Journal of Neurology, Neurosurgery, and Psychiatry 1997;63:391–393

391

SHORT REPORT

Central facial weakness due to medial medullary
infarction: the course of facial corticobulbar fibres

S Terao, S Takatsu, M Izumi, J Takagi, T Mitsuma, A Takahashi, A Takeda, G Sobue

Abstract
Two patients are reported with contralateral hemiparesis including a face of
supranuclear type, caused by an infarct of
the unilateral ventromedial part of the
upper medulla. Data from these patients
support the hypothesis that part of the
corticobulbar fibres supplying the lower
facial muscles descend ipsilaterally in the
ventromedial part of the upper medulla
and then, after decussation, ascend rostrally to the contralateral facial nucleus.
(J Neurol Neurosurg Psychiatry 1997;63:391–393)

Division of Neurology,
Fourth Department of
Internal Medicine,
Aichi Medical
University, Nagakute,
Aichi, Japan
S Terao
S Takatsu
M Izumi
J Takagi
T Mitsuma
Tokai Central Hospital,
Kakamigahara, Gifu,
Japan
A Takahashi
Department of
Neurology, Chubu
National Hospital,
Obu, Aichi, Japan
A Takeda
Department of
Neurology, Nagoya
University School of
Medicine, Nagoya,
Japan
G Sobue
Correspondence to:
Dr Shin-ichi Terao, Division
of Neurology, Fourth
Department of Internal
Medicine, Aichi Medical
University, Nagakute, Aichi
480–11, Japan.
Received 21 January 1997
and in revised form 25
March 1997
Accepted 27 March 1997

Keywords: facial nerve; corticobulbar tract; brain stem
infarction; magnetic resonance imaging

The anatomical distribution and the function
of human peripheral facial nerves are well
known, but little is known of the course of the
corticobulbar fibres that connect the motor
cortex with the facial nucleus.1–3 The facial corticobulbar fibres provide strongly unilateral
innervation to the contralateral lower facial
muscle and bilateral innervation to the upper
facial muscles.1–3 Classic symptomatic localisation postulates that lesions rostral to the upper
mid-pons result in contralateral facial weakness
of a central type, whereas ipsilateral facial
weakness of the peripheral type ensues from
lesions involving the inferolateral portion of the
pons.3 4 We report two patients in whom
contralateral lower facial weakness of central
type, in addition to contralateral hemiparesis of
the limbs, resulted from unilateral medial
medullary infarction.
Case reports
PATIENT 1

A 40 year old man presented to our hospital
with a weakness of the right limbs and
dysarthria which began while he was driving a
car five days previously. At the age of 30 he was
noted to have hypertension. On admission he
was alert, mildly obese, with a blood pressure
of 134/80 mm Hg and a regular heart rate of 70
beats/min. Neurologically, there were no abnormalities of eye movement or pupillary function, and the strength of the frontalis and

orbicularis oculi muscles was well preserved.
However, he had right lower facial weakness
and mild flattening of the right nasolabial fold.
There was weakness of the left half of the
tongue. Slight paralytic dysarthria was also
present, although dysgeusia, paresis of the soft
palate, sensory impairment of the face, hypoacousis, and dysphagia were absent. Right
hemiparesis with prominent weakness of the
arm was noted. Deep tendon reflexes were
exaggerated in the right limbs and Babinski’s
sign was present on the right side. Light touch
and vibratory sensation were slightly diminished in the right leg, whereas temperature and
pain sensation were well preserved. Transthoracic echocardiogram, ECG, and Holter monitoring findings were normal. Brain MRI
performed on day 10 after onset of disease disclosed a small area of infarction in the left ventromedial part of the upper medulla (fig 1A)
and no other lacunar infarctions of the deep
white matter. Cerebral angiography at 12 days
post-onset showed mild atherosclerotic
changes of the vertebrobasilar arteries and
non-visualisation of the anterior spinal artery.
The right vertebral artery exhibited hypoplastic
occlusion. Although the hemiparesis of the
right arm remained, the right facial weakness
and left tongue paralysis improved gradually
and resolved within one month of onset.
PATIENT 2

