation of abducens nerve paraly¬

sis. Arch Ophthalmol 1960;63:84-91.

12. Lane RJ, Weisman RA, Savino PJ, et al:
Aneurysm of the internal carotid artery at the

base of the skull: An unusual cause of cranial
neuropathies. Otolaryngol Head Neck Surg

1980;88:230-232.

Ataxic Hemiparesis From
Lesions of the Corona Radiata
Jacob I. Sage, MD, Frederick E. Lepore, MD

• Ipsilateral cerebellar and pyramidal
signs suddenly developed in three
patients. Computed tomography revealed

signs in the limbs are more prominent
than pyramidal signs, and dysarthria
is described in many of the published

small infarcts of the corona radiata in two
patients and a small infarct in the posteri¬
or limb of the internal capsule in the third.
Ataxic hemiparesis can result from
lesions of the corona radiata as well as
many other points along the corticopontine pathways.
(Arch Neurol 1983;40:449-450)

reports.2·6
In 1965, Fisher and Cole2 argued

taxic hemiparesis is a syndrome in
which cerebellar and pyramidal
signs occur ipsilaterally.1 Cerebellar
Accepted for publication Jan 6, 1983.
From the Department of Neurology, Universi¬
ty of Medicine and Dentistry of New Jersey,
Rutgers Medical School, New Brunswick.
Reprint requests to Department of Neurology,
UMDNJ/Rutgers Medical School, Academic
Health Science Center, CN 19, New Brunswick,
NJ 08903 (Dr Sage).

that the responsible lesion was lo¬
cated in the region of the internal
capsule or corona radiata. They could
not confirm this hypothesis, as the
one autopsied patient in their series
had multiple lesions. In 1978, Fisher4
described three more patients with
ataxic hemiparesis, each of whom had
an infarct in the contralateral pons.
Since then, more patients with ataxic
hemiparesis have been described, with
tumors, infarcts, and hemorrhages
located in the pons, midbrain, and
internal capsule.710
We report three cases of ataxic
hemiparesis, two with lesions in the
corona radiata, supporting Fisher and
Cole's original hypothesis, and one

Downloaded From: http://archneur.jamanetwork.com/ by a Oakland University User on 06/02/2015

with a lesion in the posterior limb of
the internal capsule. All three
patients showed the characteristic
changes of infarction on computed

tomographic (CT) scans.

REPORT OF CASES

Case 1.—A 78-year-old, right-handed,
hypertensive woman was visiting the hos¬
pital when she experienced the sudden
onset of unsteadiness and slurred speech.
She was able to sit down without falling.

On her arrival in the emergency room ten
minutes later, she was alert, oriented, and
not aphasie. Her BP was 204/90 mm Hg.
She was dysarthric and had mild weakness
of the right lower part of the face, a
pronator drift of the right arm, and slight
weakness of the right leg. The muscle
stretch reflexes were symmetrical, but a
right Babinski sign was present. The fin¬
ger-nose and heel-knee-shin tests revealed
a marked dysmetria. The patient was
unable to stand without aid. A CT scan

1. Fisher CM: Lacunar strokes and infarcts: A
review. Neurology 1982;32:871-876.
2. Fisher CM, Cole M: Homolateral ataxia and
crural paresis: A vascular syndrome. J Neurol

Neurosurg Psychiatry 1965;28:48-55.

3. Fisher CM: A lacunar stroke: The dysarthria-clumsy hand syndrome. Neurology 1967;
17:614-617.
4. Fisher CM: Ataxic hemiparesis: A patholog¬
ic study. Arch Neurol 1978;35:126-128.
5. Iragui VJ, McCutchen CB: Capsular ataxic
hemiparesis. Arch Neurol 1982;39:528-529.
6. Perman GP, Racy A: Homolateral ataxia
and crural paresis: Case report. Neurology

1980;30:1013-1015.
7. Bendheim PE, Berg BO: Ataxic hemiparesis
from a midbrain mass. Ann Neurol 1981;9:405-

407.
8. Ichikawa K, Tsutsumishita AS, Fujioka A:
Capsular ataxic hemiparesis. Arch Neurol 1982;
39:585-586.
9. Sakai T, Murakami S, Ito : Ataxic hemi¬
paresis with trigeminal weakness. Neurology
1.—Contrast-enhanced computed tomo¬
Fig1981;31:635-636.
10. Tuhrim S, Yang(arrows)
WC, Rubinowitz
H, et al:
in left corona
gram shows infarct
and the dysarhemorrhage
pontine
Primary
near
radiata
anterior
horn of lateral ventricle.
thria-clumsy hand syndrome. Neurology 1982;
32:1027-1028.
11. Carpenter MB: Human Neuroanatomy.
& Wilkins Co, 1976,
Baltimore,
chap
done
one hour was normal.
withinWilliams
During
10.
the next four days, she became lethargic,

and her hemiparesis worsened. By the sev¬
enth hospital day, she had recovered to the
point that her neurologic status was the
same as it had been on admission. The CT
scan at that time revealed an infarct in the
left corona radiata near the anterior horn
of the lateral ventricle (Fig 1).
Case 2.—A 67-year-old, right-handed,
hypertensive man was at work when he
suddenly began to fall toward the left. He
managed to get home and remained there
for the next three days. When improve¬
ment did not occur, he came to the emer¬
gency room. He was alert and oriented on
arrival. His BP was 170/104 mm Hg. He
had no dysarthria, but a mild weakness of
the left lower part of the face was noted,
along with a mild pronator drift of the left
arm and weakness of the left leg. The
muscle stretch reflexes were symmetrical,
but a left Babinski sign was present. The
finger-nose and heel-knee-shin tests
revealed a marked dysmetria.The patient
was able to walk with assistance. A CT
scan performed on the sixth day revealed
an infarct in the right corona radiata near
the posterior horn of the lateral ventricle

(Fig 2).

