OBSERVATION

Impaired Volitional Closure of the Left Eyelid
After Right Anterior Cerebral Artery Infarction
Apraxia Due to Interhemispheric Disconnection?
Thomas Korn, MD; Wolfgang Reith, MD; Georg Becker, MD†

Background: The inability of volitional unilateral eyelid closure is an uncommon symptom of a central nervous system disorder. When it occurs as the result of a
localized brain lesion, it is debated to be a form of supranuclear facial palsy or an apraxic phenomenon.
Objectives: To report and discuss a unilateral (leftsided) higher-order movement disorder of the facial periocular musculature bearing apraxic features.
Setting: University neurology department.
Patient: A 78-year-old right-handed man was admitted to the hospital with a left-sided brachiofacial hemiparesis of sudden onset. After thrombolysis with intravenous recombinant tissue-type plasminogen activator,
the hemiparesis, including the left-sided facial weakness, disappeared. Serial computed tomographic scans
showed that the patient was left with a stroke in the right

T

From the Departments of
Neurology (Drs Korn and
Becker) and Neuroradiology
(Dr Reith), Universität des
Saarlandes, Homburg/Saar,
Germany.
†Deceased.

anterior cerebral artery territory, affecting the frontal commissural fibers of the corpus callosum. There were no
signs of upper motor neuron facial paresis on the left side
when gesturing in a natural context. Eyelid closure was
complete during sleep. However, left eyelid closure and
elevation of the left eyebrow were not possible on verbal
command. In contrast, voluntary innervation of the perioral facial musculature was performed properly.
Conclusions: The voluntary-automatic dissociation of
our patient’s eyelid closure was suggestive of an apraxic
disorder. Disconnection from a praxis center caused by
callosal damage may be assumed to be the underlying
cause. The unilaterality of the symptom might imply that
in a bilaterally organized corticonuclear system such as
upper face innervation, it is the crossing fibers that are
primarily involved in praxis tasks.

Arch Neurol. 2004;61:273-275

HE CONCEPT OF APRAXIC DIS-

orders has essentially been
worked out on a phenomenologic basis regarding errors of limb usage.1 Ideational (or conceptual), ideomotor, and
limb-kinetic apraxia are common terms to
describe different deficits in limb praxis.
Ideational apraxia was considered as agnosia for tool usage2 or more general, as
loss of the space-time plan.3 The patient
does not know what to do. Lesions most
often found with this condition were left
parieto-occiptal or parietotemporal. In
ideomotor apraxia, the space-time plan is
intact but is disconnected from the innervating motor engram. The patient knows
what to do but not how to do it. Ideomotor apraxia is commonly associated with
lesions of left parietal association areas or
intrahemispheric white matter bundles.
Limb-kinetic apraxia is eventually due to
damage of innervating motor engrams and
usually observed contralaterally to the affected hemisphere. It is often described as

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273

a loss of dexterity in complex finger movements.
Callosal lesions may produce unilateral apraxia of the nondominant limb.
Apraxic deficits in callosal apraxia may reflect ideomotor apraxic features. In a report by Geschwind and Kaplan4 that refers to interhemispheric disconnection
syndromes, pantomiming with the left
hand was impaired on verbal command
whereas there was no problem with object use. In the present report, we describe a patient with impaired voluntary
eyelid closure on the left side. The patient’s facial motor deficits clearly bore features of a higher-order motor disorder.
REPORT OF A CASE

A 78-year-old right-handed man was admitted to the hospital because of acute leftsided hemiparesis. The man lived independently and had been well until 21⁄2
hours prior to admission, when he suddenly noticed tingling and weakness in his

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A

was unable to lift his left eyebrow when told to do so nor
could he keep it elevated when it had been lifted passively by the examiner. In contrast, the involuntary eyelid closure during sleep was not affected and neither was
the blink reflex. There was no impairment of automatic
gesticulation (smiling, laughing, or blinking) outside the
clinical test setting.
Control computed tomographic scans were performed 11 hours and 10 days after thrombolysis. They
revealed an ischemic stroke in the right anterior cerebral artery territory (Figure, C). In the digital subtraction arteriogram, the proximal internal carotid artery on
the right side was found to be occluded and had not become recanalized after the thrombolysis procedure,
whereas the distal part of the internal carotid artery and
the medial cerebral artery but not the anterior cerebral
artery on the right side were refilled via the ophthalmic
artery. Regarding the initial medial cerebral artery syndrome (left-sided brachiofacial hemiparesis), we therefore hypothesize that initially, the carotis bifurcation could
have been blocked by a thrombus whose medial cerebral artery “limb” might have been lysed successfully by
rtPA, leaving part of the anterior cerebral artery territory infarcted.

B

C

COMMENT

R

L

A 78-year-old man with an apraxic movement disorder that affected
selectively the upper portion of the left face (A and B). The causative lesion
was an ischemic stroke, damaging the right rostral part of the callosal
forceps (computed tomographic scan, C).

left arm. Eight years previously, he had to be treated with
bypass surgery because of coronary heart disease. Four
years before, a pacemaker was implanted because of atrioventricular blockage. His main cardiovascular risk factor was arterial hypertension.
At examination, the patient was alert and fully oriented, with fluent speech. He had a conjugated deviation of gaze to the right but no gaze palsy to the left. A
medium-grade paresis of the left-sided lower facial muscles
was evident. The other cranial nerve functions were preserved. The left-sided hemiparesis was high grade in the
arm and minor in the leg. The deep tendon reflexes of
the left arm were increased. The left plantar response was
extensor. The initial computed tomographic scan did not
show signs of an ischemic stroke but excluded hemorrhage. Magnetic resonance imaging was not possible since
the patient had a pacemaker.
A systemic thrombolysis with intravenous recombinant tissue-type plasminogen activator (rtPA) (1 mg/
kg) was performed. One day later, the patient exhibited
normal strength in his left arm and hand. However, it
turned out to be very difficult for him to voluntarily close
his left eye. While he could easily puff up his cheeks and
hold in the air, it was virtually impossible for him to close
his left eye on verbal command (Figure, A and B). He
(REPRINTED) ARCH NEUROL / VOL 61, FEB 2004
274

