CLINICAL SIGN OF OBSTRUCTED AXOPLASMIC TRANSPORT

doi:10.1016/S0140-6736(75)90364-5

The Lancet

Volume 306, Issue 7942, 15 November 1975, Pages 954-956

https://doi.org/10.1016/S0140-6736(75)90364-5 Get rights and content

Abstract

Orthograde and retrograde axoplasmic transport in retinal ganglion-cell axons can be interrupted by axonal ischæmia. This report is believed to be the first to illustrate how this phenomenon can be observed clinically in man in cases of retinal vascular disease. The intense retinal "whiteness" of small cottonwool spots and at the periphery of larger areas of retinal ischæmia represents gross localised axonal distension secondary to the cessation axoplasmic flow.

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Cited by (15)

Evidence for an enduring ischaemic penumbra following central retinal artery occlusion, with implications for fibrinolytic therapy
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Citation Excerpt :
Of note, many CWSs are described as being “isolated” when, in fact, they are sentinels of the boundary(s) of ischaemic infarction; this mistaken impression arises because necrotic inner retina is absorbed much more quickly than the axoplasmic debris accumulating along its borders (McLeod, 1981, 2005). On occasion, axoplasmic debris will accumulate within an area of infarction instead of marking the ischaemic boundary (Fig. 2), albeit the embedded white material is always located close to that boundary (McLeod, 1975, 2009). This implies that the deeper part of the inner retina (i.e. the middle retina comprising the inner plexiform layer [IPL], INL and OPL) may be more extensively infarcted than the superficial inner retina (i.e. the GCL and NFL).
The rationale behind hyperacute fibrinolytic therapy for cerebral and retinal arterial occlusion is to rescue ischaemic cells from irreversible damage through timely restitution of tissue perfusion. In cerebral stroke, an anoxic tissue compartment (the “infarct core”) is surrounded by a hypoxic compartment (the “ischaemic penumbra”). The latter comprises electrically-silent neurons that undergo delayed apoptotic cell death within 1–6 h unless salvaged by arterial recanalisation. Establishment of an equivalent hypoxic compartment within the inner retina following central retinal artery occlusion (CRAO) isn't widely acknowledged. During experimental CRAO, electroretinography reveals 3 oxygenation-based tissue compartments (anoxic, hypoxic and normoxic) that contribute 32%, 27% and 41% respectively to the pre-occlusion b-wave amplitude. Thus, once the anoxia survival time (≈2 h) expires, the contribution from the infarcted posterior retina is irreversibly extinguished, but electrical activity continues in the normoxic periphery. Inbetween these compartments, an annular hypoxic zone (the “penumbra obscura”) endures in a structurally-intact but functionally-impaired state until retinal reperfusion allows rapid recovery from electrical silence. Clinically, residual circulation of sufficient volume flow rate generates the heterogeneous fundus picture of “partial” CRAO. Persistent retinal venous hypoxaemia signifies maximal extraction of oxygen by an enduring “polar penumbra” that permeates or largely replaces the infarct core. On retinal reperfusion some days later, the retinal venous oxygen saturation reverts to normal and vision improves. Thus, penumbral inner retina, marginally oxygenated by the choroid or by residual circulation, isn't at risk of delayed apoptotic infarction (unlike hypoxic cerebral cortex). Emergency fibrinolytic intervention is inappropriate, therefore, once the duration of CRAO exceeds 2 h.
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Preliminary CommunicationsCLINICAL SIGN OF OBSTRUCTED AXOPLASMIC TRANSPORT

Abstract

Brain Res.

Progr. Brain Res.

J. cell. Biol.

Neurology

Br. J. Ophthal.

Br. J. Ophthal.

Preliminary Communications
CLINICAL SIGN OF OBSTRUCTED AXOPLASMIC TRANSPORT