Case 3.—A 61-year-old, right-handed,
hypertensive woman found that she kept
falling to the right when she tried to get
out of bed one morning. She had stopped
taking her antihypertensive medications

three weeks earlier. When seen in the
emergency room that day, her BP was
200/120 mm Hg. She was alert, oriented,
and not aphasie. A mild weakness of the
right lower part of the face was noted. In
the opinion of her family, her speech was
slightly slurred. There was a mild pronator
drift of the right arm but no detectable leg
weakness. Muscle stretch reflexes were
symmetrical, but a right Babinski sign was
present. The finger-nose and heel-kneeshin tests showed a marked dysmetria. The
patient was ataxic but able to walk with
assistance. A CT scan performed on the

Fig 2.—Contrast-enhanced computed tomo¬
(arrow) in right corona
radiata near posterior horn of lateral ventri¬

gram shows infarct

Fig 3.—Unenhanced computed tomogram
reveals infarct (arrow) in posterior limb of left
internal capsule.

cle.

fourth day revealed an infarct in the poste¬
rior limb of the left internal capsule

(Fig 3).

COMMENT

The clinical features in each of our
three patients were similar to those in
previously described cases of ataxic
hemiparesis. Pyramidal and cerebel¬
lar signs were present on the same
side. Evidence of corticospinal dys¬
function consisted of a mild arm drift,
minimal weakness of the lower part of
the face and the leg, and a Babinski
sign on the involved side. In no case
could the weakness explain the severe
degree of limb incoordination and gait
ataxia, which was indistinguishable
from that found in cerebellar disease.
Gait ataxia was severe enough to pre¬
vent any of the patients from walking
without assistance. Two patients had
some dysarthria, and one had normal

speech.

These cases support the view that
ataxia from supratentorial lesions is
the result of interrupting corticopontocerebellar fibers. Patient 1 had an
infarct of the anterior corona radiata.
Such a lesion presumably interrupts
fibers arising from the prefrontal and
precentrai areas, which go on to form
the frontopontine tract (Arnold's bun¬
dle).11 Patient 2 had an infarct in the
posterior part of the corona radiata
near the posterior horn of the lateral
ventricle. A lesion so located inter¬
rupts fibers from the occipital and
parietal lobes, whose fibers, together
with those of the temporal lobe, join
to form Tiirck's bundle in the retrolenticular and sublenticular capsule.11
Patient 3 had an infarction of the
posterior limb of the internal capsule,

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which, again, interrupts fibers from

the precentrai cortex and has been
described by others.5·68 These three
cases confirm the idea that ataxia
with ipsilateral pyramidal signs, even
in the presence of dysarthria and
severe gait disturbance, does not

always mean a pontine lesion as was
suggested recently.1 The cases re¬
ported herein, together with previous¬
ly well-documented cases of midbrain
and pontine lesions, provide convinc¬
ing evidence that ataxic hemiparesis
can result from lesions at many points
along the corticopontine pathways,

from the corona radiata to the mid¬
pons.
References

1. Fisher CM: Lacunar strokes and infarcts: A
review. Neurology 1982;32:871-876.
2. Fisher CM, Cole M: Homolateral ataxia and
crural paresis: A vascular syndrome. J Neurol

Neurosurg Psychiatry 1965;28:48-55.

3. Fisher CM: A lacunar stroke: The dysarthria-clumsy hand syndrome. Neurology 1967;
17:614-617.
4. Fisher CM: Ataxic hemiparesis: A patholog¬
ic study. Arch Neurol 1978;35:126-128.
5. Iragui VJ, McCutchen CB: Capsular ataxic
hemiparesis. Arch Neurol 1982;39:528-529.
6. Perman GP, Racy A: Homolateral ataxia
and crural paresis: Case report. Neurology

1980;30:1013-1015.
7. Bendheim PE, Berg BO: Ataxic hemiparesis
from a midbrain mass. Ann Neurol 1981;9:405407.
8. Ichikawa K, Tsutsumishita AS, Fujioka A:
Capsular ataxic hemiparesis. Arch Neurol 1982;
39:585-586.
9. Sakai T, Murakami S, Ito : Ataxic hemi¬
paresis with trigeminal weakness. Neurology

1981;31:635-636.
10. Tuhrim S, Yang WC, Rubinowitz H, et al:
Primary pontine hemorrhage and the dysarthria-clumsy hand syndrome. Neurology 1982;

32:1027-1028.
11. Carpenter MB: Human Neuroanatomy.
Baltimore, Williams & Wilkins Co, 1976, chap
10.