Asaccadia and Ataxia after Repair of Ascending Aortic Aneurysm

Antonio-Santos, Aileen A.; Eggenberger, Eric

doi:10.1080/08820530701193275

Cited by 9 publications

(8 citation statements)

References 11 publications

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“…Similar cases have been reported without neuropathologic evaluation [ 17 – 26 ], typically with aortic valve or root surgery requiring cardiopulmonary bypass and hypothermic circulatory arrest. MRIs have not shown brainstem infarcts.…”

Section: Introductionsupporting

confidence: 67%

Saccadic Palsy following Cardiac Surgery: Possible Role of Perineuronal Nets

et al. 2015

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ObjectivePerineuronal nets (PN) form a specialized extracellular matrix around certain highly active neurons within the central nervous system and may help to stabilize synaptic contacts, promote local ion homeostasis, or play a protective role. Within the ocular motor system, excitatory burst neurons and omnipause neurons are highly active cells that generate rapid eye movements – saccades; both groups of neurons contain the calcium-binding protein parvalbumin and are ensheathed by PN. Experimental lesions of excitatory burst neurons and omnipause neurons cause slowing or complete loss of saccades. Selective palsy of saccades in humans is reported following cardiac surgery, but such cases have shown normal brainstem neuroimaging, with only one clinicopathological study that demonstrated paramedian pontine infarction. Our objective was to test the hypothesis that lesions of PN surrounding these brainstem saccade-related neurons may cause saccadic palsy.MethodsTogether with four controls we studied the brain of a patient who had developed a permanent selective saccadic palsy following cardiac surgery and died several years later. Sections of formalin-fixed paraffin-embedded brainstem blocks were applied to double-immunoperoxidase staining of parvalbumin and three different components of PN. Triple immunofluorescence labeling for all PN components served as internal controls. Combined immunostaining of parvalbumin and synaptophysin revealed the presence of synapses.ResultsExcitatory burst neurons and omnipause neurons were preserved and still received synaptic input, but their surrounding PN showed severe loss or fragmentation.InterpretationOur findings support current models and experimental studies of the brainstem saccade-generating neurons and indicate that damage to PN may permanently impair the function of these neurons that the PN ensheathe. How a postulated hypoxic mechanism could selectively damage the PN remains unclear. We propose that the well-studied saccadic eye movement system provides an accessible model to evaluate the role of PN in health and disease.

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Section: Introductionsupporting

confidence: 67%

Saccadic Palsy following Cardiac Surgery: Possible Role of Perineuronal Nets

et al. 2015

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“…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 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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“…Vertical saccades may be affected in isolation, though both vertical and horizontal saccades are typically impaired. As in most cases (summarized in Table 1), our patients’ MRIs did not reveal a brainstem injury, likely because of insufficient imaging resolution 5. Importantly, one of our cases did have an occipital infarction as evidence of posterior circulation ischemia.…”

Section: Casesmentioning

confidence: 54%