A 76-year-old woman was admitted to our emergency department for acute development of vertigo, followed by loss of consciousness. Brain MRI revealed a bilateral paramedian thalamo-mesencephalic infarction due to basilar artery occlusion (Figure). The patient underwent systemic thrombolysis and mechanical thrombectomy, with complete reperfusion of the basilar artery. After the procedure, the patient was alert and oriented, and her examination demonstrated apraxia of eyelid opening (ALO) and vertical-gaze palsy (Video 1). ALO is considered a form of eyelid dystonia. Previous electromyographic studies on affected patients demonstrated either involuntary levator-palpebrae inhibition or pretarsal orbicularis-oculi muscle motor persistence.1 Its neuroanatomic bases are still unknown, but there is evidence that this condition is linked to disorders of the basal ganglia, rostral midbrain, and frontal lobes.1 Myint et al.2 reported a case of ALO in isolated bilateral thalamic infarction, suggesting that the paramedian thalamic nuclei may have a role in the voluntary eyelid movements network.
Figure. Patient's Neuroimaging.
Brain MRI showing a bilateral paramedian thalamic (A) and mesencephalic (B) infarction in fluid-attenuated inversion recovery sequences. Digital subtraction angiography showing an occlusion of the top of the basilar artery (arrow, C).
Patient's neurological examination. [00:02]: the patient cannot open her eyes when required by the operator. Note the bilateral contraction of the frontalis muscle on attempted eye opening; [00:05]: the patient is able to perform other voluntary movements (i.e., mouth opening and closure, tongue protrusion and lateral movements) on request; [00:32]: the ability to keep the eyes open after forced opening exclude the presence of bilateral ptosis; [00:42]: the absence of spasms of the orbicularis oculi muscle and triggers prompting eye closure differentiate apraxia of eyelid opening from blepharospasm; [00:52]: the operator asks to follow his finger. Note the presence of mild ptosis and rectus medialis muscle deficit in the left eye, consistent with lesion localized in the left paramedian midbrain; [01:08]: note the presence of vertical gaze palsy, consistent with midbrain lesion.Download Supplementary Video 1 (18.2MB, mov) via http://dx.doi.org/10.1212/206799_Video_1
Acknowledgment
The authors would like to thank the patient and family for permission to share this case report.
Appendix. Authors
Footnotes
Teaching slides http://links.lww.com/WNL/C582
Study Funding
No targeted funding reported.
Disclosure
The authors report no disclosures relevant to the manuscript. Go to Neurology.org/N for full disclosures.
References
- 1.Boghen D. Apraxia of lid opening: a review. Neurology. 1997;48(6):1491-1494. doi: 10.1212/wnl.48.6.1491. [DOI] [PubMed] [Google Scholar]
- 2.Myint PK, Anderson KN, Antoun NM, Warburton EA. Eyelid apraxia associated with bilateral paramedian thalamic infarct. Age Ageing. 2008;37(3):343-344. doi: 10.1093/ageing/afn016. [DOI] [PubMed] [Google Scholar]
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Supplementary Materials
Patient's neurological examination. [00:02]: the patient cannot open her eyes when required by the operator. Note the bilateral contraction of the frontalis muscle on attempted eye opening; [00:05]: the patient is able to perform other voluntary movements (i.e., mouth opening and closure, tongue protrusion and lateral movements) on request; [00:32]: the ability to keep the eyes open after forced opening exclude the presence of bilateral ptosis; [00:42]: the absence of spasms of the orbicularis oculi muscle and triggers prompting eye closure differentiate apraxia of eyelid opening from blepharospasm; [00:52]: the operator asks to follow his finger. Note the presence of mild ptosis and rectus medialis muscle deficit in the left eye, consistent with lesion localized in the left paramedian midbrain; [01:08]: note the presence of vertical gaze palsy, consistent with midbrain lesion.Download Supplementary Video 1 (18.2MB, mov) via http://dx.doi.org/10.1212/206799_Video_1