Why cotton wool spots should not be regarded as retinal nerve fibre layer infarcts

“…Axoplasmic transport in the RNFL can be obstructed by a variety of vascular or mechanical circumstances. McLeod [10] emphasized that transient hypertension and passive hyperdistension of the thin-walled retinal venules in the peripapillary RNFL may cause compressional damage to the axonal bundles in Purtscher’s angiopathy. Behrens-Baumann et al [3] classified the clinical manifestations by 3 characteristic features: (1) yellow-white ‘Purtscher-Flecken’, which have a polygonal margin and are located in the inner nuclear layer between the arterioles; (2) white cotton-wool spots in the RNFL covering the retinal vessels; (3) spot-like or flame-shaped hemorrhages in different retinal layers.…”

Section: Introductionmentioning

confidence: 99%

Functional and Anatomical Findings in Acute Purtscher’s Retinopathy

Meyer

Callizo²,

Schmidt³

et al. 2006

Ophthalmologica

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Introduction: To determine the anatomical location and functional impairment in acute Purtscher’s retinopathy (PR). Material and Methods: A 15-year-old boy with acute PR was examined with optical coherence tomography (OCT) and microperimetry (MP). Results: His initial best corrected visual acuity was 20/30 OD and 20/80 OS, the MP demonstrated absolute scotomas in the central and peripapillary area of the cotton-wool spots. On the OCT, there was a hyporeflective area in the inner aspect of the retina, corresponding to white patches on funduscopy. After he had been treated with oral prednisolone 100 mg, his visual acuity improved to 20/20 OU within 4 weeks and there were no scotomas on the MP. The central retinal architecture returned to normal with no sub- or intraretinal fluid. Discussion: Cotton-wool spots in PR represent infarctions of the retinal nerve fiber layer. Deeper layers of the retina may also be involved, causing a breakdown of the inner blood-retina barrier with temporary intra- and subretinal edema.

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“…Although 'nonischaemic' obstruction of the central retinal vein is not infrequently complicated by cilioretinal infarction, cilioretinal ischaemia secondary to hemisphere venous obstruction has been reported only once before. 2 Importantly, cilioretinal infarction from hemisphere retinal vein occlusion provides an opportunity to remove any lingering doubt that may exist as to the interrelationship between the venous and arteriolar occlusions. 3,4 Failure of perfusion affects only that part of the cilioretinal circulation drained by the obstructed hemisphere vein so, of the two, the venous obstruction must be the instigating occlusion.…”

Section: Commentmentioning

confidence: 99%

“…3,4 Failure of perfusion affects only that part of the cilioretinal circulation drained by the obstructed hemisphere vein so, of the two, the venous obstruction must be the instigating occlusion. 2 The basis of the association between these two vascular events is said to be the lower perfusion pressure in the inner retina supplied by cilioretinal arterioles in comparison with that in the territory of the central retinal artery, 5 but this assertion tends to hide the true picture. Significant differential effects on perfusion are only manifest when blood circulation through the inner retina is seriously challenged (eg, by marked elevation of the pressure in the central retinal vein or during…”

Section: Commentmentioning

confidence: 99%