Abstract
Saccades function to bring targets of interest into the field of view. They are one of the four types of basic eye movements in humans, all of which are generated and modulated by components of a complex eye movement network, involving cortical eye fields, thalami, basal ganglia, cerebellum, and brainstem structures. Similarly, blinks are presumed to be generated by a blink center involving complex cortical and subcortical pathways. An association between saccades and blinks is well established; when these circuits are disrupted, normal saccadic parameters change. We report a case of a 48-year-old female who presented with fatigue and weakness. She had a complicated medical history, including drug-resistant epilepsy with subsequent vagus nerve stimulator (VNS) placement, right anterior temporal lobectomy, and craniotomy for a residual right temporal lobectomy and amygdalohippocampectomy. The latter was complicated by ischemic right middle cerebral artery (MCA) territory stroke with residual left hemiplegia. Her examination was unremarkable with regards to the presenting complaints, but one unique finding was observed; she demonstrated abnormal conjugate eye movements to the left associated with each blink. These eye movements continued to be present even after the patient’s ability to fixate on an object was removed. It was unclear how long this finding had been present. A review of her MRI of the brain from 10 months prior showed encephalomalacia and surrounding gliosis in the right MCA territory, right temporal laminar necrosis, right basal ganglia and parietal lobe microhemorrhages, ex vacuo dilatation of the right lateral ventricle, and a rightward midline shift. Saccadic abnormalities have been reported in a variety of conditions. The eye blink-associated saccades seen here are rare. To our knowledge, only one other patient has been reported with similar blink-associated eye movements after brain injury following a right MCA territory stroke. The exact mechanism underlying these eye movements is unclear, but may involve aberrant or disrupted neuronal signaling in cortical and/or basal ganglia components of the eye movement network, or related to an as yet unknown blink-saccadic regulatory mechanism.
Highlights
Saccades are rapid eye movements that function to bring targets of interest into a person’s field of view
She had a complicated medical history, including drug-resistant epilepsy with subsequent vagus nerve stimulator (VNS) placement, right anterior temporal lobectomy, and craniotomy for a residual right temporal lobectomy and amygdalohippocampectomy. The latter was complicated by ischemic right middle cerebral artery (MCA) territory stroke with residual left hemiplegia. Her examination was unremarkable with regards to the presenting complaints, but one unique finding was observed; she demonstrated abnormal conjugate eye movements to the left associated with each blink
Only one other patient has been reported with similar blink-associated eye movements after brain injury following a right MCA territory stroke
Summary
Saccades are rapid eye movements that function to bring targets of interest into a person’s field of view. One year later, at age 47, she underwent craniotomy for invasive EEG monitoring with subdural grid placement, followed by residual anterior-superior temporal lobectomy and frontal corticectomies Her hospital course was complicated by a perioperative ischemic stroke in the right MCA territory, with scattered foci of infarct in the right frontal lobe and right posterior parietal lobe seen on MRI (Figure 1). Review of her most recent MRI of the brain completed 10 months prior (eight months post-stroke) showed encephalomalacia and surrounding gliosis in the right MCA territory, including the right corona radiata, with right temporal laminar necrosis, microhemorrhages in the right basal ganglia and right parietal lobe, ex vacuo dilatation of the right lateral ventricle with Wallerian degeneration of the right cerebral peduncle, and interval development of a rightward midline shift secondary to the chronic right cerebral convexity volume loss (Figure 2). Images shown in two different planes each (A, inferior; B, superior; C, anterior; D, posterior)
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