The impossibility of voluntary unilateral eyelid closure
due to a localized brain lesion was observed in our patient. Previous reports about the bilateral lack of volitional eyelid closure as a pseudobulbar phenomenon resulting from generalized or disseminated brain lesions
are abundant.5 The number of cases is getting rarer when
a localized lesion—especially in the right hemisphere—is supposed to be the underlying cause.6-8 Ghika
et al5 considered cortical damage and loss of association
fibers between supplementary motor regions and the premotor or primary motor areas responsible for the bilateral inability of 2 patients with ischemic lesions involving Brodmann areas 4 and 6 of the right parietal lobe to
close their eyes voluntarily. Disconnection between these
areas would lead to failure of volitional eyelid closure.
The failure would be bilateral since eyelid closure is supposed to be an axial movement with bilateral innervation. A systematic investigation of patients with lateralized brain lesions for (bilateral) face apraxia has recently
been conducted, illustrating that 46% of left-hemispheredamaged and 44% of right-hemisphere-damaged patients showed apraxic upper face movements.9
Here we describe a patient with a disorder of voluntary movement in the upper portion of the left face after right anterior cerebral artery stroke. The intact spontaneous facial gesturing revealed no evidence for left facial
weakness due to upper motor neuron damage. Also, a
supranuclear palsy of cranial nerve VII could hardly be
present on theoretical grounds since it is commonly true
for the innervation of the periocular and forehead musculature to be spared in contralateral stroke due to uncrossed innervation of the corresponding part of the facial nucleus. If ever there is some variability in the
organization of the corticonuclear pathway to the facial
nucleus, it is in the way that the motoneurons of the lower
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facial muscles (in addition to the upper ones) may receive bilateral corticonuclear input.10 Therefore, it is quite
unlikely that the impaired voluntary movement of the
left periocular muscles was due to right pyramidal (corticonuclear) tract damage.
Rather, we suggest that the lesion of the right limb
of the frontal callosal forceps (Figure, C) led to disconnection of the right hemispheric motor system from the
praxis center in the left hemisphere. The disconnection
from the left intraparietal cortex (intraparietal sulcus) or
the left dorsolateral frontal cortex is believed to be a substrate of ideomotor apraxia in right-handed subjects.11-13 The observed left-sided facial movement disorder was reminiscent of ideomotor apraxic features since
there was a clear dissociation between impaired voluntary closure of the left eyelid on verbal command and perfectly normal blinking and automatic eyelid closure in a
natural context. In our patient, the disturbance of voluntary gesturing was unilateral (confined to the left half
of the face). Given the commonly accepted truth that the
innervation of the upper face is bilateral with a contralateral predominance,14 we would like to hypothesize that
the predominance of the crossing corticonuclear fibers
is unmasked more clearly in volitionally evoked movements of the periocular musculature as compared with
reflex movements.
Nevertheless, we cannot exclude that the described phenomenon is the facial equivalent of a limbkinetic apraxia (loss of deftness), which may result from
right-sided damage to intrahemispheric premotor cortex connections, with subsequent alteration of motor engrams. However, a certain dominance of the left hemisphere has recently been shown.15 In contrast with the
present case, a voluntary-automatic dissociation of motor performance is usually not observed in limb-kinetic
apraxia. In addition, according to the bilateral projections of the upper facial corticonuclear tract neurons, we
would predict more prominent bilateral clinical signs if
the intrahemispheric motor engram for the movement
of the upper face was lesioned.
It has long been known that lesions of the callosal
splenium can make individuals lose the very concept of
skilled movements. This has been referred to as agnosia
for tool usage16 and is associated with disconnection from
the dominant posterior parietal lobe, whose projections
cross over in the splenium. Isolated defects of the callosal trunk result in poor performance of a particular motor act in response to a verbal command (ideomotor
apraxia).17 This type of apraxia is seen unilaterally in the
left hand when the anterior callosal trunk is lesioned
(“alien hand syndrome”).18,19
As a conclusion from this case, the hypothesis might
be raised that lesions involving the anterior parts of the
callosal body could selectively cause left-sided dyspraxia that presents as isolated higher-order disturbance of facial movement. In this sort of “disconnection
syndrome,” the preformed lateralization of the bilater-

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275

ally organized corticonuclear tract for upper face innervation may be unmasked.
Accepted for publication August 13, 2003.
Author contributions: Study concept and design (Drs
Korn and Becker); acquisition of data (Drs Korn, Reith,
and Becker); analysis and interpretation of data (Drs Korn,
Reith, and Becker); drafting of the manuscript (Drs Korn
and Becker); critical revision of the manuscript for important intellectual content (Drs Korn, Reith, and Becker); administrative, technical, and material support (Drs Korn,
Reith, and Becker); study supervision (Dr Becker).
This study was supported by the Universität des Saarlandes, Homburg/Saar, Germany.
During the review period, Dr Becker died in an accident. We are mourning for him.
Corresponding author: Thomas Korn, MD, Department of Neurology, Universität des Saarlandes, Kirrberger
Str, 66421 Homburg/Saar, Germany (e-mail:
netkor@uniklinik-saarland.de).
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