Abstract Details

Title Eyelid Closure Apraxia: A Novel Presentation of Unilateral Striatocapsular Infarction

Topic Cerebrovascular Disease and Interventional Neurology

Presentation(s) P2 - Poster Session 2 (11:45 AM-12:45 PM)

Poster/Presentation
Number 4-021

Objective To describe a novel case of unilateral putaminal ischemic stroke presenting with contralateral eyelid closure apraxia.

Background Apraxia of eyelid closure (impaired voluntary eyelid closure with preserved blink reflex) typically localizes to the contralateral parietal cortex. In contrast, apraxia of eyelid opening is well-documented with subcortical lesions. While eyelid closure apraxia has been reported in degenerative diseases and bilateral subcortical pathology, it is not as well documented following unilateral striatocapsular infarction.

Design/Methods Single case report. Methods included neurologic examination, laboratory testing, and multimodal neuroimaging.

Results A 76-year-old right-handed male with atrial fibrillation on dabigatran presented with acute dysarthria and left hemiparesis. He was not a thrombolysis candidate due to anticoagulation and presentation beyond the time window. CT angiography revealed right MCA M1 branch occlusion with significant perfusion-diffusion mismatch. He underwent successful mechanical thrombectomy (TICI 2B). Post-procedure examination revealed left eyelid closure apraxia, left hemiparesis (upper extremity 0/5 distally, 3/5 proximally; lower extremity 4-/5 proximally and distally), and left tactile extinction. Brain MRI demonstrated right putaminal and corona radiata ischemic infarction without cortical involvement. At 72 hours post-thrombectomy, he showed partial recovery: distal upper extremity strength improved to 3/5, and he could partially close his eyelid on command with effort.

Conclusions To the best of our knowledge, this is the first report of eyelid closure apraxia from unilateral striatocapsular stroke. This expands our understanding of subcortical localization for traditional cortical signs. We hypothesize the clinical presentation reflected dual mechanisms: permanent injury to putaminal-corona radiata pathways and transient cortical hypoperfusion prior to recanalization. Without follow-up perfusion imaging, we cannot definitively distinguish this from standard penumbral recovery or diaschisis resolution. Nonetheless, this case highlights that eyelid closure apraxia can arise from isolated subcortical lesions and should be recognized as a rare but possible manifestation of striatocapsular infarction.

Authors/Disclosures
Zemen Abu, MD (Broward Health North Neurology department) PRESENTER	Dr. Abu has nothing to disclose.
Poojitha Koppu, MD	Poojitha Koppu has nothing to disclose.
Belinda Philip, MD	Dr. Philip has nothing to disclose.
Danisette Torres, MD (Florida Atlantic University)	Dr. Torres has nothing to disclose.
Damon Salzman, MD (Sunrise Medical Group)	Dr. Salzman has nothing to disclose.

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