Spontaneous Pulsation of the Retinal Veins

Levine, David N.

doi:10.1006/mvre.1998.2098

Cited by 53 publications

(47 citation statements)

References 14 publications

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“…A downstream modulation of the outflow resistance by the IOP has indeed been postulated, mediated, e.g., by IOP evoked deformation of the lamina cribrosa. 23 This is not supported by the observed correlation between the retrobulbar velocity and IOP waveforms. 53 This correlation suggested to those authors a dependence of the velocity over the IOP, and that outflow resistance remains constant throughout the pulse cycle in the subject shown.…”

Section: Type 1: Venous Pulsations As Windkessel Waveforms?contrasting

confidence: 49%

“…Since SVP was first observed, it has been reported that a collapse, partial or total, coincides with the systole. 20, 21 Several hypotheses have been proposed based on this observation: (1) blood volume pulsation induces intraocular pressure (IOP) pulsation, occasionally overcoming intralumi-nal venous pressure and thus collapsing veins, 21 (2) increased blood velocity during the systole induces intraluminal pressure reduction through the Venturi effect, leading to collapse, 22 (3) venous flow is constant while the IOP/ICP pressure-gradient pulsates, leading to translaminar pressure pulsation inducing collapse, 23 and (4) pulsation is a self-excited oscillation as observed in collapsible tube, modelocking on external periodic pressure fluctuations when present. 24 The latter hypothesis does not require IOP or ICP pulsation: SVP occurs just because of the IOP/ICP pressure gradient.…”

Section: Introductionmentioning

confidence: 99%

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Quantitative Analysis of Fundus-Image Sequences Reveals Phase of Spontaneous Venous Pulsations

Moret

Reiff

Lagrèze

et al. 2015

Trans. Vis. Sci. Tech.

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Purpose: Spontaneous venous pulsation correlates negatively with elevated intracranial pressure and papilledema, and it relates to glaucoma. Yet, its etiology remains unclear. A key element to elucidate its underlying mechanism is the time at which collapse occurs with respect to the heart cycle, but previous reports are contradictory. We assessed this question in healthy subjects using quantitative measurements of both vein diameters and artery lateral displacements; the latter being used as the marker of the ocular systole time.Methods: We recorded 5-second fundus sequences with a near-infrared scanning laser ophthalmoscope in 12 young healthy subjects. The image sequences were coregistered, cleaned from microsaccades, and filtered via a principal component analysis to remove nonpulsatile dynamic features. Time courses of arterial lateral displacement and of diameter at sites of spontaneous venous pulsation or proximal to the disk were retrieved from those image sequences and compared.Results: Four subjects displayed both arterial and venous pulsatile waveforms. On those, we observed venous diameter waveforms differing markedly among the subjects, ranging from a waveform matching the typical intraocular pressure waveform to a close replica of the arterial waveform. Conclusions:The heterogeneity in waveforms and arteriovenous phases suggests that the mechanism governing the venous outflow resistance differs among healthy subjects.Translational relevance: Further characterizations are necessary to understand the heterogeneous mechanisms governing the venous outflow resistance as this resistance is altered in glaucoma and is instrumental when monitoring intracranial hypertension based on fundus observations.

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Section: Type 1: Venous Pulsations As Windkessel Waveforms?contrasting

confidence: 49%

Section: Introductionmentioning

confidence: 99%

Quantitative Analysis of Fundus-Image Sequences Reveals Phase of Spontaneous Venous Pulsations

Moret

Reiff

Lagrèze

et al. 2015

Trans. Vis. Sci. Tech.

