Eyelid apraxia associated with subthalamic nucleus deep brain stimulation

Abstract

Eyelid apraxia, an inability to open the eyelid secondary to involuntary nonparalytic levator palpebrae inhibition, is thought to occur in up to 5% of patients with chronic subthalamic nucleus (STN) stimulation.1 Basal ganglia pathways have been linked to eyelid apraxia, as pallidal stimulation and pallidotomies have resulted in symptomatic improvement.2 Of note, both improvement in and initiation of eyelid apraxia have been reported with STN stimulation.3 However, the precise relationship between these structures/pathways and levator palpebrae inhibition has not been elucidated.4,5 As observed in our patient, bilateral eyelid apraxia during deep brain stimulation may be a result of electric current spread to pathways (including the dorsal trigeminothalamic tract) adjacent to the STN. This 62-year-old right-handed woman reported onset of symptoms approximately 10 years before when she began having difficulty walking. With l-dopa administration, improvements in her gait, stiffness, dyskinesias, and tremor were evident; however, she was later approved for bilateral deep brain stimulator placement as increased dosages were required for symptomatic control. On the date of surgery, she …