Indian Journal of Ophthalmology

: 1968  |  Volume : 16  |  Issue : 1  |  Page : 12--18

Vascular pseudoneuritis and atrophy of the optic nerve

G Goder 
 Humboldt University Clinic, E:. Berlin (G.D.R.)

Correspondence Address:
G Goder
Humboldt University Clinic, E:. Berlin (G.D.R.)

How to cite this article:
Goder G. Vascular pseudoneuritis and atrophy of the optic nerve.Indian J Ophthalmol 1968;16:12-18

How to cite this URL:
Goder G. Vascular pseudoneuritis and atrophy of the optic nerve. Indian J Ophthalmol [serial online] 1968 [cited 2020 Apr 1 ];16:12-18
Available from:

Full Text

The so called vascular pseudoneuritis or pseudopapillitis is going to become more and more common in European countries increasing with rising life-expectation.

PARSONS-SMITH in 1959 found 7 bilatral blind people on account of vascular atrophy among 1 million of the population. In our experience it is thrice as much. The incidence is substantially higher if the cases of unilateral blindness due to it are also accounted.

There is a dispute about the patho­logical causes. Through KREIBIG [10] we know that there takes place a noncoagulative necrosis of the optic nerve in a circumscribed field. In most cases it is situated near the la­mina cribrosa and surrounded by a collateral oedema. This appears as a papilledema. The more anterior this necrosis lies, the more strongly mark­ed is the papilledema, which may overlap even the retina, causing an ophthalmoscopic picture quite simi­lar or even indistinguishable from the picture of an occlusion of the central retinal artery. (Plate 1)-[Figure 2]. FRANCOIS, VERRIEST, NEETENS de RAVEK and HANSSEN [4]

What is the reason for this optic necrosis? FRANCOIS AND NEET­ENS [2] and FRANCOIS AND COLET­TE [3] put the blame on an obstruction of the so called central artery of the optic nerve. The existence of this vessel was already postulated in 1879 by KUHNT. [11] In agreement with SINGH AND DASS [13] we could find this vessel in only 25% of cases of post mortem studies as a somewhat thicker branch of the ophthalmic artery, about a sixth of the diameter of the central retinal artery. The optic nerve is supplied by capillaries, arising from branches of the ophthal­mic artery, perforating the sheaths of the optic nerve. We filled the capillaries with polyethylen, digested the tissue and found that in some older people there was a lack of capilla­ries just near the lamina cribrosa and in the scteral part of the optic nerve. We could prove this fact also by counting the capillaries in histo­logical serial sections, coloured for example with dialysed iron. (Plates 2 A and B)-[Figure 3]-(GODER [5] ).

Only these areas are meeting points of the blood supply, the first between the capillaries from the arch of Zinn and the capillaries entering the optic nerve with the central retinal artery, and the second between the intra­orbital and intracranial vessels. At­rophy of such tops of the capillary tree is already well known in the brain and spinal chord. It also takes place in the optic nerve. We call this process according to BURGER [1] "Wipfeldurre", which means tree top dryness.

This tree top dryness in the optic nerve is the main cause of ischemic necrosis. When the blood supply becomes diminished on account of an arteriosclerotic or inflammatory narrowing of the ophthalmic artery, then there is a lack in reserve capilla­ries in this part, and necrosis starts. The reserve capillaries open in mo­ments of distress. This necrosers was called opticomalacia KREIBIG [9],[10] .

What about the practical meaning of this knowledge?

Sometimes it is difficult to diag­nose a vascular atrophy of the optic nerve only by clinical means espe­cially in older stages. We carried out cadaver studies in 100 cases com­paring the changes of the tree of the ophthalmic artery with other parts of the vascular system and we found that the tightest correlation exists with the superficial temporal artery. In every case of well marked arteriosclerosis of the ophthalmic artery with reduction of the capilla­ries in the mentioned parts, there exists a strongly marked arterioscle­rosis of the temporal artery; but not in every case the opposite is true. The arteriosclerosis proceeds to the peri­phery. The thickness of the intima in these cases is two or three times that of the normal for that age. [Figure 1]-(GODRR [6] )

Most commonly we find a so call­ed stratified sclerosis which means, we find three layers in the intima: in the innermost one the small elas­toid fibres predominate, in the mid­dle, mainly collagen fibres can be found and near the media there are muscle cells, which grow through enlarged pores of the elastic mem­brane Plates 3-[Figure 4] and Plate 4-[Figure 5]. The latter is a very important step in the be­ginning of arteriosclerosis of vessels of the caliber of the ophthalmic artery and the temporal artery as our electron microscopic investigations have shown. The muscle cells play an important role in sclerosis of these vessels. In the capillaries the most important event is the thickening of the basal membranes. In the greater vessels we find changes of the mus­cular cells together with fibrous material.

