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if the patient is comparatively young. In older patients this sign is not a reliable sign of chronic nephritis, but it must still be regarded as a sign pointing to the danger of possible cerebral hæmorrhage.

Gunn records some cases where marked arterial disease with albuminuria appeared quickly after influenza. He considers these to be cases of somewhat rapid poisoning similar to those occurring in pregnancy, but more acute.

Nettleship insists that there is only one sort of renal retinitis, and the varieties of appearances seen are only different stages and degrees of

(a) General ædema ;
(b) Exudation into the nerve fibre layer; and
(c) Spots or patches of opacity in the deeper layers, due

to degeneration of fibrinous or albuminous effusion in
the inter-granule layer, and perhaps to changes in

Muller's fibres. The optic neuritis and retinal hæmorrhages so often present in varying degrees are not characteristic. The general appearance of the retinitis does not afford any guide to the kind of chronic nephritis which is the cause of it. West, however, considers that the inflammatory or exudative retinitis indicates parenchymatous nephritis, whilst the degenerative variety-star figures and white dots in the macular region—with little or no general retinal haze and often with decided thickening of retinal arteries, points to granular kidney. Diabetic retinitis closely resembles albuminuric retinitis in ophthalmoscopic appearances. It differs from the latter in the absence of the soft-edged or woolly patches and of the radially-arranged figures in the yellowspot region, and there is usually no ædema of the retina. The hæmorrhages so often present in diabetic retinitis are more often punctate and deeply seated than linear and superficial, as is usual in renal retinitis. The white deposits take the form of irregular masses or clumps rather than dots, and are often arranged in a more or less complete ring around the macular area. Though albumen is often present in the urine, as well as sugar, there can be no doubt but that

retinitis can be caused by diabetes alone. Diabetic retinitis seldom occurs before the age of thirty, and is generally noticed between fifty and seventy. The prospect as to life is better in diabetic than in albuminuric retinitis.

Renal retinitis, though generally symmetrical, may be unilateral, especially when hæmorrhage is the chief sign. Pigmentation of the retina, night-blindness, formation of new blood-vessels in the vitreous, choroiditis, and iritis have been noted in connection with albuminuric retinitis. Such signs are anomalous, and in no way characteristic of renal disease.



J. Herbert Parsons and Thos. Snowball (Royal London Ophthalmic Hospital Reports, January, 1903).- In this series of observations the blood-pressure was taken in the femoral artery, and occasionally in the carotid of the side opposite to the eye observed. The intra-ocular pressure was taken by means of a fine canula inserted into the anterior chamber, and occasionally into the vitreous. This canula was connected with a Hürthle manometer and

pressure bottle. Sources of variation in intra-ocular blood pressure other than variable blood-pressure-e.g., contraction of the extrinsic muscles of the eye—were carefully eliminated. Stimulation of the peripheral end of the sympathetic in the cat was invariably followed by a rise in intra-ocular pressure, irrespective of any change in blood-pressure. This was found not to be due to vascular changes in the eye or changes in the iris, but to contraction of nonstriped muscle in the orbit; stimulation of the peripheral end of the fifth nerve gave no result. The blood supply of the eye in the dog and cat is mainly derived from the terminal branch of the external carotid (internal maxillary). Tying the external carotid-cutting off the main blood supply to the eyecaused a slight rise in general blood-pressure, but a well-marked fall in intra-ocular pressure. Ligature of the internal carotid, which is much smaller than the external carotid, caused no change in intra-ocular pressure if the external was patent. Changes in general

blood-pressure affected the eye after ligature of the external carotid, through anastomotic branches from the internal carotid and through the circle of Willis. Intra-ocular tension responded passively to all variations in general blood-pressure, even when the external carotid was tied or the skull laid freely open. The respiratory and cardiac oscillations were usually clearly represented by the air bubble in the connecting tube, but were not recorded by the manometer. The general curve of the blood-pressure was reproduced in a

damped ” form by the intra-ocular manometer, i.e., there was a short latent period of one to two seconds; the changes were slower and the curve flatter. Variations of bloodpressure by mechanical pressure of the aorta, stimulation of the central end of sensory and mixed nerves, the vagus, the cord, or vasometer centre, were accompanied by rise in intraocular tension. Drugs which modify blood-pressure (e.g., adrenalin, nicotine, strychnine, pilocarpin, quinine, amyl nitrite, and large doses of chloroform) have a similar influence over intra-ocular tension. Asphyxia caused increase in blood and intra-ocular pressure, followed by a fall in both pressures.

The authors do not regard the experiments, as performed, to have been influenced by the elasticity of the sclerotic or by active vasomotor changes.



Brown Pusey (Archives of Ophthalmology, March, 1904) found that fresh sheep's eyeballs immersed in solutions of either salt or sugar of the concentration of m/32, m/16, m/8 increased in weight, whilst in similar solutions of concentration m and m/2 they lost weight. From these experiments he concludes that variations in tension may take place under varying osmotic pressures, and may be the explanation of the primary cause of glaucoma.

In carrying out these experiments the author found that the lenses of the eyes placed in m and m/2 solutions of salt

and sugar became cataractous after one and a half to two and a half hours' immersion in the salt solutions, and after twenty-four hours in the sugar solutions. The lenses which became cataractous in the salt solution could be cleared again by putting them in an m/32 solution of salt, or by leaving them in distilled water for some hours.



Ophthalmological Anatomy, with some illustrative cases. By

J. HERBERT FISHER, M.B., B.S., F.R.C.S. London :

Hodder and Stoughton. 1904. THIS volume contains an excellent selection of anatomical information concerning the eye and its adnexa. The subject matter is divided into nine chapters. The first four deal with the origins, courses, and distributions of the ocular nerves. The fifth chapter deals with the cutaneous nerves of the head and face and cerebral topography. The sixth deals with ocular muscles and movements; the seventh is concerned with the eyelids and lachrymnal apparatus ; the eighth is devoted to the ophthalmic blood-vessels and intracranial venous sinuses; and the ninth includes the anatomy of the orbit and the surrounding air cells, and some points in development. It is not to be supposed that this represents the whole field of ophthalmological anatomy, and the author's expressed intention is that it should be a * useful supplement to students' text-books, and prove a practical help to the clinical ophthalmologist."

In this the author has been eminently successful, as the work before us contains a large amount of information which it would be almost impossible for the busy practitioner to acquire and retain in his mind were it not presented to him in so accessible a form. The contents of this book are essentially useful and practical, and the application in practice of many of the points mentioned is demonstrated in the list of illustrative cases described at the end of the book. It is hardly necessary to say that the anatomical and clinical descriptions are tersely and lucidly given, and their correctness is only what we should expect from an author so experienced in anatomical teaching and practical ophthalmology. Ophthalmic surgeons should be much indebted to Mr. Fisher

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