Concerning central retinal artery occlusion (CRAO) and cerebral stroke

Sir,

I read with interest the correspondence on central retinal artery occlusion (CRAO) and cerebral stroke regarding Varma et al's article ‘A review of central retinal artery occlusion: clinical presentation and management.'¹ In a paper published in this journal in 1992 we looked at the relationship between central retinal artery and ocular neovascularisation in eight patients.²

We agree with McLeod³ that penumbral retinal tissue viability can persist as half of our patients did not fall into the carotid occlusive disease group. This concurs with Kottow and Hendrickson,⁴ who found anterior segment neovascularisation following CRAO, as well as Brown,⁵ who reported a case of neovascularisation following CRAO due to presumed single mitral valve embolus in the absence of carotid disease.

Varma et al also refer to preventing ocular neovascularisation following CRAO. The relationship between these two events is more complex than this paper implies, as we described in a table which I reproduce here for the sake of clarity (Table 1). As well as considering CRAO alone, it considers the concept of double embolism as reported by Wolter⁶ as well as CRAO in a setting of chronic ocular ischaemia due to carotid occlusive disease.^{7, 8}

Table 1. A classification of the proposed mechanisms relating central retinal artery occlusion (CRAO) to ocular neovascularisation (NVN).

1. Chronic ocular ischaemia alone leading to ocular NVN	→Rubeotic glaucomaa
	↓
Low CRA perfusion pressure	→CRAO
2. Chronic ocular ischaemia+coincidental CRAO	→Ocular NVN
3. Double embolism: CRAO+PCAO	→Ocular NVN
4. CRAO alone	→Ocular NVN

Abbreviation: PCAO, posterior ciliary artery occlusion.

^aRubeotic glaucoma is usually characterised by a low intraocular pressure.

We do, however, strongly agree with Varma et al that such patients should be reviewed at regular intervals for at least 3 months following the diagnosis of CRAO.

The author declares no conflict of interest.