In the socalled giant cell arteritis the lumen of the ophthalmic artery is rapidly narrowed and there quick­ly starts an optical necrosis in cases of tree top dryness. The clinical picture of this disease is well known nowadays. It was rediscovered in the last thirty years but it was al­ready described in the last century by HUTCHINSON, but it must have been known already to the doctors of antiquity, as we learn out of the diary of an eye doctor of the 9th century, the tadhkivat al kahhalin of Ali Ibn Iza of Bagdad.

We see every year 3-4 cases of temporal arteritis with involvement of the eye, because we immediately perform a resection of the temporal artery in every case of suspected disturbance of the blood flow in the optic vessels. There is a large num­ber of cases without the typical cli­nical symptoms and signs of tempo­ral arteritis which would not be diag­nosed without routinely done biopsy of the temporal artery. This is the so called occult form of arteritis tem­poralis.

The biopsy is not only of diagnos­tic importance but also of therapeu­tic value, because it stops a vaso­vasal reflex, which perhaps causes spastic narrowing of the ophthalmic artery. After establishing the diag­nosis, it is necessary to begin imme­diately a course of cortisone intra­venously.

The electron-microscopical picture of the arteritis temporalis we des­cribed extensively in a former paper. (GODER [8] ). It is remarkable that all inflammatory cells develop from mus­cle cells, but they show changes diffe­rent than in arteriosclerosis. The first step is a break in the connection of the clastic fibres with the muscle cells. Then the muscle cells undergo variations into macrophages which phagocytose elastic material. Some­times macrophages are lying so close together that they appear as multi­nucleated giant cells in the histolo­gical picture. (Plate 5)-[Figure 6] These cells do not show a great phagocytic acti­vity in contrast to the single macro­phages. (Plate 6)-[Figure 7]


Pseudo-neuritic with atrophic chan­ges in the optic nerve as a result of retinal vasculities is a clinical mani­festation which is increasingly be­coming known. Its association with temporal arteritis is of diagnostic and therapeutic value, because biopsy of an excised piece of superficial tempo­ral artery not only shows typical thickening but relieves the condition by breaking the vaso - vasal reflex which causes spastic narrowing of the ophthalmic artery.[14]


1BURGER M.: Age and Disease (Ger­man) Publ. G. Thieme, Leipzig (1954).
2FRANCOIS J. AND NEETENS A.: Central Retinal Artery and Central Optic Nenve Artery. Brit. J. Ophth. 47, 21 (1963)
3FRANCOIS J AND COLETTE M.: Ocular Microangiography (French) Ophthalmologica, Basel, 129, 145 (1955).
4FRANCOIS J., VERRIEST G., NEE­TENS A., DE ROUCK A AND HANSSENS M.: Vascular Pseudo­papillitis (French) Annal. Ocul. 1. Paris 195, 830 (1962).
5GODER G.: The Changcs in Capilla­ries of the Optic Nerve and their Pa­thogenic Significance (German) Angio­logica 3, 59 (1965).
6GODER C.: Vascular Disturbances of the Eyes and Biosy of the Temporal Artery (German), - Publ G. Thieme. Leipzig (1968).
7GODER G.: On the History of Arte­ritis Temporalis Ind. J. Hist, Med., (in Press).
8GODER G.: David H. and Uerlings. Electron-microscopic Findings in the Vessel Wall in Temporal Arteritis (German) v. Graefes Arch. Ophth. 169, 12 (1966).
9KREIBIG W.: On Opticomalacia (German) Ber. Dtsch. Ophth. Ges. 53, 173 (1940).
10KREIBIG W.: Opticomalacia, the re­sult of occlusion of the Vessels in the retrobulbar segment of the Optic Nerve. Klin. Mbl. Agenheilk 122, 719 (1953).
11Kuhnt: Quoted by Vail in 14.
12PARSON-SMITH: G Sudden Blind­ness in Oranial Arteritis. Brit. J. Ophth. 43, 204 (1959).
13SINGH S. AND DASS A.: The Cen­tral Artery of the Retina. Brit. J. Ophth. 44, 195 and 280 (1960).
14VAIL D.: The Blood Supply of the Optic Nerve and its Clinical Signifi­cance. Amer. J. Ophth, 31, 1 (1948).