Ipsilateral Hemiplegia and
the Wallenberg Syndrome
Surjit K. Dhamoon, MD; Javaid Iqbal, MD; George H. Collins, MD
\s=b\ We documented the anatomic basis
for hemiplegia occurring on the same side
of the body as the lateral medullary infarction. Extension of the zone of ischemia
into the rostral spinal cord involves corti-$
cospinal fibers after they cross from the
opposite side.
(Arch Neurol 1984;41:179-180)

T^he occurrence of pyramidal tract
signs as part of the syndrome asso¬

ciated with lateral medullary infarc¬
tion is unusual.1 Autopsy studies of
most of these cases found that the
medullary pyramid ipsilateral to the
lateral medullary infarction was
involved.2 In some cases, however, the
pyramidal signs have been ipsilateral
to the medullary infarction.3"6 Most of
these cases have been clinical reports
without autopsy. In only one report
did pathologic studies verify that the
ischemie effect extended caudally into
the cervical spinal cord and that it
involved the corticospinal fibers cau¬
dal to the pyramidal decussation.6
Because of the rarity of such an occur¬
rence and the lack of complete photo¬
graphic documentation of this phe¬
nomenon, we present this case.
REPORT OF A CASE

78-year-old man with a history of
hypertension, diabetes, and angina was
admitted to the hospital with complaints
of nausea, vomiting, and hoarseness. Two
weeks prior to admission, he had begun to
A

Accepted for publication April 21, 1983.
From the Departments of Neurology (Drs

Dhamoon and Iqbal) and Pathology (Dr Collins),

State University of New York, Upstate Medical
Center, Syracuse.
Reprint requests to Department of Pathology,
Upstate Medical Center, 766 Irving Ave, Syracuse, NY 13210 (Dr Collins).

have a productive cough without fever or
chest pain. He was recovering from these
symptoms until the evening of his admis¬
sion, when nausea, vomiting, and hoarse¬
ness suddenly developed. He was unable to
get out of bed and was brought to the
emergency room.

On admission, his vital signs were nor¬
mal, but his BP was 190/100 mm Hg.
Extraocular movements were normal, and
his pupils were equal in size and were
reactive to light and accommodation. A
low-pitched bruit in the right carotid area
and a grade 2/6 systolic murmur in the
aortic area were heard. The neurologic
examination found that the patient was
verbal and responsive but drowsy. Cranial
nerves II, III, IV, and VI were intact. Facial
sensation and jaw mobility were not evalu¬

ated. A flattened nasolabial fold was noted
on the right side of the face. The patient
had no gag reflex bilaterally, and his voice
was hoarse. There was no tongue deviation,
but weakness of head turning to the left
was found. A right hemiparesis was
present with symmetric tendon reflexes
and a bilateral Babinski's sign. Sensory
(including hearing) and cerebellar func¬
tions could not be tested.
Findings from routine studies, including
blood chemistry and enzymes, were normal
except for a blood glucose level of 274
mg/dL. Chest roentgenogram showed mild
cardiomegaly and increased markings at
the base of the right lung. An ECG showed
left bundle-branch block and a normal
sinus rhythm. No mural thrombus was
found from M-mode and two-dimensional

echocardiography.
A neurologist found a right central
facial palsy and a dense right hemiplegia
(arm and leg weakness was equal). The
patient's speech was slightly slurred. A
deep left cerebral infarct was suggested,
but the computed tomographic scan was
normal. The patient's condition was stable
for two days. On the third hospital day,
respiratory arrest developed. He was intu¬
bated and resuscitated, but was found
without respiration or pulse on the 12th
day. He died the following day.