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“…When CSF pulse pressure equals retinal venous pulse pressure, the SVP is extinguished. 3 The absence of SVP, however, is not solely associated with raised ICP. SVP is reported to occur in 90% of healthy individuals and therefore is absent in 10%.…”

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confidence: 99%

“…The pulse is only manifest at the distal vein over the optic disc since, due to the inherent resistance to fluid flow within the retinal venous system (to which the viscosity of blood is a contributory factor), the pressure difference between intraocular and extraocular veins is only transmitted a short distance into the eye. 3 The outflow theory better explains the etiology of SVP than the classic theory, which suggests that the vein collapses in response to the ocular arterial pulse. In fact, this should not occur since the retinal venous pressure is consistently higher than intraocular pressure throughout the cardiac cycle.…”

mentioning

confidence: 99%

“…1 Since the variation of intraocular venous pressure between systole and diastole (the ocular pulse pressure) is greater than the CSF pulse pressure, the velocity of venous outflow from the eye increases during systole and decreases during diastole. 3 This leads to the systolic collapse of the retinal vein as it exits the eye characteristic of SVP. The pulse is only manifest at the distal vein over the optic disc since, due to the inherent resistance to fluid flow within the retinal venous system (to which the viscosity of blood is a contributory factor), the pressure difference between intraocular and extraocular veins is only transmitted a short distance into the eye.…”

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confidence: 99%

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Pearls & Oy-sters: Spontaneous venous pulsation and its role in differentiating papilledema from pseudopapilledema

Lascaratos

Ahmed²,

Madill³

2010

Neurology

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Spontaneous venous pulsation (SVP) of the optic disc can be used as a surrogate marker of intracranial pressure (ICP) in patients with discs of normal morphology. The presence of SVP can suggest an ICP within normal limits.1 Based on this premise, SVP is also referred to when differentiating anomalous pseudopapilledematous optic nerves from true papilledema. However, this application may be limited by the fact that anomalous discs are less likely to demonstrate SVP.2 The case detailed below supports this contention.CASE REPORT A 48-year-old white woman presented to our hospital complaining of a recent onset of blurred vision. She was known to have migraine with aura and had a past ocular history of unilateral disc drusen (left eye only). On examination, the bestcorrected visual acuity was 0.7 in the right and 0.5 in the left. Anterior segment examination was unremarkable in both eyes. Color vision was normal in the right and slightly reduced in the left (10/13 Ishihara) and there was a left relative afferent pupillary defect. Funduscopy revealed left optic nerve drusen with a clearly elevated drusenoid left optic disc and a normal-appearing right optic disc (figure). Both maculae and peripheral fundi were normal. Goldmann visual fields demonstrated a left superior scotoma. Fundus fluorescein angiography confirmed the presence of disc autofluorescence in the left eye without leakage (figure). MRI scanning failed to demonstrate any intracranial pathology. Left optic neuropathy secondary to disc drusen was diagnosed. Interestingly, SVP was noted in the right eye but was absent from the left (videos 1 and 2 on the Neurology ® Web site at www.neurology.org).DISCUSSION Spontaneous retinal venous pulsation is the rhythmic change in the caliber of one or more retinal veins at the optic disc caused by variation in the pressure gradient between the intraocular retinal veins and the retrolaminar portion of the central retinal vein, which is subjected to ICP as it passes through the subarachnoid space.1 Since the variation of intraocular venous pressure between systole and diastole (the ocular pulse pressure) is greater than the CSF pulse pressure, the velocity of venous outflow from the eye increases during systole and decreases during diastole. 3 This leads to the systolic collapse of the retinal vein as it exits the eye characteristic of SVP. The pulse is only manifest at the distal vein over the optic disc since, due to the inherent resistance to fluid flow within the retinal venous system (to which the viscosity of blood is a contributory factor), the pressure difference between intraocular and extraocular veins is only transmitted a short distance into the eye. 3 The outflow theory better explains the etiology of SVP than the classic theory, which suggests that the vein collapses in response to the ocular arterial pulse. In fact, this should not occur since the retinal venous pressure is consistently higher than intraocular pressure throughout the cardiac cycle. 4 The venous outflow theory also explains how SVP and IC...

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