On optic neuritis in intracranial disease / by J. Hughlings Jackson.

  • Jackson, J. Hughlings (John Hughlings), 1835-1911.
Date:
1881
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Licence: Public Domain Mark

Credit: On optic neuritis in intracranial disease / by J. Hughlings Jackson. Source: Wellcome Collection.

Provider: This material has been provided by UCL Library Services. The original may be consulted at UCL (University College London)

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    are no thickened sheaths, except a trace in the case of one retinal vein on the left disc. The maculae and their regions are healthy and free from greyness and oedema. Either his accommodation was unduly active, or a slight myopia has developed in the right. It requires— 72 spherical to get |§. Even the left got |g more easily with - 72. The amount of myopia, even if real, is of no importance. It thus appears that a very satisfactory improvement has come in the discs and retinae.^' Not unfrequently patients come to physicians for such a nervous symptom as localised convulsion, giving a more or less vague account of some illness with headache and vomiting months before. The discovery of relics of past neuritis might help us in determining whether the symptom we are consulted for depends on gross organic brain disease or not. Let me put the matter in another way. It is stated by Mr. Couper that prolonged use of the eyes in some cases of hypermetropia induces oedema and swelling of the discs, occasionally mistaken for, and treated as, slight optic neuritis depending on cerebral disease. Is it possible that swelling of the discs thus caused may leave behind it traces like those left on what we call recovery from neuritis ? Unfortunately, the discs do not always go back to health, but, so to speak, down to atrophy, partial or total. In most cases we can tell by the ophthalmoscope whether the atrophy is the sequel of some neuritis, although, maybe, not that there had been the neuritis which is commonly called optic neuritis. And, if we could not diagnose past neurosis, we could in most cases infer it. But I am not speaking of inference. The question I put is this :— What are the best ophthalmoscopical signs to rely on in the diagnosis betwixt atrophy after a neuritis and the atrophy in locomotor ataxy, disseminated sclerosis, etc., apart from collateral evidence ? The signs generally given as diagnostic of past neuritis are veiling of the lamina cribrosa, white marks along the vessels, ill-margined disc, irregularity of veins. Are such signs always present in very long standing cases of post-neuritic atrophy ? [I omitted speaking of conditions of the pupils in cases of double optic neuritis, and now I speak on but one point. Supposing, Avhen blindness, with atrophy of the discs, has come on, the pupils do not act to light, do they act during accommodation ? I have seen two patients, each with mere perception of light, in the different atrophy of tabes dorsalis, whose pupils did not contract to light (which is not perhaps remarkable), but did contract well during accommodation.