Abstract
Objective: Cortical activity, including cognitive and emotional processes, may influence pupillary function. The exact pathways and the site of cortical pupillary innervation remain elusive, however. We investigated the effects of select cortical strokes, i.e. ischemic infarcts affecting the insular cortex and prefrontal eye field, on pupillary function.Methods: Seventy-four patients with acute ischemic stroke, consecutively admitted to our institution from March to July 2018, were assessed 24 h after endovascular recanalization therapy (i.e., day 2 after the stroke), using automated pupillometry. Stroke location and volume and clinical severity (estimated by the Alberta Stroke Program Early CT Score and National Institute of Health Stroke Scale) were recorded. We excluded patients with posterior circulation stroke, intracranial pathology other than ischemic stroke, midline shift on computed tomography exceeding 5 millimeters or a history of eye disease. Pupillometry data from 25 neurologically normal patients with acute myocardial infarction were acquired for control.Results: Fifty stroke patients after thrombectomy were included for analysis. Twenty-five patients (50%) had insular cortex or prefrontal eye field involvement (group 1, strategic infarcts); 25 patients had infarcts located in other cerebral areas (group 2, other infarcts). The pupillary light reflex, as measured by constriction velocity and maximal/minimal pupillary diameters, was within physiological limits in all patients, including controls. However, while pupillary size and constriction velocities were correlated in all subjects, the correlation of size and dilatation velocity was absent in right-hemispheric infarcts (left hemisphere infarcts, group 1 (r2 = 0.15, p = 0.04), group 2 (r2 = 0.41, p = 0.0007); right hemisphere infarcts, group 1 (r2 = 0.008, p = 0.69); group 2 (r2 = 0.12, p = 0.08); controls (r2 = 0.29, p ≤ 0.0001).Conclusions: Cortical infarcts of the prefrontal eye field or insula do not impair the pupillary light reflex in humans. However, subtle changes may occur when the pupils dilate back to baseline, probably due to autonomic dysfunction. Replication is needed to explore the possible influence of hemispheric lateralization. We suggest that endovascular therapy for acute ischemic stroke may serve as a clinical research model for the study of acquired cortical lesions in humans.
Highlights
The pupillary light reflex is a polysynaptic reflex that requires cranial nerves II and III, as well as central brainstem connections [1]
The human pupillary light reflex, as assessed by the speed of pupillary constriction and diameters before and after constriction, does not seem to be affected by strategic infarcts of the prefrontal eye field or insular cortex. This finding does not support the hypothesis of strategic strokes altering pupillary function, probably because the present model is a model of cortical lesioning as opposed to cortical activation
Patients with strategic infarcts had larger stroke volumes and more severe neurological deficits compared to patients without strategic infarcts, and, strokes producing mass effects were excluded, this may have influenced pupillary function either by accumulative neuronal loss or damage to still unidentified neuronal groups that may be important for pupillary function
Summary
The pupillary light reflex is a polysynaptic reflex that requires cranial nerves II and III, as well as central brainstem connections [1]. Light falling into one eye stimulates retinal photoreceptors, bipolar cells and subsequently retinal ganglion cells, whose axons form the optic nerve Some of these axons terminate in the pretectum of the mesencephalon; and pretectal neurons project further to the Edinger-Westphal nuclei. Via connections with the intermediate layer of the superior colliculus, the frontal eye field appears to be able to modulate pupillary diameters, resulting in pupillary dilation during cognitive processes [10]. Another gray matter region that may contribute to pupillary function is the insular cortex. The exact pathways of cortical modulation of human pupillary function remain elusive
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