A 65 year old man was admitted to our hospital after the onset of weakness in his right leg
two days earlier, with consequent diYculty in
walking. He was noted to have diabetes
mellitus and hypertension two years previously,
and had been on an antihypertensive drug. On
admission he was alert and had a blood
pressure of 154/72 mm Hg with no arrhythmia.
Neurologically, there were no abnormalities of
eye movement or pupillary function. The
strength of the frontalis and orbicularis oculi
muscles was well preserved, but he had a right
lower facial weakness with mild flattening of
the right nasolabial fold and paralytic dysarthria. There was no paralysis of the tongue nor
other cranial nerve deficit. He exhibited a
severe right hemiparesis and hyperreflexia with
a Babinski’s sign. Sensory testing was normal
to all modalities. Transthoracic echocardio-

392

Terao, Takatsu, Izumi, Takagi, Mitsuma, Takahashi, et al

Figure 1 (A) Axial (left) and coronal (right) T2 weighted (5000/96, TR/TE) MRI of patient 1. A high signal intensity
area (arrow) is present in the left ventromedial part of the upper medulla. (B) Axial (left) and coronal (right) T2 weighted
(4000/96, TR/TE) MRI of patient 2. A high signal intensity area (arrow) is present in the left ventromedial part of the
upper medulla.

gram, ECG, and Holter monitoring findings
were all normal. Brain MRI performed 10 days
after onset showed an infarct of the left ventromedial part of the upper medulla (fig 1B) and
old multiple lacunar infarctions of the deep
white matter of the cerebral hemispheres. Two
weeks after onset MR angiography disclosed
atheromatous changes involving the left vertebrobasilar arteries, although no apparent stenosis or occlusion was found. The right hemiparesis remained two months after the onset,
yet the right facial weakness resolved within
three weeks.

Discussion
Although contralateral facial weakness is usually caused by lesions rostral to the facial
nucleus, it is important to realise that lesions
caudal to the facial nucleus can also cause contralateral facial weakness.
There have also been several reports of mild
facial weakness caused by medial medullary
infarction,5–11 but there were few details on the
responsible lesion. Currier6 hypothesised that
the corticobulbar fibres to the lower facial
nucleus leave the pyramid at the pontomedullary junction and descend caudally to at least

Central facial weakness due to medial medullary infarction: the course of facial corticobulbar fibres

393

give rise to right central facial weakness
because the corticobulbar fibres are aVected at
predecussation levels (fig 2A). On the other
hand, the lateral medullary infarction is likely
to result in ipsilateral central facial weakness
because the corticobulbar fibres are interrupted at postdecussation levels (fig 2B).
Therefore, it is suggested that part of the pathways of the facial corticobulbar fibres descend
ipsilaterally adjacent to the ventromedial part
of the corticospinal tract to the upper medulla
before decussating, and ascend contralaterally
in the dorsolateral part of the medulla to the
facial nucleus.
MRI allows a clear delineation of lesions of
the brain stem and spinal cord. It is hoped that
further neuroanatomical study will clarify in
detail the courses of central pathways including
the corticobulbar and corticospinal tracts.
This work was supported in part by a grant from the Aichi
Health Promotion Foundation and a grant from the Ministry of
Health and Welfare of Japan.

Figure 2 Schematic diagram of the pathways of the facial corticobulbar fibres. (A) (our
patients) and (B) (lateral medullary infarction) show aVected sites of the corticobulbar
fibres. CST represents corticospinal tract; CF represents facial corticobulbar fibres.

mid-medullary levels, and then most fibres
cross to the opposite facial nucleus. It has been
postulated that interruption of these fibres by
infarction at a predecussation level results in
the contralateral central facial weakness. There
have been some reports of facial weakness
resulting from a similar mechanism by medial
medullary infarction,7 8 12 13 although it has
been established pathologically that the facial
nucleus received such corticobulbar fibres.1 14
Recently, Cavazos et al10 reported a patient with
an infarction of the medullary pyramid with
pure motor hemiparesis including the lower
face. Based on the MRI findings, they hypothesised that some of the facial corticobulbar
fibres descend ipsilaterally, making a loop as
low as the upper medulla before decussating
and ascending to the contralateral facial
nucleus. We suggest that the findings in our
present patients serve to support Cavazos’s
description on the course of the facial corticobulbar fibres.
The absence of facial weakness in several
reported cases may be consistent with a more
caudal medullary lesion.12 15 16 On the other
hand, lateral medullary infarction relatively
often results in facial weakness on the side of
the lesion.14 17–20 It has also been postulated that
facial weakness on the side of the lesion results
from corticobulbar fibres being interrupted
while they ascend contralaterally after
decussating.13 17 20
We have proposed a scheme for the facial
corticobulbar fibres (fig 2). In our patients, left
ventromedial lesion of the upper medulla may

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