Saccadic palsy following cardiac surgery: a review and new hypothesis

Eggers, Scott D.Z.; Horn, Anja K.E.; Roeber, Sigrun; Härtig, Wolfgang; Nair, Govind; Reich, Daniel S.; Leigh, R. John

doi:10.1111/nyas.12666

Cited by 9 publications

(7 citation statements)

References 41 publications

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“…As previously reported, gross inspection of the brain was unremarkable ( Fig 1B and 1C ) and was consistent with in vivo and ex vivo 7 tesla MRI studies [ 27 ]. Atherosclerotic plaques were noted at the bifurcation of the basilar into the posterior cerebral arteries.…”

Section: Resultssupporting

confidence: 90%

“…The whole brain was collected the day of death and fixed in 10% formalin for 2 weeks. Next, the brain was suspended in Fomblin (Solvay Solexis, West Deptford, NJ) for ex vivo 7 tesla MRI, as previously described [ 27 ]. After refixation in formalin, the brain was dissected, and the brainstem was cut transversely into several 2cm thick slices, which were embedded in paraffin.…”

Section: Methodsmentioning

confidence: 99%

“…Thus, the process causing selective saccadic palsy following cardiac surgery remains uncertain. Although ischemic damage to PBN and OPN remains possible, we recently studied one such patient in whom autopsy demonstrated preserved PBN and OPN [ 27 ]. Since experimental work has demonstrated that PN are vulnerable to ischemia [ 28 ], we investigated whether damage to brainstem saccadic network PN could account for her selective saccadic palsy.…”

Section: Introductionmentioning

confidence: 99%

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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: Resultssupporting

confidence: 90%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Saccadic Palsy following Cardiac Surgery: Possible Role of Perineuronal Nets

et al. 2015

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“…Ischemic injury is considered most likely, given the temporal relationship with cardiac surgery. A recent theory proposes injury to perineural nets that surround brainstem burst neurons ( 51 , 52 ).…”

Section: Differential Diagnosis Of Sgpmentioning

confidence: 99%

Clinical Approach to Supranuclear Brainstem Saccadic Gaze Palsies

2017

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Failure of brainstem supranuclear centers for saccadic eye movements results in the clinical presence of a brainstem-mediated supranuclear saccadic gaze palsy (SGP), which is manifested as slowing of saccades with or without range of motion limitation of eye movements and as loss of quick phases of optokinetic nystagmus. Limitation in the range of motion of eye movements is typically worse with saccades than with smooth pursuit and is overcome with vestibular–ocular reflexive eye movements. The differential diagnosis of SGPs is broad, although acute-onset SGP is most often from brainstem infarction and chronic vertical SGP is most commonly caused by the neurodegenerative condition progressive supranuclear palsy. In this review, we discuss the brainstem anatomy and physiology of the brainstem saccade-generating network; we discuss the clinical features of SGPs, with an emphasis on insights from quantitative ocular motor recordings; and we consider the broad differential diagnosis of SGPs.

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“…No neuroimaging abnormalities were identified. However, it has been proposed that the loss of cerebellar Purkinje cells [198] or perineuronal nets (PN) dysfunction, due to their vulnerability to ischemia, are responsible for the saccadic palsy [204, 205, 206]. It is postulated that the abnormality is likely to be due to a brainstem process that singles out the saccadic burst generation in pons and mesencephalon.…”

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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Saccadic palsy following cardiac surgery: a review and new hypothesis

Cited by 9 publications

References 41 publications

Saccadic Palsy following Cardiac Surgery: Possible Role of Perineuronal Nets

Saccadic Palsy following Cardiac Surgery: Possible Role of Perineuronal Nets

Clinical Approach to Supranuclear Brainstem Saccadic Gaze Palsies

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

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