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General autopsy studies found athero¬
sclerosis of the coronary artery; a healed
infarct of the anterior wall of the left
ventricle; left ventricular hypertrophy (590
g); and nodular hemorrhagic areas of the
left lower lobe consistent with pulmonary
infarcts.
The formaldehyde-fixed brain weighed
1,140 g. On gross inspection, cerebral gyri
and sulci appeared normal in size and
configuration. Examination of the cerebral
vessels showed thrombosis and occlusion
of the terminal 3 cm of the right vertebral
artery that included the origin of the pos¬
terior inferior cerebellar artery (PICA), 1.5
cm from the vertebrobasilar junction (Fig
1, top). The left vertebral artery was scle¬
rotic, dilated, and patent. The basilar
artery was severely atherosclerotic. Arter¬
ies of the circle of Willis were also athero¬
sclerotic, with a 50% narrowing of the
Fig 1.—Top, Ventral aspect of brain stem and
cerebellum showing tortuous and thrombotic
right vertebral artery. Bottom, Cross section of
infarcted zone in right superolateral aspect of
medulla.

unusual features, including right
facial paresis, right sternocleidomastoid weakness, and right hemiplegia.
The right facial paresis, an occasional
occurrence in this syndrome,4 has
been explained by involvement of corticobulbar fibers coursing from the
pyramidal tract to the facial nucleus
through the rostral medulla.7 Involve¬
ment of sternocleidomastoid muscle
function implies caudal extension of
the infarction to the level of the 11th
cranial nerve, with an interruption of
its motor fibers within the neuraxis.
The right hemiplegia, which devel¬
oped from an initial right hemipare-

sis, indicates an evolution of the pri¬

Fig 2.—Infarct distribution in cross sections of high, middle, and low medulla (top left, top right,
and bottom left). Bottom right, Pale area of myelinated fiber loss affecting decussated fibers of
pyramidal tract on right side at level of junction of medulla and spinal cord (Klüver-Barrera
stain).
middle and anterior cerebral arteries. On
coronal sectioning, the lateral ventricles
appeared normal in size and shape. The
left cerebral hemispheric white matter had
a small (5X2 mm) cavity in the border
zone between the cortical and central cir¬
culation. A similar cavity, 2X2 mm, was
seen in the anterior limb of the right
internal capsule. Midbrain and pons sec¬
tions appeared normal. Coronal sections of
the medulla showed infarction in the right
lateral medullary region, but not in the
pyramids nor in the remaining paramedian tissue (Fig 1, bottom). Coronal sections
of the cerebellum appeared normal. In the
proximal and distal sections of the right
vertebral artery, severe atherosclerosis
and a recent thrombus were present with
early organization of the thrombus. A
right lateral medullary infarction was seen
in the rostral medulla (Fig 2, top left).
Pallor, necrosis, and hemorrhages were
seen that involved the nucleus and tract of

cranial nerve V, the ambiguous nucleus,
the solitary tract, the spinocerebellar and
spinothalamic tracts, and other structures
in this region (Fig 2, top left and right).
Paramedian structures were spared. In the
caudal medulla and medullocervical re¬
gion, the right lateral medullary infarct
persisted (Fig 2, bottom left and right).
The crossed pyramidal tract was affected
by the infarct immediately at the point of
decussation from the left pyramid to the
right lateral white columns in the rostral
cervical cord (Fig 2, bottom right).
COMMENT

Because the clinical information is

incomplete in our case, many of the
typical features of a lateral medullary
infarction are lacking. Nevertheless,
on clinical grounds alone, it is still
possible to identify the lateral medul¬
la as the target area despite some

mary process so as to involve either
the contralateral pyramid or the ipsi¬
lateral corticospinal tract after decus¬
sation of the pyramids. The pathologic
data clearly demonstrate involvement
of the ipsilateral corticospinal tract.
We probably cannot determine the
precise vascular mechanism responsi¬
ble for such an occurrence because of
the marked variability in the blood
supply to the affected areas.8 Howev¬
er, because of the restricted nature of
the infarct in this area, relative ische¬
mia was probably a causal factor. The
thrombosis in the vertebral artery
occluded the lateral medullary
branches, the PICA, and the anterior
spinal artery. The distribution of the
main body of the infarct can be
explained by a vertebral artery effect,
alone or in combination with the
PICA. There was no evidence of tissue
damage in the distribution of the
anterior spinal artery at the level of
the medulla, nor in the distribution of
the posterior spinal artery at the level
of the spinal cord. The area of spinal
cord that was involved, however, can
be regarded as a junctional zone
between the anterior and posterior
spinal artery and between the verte¬
bral and spinal artery supplies.911 We
can thereby identify a potential mech¬
anism for the occurrence of relative
ischemia in this area that may
account for this unusual extension of
the infarct into the spinal cord.

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