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Pure Motor Hemiplegia due to Infarction
of the Cerebral Peduncle
Khang-Loon Ho, MD
\s=b\ Pure motor hemiplegia caused by
lacunar infarction of the left cerebral
peduncle occurred in a 57-year-old hypertensive man. This case seems to fulfill the
postulate and expectation that a lesion
anywhere along the corticospinal pathway could result in pure motor hemiple-

gia.
(Arch Neurol 1982;39:524-526)

their initial report of 50 cases,
which included nine autopsies,
Fisher and Curry concluded that pure
motor hemiplegia resulted from lacu¬
nar infarctions in the internal capsule
or the basis pontis, probably because
of thrombotic occlusion of the small
penetrating vessels.1 Subsequent case
reports of pure motor hemiplegia
caused by lesions in the cerebral cor¬
tex,2 centrum semiovale,' and medul¬
lary pyramid45 have been described.
We describe a patient with pure motor
hemiplegia secondary to infarction of
the cerebral peduncle of the mid¬
brain.

Accepted for publication Aug 17, 1981.
From the Department of Pathology, Wayne
State University School of Medicine, Detroit. Dr
Ho is now with the Henry Ford Hospital,
Detroit.
Reprint requests to Department of Pathology,
Henry Ford Hospital, 2799 W Grand Blvd,
Detroit, MI 48202 (Dr Ho).

REPORT OF A CASE

A 57-year-old man was hospitalized in
1969 because of sudden weakness of the
right upper and lower extremities. There
was no impairment of consciousness, head¬
ache, convulsion, vertigo, diplopia, or par¬
esthesia. The history included hyperten¬
sion and coronary heart disease with a
mild myocardial infarction two years
before. He was alert and oriented and had
no mental impairment. The BP was 185/
100 mm Hg. All pulses were palpable and
symmetrical. The visual fields were intact.
The pupils were equal and reactive to light.
The extraocular movements were normal,
and there was no nystagmus. There was a
right-sided central facial weakness and
flattening of the right nasolabial fold.
There was no palatal or lingual weakness.
The patient had a right hemiplegia that
was equally severe in the leg and the arm.
The hémiplégie limbs were flaccid. The
muscle stretch reflexes were greater on the
right than on the left. Plantar response
was extensor on the right but flexor on the
left. Perceptions of pinprick, temperature,
light touch, vibration position, and stere-

ognosis were normal bilaterally. There was

no dysarthria or cerebellar ataxia. The
CSF was clear and contained no cells.
Protein concentration was 35 mg/dL, and
the glucose level was 110 mg/dL. The clini¬
cal impression was a left-sided capsular
infarction. His condition improved gradu¬
ally during the succeeding weeks. At the
time of discharge from the hospital, he was
able to walk with assistance and to carry
out discrete movement of the right arm.
His final admission in 1979, at the age of
67 years, was due to cirrhosis of the liver
with jaundice and ascites. He was moder¬
ately demented. The cranial nerve fune-

tions seemed to be intact. There was resid¬
ual paresis of the right leg and arm.
The right hemiparesis was spastic,
with increased reflexes and Babinski's
sign. He died of bilateral confluent bronchopneumonia ten years after the onset of

hemiplegia.

PATHOLOGIC FINDINGS

Necropsy showed moderately severe
atherosclerosis and an enlarged heart
with focal myocardial fibrosis in the
left ventricle. The atrophie brain
weighed 1,150 g, and the ventricular
system was moderately dilated. There
were several 2- to 4-mm lacunar
infarcts in the centrum semiovale, the
head of the caudate nucleus, putamen,
and both thalami. There were no lacu¬
nae in the internal capsules. In the
midbrain, the left cerebral peduncle
was shrunken and smaller than on the
right side.
There was an irregular, loose, col¬
lapsed, 3 X 3-mm lesion in the central
segment of the left cerebral peduncle
at the level of the oculomotor nerve
(Fig 1). The lesion was confined to the
midbrain and did not extend to the
internal capsule or to the upper pons.
Microscopically, the lesion was char¬
acteristic of a lacunar infarct; it con¬
tained debris of necrotic tissue, neuroglial fibers, reactive astrocytes, scat¬
tered macrophages, and hemosiderin
pigments (Fig 2). Several hyalinized
arterioles with stenotic lumens were
present in the astroglial tissue close to
the infarct (Fig 3). Similar hyalinized

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Fig 1.

