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Appendix A. Supplementary material
Supplementary data associated with this article can be found, in
the online version, at doi:10.1016/j.jocn.2011.03.001.
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Rubenstein LJ, editors. Pathology of tumors of the central nervous system, 1st
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3. Love JG, Kernohan JW. Dermoid and epidermoidal tumors of the central
nervous system (cholesteatomas). JAMA 1936;107:1876–83.
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doi:10.1016/j.jocn.2010.12.055

Can subcortical infarction cause apraxia of eyelid opening?
Sang-Soo Lee ⇑, Hyung-Suk Lee
Department of Neurology, Chungbuk National University School of Medicine, 52 Naesudong-ro, Cheongju-si, Chungbuk 361-711, South Korea

a r t i c l e

i n f o

Article history:
Received 5 July 2010
Accepted 11 December 2010

a b s t r a c t
Apraxia of eyelid opening is the inability to voluntarily open the eyes in the absence of motor dysfunction
or blepharospasm. It has been described mostly in association with extrapyramidal diseases and only
rarely in cortical lesions. We report a right-handed woman with a right subcortical lesion due to borderzone infarction showing eyelid opening apraxia.

Keywords:
Borderzone infarction
Eyelid apraxia
Perfusion CT scans
Subcortical infarction

1. Introduction
Apraxia of eyelid opening (AEO) is a non-paralytic inability to
voluntarily open the eyes and the absence of orbicularis oculi contraction, despite frontalis muscle contraction, normal spontaneous
lid elevation, no ocular motor nerve dysfunction, no ocular sympathetic dysfunction and no ocular myopathy.1 This syndrome has
mostly been described in extrapyramidal diseases such as multiple
system atrophy, Parkinson’s disease, progressive supranuclear
palsy, blepharospasm and motor neuron disease. It has been less
frequently reported after bilateral or non-dominant hemisphere

⇑ Corresponding author. Tel.: +82 43 269 6336; fax: +82 43 275 7591.
E-mail address: sslee@chungbuk.ac.kr (S.-S. Lee).

Ó 2011 Elsevier Ltd. All rights reserved.

vascular lesions. Most of these reported vascular lesions were cortical infarctions in the territory of the middle cerebral artery
(MCA),2–4 AEO has rarely been reported with deep-seated vascular
lesions.5,6 We present a right-handed woman who developed AEO
after a right frontal subcortical lesion due to borderzone infarction.

2. Case report
A 76-year-old right-handed woman with no significant past
medical history woke up in the early morning with dysarthric
speech and left-sided weakness. She was alert and well oriented
with left-sided neglect. She had no evidence of orofacial or limb
apraxia. She had minimal left central facial weakness and left hemiparesis. The plantar response was flexor bilaterally. The pupils

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Case Reports / Journal of Clinical Neuroscience 18 (2011) 1399–1400

Fig. 1. (A) Day 1: axial diffusion-weighted MRI showing high signal intensity in the right frontal subcortical area; (B) day 3: CT scan showing low density in the same area;
and (C) day 1: perfusion CT scan showing an increase in the mean transit time in the right frontal lobe. This figure is available in colour at www.sciencedirect.com.

were 4 mm, symmetrical, and equally reactive. She had full extraocular movement, although she revealed right conjugate gaze preference. She could not open her eyes on command, despite frontalis
muscle contraction. Although she kept her eyes closed most of
time, she opened them spontaneously at times. There was no evidence of ptosis. Eye closure was normal. No involuntary contraction of the orbicularis oculi was seen. Diffusion-weighted MRI
and follow-up CT scans showed a deep right frontal subcortical
lesion consistent with an internal carotid artery borderzone
infarction (Fig. 1). There was no evidence of a basal ganglia lesion
on imaging studies. Magnetic resonance angiography revealed
occlusion in the distal main trunk of the right MCA and multifocal
luminal irregularities in the posterior cerebral and vertebral arteries. Her symptoms had disappeared completely 6 days after
infarction.

cardiac thrombus, the occlusion in the MCA was likely to be
atherosclerotic.
Two mechanisms could be suggested in our patient. The first is
that cortical dysfunction caused AEO, because she had hemineglect
and hypoperfusion in the frontal cortex as detected by perfusion CT
scan (Fig. 1), despite the internal borderzone infarction on CT scan
and diffusion-weighted MRI. This could result from a functional
frontal lobe lesion of greater magnitude than appears on anatomical imaging such as CT scans or MRI. The second mechanism might
be abnormal interruption of striatofrontal ganglionic connections
for supranuclear control of eyelid opening.
Our patient exhibited AEO without other ocular or lid abnormalities and radiographical examinations indicated unilateral right
hemispheric subcortical involvement. This case suggests that AEO
could be associated with subcortical lesions. Thus, clinicians confronted with acute AEO should consider a subcortical lesion as well
as focal cortical lesions.

3. Discussion
Acknowledgement
The transient eyelid opening difficulty in our patient is consistent with AEO. This syndrome has been described only rarely in
acute stroke lesions. However, AEO is an underestimated syndrome
that should be taken into consideration in clinical practice with the
frequent occurrence of MCA stroke. The precise neuroanatomical
lesion responsible for AEO is unclear. Dysfunctions in the basal
ganglia, rostral brainstem, or frontal lobe, especially the medial
frontal lobe, have been suggested.7 Supranuclear control of eyelid
opening seems to be so unequally distributed such that non-dominant hemisphere lesions are more common than dominant hemisphere lesions.2,3
As well as being associated with extrapyramidal diseases, AEO
has been described in bilateral or unilateral cortical dysfunction,
but very rarely in patients with deep-seated lesions.5,6 Our patient
is unique because she had a subcortical lesion due to a borderzone
infarction. Given the angiographical findings and the absence of
doi:10.1016/j.jocn.2010.12.055

The authors thank Dr. Earl Lee for the helpful review of the
manuscript.
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