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Disturbance of posterior ciliary arterial circulation is primarily responsible for common ischaemic disorders of the optic nerve head (ONH) such as anterior ischaemic optic neuropathy and glaucomatous optic neuropathy.1 Much of the attention given to the vasculature of the ONH stems from an interest in these conditions. Anatomical studies using vascular casts or serial histological sections and angiography have provided a basis for understanding blood supply but, because the feeding arteries could not be visualised hitherto, knowledge of the vascular dynamics remained uncertain. Moreover, disagreements on vascular structure persist; two examples concern the roles of the Zinn–Haller circle and the choroidal arteries. Accepting that ONH blood supply is substantially centripetal and derived from the short posterior ciliary arteries (SPCAs), to what extent does the Zinn–Haller circle function as an intermediary? In the recent past some observers reported the circle to be incomplete or commonly absent and claimed that direct centripetal branches from SPCAs provide the lamina cribrosa blood supply.2 3 Now, the weight of evidence, obtained mainly from cast studies, indicates that it is regularly present with medial and lateral SPCAs or their branches turning within the plane of the peripapillary sclera to run in an arcuate fashion. They anastomose, forming a complete circle in a majority of eyes and arterioles issue at intervals from the circle passing centripetally to the laminar ONH, possibly also to the prelaminar ONH or as pial arterioles to the post-laminar ONH.4-7 Regarding the choroidal supply to the ONH, those peripapillary choroidal arteries supplying recurrent branches to the laminar or post-laminar ONH either issue from SPCAs directly1 or from the Zinn–Haller circle5 6but the main debate turns on the question of whether choroidal branches penetrate the border tissue of Jacoby to enter the prelaminar ONH1 or enter from the level of the sclera.4 8
Returning to the first of these problems, if the circle is completed or nearly completed by anastomoses then the ONH vascular supply is not an end arterial system, and potentially a reduction in the perfusion pressure in one of the feeding arteries would be compensated by the contribution from others, avoiding segmental ONH deficit. But as Hayreh1 makes clear, one cannot conclude that a functional connection exists on the evidence of plastic casts of cadaver eyes. In this issue of the BJO (p 1357) Ohno-Matsui and colleagues report a further development of indocyanine green angiography9 10 enabling them to visualise the circle fully in myopic eyes with an annular crescent. They find an incomplete Zinn–Haller circle supplied by medial and lateral SPCAs in half of the 44 eyes studied, and only by medial or lateral arteries in others. Anastomotic channels between medial and lateral SPCAs were not observed indicating that the circle functions as an end arterial system. Olveret al,11 noting two instances among 18 eyes of a circle supplied by a single SPCA, commented that in such eyes there may be potential vascular vulnerability. Ohno-Matsui and others’ results indicate that a unilateral input to the circle is functionally quite common.
Results from highly myopic eyes may not be representative but not withstanding, Ohno-Matsui and colleagues’ report is a significant advance in knowledge and it may have some bearing on the development of segmental defects of the ONH.
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