Section of midbrain at level of oculomotor nerve showing small infarct confined to central

segment of left cerebral peduncle (hematoxylin-eosin, X3).
—

Fig 2.—Higher magnification of peduncular infarct showing cystic,
collapsed features. Fibers of oculomotor nerve are intact (hematox¬
ylin-eosin, X8).

vessels

were also present at the
periphery of the lacunar infarcts in
the basal ganglia. However, examina¬
tion of serial sections of the peduncu¬

lar infarct failed to demonstrate an
occluded vessel.
The medial and lateral segments of
the left cerebral peduncle were intact,
and there was no involvement of the
nucleus and fibers of the oculomotor
nerve, red nucleus, superior cerebellar
peduncle, or other tegmental struc¬
tures (Figs 1 and 2). The basis pontis
and the medullary pyramid on the left
side were atrophie, because of Wallerian degeneration of the corticospinal tracts (Fig 4). The cerebellum was

Fig 3. Several arterioles in astroglial tissue of peduncular infarct
showing hyalinosis of wall and narrowing of lumen (hematoxylineosin, X120).
—

unremarkable. The vessels of the cir¬
cle of Willis showed patchy areas of
atherosclerosis and narrowed lumina.
The rostral portion of the basilar
contained
atheromatous
artery
plaques; however, the lumen was

patent.
COMMENT

Fisher and

Curry1 defined pure
motor hemiplegia as a paralysis, com¬
plete or incomplete, of the face, arm,
and leg on one side unaccompanied by
sensory signs, visual field defect, dysphasia, or apractognosia. In the case
of brainstem lesions, the hemiplegia
will be free of vertigo, deafness, tinnì-

tus, diplopia, cerebellar ataxia, and

gross nystagmus. The clinical features

of our case were consistent with this
definition. The good recovery of motor
deficit in the right arm and leg years
after infarction was also in keeping
with the clinical course of pure motor

hemiplegia.1·67

Infarcts that are limited to the mid¬
brain are less common than those of
the pons or the medulla.89 To my
knowledge, there are few clinicopathologic studies of infarction of the cere¬
bral peduncle, and in most of these
cases, the lesion extended beyond the
peduncle to other tegmental struc¬
tures, resulting in various clinical

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References

1. Fisher CM, Curry HB: Pure motor hemiplegia of vascular origin. Arch Neurol 1965;13:30\x=req-\
44.
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motor hemiplegia due to cerebral cortical infarc-

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5. Ho KL, Meyer KR: The medial medullary
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8. Hiller F: The vascular syndromes of the

Fig 4. Section of medulla showing Wallerian degeneration of left pyramid (hematoxylineosin, X5).
—

appearances.912 In the present case,
the lacunar infarction of the midbrain
was approximately in the central seg¬
ment of the left cerebral peduncle,
where the corticospinal and corticobulbar tracts are located. To my
knowledge, the present case demon¬
strates for the first time that an
infarction confined to the cerebral
peduncle can produce the syndrome of
pure motor hemiplegia. This case
seems to fulfill the original postulate

and expectation of Fisher and Curry1
that a lesion anywhere along the cor¬
ticospinal pathway from the cortex to
the medullary pyramid could result in

pure motor hemiplegia.

Although it has been shown that
the cerebral peduncles are supplied by
branches from the basilar artery
bifurcation and the proximal posteri¬
or cerebral arteries,1315 there is dis¬
agreement about their actual angioarchitecture, as shown both by injection
techniques and by infarction after
vascular occlusion.1618 In the present
case, cerebral angiography was not
performed. The basilar artery at ne¬
cropsy was patent although athero¬
sclerotic, and available sections of the
midbrain failed to demonstrate an
occluded vessel. The presence of hya¬
linized vessels in the astroglial tissue
close to the infarct suggests that
thrombosis of a small penetrating
artery was the likely pathophysiologic
mechanism of the peduncular infarc¬
tion.1920 However, as Gillilan17 pointed
out, brainstem vascularization is so
variable that in localizing a brainstem

vascular syndrome clinically, it is far
better to identify the region involved
rather than the suspected named or
unnamed artery.
The lacunar state, as demonstrated
by Fisher and Curry,1 is closely linked
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atherosclerosis, and in all lacunar
states, death rarely follows a single
infarct. By the time the case comes to
autopsy, the brain is usually riddled
with multiple small infarcts.19·20 This
characteristic is also true of the
present case. The small lacunar
infarcts in the basal ganglia, thalami,
and central semiovale of our patient
were
probably asymptomatic. Al¬
though Fisher and Curry in their orig¬
inal article pointed out that, as a rule,
a pure motor hemiplegia is the prod¬
uct of small-vessel thrombosis and
other diagnoses need not be strongly
considered,1 other causes, such as epidural hematoma,21 cerebral cortical
infarct,2 brain abscess,3 intracerebral

hemorrhage,22 pontine hemorrhage,23

occlusion of the extracranial carotid
artery,24 demyelinating disorder,25 and
metastasis,25 have been reported in
recent years. In a computed tomo¬
graphic study of 33 patients with pure
motor hemiplegia, Weisberg25 found
that 14 patients had lesions other
than an infarct, but none were located
in the cerebral peduncle.
This study was supported in part by the
Research Corporation of Detroit Receiving Hos¬

pital.

Florence Rempala provided secretarial assis¬

tance.

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