Selective Saccadic Palsy After Cardiac Surgery

Kim, Eui–Jung; Oh, Sun-Young; Choi, Ha-Cheol; Shin, Byoung‐Soo; Seo, Man-Wook; Choi, Jong-Bum

doi:10.1097/wno.0b013e3181e08b20

Cited by 7 publications

(6 citation statements)

References 15 publications

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“…The syndrome of saccadic palsy following cardiac or aortic surgery is now well recognized, but its pathogenesis is poorly understood. The initial case of Hanson et al .…”

Section: Discussionmentioning

confidence: 99%

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Saccadic palsy following cardiac surgery: a review and new hypothesis

Eggers

Horn

Roeber

et al. 2015

Annals of the New York Academy of Sciences

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The ocular motor system provides several advantages for studying the brain, including well-defined populations of neurons that contribute to specific eye movements. Generation of rapid eye movements (saccades) depends on excitatory burst neurons (EBNs) and omnipause neurons (OPNs) within the brain stem; both types of cell are highly active. Experimental lesions of EBNs and OPNs cause slowing or complete loss of saccades. We report a patient who developed a permanent, selective saccadic palsy following cardiac surgery. When she died several years later, surprisingly, autopsy showed preservation of EBNs and OPNs. We therefore considered other mechanisms that could explain her saccadic palsy. Recent work has shown that both EBNs and OPNs are ensheathed by perineuronal nets (PNs), which are specialized extracellular matrix structures that may help stabilize synaptic contacts, promote local ion homeostasis, or play a protective role in certain highly active neurons. Here, we review the possibility that damage to PNs, rather than to the neurons they support, could lead to neuronal dysfunction—such as saccadic palsy. We also suggest how future studies could test this hypothesis, which may provide insights into the vulnerability of other active neurons in the nervous system that depend on PNs.

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“…The syndrome of saccadic palsy following cardiac or aortic surgery is now well recognized, but its pathogenesis is poorly understood. The initial case of Hanson et al .…”

Section: Discussionmentioning

confidence: 99%

“…A number of similar saccadic palsy cases have been reported without pathologic evaluation, most commonly in the setting of aortic valve or root surgery requiring cardiopulmonary bypass and hypothermic circulatory arrest. MRIs have failed to show evidence of brainstem infarcts.…”

Section: Casesmentioning

confidence: 99%

Saccadic palsy following cardiac surgery: a review and new hypothesis

Eggers

Horn

Roeber

et al. 2015

Annals of the New York Academy of Sciences

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“…The most common finding in patients with neurological deficits after cardiac surgery is selective horizontal and vertical saccadic palsy. 1 , 2 , 3 , 4 , 5 Two types of saccadic generator have been reported. First, premotor excitatory burst neurons (PBNs) in the paramedian pontine reticular formation at the level of the abducens nuclei generate horizontal saccades, while PBNs in the rostral interstitial nuclei of the medial longitudinal fasciculus of the midbrain produce vertical saccades.…”

Section: Discussionmentioning

confidence: 99%

“…There are few reports of patients who develop neurological deficits after cardiac surgery in the literature. 1 , 2 , 3 , 4 , 5 Although there are differences in the clinical manifestations of each case, most patients exhibit both horizontal and vertical saccadic palsy.…”

Section: Introductionmentioning

confidence: 99%

Saccadic Palsy after Cardiac Surgery: Serial Neuroimaging Findings during a 6-Year Follow-Up

et al. 2014

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BackgroundPatients who develop horizontal and vertical saccadic palsy after cardiac surgery have rarely been described. Although most such patients exhibit distinct neurological deficits, their brain MRI findings are almost normal. In addition, functional neuroimaging of such patients has never been reported.Case ReportA 43-year-old woman with dysarthria, dysphagia, and horizontal and vertical saccadic palsy after cardiac surgery was followed up for about 6 years; serial brain MRIs has been performed during this period, including susceptibility-weighted imaging (SWI) and [18F]-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET). Multiple microbleeds in the cerebral cortex, cerebellum, and brainstem, and glucose hypometabolism in the brainstem, cerebellum, and multiple cortical areas.ConclusionsTo the best of our knowledge, this is the first reported case of saccadic palsy after cardiac surgery with serial SWI and [18F]-FDG-PET performed to explore the possible cerebral lesions.

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“…Characteristic findings range from slow or hypometric saccades in both horizontal and vertical directions to complete saccade palsy [200, 201, 202]. Quick phases of both optokinetic and vestibular nystagmus are slow to absent [197, 203]. The pathophysiology is not well understood however, a likely mechanism is the selective loss of omnipause and premotor burst neurons in the paramedian pons with sparing of cerebral hemisphere and other parts of the neuraxis [200].…”

Section: Disorders Of Mid-brainmentioning

confidence: 99%

Basic and translational neuro-ophthalmology of visually guided saccades: disorders of velocity

Puri

Shaikh

2017

Expert Review of Ophthalmology

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Introduction: Saccades are rapid, yoked eye movements in an effort to direct a target over fovea. The complex circuitry of saccadic eye movements has been exhaustively described. As a result clinicians can elegantly localize the pathology if it falls on the neuraxis responsible for saccades. Traditionally saccades are studied with their quantitative characteristics such as amplitude, velocity, duration, direction, latency and accuracy. Areas covered: Amongst all subtypes, the physiology of the visually guided saccades is most extensively studied. Here we will review the basic and pertinent neuro-anatomy and physiology of visually guided saccade and then discuss common or classic disorders affecting the velocity of visually guided saccades. We will then discuss the basic mechanism for saccade slowing in these disorders. Expert commentary: Prompt appreciation of disorders of saccade velocity is critical to reach appropriate diagnosis. Disorders of midbrain, cerebellum, or basal ganglia can lead to prolonged transition time during gaze shift and decreased saccade velocity.

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Selective Saccadic Palsy After Cardiac Surgery

Cited by 7 publications

References 15 publications

Saccadic palsy following cardiac surgery: a review and new hypothesis

Saccadic palsy following cardiac surgery: a review and new hypothesis

Saccadic Palsy after Cardiac Surgery: Serial Neuroimaging Findings during a 6-Year Follow-Up

Basic and translational neuro-ophthalmology of visually guided saccades: disorders of velocity

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